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Magnesium Deficiency; What is Magnesium Deficiency Syndrome?

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Magnesium deficiency or hypomagnesia (not to be confused with hypomagnesemia) refers to inadequate intake of dietary magnesium or impaired absorption of magnesium, which can result in numerous symptoms and diseases. It is generally corrected by an increase of magnesium in diet, oral supplements, and in severe cases, intravenous supplementation.

‘Normal’ serum magnesium levels

0.75–0.95 mmol/L

  • A serum magnesium <0.82 mmol/L (2.0 mg/dL) with a 24-hour urinary magnesium excretion of 40–80 mg/day is highly suggestive of magnesium deficiency.
  • One group of experts has recommended magnesium supplementation in subjects experiencing symptoms that reflect magnesium deficiency if the serum level is below 0.9 mmol/L, with levels less than 0.8 mmol/L necessitating magnesium.
  • Serum magnesium levels above 0.95 mmol/L may indicate hypermagnesaemia.

Magnesium requirements based on older balance studies

Age Requirement
Infants 150–200 mg/day
Children 200–250 mg/day
Adults 250–300 mg/day
Lactating women 400 mg/day

Causes of magnesium deficiency

Magnesium: Deficiency signs and symptoms [].

  • General  – Anxiety, lethargy, weakness, agitation, depression, dysmenorrhea, hyperactivity, headache, irritability, dysacusis, low stress tolerance, loss of appetite, nausea, sleep disorders, impaired athletic performance.
  • Musculature – Muscle spasm, cramps in the soles of the feet, leg cramps, facial muscles, masticatory muscles, and calves, carpopedal spasm, back aches, neck pain, urinary spasms, magnesium deficiency tetany.
  • Nerves/CN – Nervousness, increased sensitivity of NMDA receptors to excitatory neurotransmitters, migraine, depression, nystagmus, paraesthesia, poor memory, seizures, tremor, vertigo.
  • Gastrointestinal tract – Constipation.
  • Cardiovascular syste – Risk of arrhythmias, supraventricular or ventricular arrhythmias, hypertension, coronary spasm, decreased myocardial pump function, digitalis sensitivity, Torsade de pointes, death from heart disease.
  • Electrolytes – Hypokalaemia, hypocalcaemia, retention of sodium.
  • Metabolism – Dyslipoproteinemia (increased blood triglycerides and cholesterol), decreased glucose tolerance, insulin resistance, increased risk of metabolic syndrome, disturbances of bone and vitamin D metabolism, resistance to PTH, low circulating levels of PTH, resistance to vitamin D, low circulating levels of 25(OH)D, recurrence of calcium oxalate calculi.
  • Miscellaneous – Asthma, chronic fatigue syndrome, osteoporosis, hypertension, altered glucose homeostasis.
  • Pregnancy -m Pregnancy complications (e.g., miscarriage, premature labor, eclampsia).
  • Acetaminophen toxicity.
  • Alcoholism.
  • Aluminium (environmental and dietary).
  • Aldosteronism.
  • Alcohol.
  • Ageing  (hypochlorhydria, ie, decreased acid in the stomach).
  • Antacid (including ranitidine and famotidine).
  • Bariatric surgery (small intestinal bypass surgery).
  • Calcium supplements (or a high calcium to magnesium diet).
  • Caffeine.
  • Cancer.
  • Coeliac disease.
  • Colon removal
  • Chronic stress
  • Cisplatin
  • Crohn’s disease.
  • Ciclosporin.
  • Type 1 and type 2 diabetes (uncontrolled glucose levels).
  • Diarrhoea.
  • Diet high in fat or sugar.
  • Digoxin
  • Diuretics non-potassium-sparing diuretics (thiazide and loop diuretics).
  • Excessive ingestion of poorly absorbable magnesium (such as magnesium oxide), leading to diarrhoea and magnesium loss.
  • Emotional and/or psychological stress (overactivation of the sympathetic nervous system).
  • Enzymatic dysfunction (impaired magnesium distribution).
  • Oestrogen therapy (shifts magnesium to soft and hard tissues lowering serum levels).
  • Excessive or prolonged lactation
  • Excessive menstruation.
  • Fasting (or low magnesium intake).
  • Foscarnet
  • Gentamicin and tobramycin.
  • Hyperparathyroidism and hypoparathyroidism.
  • Hyperthyroidism.
  • Kidney diseases (glomerulonephritis, pyelonephritis, hydronephrosis, nephrosclerosis and renal tubular acidosis).
  • Heart failure.
  • Haemodialysis.
  • High phosphorus in the diet (soda, inorganic phosphates contained in many inactive ingredients in processed foods).
  • Hyperinsulinaemia (and insulin therapy).
  • Insulin resistance (intracellular magnesium depletion).
  • Laxatives.
  • Low salt intake.
  • Low selenium intake.
  • Gastrointestinal disorders—malabsorption syndromes (coeliac disease, non-tropical sprue, bowel resection, Crohn’s disease, ulcerative colitis, steatorrhoea), prolonged diarrhoea or vomiting.
  • Liver disease (acute or chronic liver disease, including cirrhosis).
  • Metabolic acidosis (latent or clinical).
  • Pancreatitis(acute and chronic).
  • Parathyroidectomy.
  • Pentamidine.
  • Peritoneal dialysis.
  • Porphyria with inappropriate secretion of antidiuretic hormone.
  • Pregnancy.
  • Proton pump inhibitors.
  • Strenuous exercise.
  • Tacrolimus.
  • Vitamin B6 (pyridoxine) deficiency.
  • Vitamin D excess or deficienc (chronic kidney disease and liver disease can prevent the activation of vitamin D).

Potential clinical signs of magnesium deficiency

Less severe signs

  • Aggression.
  • Anxiety.
  • Ataxia.
  • Chvostek sign (twitching of the facial muscles in response to tapping over the area of the facial nerve).
  • Confusion.
  • Cramps (spontaneous carpopedal spasm or painful cramps of the muscles in your hands and feet).
  • Disorientation.
  • Fasciculations (‘a brief, spontaneous contraction affecting a small number of muscle fibres, often causing a flicker of movement under the skin. It can be a symptom of disease of the motor neurons)’.
  • Hyper-reflexia.
  • Irritability.
  • Muscular weakness.
  • Neuromuscular irritability.
  • Pain or hyperalgesia (decreases the nociceptive threshold).
  • Photosensitivity.
  • Spasticity.
  • Tetany (involuntary muscle spasms).
  • Tinnitus (ringing in the ears).
  • Tremors.
  • Trousseau sign.
  • Vertigo.
  • Vitamin D resistance.

Severe signs

  • Arrhythmias (caused by over-excitation of the heart due to enhanced depolarisation susceptibility, especially torsades de pointes or ventricular tachycardia with a prolonged QT interval).
  • Calcifications (soft tissue).
  • Cataracts.
  • Convulsions.
  • Coronary artery disease.
  • Depressed immune response.
  • Depression.
  • Hearing loss.
  • Heart failure.
  • Hypertension.
  • Migraines/headaches.
  • Mitral valve prolapse.
  • Osteoporosis.
  • Parathyroid hormone resistance and impaired parathyroid hormone release/function.
  • Psychotic behavior.
  • Seizures (overexcitation of the nervous system (nerve cells), which are more likely to fire due to a reduced electric potential difference between the outer and inner surfaces of the membrane).
  • Sudden cardiac death.
  • Tachycardia.

Lab and ECG signs of magnesium deficiency

  • Hypomagnesaemia.
  • Hypocalcemia.
  • Hypokalaemia.
  • Prolonged QTc.
  • ST segment depression (in animals).

Measurements to diagnose magnesium deficiency (best to worst)

Reliable methods

  • Retention of magnesium load (intravenous or oral) after its administration is likely the best indicator of magnesium deficiency. However, the retention test assumes normal kidney function for intravenous magnesium loads and normal gastrointestinal and renal function for oral load tests and is cumbersome and invasive.
  • Mononuclear cell magnesium and muscle magnesium content (muscle biopsy).

Less reliable methods

  • Hair magnesium content (one study concluded: ‘magnesium hair concentration may be an easier, cheaper and less invasive indicator of body magnesium depletion’).
  • Bone magnesium (magnesium depletion in the coccyx may indicate magnesium deficiency).
  • The ratio of ionized magnesium to total magnesium (serum or plasma).
  • Ionized magnesium levels (serum or erythrocytes, ionized magnesium is the physiologically active magnesium not bound to proteins). However, this biomarker is controversial and not always available in clinical labs and hard to measure reliably.
  • Lymphocyte magnesium.
  • Urinary or fecal magnesium excretion (low or high levels may indicate deficiency).
  • Urinary fractional magnesium excretion >4% (some authors have suggested >2% in those with normal kidney function).
  • Total erythrocyte magnesium levels (magnesium deficiency has been suggested when erythrocyte magnesium levels are <1.65 mmol/L).
  • Total serum magnesium levels.
  • It is important to note that choosing only one of the aforementioned methods of measuring magnesium deficiency is not appropriate for diagnosing magnesium deficiency. In general, either symptom of magnesium deficiency must accompany the more reliable methods to diagnose magnesium deficiency (eg, intravenous/oral magnesium load, mononuclear cell or muscle), or two or more of the reliable measurements (eg, intravenous/oral magnesium load, mononuclear cell or muscle) should be used in supporting a diagnosis of magnesium deficiency.

Causes of hypermagnesaemia

  • Oversupplementation (mainly from magnesium-containing antacids).
  • Kidney damage.
  • Inflammation and cellular injury (significant increases in total and ionized magnesium in animals during endotoxin challenge).

 Magnesium Deficiency & it Basic Role in Human Body

It is an antidote to stress, the most powerful relaxation mineral available, and it can help improve your sleep.

I find it very funny that more doctors aren’t clued in to the benefits of magnesium, because we use it all the time in conventional medicine. But we never stop to think about why or how important it is to our general health or why it helps our bodies function better.

I remember using magnesium when I worked in the emergency room. It was a critical “medication” on the crash cart. If someone was dying of a life-threatening arrhythmia (or irregular heart beat), we used intravenous magnesium. If someone was constipated or needed to prepare for colonoscopy, we gave them milk of magnesia or a green bottle of liquid magnesium citrate, which emptied their bowels.

Magnesium Deficiency

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If pregnant women came in with pre-term labor, or high blood pressure of pregnancy (pre-eclampsia) or seizures, we gave them continuous high doses of intravenous magnesium.

But you don’t have to be in the hospital to benefit from getting more magnesium. You can start taking regular magnesium supplementation today and see results.

The Relaxation Mineral

Think of magnesium as the relaxation mineral. Anything that is tight, irritable, crampy, and stiff — whether it is a body part or an even a mood — is a sign of magnesium deficiency.

This critical mineral is actually responsible for over 300 enzyme reactions and is found in all of your tissues — but mainly in your bones, muscles, and brain. You must have it for your cells to make energy, for many different chemical pumps to work, to stabilize membranes, and to help muscles relax.

When was the last time you had a good dose of seaweed, nuts, greens, and beans? If you are like most Americans, your nut consumption mostly comes from peanut butter.

That is why the list of conditions that are found related to magnesium deficiency is so long. In fact, there are over 3,500 medical references on magnesium deficiency!

Even so, this mineral is mostly ignored because it is not a drug, even though it is MORE powerful than drugs in many cases. That’s why we use it in the hospital for life-threatening and emergency situations like seizures and heart failure.

Magnesium Deficiency Symptoms

Magnesium deficiency has even has been linked to inflammation in the body and higher CRP levels.

  • In our society, magnesium deficiency is a huge problem. By conservative standards of measurement (blood, or serum, magnesium levels), 65 percent of people admitted to the intensive care unit — and about 15 percent of the general population — have a magnesium deficiency.
  • But this seriously underestimates the problem, because a serum magnesium level is the LEAST sensitive way to detect a drop in your total body magnesium level. So rates of magnesium deficiency could be even higher!
  • The reason we are so deficient is simple: Many of us eat a diet that contains practically no magnesium — a highly-processed, refined diet that is based mostly on white flour, meat, and dairy (all of which have no magnesium).
  • When was the last time you had a good dose of sea vegetables (seaweed), nuts, greens, and beans? If you are like most Americans, your nut consumption mostly comes from peanut butter, and mostly in chocolate peanut butter cups.
  • Much of modern life conspires to help us lose what little magnesium we do get in our diet. Magnesium levels are decreased by excess alcohol, salt, coffee, phosphoric acid in colas, profuse sweating, prolonged or intense stress, chronic diarrhea, excessive menstruation, diuretics (water pills), antibiotics and other drugs, and some intestinal parasites. In fact, in one study in Kosovo, people under chronic war stress lost large amounts of magnesium in their urine.
  • This is all further complicated by the fact that magnesium is often poorly absorbed and easily lost from our bodies. To properly absorb magnesium we need a lot of it in our diet, plus enough vitamin B6, vitamin D, and selenium to get the job done.
  • A recent scientific review of magnesium concluded, “It is highly regrettable that the deficiency of such inexpensive, low-toxicity nutrient results in diseases that cause incalculable suffering and expense throughout the world.” (ii) I couldn’t’ have said it better myself.
  • It is difficult to measure and hard to study, but magnesium deficiency accounts for untold suffering — and is simple to correct. So if you suffer from any of the symptoms I mentioned or have any of the diseases I noted, don’t worry — it is an easy fix!! Here’s how.
  • Magnesium deficiency can be harmful! Low magnesium levels can cause fatigue, seizures, high blood pressure, blood clots, muscle cramps and so on.
  • It’s estimated that 80 percent of Americans have a magnesium deficiency. And this is not a good thing since this mineral affects every organ in the body.
  • According to the Institute of medicine, adult men should consume 400 –
  • 420 mg of magnesium while women should aim for 310 – 360 mg per day. Now, the foods below can help get the recommended amount of magnesium without supplementation.

Magnesium Rich Food to Improve Your Overall Health

Functions of magnesium (selection) [,,,,].

  • Magnesium is involved in more than 300 essential metabolic reactions (e.g., all Adenosine Triphosphate (ATP)-dependent reactions).
Energy production (→ ATP production)
  • Breakdown and energetic utilization of carbohydrates, proteins and fats in intermediate metabolism (e.g., glycolysis, respiratory chain phosphorylation). ATP exists primarily as a complex with magnesium (MgATP).
Enzyme activation (examples)
  • Mitochondrial ATP synthase, Na+/K+-ATPase, Hexokinase, Creatine kinase, Adenylate cyclase, Phosphofructokinase, tyrosine kinase activity of the insulin receptor.
Calcium antagonist/NMDA-receptor antagonist
  • Control of calcium influx at the cell membrane (course of contractions, regulation of vascular muscle tone): muscle contraction/relaxation, neurotransmitter release, action potential conduction in nodal tissue, neuromuscular impulse conduction (inhibition of calcium-dependent acetylcholine release at the motor end plate), maintenance and stabilization of membrane physiology, muscle contraction.
Cardiovascular system
  • Economization of cardiac pump function, regulation of potassium movement in myocardial cells, protection against stress, vasodilation of the coronary and peripheral arteries, reduction of platelet aggregation.
Membrane function
  • Transmembrane electrolyte flux, active transport of potassium and calcium across cell membranes, regulation of cell adhesion and cell migration.
Structural roles
  • Component of mineralized bone (structure, microarchitecture), multiple enzyme complexes, mitochondria, proteins, polyribosomes, and nucleic acids.
Nutrient metabolism
  • Metabolic activation and the utilisation of vitamin D, B-vitamins (e.g., thiamine) and glutathione.

Magnesium Deficiency

  • Okra –  One cup of okra has 70 mg of magnesium – approx. 15 percent of the recommended daily intake. Avoid fried okra, boil or roast it.
  • Dark chocolate – A bar of chocolate has more than half of the daily recommended magnesium.
  • Pumpkin – A cup of chopped pumpkin has 60 mg of magnesium. This food also other numerous benefits so eat it as often as possible.
  • Brown rice – A cup of brown rice supplies about 20 percent of recommended magnesium.
  • Avocado – This alkaline food is a great magnesium source. One medium-size avocado has about 15 percent of the magnesium you need in a day.
  • Almonds – One ounce of this healthy nut has approx. 20 percent of magnesium you need.
  • Beet greens – Beet greens may not be popular, but they have lots of magnesium. One cup has 100 mg of magnesium.
  • Spinach – A cup of spinach has 150 mg of magnesium. This is definitely one of the best sources of this mineral.
  • Squash – This pumpkin-like will give lots of magnesium. One cup has about 40 mg.
  • Broccoli – If you’ve never liked broccoli, its magnesium content might change your mind. A cup has 33 mg.
  • Figs – 4 cups of dried figs can give you all the magnesium you need in a day.
  • Cashew nuts – An ounce of cashew nuts has about 20 percent of the magnesium you need.
  • Bananas – Bananas may be known for being potassium-rich, but they also contain some magnesium.
  • Pumpkin seeds – Pumpkin and squash seeds contain about 19 percent of recommended magnesium per ounce.
  • Lentils – A cup of lentils will give you 18 percent of recommended magnesium.
  • Cucumbers – A cup of cucumbers has about 40 mg of magnesium.
  • Peas – You can get 70 mg of magnesium from a cup of peas.

Magnesium and drug interactions. 

Medications that reduce magnesium levels:
(i) H2 blockers: for example, cimetidine and nizatidine
(ii) Proton pump inhibitors: for example, esomeprazole, omeprazole, and pantoprazole (FDA WARNING: supplementing magnesium will not correct deficiency; you must stop the drug)
(iii) Antacids: aluminum and magnesium hydroxide and sodium bicarbonate
(iv) Antibiotics: for example, amoxicillin, azithromycin, doxycycline, minocycline, levofloxacin, ciprofloxacin, cephalexin,
sulfamethoxazole and trimethoprim, and tetracycline
(v) Antihistamines: for example, astemizole and terfenadine
(vi) Antivirals: for example, delavirdine, lamivudine, and zidovudine
(vii) Antiepileptic medications: phenytoin and phenobarbital
(viii) Blood pressure drugs: hydralazine and combination of ACE inhibitors with HCTZ (enalapril and HCTZ)
(ix) Diuretics: for example, furosemide, ethacrynic acid, chlorothiazide, chlorthalidone, metolazone, and indapamide
(x) Cardiac glycoside: digoxin
(xi) Cardiac drugs: sotalol, amiodarone, bretylium, and quinidine
(xii) CNS stimulants: methylphenidate
(xiii) Cholesterol agents: cholestyramine and colestipol
(xiv) Corticosteroids: betamethasone, dexamethasone, hydrocortisone, prednisone, and triamcinolone
(xv) Inhaled corticosteroids: fluticasone, flunisolide, and triamcinolone
(xvi) Estrogens: DES, estradiol, estring, and estrogen-containing drugs: HRT and BCP
(xvii) Immunosuppressants: cyclosporine and tacrolimus
(xviii) Nonsteroidal aromatase inhibitors for breast cancer: anastrozole
(xix) Osteoporosis: raloxifene
(a) On the other hand, magnesium decreases bisphosphonate absorption
(xx) SERMs (selective estrogen receptor modulators): raloxifene, tamoxifen, and toremifene
(xxi) Sulfonamides: antibiotics and some diabetic medications
(xxii) Nutraceuticals: for example, high-dose calcium, high-dose vitamin D, and caffeine

Medications that may increase serum magnesium:
(i) Lithium carbonate
(ii) Antidepressants: for example, sertraline and amitriptyline
(iii) Potassium sparing diuretics: amiloride and spironolactone reduce magnesium excretion

References

Magnesium Deficiency

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Ankle Sprain; Types, Causes, Symptoms, Diagnosis, Treatment

Ankle sprain also known as a twisted ankle or rolled ankle, is a common injury where sprain occurs on one or more ligaments of the ankle. A sprained ankle is an injury that occurs when you roll, twist or turn your ankle in an awkward way. This can stretch or tear the tough bands of tissue (ligaments) that help hold your ankle bones together. Ligaments help stabilize joints, preventing excessive movement. A sprained ankle occurs when the ligaments are forced beyond their normal range of motion. Most sprained ankles involve injuries to the ligaments on the outer side of the ankle.

A strain refers to a painful condition of the ankle joint brought about by inflammation, overuse or simply awkward (or unbalanced) use. It includes inflammation of muscles and tendons such as the Achilles tendon at the back of the heel.

A sprain is an injury to the band which connects two or more bones to a joint. This band is called a ligament. A sprain is usually caused by the joint being forced suddenly outside its usual range of movement. Most sprains heal within a few weeks. A severe sprain may look and feel like a fracture, and it can be difficult for health professionals to tell the difference between the two.

A fracture is a break in one of the bones which make up the ankle joint. These are the leg bones (the tibia and fibula) and the heel and forefoot bones (the calcaneus and talus). Depending upon the exact cause of the fracture, one or more bones may be involved.

Ankle pain may also arise from existing conditions of the joint itself, such as arthritis or gout, which may be aggravated by movement, impact or strain

 

 

Anatomy  of Ankle Sprain / Strain

Ligaments > distal tibiofibular syndesmosis includes

Anterior-inferior tibiofibular ligaments (AITFL)

  • originates from anterolateral tubercle of the tibia (Chaput’s)
  • inserts on anterior tubercle of the fibula (Wagstaffe’s)

Posterior-inferior tibiofibular ligament (PITFL)

  • originates from posterior tubercle of the tibia (Volkmann’s)
  • inserts on the posterior part of the lateral malleolus
  • the strongest component of the syndesmosis
  • interosseous membrane

Interosseous ligament (IOL)

  • distal continuation of the interosseous membrane
  • the main restraint to proximal migration of the talus
  • inferior transverse ligament (ITL)

Syndesmosis Biomechanics

  • function > maintains integrity between the tibia and fibula & resists axial, rotational, and translational forces
  • normal gait >syndesmosis widens 1mm during gait
  • deltoid ligament >indirectly stabilizes the medial ankle mortise

Classifications are based on particular patterns of breakage which are seen after particular types of injury. These include

  • Pott’s fracture: involving both the tibia and fibula leg bones (bimalleolar fractures). These fractures are unstable and require urgent treatment.
  • Pilon fracture: a fracture of the very end of the tibia and top of the talus forefoot bone. The talus is ‘driven’ into the tibia as may happen in a fall from a height or a foot braced against the floor of a car in a collision.
  • Snowboarder’s fracture: this is a fracture of the outer side of the talus produced by forced turning down and inwards of the foot at the ankle.
  • Stress fracture: this is a small crack in a bone. Stress fractures often develop from overuse, such as from high-impact sports like distance running – the repeated stress of the foot striking the ground can cause problems. Stress fractures differ from other ankle fractures in that they result from overuse rather than sudden trauma. The cracks are small (although they may be multiple) so that, although they are painful, the swelling may be only slight. In the ankle, the heel (calcaneus) and the lower leg (fibula) are most commonly affected.
  • Related image

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Grade of Ankle Sprain

Depending on the severity of the injury, an ankle sprain is classified as:

  • Grade I — The ankle is painful, but there is little ligament damage and little loss of function.

Ankle Sprain

  • Grade II — There is moderate ligament damage, and the ankle joint is somewhat loose.
  • Grade III — One or more ligaments are torn, and the ankle joint is very loose or unstable.

Classification of Ankle Sprains

GRADE SIGNS AND SYMPTOMS

I: partial tear of a ligament

Mild tenderness and swelling

Slight or no functional loss (i.e., patient is able to bear weight and ambulate with minimal pain)

No mechanical instability (negative clinical stress examination)

II: incomplete tear of a ligament, with moderate functional impairment

Moderate pain and swelling

Mild to moderate ecchymosis

Tenderness over involved structures

Some loss of motion and function (i.e., patient has pain with weight-bearing and ambulation)

Mild to moderate instability (mild unilateral positivity of clinical stress examination)

III: complete tear and loss of integrity of a ligament

Severe swelling (more than 4 cm about the fibula)

Severe ecchymosis

Loss of function and motion (i.e., patient is unable to bear weight or ambulate)

Mechanical instability (moderate to severe positivity of clinical stress examination)

The grade of scientific evidence and level of evidence according to the Eastern Association for the Surgery of Trauma (EAST) (2001).
A grade of scientific evidence
Class I
  • Prospective randomized controlled trials – may be poorly designed, have inadequate numbers, or suffer from other methodological inadequacies
Class II
  • Prospective clinical studies and retrospective analyses based on clearly reliable data (observational studies, cohort studies, prevalence studies

and case control studies)

Class III
  • Retrospective studies (clinical series, database or registry review, large series of case reviews, expert opinion)

Level of recommendation

1
  • Convincirecommendation levelsed on the available scientific information, usualli Class I data or strong Class II evidence, especially if the issue does not lend itself to testing in a randomized format. Conversely, low quality or contradictory Class I data may not be able to support a level 1 recommendation.
Level 2
  • Reasonably justifiable by available scientific evidence and strongly supported by experts opinion. Usually supported by Class II data or a preponderance of Class III evidence.
Level 3
  • Supported by available data but adequate scientific evidence is lacking, generally Class III data. Useful for educational purposes and in guiding future clinical research.

Causes of Ankle Sprain

These are the main causes that can lead to the appearance of high ankle sprain:

  • Walking or exercising on an uneven surface
  • Falling down
  • Participating in sports that require cutting actions or rolling and twisting of the foot—such as trail running, basketball, tennis, football, and soccer
  • During sports activities, someone else may step on your foot while you are running, causing your foot to twist or roll to the side.

Rotational injuries

  • Ankle fractures

Impact sports

  • Football tackles
  • Falling or being pushed forward
  • Side-to-side running
  • Starting and stopping feet in a repetitive manner
  • Turning while moving
  • Other sports: hockey, wrestling, soccer

Mechanism

  • Foot is planted on the ground
  • Foot is then twisted outward (excessively)
  • Bones pull away from each other and the syndesmotic ligaments that connect them are torn

Increased risk

  • Severe load on the ankle
  • Excessive dorsiflexion of the foot – toes go beyond their normal range of motion, towards the shin
  • When a person is tangled under another person.

Symptoms of an ankle sprain

In an ankle sprain, the following signs and symptoms may occur

  • Localized pain at the site of the sprain – For example, if the deltoid ligament has been sprained, pain would be localized to the inside of the ankle. Pain is often described as sudden and sharp, and worsens with movement or placing weight on the ankle. Pain may be relieved somewhat by rest and elevation of the ankle.
  • Swelling at the site of the sprain – In the case of a deltoid ligament sprain, the inside of the ankle may be noticeably swollen. Or swelling may occur on the outside of the ankle if one or more ligaments in the lateral ligament complex are sprained.
  • Bruising over the site of the sprain – In addition to swelling, patients may notice bluish, reddish, or purplish skin discolorations over the sprain site as an indication that ligaments have torn and blood is rushing to the area.
  • Limited ability to move the ankle – In more severe sprains, patients may not be able to turn, bend, or flex the foot. Weight-bearing activities such as walking may become difficult or impossible.
  • Popping sound or sensation – When the injury occurs, patients may hear or feel a “pop” as the ligament is stretched or torn.
  • Intense pain at the time of the trauma – In cases of severe sprains when the ligament(s) is partially or completely torn, the pain is sudden and severe enough to make patients stop whatever they are doing and become immobile.
  • Sensibility affected – This is due to the inflammation which increases the pressure in the area.
  • Stiffness – Mainly after some time without moving your ankle.
  • Limited range of motion – All movements are going to be limited, although the most restricted (as it will cause pain) is ankle inversion.
  • Instability – When the ankle sprain is a severe one.
  • Difficulty or impossibility of bearing your weight – The more severe the ankle sprain, the more difficult to bear your weight and walk.
  • Pop sound in some severe ankle sprains

Ankle Sprain assessment

Image result for ankle sprain hd

The therapist will perform a series of tests which may include the following

Observation

  • Observation is usually the first stage of any injury assessment.
  • The therapist will usually observe the patient in both standing and lying down and will be looking closely for swelling, bruising and deformity, as well as postural issues such as over pronation of the feet or problems putting the foot on the floor.

Palpation

  • The therapist will then palpate the entire ankle joint and surrounding area to assess if the joint is warm (due to acute inflammation) and swollen and if the ligaments are painful to touch.

Range of Motion

  • The therapist will usually assess both active (the patient moves) and passive (the therapist moves the joint) movements of the ankle with the knee both straight and then bent.
  • The ankle is often painful to move after an ankle sprain.
  • Passive range of motion is usually pain-free as the muscles are not contracting, although the end of range into dorsiflexion (toes pointing upwards) may be painful as the muscles stretch.

Assessing Ankle flexibility

  • Depending on the severity of the ankle injury, the therapist may assess the patient in standing to test the movement of the ankle when weight bearing.

Resisted Muscle Tests

  • These tests are used to assess strength of the muscles around the ankle joint compared to the other side.
  • They may be tested with the knee straight and then bent.

Special Tests

Special tests are used to assess the integrity of the ligaments and how badly damaged they are.

  • “Anterior drawer test” will be used to assess the ATFL ligament
  • “Talar Tilt” test will be used to test the CFL ligament
  • External rotation and squeeze tests will be used to assess the high ankle ligaments (syndesmosis complex)

Imaging of Ankle Sprain

Radiographs > indications for radiographs with an ankle injury include (Ottawa ankle rules)

  • inability to bear weight
  • medial or lateral malleolus point tenderness
  • 5MT base tenderness
  • navicular tenderness

Radiographic views to obtain > standard ankle series (weight bearing)

  • AP
  • lateral
  • mortise

ER rotation stress view

  • useful to diagnosis syndesmosis injury in high ankle sprain
  • look for asymmetric mortise widening
  • medial clear space widening > 4mm
  • tibiofibular clear space widening of 6 mm

Varus stress view

  • used to diagnose injury to ATFL or CFL
  • measures ankle instability by looking at talar tilt and anterior talar translation

Radiographs more

  • X-rays – X-rays provide images of dense structures, such as bone. Your doctor may order x-rays to rule out a broken bone in your ankle or foot. A broken bone can cause similar symptoms of pain and swelling.
  • Stress x-rays – In addition to plain x-rays, your doctor may also order stress x-rays. These scans are taken while the ankle is being pushed in different directions. Stress x-rays help to show whether the ankle is moving abnormally because of injured ligaments.
  • Magnetic resonance imaging (MRI) scan – Your doctor may order an MRI if he or she suspects a very severe injury to the ligaments, damage to the cartilage or bone of the joint surface, a small bone chip, or another problem. The MRI may not be ordered until after the period of swelling and bruising resolves.
  • Ultrasound – This imaging scan allows your doctor to observe the ligament directly while he or she moves your ankle. This helps your doctor to determine how much stability the ligament

Sonography

Sonography is a valuable tool for examining the tendons of the ankle joint such as the Achilles or the peroneal tendons for rupture or displacement. Only a few studies have evaluated the capacity of sonography to diagnose injuries of the lateral ligaments of the ankle. Milz et al. performed the sonographic evaluation in 20 patients using MRI as the gold standard with a sensitivity of 92% and a specificity of 83% for injury and rupture of ATFL. In 34 patients, sonography was confirmed at arthroscopy with a sensitivity of 100% and a specificity of 33%. However, sonographic evaluation is strongly dependent on the expertise of the technician. Furthermore, state of the art equipment and examination techniques are the prerequisite to assess ligament integrity.

Arthrography

Rupture of the ATFL can be diagnosed with a sensitivity of 96–100% using arthrography. For the PTFL, sensitivity decreases to 75% for anatomical reasons. Further arthrography is invasive and is not able to provide images of the ligament itself, but it is an indirect tool for the diagnosis of rupture. Therefore, it should not be considered a standard tool for diagnosis of ligament rupture in the ankle.

Recommendation: arthrography shows a similar sensitivity only in diagnosing injuries of the ATLF compared to delayed physical examination. It is, however, an invasive procedure and should not, therefore, be recommended for routine practice.

Treatment of Ankle Sprain

PRICE therapy

PRICE stands for

Protection – protect the affected area from further injury by using a support or, in the case of an ankle injury, wearing shoes that enclose and support your feet, such as lace-ups.

Rest – stop the activity that caused the injury and rest the affected joint or muscle. Avoid activity for the first 48 to 72 hours after injuring yourself. Your GP may recommend you use crutches.

Ice – Ice helps decrease swelling, bruising, pain, and muscle spasms. Putting ice on your ankle is helpful, but you need to be careful. The cold can damage your nerves if you leave ice in place too long. You should only use ice for up to 20 minutes at a time. If your skin feels numb, it’s time to remove the ice. Use ice treatments every 2 to 4 hours for the first 3 days after your injury. Ice treatments can consist of ice packs, ice baths, or ice massages.

  • To make an ice pack, partly fill a plastic bag with ice. Put a thin, damp cloth on your ankle to create a layer between your skin and the ice. Wrap an elastic bandage around the ice pack to hold it in place.
  • For an ice bath, fill a large bucket with water and ice. Place your ankle in the bucket until the skin starts to get numb.
  • Ice massages can work well for small areas. Freeze water in 4- to 8-ounce Styrofoam (coffee) cups. Tear the top part of the cup away from the ice. Hold the covered end and slowly rub the ice over the sprained area in a circular motion. Don’t hold the ice on one spot for more than 30 seconds.

Compression – compress or bandage the injured area to limit any swelling and movement that could damage it further. You can use a simple elastic bandage or an elasticated tubular bandage available from a pharmacy. It should be wrapped snuggly around the affected area, but not so tightly that it restricts blood flow. Remove the bandage before you go to sleep.

Elevation – keep the injured area raised and supported on a pillow to help reduce swelling. If your leg is injured, avoid long periods of time where your leg isn’t raised.

Support devices – such as a brace, cast, or splint, may be needed to limit your movement and protect your joint. You may need to use crutches to decrease your pain as you move around.

Acute care/immobilization – Immediately after a LAS the primary goals are to manage pain, control inflammation and protect the joint so that the healing process can begin. In the acute phase of healing, the most important structures to protect are the lateral ligaments of the ankle because the traumatic mechanism has caused increased laxity. In the past, the majority of the literature has focused on functional rehabilitation after a LAS. But with the high recurrence rates of LAS, development of CAI and potential for the development of ankle OA, functional rehabilitation may not allow adequate time for the ligaments of the ankle to heal and stability to be restored. Indeed, increased laxity has been reported using both subjective (ankle giving way, or feelings of instability) and objective (manual stress tests, radiographs) outcome measures.

Cryotherapy – Cryotherapy has been proved to be effective in the treatment of soft tissue injuries. The quality of studies of sprained ankles is poor, as cryotherapy has usually been combined with other treatments. However, it seems to reduce swelling and the need for painkillers, particularly when used soon after the injury, and it should, therefore, be part of the initial standard regimes. Furthermore, it improves the reliability of the clinical examination. The duration, frequencies and the technique of ice application remain controversial.

Medicines

  • NSAIDs – such as ibuprofen, help decrease swelling, pain, and fever. This medicine is available with or without a doctor’s order. NSAIDs can cause stomach bleeding or kidney problems in certain people. If you take blood thinner medicine, always ask your healthcare provider if NSAIDs are safe for you. Always read the medicine label and follow directions.
  • Acetaminophen – decreases pain. It is available without a doctor’s order. Ask how much to take and how often to take it. Follow directions. Acetaminophen can cause liver damage if not taken correctly.
  • Prescription pain medicine –  may be given. Ask how to take this medicine safely.

Avoiding HARM

For the first 72 hours after a sprain or muscle strain, you should avoid HARM. This means you should avoid:

  • Heat – such as hot baths, saunas or heat packs.
  • Alcohol – drinking alcohol will increase bleeding and swelling, and slow healing.
  • Running – or any other form of exercise that could cause more damage.
  • Massage – which may increase bleeding and swelling.

Other treatments

  • Laser therapy, ultrasound, electrotherapy, homeopathic therapy, hyperbaric oxygen therapy, prolotherapy, platelet-rich plasma, hyaluronic acid or topical nitroglycerin injection were not effective, or available data were insufficient to prove their benefit in the treatment of acute ankle injuries. In order to prove their benefit, new treatment options must be superior to placebo and to the current gold standard, i.e. functional treatment. Consequently, they should not be part of a standard protocol for the treatment of acute ankle sprains.
  • Recommendation: so far, none of these treatments have been shown to enhance recovery from acute ankle injuries. Therefore, they should not be considered as part of the standard regime in treating acute ankle injuries.

Balance exercises

  • One of the most commonly examined sensorimotor outcome measures following a LAS is single leg postural control. A prospective investigation has shown that single leg postural control is impaired for at least four weeks after injury. Further, recent systematic reviews have demonstrated that postural control is impaired on both the involved limb and the uninvolved limb relative to an uninjured control group within six weeks of a LAS. The presence of bilateral balance impairments (ie, impaired balance on the involved and uninvolved limb relative to a healthy reference group), as well as bilateral alterations at joints proximal to the ankle7,68, suggest changes in motor control patterns that are centrally mediated (ie, feed-forward neuromuscular control) have occurred.

Joint mobilizations

  • To date, manipulative therapy techniques; including Maitland’s mobilizations,Mulligan’s mobilizations with movement, and high-velocity low-amplitude (HVLA) thrusts,have all been postulated to be effective treatments for acute LAS. Indeed, manipulative therapy techniques are theorized to reduce pain, improve function and increase ROM via the restoration of arthrokinematic motions (ie, roll, glide, spin), thus recommendations to use these techniques make intuitive sense. Further, there is a great deal of anecdotal evidence in the form of published case studies supporting the use of manipulative therapies to improve various outcome measures in acute LAS.

Physiotherapy for Ankle Sprain

  • Reduce Pain and Swelling –  You will learn how to avoid or modify your daily and sports activities to allow healing to begin. Your physical therapist may use different types of treatments and technologies to control and reduce your pain and swelling, including ice, heat, ultrasound, electrical stimulation, taping, specific exercises, and hands-on therapy, such as specialized massage.
  • Improve Motion – Your physical therapist will choose specific activities and treatments to help restore normal movement in the ankle. These might begin with “passive” motions that the physical therapist performs for you to gently move your ankle and foot, and progress to “active” exercises and stretches that you do yourself.
  • Improve Flexibility – Your physical therapist will determine if any foot, ankle, or lower leg muscles are tight, begin to stretch them, and teach you how to stretch them.
  • Improve Strength – Ankle sprains may be related to weak, injured, or uncoordinated leg muscles. Certain exercises will aid healing at each stage of recovery; your physical therapist will choose and teach you the correct exercises and equipment to use, to steadily and safely restore your strength. These may include using cuff weights, stretch bands, and weight-lifting equipment.
  • Improve Endurance – Regaining your muscular endurance in the ankle and leg is important after an injury. Your physical therapist will teach you exercises to improve endurance, so you can return to your normal activities. Cardio-exercise equipment may be used, such as treadmills or stationary bicycles.
  • Improve Balance – Regaining your sense of balance is important after an injury. Your physical therapist will teach you exercises to improve your balance ability.
  • Restore Agility – Speed and accuracy of leg movement is important in athletics and in many daily activities. Your physical therapist will help you regain these skills in preparation for a return to sports and to your daily routine.
  • Learn a Home Program – Your physical therapist will teach you strengthening and stretching exercises to perform at home. These exercises will be specific for your needs; if you do them as prescribed by your physical therapist, you can speed your recovery.
  • Return to Activities – Your physical therapist will discuss activity goals with you and use them to set your work, sport, and home-life recovery goals. Your treatment program will help you reach your goals in the safest, fastest, and most effective way possible. Your physical therapist will teach you exercises, work retraining activities, and sport-specific techniques and drills to help you achieve your goals.
  • Speed Recovery Time – Your physical therapist is trained and experienced in choosing the best treatments and exercises to help you safely heal, return to your normal lifestyle, and reach your goals faster than you are likely to do on your own.

Exercises for Ankle Sprain

Exercise to Improve Range of Motion Following Syndesmotic Sprain or Syndesmotic Ankle Sprain

  • Sit straight and try and bring the ankle and foot up as much as possible so that a stretch to the calf is felt. Hold this position for about 10 seconds and repeat this around 10 times.

Exercise-1 for Syndesmotic Sprain or Syndesmotic Ankle Sprain

Exercise to Improve Range of Motion Following Syndesmotic Sprain or Syndesmotic Ankle Sprain 

  • In this exercise, while seated bring and the ankle down and bend it inwards. Maintain this position for about 10 seconds and repeat it about 10 times.

Exercise-2 for Syndesmotic Sprain or Syndesmotic Ankle Sprain

Exercise to Improve Range of Motion Following Syndesmotic Sprain or Syndesmotic Ankle Sprain 

  • In this exercise, from a seated position bring the ankle up in an outwards position and maintain this position for about 10 seconds. Repeat this exercise again 10 times.

Exercise-3 for Syndesmotic Sprain or Syndesmotic Ankle Sprain

Exercise  to Improve Range of Motion Following Syndesmotic Sprain or Syndesmotic Ankle Sprain

  • In this exercise, while in a seated position point the toes down and maintain the position for about 10 seconds and repeat this again 10 times.

Exercise-4 for Syndesmotic Sprain or Syndesmotic Ankle Sprain

Strengthening Exercises for Syndesmotic Sprain or Syndesmotic Ankle Sprain

  • The below mentioned exercises should only be done once there has been a substantial improvement in the ankle pain following a syndesmotic sprain or syndesmotic ankle sprain (SAS).

Strengthening Exercise for Syndesmotic Sprain or Syndesmotic Ankle Sprain

  • Stand on the edge of a stair, drop the ankles down and maintain this stretching position for about 10 seconds and repeat the exercise about 10 times.

Strengthening Exercise #1 for Syndesmotic Sprain or Syndesmotic Ankle Sprain

Strengthening Exercise for Syndesmotic Sprain or Syndesmotic Ankle Sprain

  • Stand about 10 inches from a wall with the toes pointing towards the wall. Now squat down and maintain this position for about 10 seconds and repeat this maneuver about 10 times.

Strengthening Exercise #2 for Syndesmotic Sprain or Syndesmotic Ankle Sprain

Isometirc Exercises for Syndesmotic Sprain or Syndesmotic Ankle Sprain

  • After achieving near normal range of motion and strength following syndesmotic sprain or a syndesmotic ankle sprain (SAS) then you can start with some isometric exercises by first pushing at a fixed object with the injured ankle. Once this is able to be done with minimal to no pain then the exercises can be advanced by placing resistance and then doing ankle range of motion.
  • Place the ankle down and inwards against a fixed object like a couch Place your ankle in the “down and in” position against a fixed object such as a couch. Maintain this position for about 10 seconds and repeat it about 10 times.
  • In this exercise, position the ankle upwards and bring it out against a stationary object. Maintain this position for about 10 seconds and repeat it about 10 times.
  • This exercise makes use of a resistance band. Take a resistance band and hold the ends of the band in the hands while the band it placed around the foot. Now, try and bring the ankle down as much as possible. Do this for about 10 seconds and repeat it about 10 times. This can also be done by typing the band around a fixed object and then doing this exercise.

Ankle sprain risk factors

  • Limited dorsiflexion – (click on the word to see explanation). If your dorsiflexion is limited,  this could result in an increase of chance of twisting your ankle.
  • High navicular- medial malleolus distance (NMM distance) – If you have a look at the photo below, it is the distance between “D” and the lowest part of “B”. Have a look at this paper.
  • Poor proprioception – This will mean that the receptors of your ankle/foot will not inform properly your brain about the position of your foot and, therefore, the risk of getting injured will be higher.
  • Higher extension range of motion at the first metatarsophalangeal joint – This means that you can move your toe upwards quite a lot.
  • Reduced balance – It can be the result of poor proprioception or due to different conditions.
  • Previous ankle sprains – Apparently people who have had previous ankle sprains are prone to have a new one.
  • Sport practised – To be a football/soccer player, due to contact with opponents and to play volleyball or basketball, as they imply a lot of jumping are risk factors, as well.

Living with an ankle sprain

Ankle sprains are common problems, but they do heal. However, you may not be able to return to normal activities right away. It will depend on the grade of your ankle sprain. If your sprain is mild, it might only be 1 to 3 days. If your sprain is moderate or severe, it could be a few weeks. Your doctor can help provide a timeframe for your condition. Once you return, you still may need to wear an ankle brace or bandage for support and protection.

Your doctor or therapist also will provide a list of ankle exercises to do. This will help strengthen your muscles and prevent future sprains. Try the following exercises:

  • Ankle circles – Sit on the floor with your legs stretched out in front of you. Move your ankle from side to side, up and down, and around in circles. Do 5 to 10 circles in each direction at least 3 times per day.
  • Alphabet letters – Using your big toe as a “pencil,” write the letters of the alphabet in the air. Do the entire alphabet 2 or 3 times.
  • Toe raises – Flex your toes back toward you while keeping your knee as straight as you can. Hold for 15 seconds. Do this 10 times.
  • Heel raises – Point your toes away from you while keeping your knees as straight as you can. Hold for 15 seconds. Do this 10 times.
  • In and out – Turn your injured foot inward until you can’t turn it anymore and hold for 15 seconds. Straighten your foot again. Turn it outward until you can’t turn it anymore and hold for 15 seconds. Do this 10 times in both directions.
  • Resistance in and out – Sit on a chair with your leg straight in front of you. Tie the ends of a large elastic exercise band together to make a knot. Wrap the end of the band around the chair leg. Wrap the other end around the bottom of your injured foot. Keep your heel on the ground and slide your foot outward and hold for 10 seconds. Put your foot in front of you again. Slide your foot inward and hold for 10 seconds. Repeat at least 10 times each direction 2 or 3 times per day.
  • Step up – Put your injured foot on the first step of a staircase and your other foot on the ground. Slowly straighten the knee of you injured leg while lifting your other foot off the ground. Return to your starting position. Do this 3 to 5 times at least 3 times per day.
  • Sitting and standing raises – Sit in a chair with your feet on the ground. Slowly raise your heels while keeping your toes on the ground. Return your heels to the floor. Repeat 10 times at least 2 or 3 times per day. As you get stronger, you can stand on your feet instead of sitting in a chair and raise your heels.
  • Balance Exercises – Stand and place a chair next to your uninjured leg to balance you. To start, stand on your injured foot for 30 seconds. You can slowly increase this to up to 3 minutes at a time. Repeat at least 3 times a day. To increase the difficulty, repeat with your eyes closed

Most ankle breaks (fractures) heal uneventfully. Possible early complications include:

  • Infection (especially after open fracture).
  • Damage to nerves and blood vessels (especially after displaced fracture).
  • Compartment syndrome (severe swelling in the leg soon after the injury, putting pressure on nerves and blood vessels).
  • Poor healing.
  • Damage to skin and soft tissues by a tight or poorly finished cast.
  • Burns to the skin as the plaster hardens.
  • Failure of bones to knit together and heal well. This can lead to delayed union, union with poor alignment, or complete non-union even after six months.
  • Temporary complications of wearing a cast include thinning of the bones and wasting of the muscles, both of which occur significantly even in a 4-6 week period of casting.
  • Inflammation of the veins of the lower leg (thrombophlebitis).
  • Clotting (thrombosis) of the deep veins of the leg (deep vein thrombosis) which can relate both to reduced mobility and to pressure on the leg veins from swelling and casting.
  • Complications of surgical treatment of ankle fracture can include pain from, and infection around, surgical pins (which can in themselves be distressing and frightening).

Possible later complications include

  • Osteoarthritis of the ankle.
  • Stiffness and loss of flexibility in the ankle.
  • Long-term instability of the ankle joint, needing later correction.
  • Algodystrophy (also called Sudeck’s atrophy, or complex regional pain syndrome) is a nerve abnormality which can develop after fracture and which leads to continuous burning pain and gradual loss of strength. Treatment is prolonged and difficult.
  • In children, damage to the growing parts of the bones of the ankle can affect overall growth

References

By

Myocardial Infarction; Causes, Symptoms, Diagnosis, Treatment

Myocardial infarction also called a heart attack happens when a blood vessel in the heart suddenly becomes blocked. Blood vessels carry blood and oxygen. When a blood vessel in the heart gets blocked, blood cannot get to the part of the heart. This part of the heart does not get enough oxygen. This is called ischemia. When the heart muscle becomes ischemic (does not get enough blood and oxygen), the ischemia often causes chest pain. This is called angina pectoris. If the ischemia lasts long enough, the heart muscle that is not getting enough oxygen dies. This is called an infarction. “Myocardial infarction” means “infarction (muscle death) in the heart muscle.

Myocardial infarction (MI) is a term used for an event of a heart attack which is due to the formation of plaques in the interior walls of the arteries resulting in reduced blood flow to the heart and injuring heart muscles because of lack of oxygen supply. The symptoms of MI include chest pain, which travels from left arm to neck, shortness of breath, sweating, nausea, vomiting, abnormal heart beating, anxiety, fatigue, weakness, stress, depression, and other factors. The immediate treatment of MI include taking aspirin, which prevents blood from clotting, and nitro-glycerin to treat chest pain and oxygen. The heart attack can be prevented by taking an earlier action to lower those risks by controlling diet, fat, cholesterol, salt, smoking, nicotine, alcohol, drugs, monitoring of blood pressure every week, doing exercise every day, and losing body weight. The treatment of MI includes, aspirin tablets, and to dissolve arterial blockage injection of thrombolytic or clot-dissolving drugs such as tissue plasminogen activator, streptokinase or urokinase in blood within 3 h of the onset of a heart attack. The painkillers such as morphine or meperidine can be administered to relieve pain. Nitroglycerin and antihypertensive drugs such as beta-blockers, ACE inhibitors or calcium channel blockers may also be used to lower blood pressure and to improve the oxygen demand of heart. The ECG, coronary angiography and X-ray of heart and blood vessels can be performed to observe the narrowing of coronary arteries. [Rx]

A heart attack is a medical emergency. The first few minutes are very important for keeping the person alive. Some of the damage from the heart attack can be repaired if the person gets treatment during the first hour of the attack

Types of Myocardial Infarction

Third universal classification of myocardial infarction

Type 1: Spontaneous MI
  • Spontaneous MI due to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe CAD, non-obstructive coronary disease or no CAD
Type 2: MI secondary to an ischemic imbalance
  • Myocardial injury with necrosis occurs due to conditions other than CAD that contribute to an imbalance between myocardial oxygen supply and/or demand such as coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachycardia-bradycardia arrhythmias, anemia, respiratory failure, hypotension, and hypertension
Type 3: MI resulting in death when biomarker values are unavailable
  • Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new LBBB, but death occurs before blood samples can be obtained before cardiac troponins biomarkers rise, or when cardiac biomarkers were not collected
Type 4A: MI related to percutaneous coronary intervention
  • I associated with PCI is defined by elevation of cTn values greater than five times the 99th percentile upper normal reference limit (URL) in patients with normal baseline values (< 99th percentile URL) or a rise of cTn values by > 20% if the baseline troponins are elevated and are stable or falling. In addition one of the following criterion are required: (1) symptoms suggestive of myocardial ischemia; (2) new ischemic ECG changes or new LBBB; (3) angiographic loss of patency of a major coronary artery or a side branch or persistent slow- or no coronary flow or coronary embolization; or (4) demonstration with imaging of a new loss of viable myocardium or new regional wall motion abnormality
Type 4B: MI related to stent thrombosis
  • I associated with stent thrombosis detected by coronary angiography or autopsy in the presence of myocardial ischemia with a rise and/or fall of troponin biomarkers. One troponin measurement should be above the 99 percentile UR
Type 4C: MI related to restenosis
  • I associated with restenosis defined as ≥ 50% stenosis or a complex lesion demonstrated at coronary angiography after (1) initial successful stent deployment; or (2) dilatation of a coronary artery stenosis with balloon angioplasty. These coronary angiographic changes should be associated with an increase and/or decrease of cTn values > 99th percentile URL and no other significant obstructive CAD
Type 5: MI related to coronary artery bypass grafting
  • MI associated with CABG is defined by elevation of cardiac troponins greater than ten times the 99thpercentile URL in patients with normal baseline cTn values (< 99th percentile URL). In addition, one of the following should be present: (1) new pathological Q waves or new LBBB; or (2) angiographic documented new graft or new native coronary artery occlusion; or (3) new loss of viable myocardium or new regional wall motion abnormality as shown by an imaging modality

Myocardial infarction is classified into two types

  • ST-segment elevation myocardial infarction (STEMI) – It occurs by complete occlusion of a major coronary artery that produces entire thickness damage of heart muscle. STEMI is also called transmural infarction due to its full thickness involvement. This entire thickness damage of heart muscle produces an ECG (electrocardiography) change of ST-segment elevation. It can be subclassified into anterior, anteroseptal, posterior, inferior, lateral, high lateral or anterolateral myocardial infarction (according to left ventricular wall damage), and RV type (according to right ventricular wall damage).
  • Non-ST-segment elevation myocardial infarction (NSTEMI) – NSTEMI is usually due to complete occlusion of a minor coronary artery or partial occlusion of a major coronary artery that produces partial thickness damage of heart muscle. Here, the damage of heart muscle is confined to the inner ⅓ rd – ⅔ rd of the left ventricular wall. For this reason, it is also called subendocardial infarction. ST-segment elevation in ECG is not developed in this myocardial infarction because of partial thickness damage of heart muscle. Here, this muscle damage is demonstrated by an elevation of cardiac markers (CK-MB or Troponin) in the blood.

Types

Myocardial infarctions are generally clinically classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). These are based on changes to an ECG.[Rx] STEMIs make up about 25 – 40% of myocardial infarctions.[Rx] A more explicit classification system, based on international consensus in 2012, also exists. This classifies myocardial infarctions into five types:[Rx]

  • Spontaneous MI related to plaque erosion and/or rupture, fissuring, or dissection
  • MI related to ischemia, such as from increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, high blood pressure or low blood pressure
  • Sudden unexpected cardiac death, including cardiac arrest, where symptoms may suggest MI, an ECG may be taken with suggestive changes, or a blood clot is found in a coronary artery by angiography and/or at autopsy, but where blood samples could not be obtained, or at a time before the appearance of cardiac biomarkers in the blood
  • Associated with coronary angioplasty or stents
    • Associated with percutaneous coronary intervention (PCI)
    • Associated with stent thrombosis as documented by angiography or at autopsy
  • Associated with CABG
  • Associated with spontaneous coronary artery dissection in young, fit women

Causes of Myocardial Infarction

The factors that lead to anterior MI are similar to those causing damage in other parts of the heart which are supplied by other branches of the coronary arteries. Risk factors which may predispose one to develop a heart attack include

  • Age greater than 45 years (although younger people may also experience it)
  • The family history of heart attack
  • Male gender
  • Smoking
  • High cholesterol levels in the blood
  • High blood pressure that is poorly controlled
  • Type A personality
  • Lack of exercise

Causes of anterior MI as well as in any part of the heart include

  • Atherosclerosis leading to plaque formation in the coronary arteries – the most common cause
  • Coronary artery vasospasm (constriction)
  • Embolism or blood clots
  • Carbon monoxide poisoning
  • Left ventricular hypertrophy (enlargement)
  • Drugs containing cocaine, amphetamines, and ephedrine
  • Arteritis
  • Aortic dissection
  • A coronary aneurysm

Symptoms of Myocardial Infarction

A heart attack involving the left ventricle can compromise the pumping action of the heart and the blood supply to the rest of the body. This can lead to symptoms like:

  • Chest pains – constricting, stabbing, squeezing type of pain under the breastbone or the left side of the chest; pains may radiate to the neck, back, shoulder and left arm
  • Shortness of breath or difficulty in breathing
  • Lightheadedness may be accompanied by fainting
  • Anxiety and a sense of impending doom
  • Extreme paleness, with cold and clammy skin
  • General weakness or fatigue
  • Squeezing pain, heaviness, tightness, pressure in the center of the chest
  • Pain that spreads to your back, left arm, jaw, neck
  • Dizziness, weakness
  • Nausea, vomiting
  • Irregular heartbeat
  • Sweating
  • Feeling of doom

Women may experience different symptoms than men. In women, along with chest pain, symptoms can include:

  • Heartburn or pain in the abdomen
  • Unusual fatigue
  • Clammy skin

Women’s symptoms sometimes differ

Although most women and men report symptoms of chest pain with a heart attack, women are slightly more likely than men to report unusual symptoms. Those who have more vague or less typical “heart” symptoms have reported the following:

  • Upper back or shoulder pain
  • Jaw pain or pain spreading to the jaw
  • Pressure or pain in the center of the chest
  • Light headaches
  • Pain that spreads to the arm
  • Unusual fatigue for several days

Risk factors for Myocardial Infarction

The following risk factors have been associated with a higher incidence of myocardial infarction. Some of these risk factors are controllable (such as smoking and physical activity) while others are uncontrollable (such as age, genetics, family history).

  • Age –  Four out of five patients with coronary artery disease are 65 years of age or older. After menopause, females are more likely to die within the first year of having a myocardial infarction than males.
  • Gender –  Males are at higher risk of myocardial infarction than women, and males are also more likely to suffer myocardial infarction earlier in life. However, heart disease kills more females each year than any other disease, including breast cancer. An alarming survey reported by the American Heart Association found that only 8% of women perceive heart disease as the greatest threat to their health despite the fact that heart disease is the leading cause of death among both women and men. Over 500,000 American women die from cardiovascular disease each year twice the number of deaths from all cancers combined. Also, women are more likely to die within the first year of a heart attack than men.
  • Family history/race –  A family history of heart disease increases the risk of coronary artery disease and myocardial infarction. In the United States, African Americans tend to have more severe high blood pressure than Caucasians, increasing coronary artery disease/myocardial infarction risk. The incidence of heart disease is also higher among certain population groups such as Mexican Americans, American Indians, native Hawaiians, and some Asian Americans.
  • Smoking –  Cigarette smokers are twice as likely to experience myocardial infarction compared to non-smokers. Smokers also have a two to four time higher risk of sudden cardiac death (within an hour of a heart attack).
  • High blood pressure (hypertension) –  Alone or in association with obesity, smoking, high blood cholesterol levels or diabetes, high blood pressure increases the risk of myocardial infarction and stroke.
  • High blood cholesterol – High total and low-density lipoprotein (LDL cholesterol) levels and low HDL cholesterol levels increase the risk of myocardial infarction Cholesterol levels can be lowered with dietary/lifestyle modifications such as exercise or medications.
  • Obesity – Obesity increases coronary artery disease, myocardial infarction, and stroke risk. Obesity increases strain on the heart, raises blood pressure and cholesterol, and increases diabetes risk. Weight reduction can be achieved with modifications to diet and increased physical activity.
  • Diabetes – Approximately two-thirds of patients with diabetes die from heart or blood vessel disease. Adults with diabetes are three to seven times more likely to develop heart disease. A recent recommendation from the U.S. government advocates aggressive treatment of high cholesterol in people with diabetes.
  • Lack of physical activity – Regular exercise reduces the risk of coronary artery disease and myocardial infarction by controlling blood cholesterol levels, decreasing the risk of obesity or diabetes, and lowering blood pressure levels in some patients.
  • Stress –  Research indicates a possible relationship between stress and coronary artery disease, which may lead to myocardial infarction Hypertension (high blood pressure) and high cholesterol are associated with stress, as are increased tendencies to smoke, gain weight and/or decrease physical activity.

Diagnosis of Myocardial Infarction

Treating a heart attack quickly can save your life, while delay can be fatal. In the emergency room, a doctor will ask you about your symptoms and perform a physical examination. The doctor will immediately run tests to determine your heart function. They may include

  • Echocardiogram (heart ultrasound) – This diagnostic technique is an excellent first step in investigating congenital heart disease or in evaluating abnormalities of the heart wall. Echocardiography is a non-invasive exam in which images are acquired and viewed in real time without the use of radiation. Echocardiography is often useful in studying the beating heart and provides some information on the functional abnormalities of the heart wall, valves, and blood vessels. Doppler ultrasound can be used to measure blood flow across a heart valve. Abnormal operation of the valves can be detected by studying the opening and closing function versus normal valve function. Echocardiography may also be used to study congenital heart defects such as a septal defect (a hole in the wall that separates the two chambers of the heart).
  • Blood tests – Your doctor may look for certain enzymes that are released into your blood when you have a heart attack.

Other tests include

  • CBC, ESR,Hb
  • Serum cholesterol, C-reactive protein, Serum creatine,
  • Chest x-ray
  • Echocardiogram – (uses sound waves to take a picture of your heart)
  • Coronary catheterization or angiogram –  (uses a liquid dye inserted through a catheter to see whether your arteries are blocked)
  • Stress test –  (involves walking on a treadmill while hooked up to an ECG machine to see how your heart responds to exercise)
  • Coronary angiogram – an x-ray imaging technique to show if the coronary arteries are narrowed or blocked
  • Exercise stress test –  involves conducting an ECG during exercise since problems with the heart are more likely to be revealed when the heart is working harder
  • Cardiac computerized tomography (CT) – or magnetic resonance imaging (MRI), involves the use of high-tech machines to reveal problems with the heart and coronary arteries by taking a series detailed images of the heart.
  • Nuclear medicine –  Nuclear medicine (also called radionuclide scanning) allows visualization of the anatomy and function of an organ. The patient will be given a radionuclide which will assist in the acquisition of clear images of the heart with a gamma camera. Nuclear medicine imaging may be used to detect coronary artery disease, myocardial infarction, valve disease, heart transplant rejection, check the effectiveness of bypass surgery, or to select patients for angioplasty or coronary bypass graft.

Treatment of Myocardial Infarction

  • Arrange an emergency ambulance if an AMI is suspected – Take an ECG as soon as possible but do not delay transfer to hospital, as an ECG is only of value in pre-hospital management if pre-hospital thrombolysis is being considered.
  • Advise any patient known – to have coronary heart disease to call for an emergency ambulance if the chest pain is unresponsive to glyceryl trinitrate (GTN) and has been present for longer than 15 minutes or on the basis of general clinical state – eg, severe dyspnoea or pain.
  • Cardiopulmonary resuscitation – and defibrillation in the event of a cardiac arrest.
  • Oxygen – do not routinely administer oxygen but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to
  • People with oxygen saturation – less than 94% who are not at risk of hypercapnic respiratory failure, aiming for saturation of 94-98%.
  • People with the chronic obstructive pulmonary disease – who are at risk of hypercapnic respiratory failure, to achieve a target saturation of 88-92% until blood gas analysis is available.
  • Pain relief with GTN sublingual/spray and/or –  an intravenous opioid 2.5-5 mg diamorphine or 5-10 mg morphine intravenously with an anti-emetic.Avoid intramuscular injections, as absorption is unreliable and the injection site may bleed if the patient later receives thrombolytic therapy.
  • Aspirin 300 mg orally – (dispersible or chewed).
  • Insert a Venflon for intravenous access and take blood tests for FBC, – renal function and electrolytes, glucose, lipids, clotting screen, C-reactive protein (CRP) and cardiac enzymes (troponin I or T).
  • Pre-hospital thrombolysis is indicated – if the time from the initial call to arrival at the hospital is likely to be over 30 minutes. When primary percutaneous coronary intervention cannot be provided within 120 minutes of ECG diagnosis, patients with an ST-segment-elevation acute coronary syndrome should receive immediate (pre-hospital or admission) thrombolytic therapy.
  • National Institute for Health and Care Excellence (NICE) – recommends using intravenous bolus (reteplase or tenecteplase) rather than an infusion for pre-hospital thrombolysis.
  • The goals of therapy in acute MI – are the expedient restoration of normal coronary blood flow and the maximum salvage of functional myocardium. These goals can be met by a number of medical interventions and adjunctive therapies. The primary obstacles to achieving these goals are the patient’s failure to recognize MI symptoms quickly and the delay in seeking medical attention. When patients present to a hospital, there are a variety of interventions to achieve treatment goals. “Time is muscle” guides the management decisions in acute STEMI, and an early invasive approach is the standard of care for acute NSTEMI.

Medical Options

  • Aspirin Helps stop blood from clotting. You may be given aspirin in the ambulance or as soon as you get to the hospital. Aspirin should be continued indefinitely at a dose of 81 mg per day, or as directed by your physician.
  • Warfarin (INR 2-3) – or dabigatran can be considered for patients unable to take aspirin or clopidogrel.
  • Nitroglycerin – Helps dilate (widen)or used to widen your blood vessels. You may be given nitroglycerin in the ambulance or as soon as you get to the hospital.
  • Pain reliever Helps relieve pain and is often given intravenously (IV).
  • Thrombolytics – Work to break up clots. They are most effective when taken within 2 hours of the heart attack, and are not given after 12 hours have elapsed. These drugs may be given with other anticoagulants (blood thinners).
  • Anticoagulants (blood thinners) – Make your blood less likely to form clots. Heparin is often given by injection while you are in the hospital..
  • Antiplatelet – drugs, such as clopidogrel, can be used to prevent new clots from forming and existing clots from growing.
  • Beta-blockers – lower your blood pressure and relax your heart muscle. This can help limit the severity of damage to your heart.
  • ACE inhibitors – can also be used to lower blood pressure and decrease stress on the heart.
  • Bronko dilator – group of medicine(montelukast) can be used to accelerate the normal breathing.
  • Anti-depressants – the drug can be used to sleep normally.
  • Antibiotic & prednisolone/methylprednisolone –  in some cases can be used to erase the inflammation in the supervision of a cardiologist.
  • Lipid-lowering agent – (atorvastatin, pitavastatin)can be used in case of controlling blood pressure & removed excess fat from the body.

Other Treatment

  • Heparin infusion is used as an adjunctive agent in patients receiving alteplase but not with streptokinase. Heparin is also indicated in patients undergoing primary angioplasty.
  • Prophylaxis against thromboembolism: if not already receiving heparin by infusion, then patients should be given regular subcutaneous heparin until fully mobile.
  • Insulin-glucose infusion followed by intensive glucose control with subcutaneous insulin for all people with type 1 and type 2 diabetes.
  • The routine use of nitrates, calcium antagonists, magnesium, and the high-dose glucose-insulin-potassium infusion is not currently recommended during the acute phase of treatment of AMI.

Antiplatelet Agents

  • The use of aspirin has been shown to reduce mortality from MI. Aspirin in a dose of 325 mg should be administered immediately on recognition of MI signs and symptoms. The nidus of an occlusive coronary thrombus is the adhesion of a small collection of activated platelets at the site of intimal disruption in an unstable atherosclerotic plaque.
  • Aspirin irreversibly interferes with the function of cyclooxygenase and inhibits the formation of thromboxane A2. Within minutes, aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion. This effect benefits all patients with acute coronary syndromes, including those with amyocardial infarction. Aspirin alone has one of the greatest impacts on the reduction of MI mortality.
  • Its beneficial effect is observed early in therapy and persists for years with continued use. The long-term benefit is sustained, even at doses as low as 75 mg/day.

Statins  – Help lower cholesterol. People who are pregnant or have liver disease should not take statins. They include:

  • Lovastatin (Mevacor)
  • Simvastatin (Zocor)
  • Pravastatin (Pravachol)
  • Atorvastatin (Lipitor)
  • Fluvastatin (Lescol)
  • Rosuvastatin (Crestor)

Niacin (nicotinic acid)  – In prescription form, is sometimes used to lower cholesterol. Dietary supplements of niacin should not be used instead of prescription niacin, as it can cause side effects. Take niacin for high cholesterol only with your doctor’s supervision.

Table 1: Antiplatelet Medications

Treatment Modality Aspirin Clopidogrel
Medical management 75-162 mg/day indefinitely Optional: 75 mg/day × 1 month
Bare Metal stent 162-325 mg/day × 1 month, then 75-162 mg/day indefinitely 300 mg loading dose,* then
75 mg/day × 1 month
Sirolimus-eluting stent
(Cypher)
162-325 mg/day × 3 months, then 75-162 mg/day indefinitely 300 mg loading dose,* then
75 mg/day × 1 year
Paclitaxel-eluting stent
(Taxus)
162-325 mg/day × 6 months, then 75-162 mg/day indefinitely 300 mg loading dose,* then
75 mg/day × 1 year

 * Note: No loading dose in patients older than 75 years.

Supplemental Oxygen

  • Oxygen should be administered to patients with symptoms or signs of pulmonary edema or with pulse oximetry less than 90% saturation. The rationale for using oxygen is the assurance that erythrocytes will be saturated to maximum carrying capacity. Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and by other tissues may be diminished. In some cases, elevated pulmonary capillary pressure and pulmonary edema can decrease oxygen uptake as a result of impaired pulmonary alveolar-capillary diffusion. Supplemental oxygen increases the driving gradient for oxygen uptake.

Nitrates

  • Intravenous nitrates should be administered to patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI. The primary benefit of nitrates is derived from its vasodilator effect. Nitrates are metabolized to nitric oxide in the vascular endothelium. Nitric oxide relaxes vascular smooth muscle and dilates the blood vessel lumen.
  • Vasodilatation reduces cardiac preload and afterload and decreases the myocardial oxygen requirements needed for circulation at a fixed flow rate. Vasodilatation of the coronary arteries improves blood flow through the partially obstructed vessels as well as through collateral vessels. Nitrates can reverse the vasoconstriction associated with thrombosis and coronary occlusion.
  • When administered sublingually or intravenously, nitroglycerin has a rapid onset of action. Clinical trial data have supported the initial use of nitroglycerin for up to 48 hours in MI. There is little evidence that nitroglycerin provides substantive benefit as long-term post-MI therapy, except when severe pump dysfunction or residual ischemia is present. Low BP, headache, and tachyphylaxis limit the use of nitroglycerin. Nitrate tolerance can be overcome by increasing the dose or by providing a daily nitrate-free interval of 8 to 12 hours. Nitrates must be avoided in patients who have taken a phosphodiesterase inhibitor within the previous 24 hours.

Pain Control

  • Pain from MI is often intense and requires prompt and adequate analgesia. The agent of choice is morphine sulfate, given initially IV at 5 to 15 minute intervals at typical doses of 2 to 4 mg. Reduction in myocardial ischemia also serves to reduce pain, so oxygen therapy, nitrates, and beta blockers remain the mainstay of therapy. Because morphine can mask ongoing ischemic symptoms, it should be reserved for patients being sent for coronary angiography. This was downgraded to a IIa recommendation in the latest STEMI guidelines.

Beta Blockers

  • Beta-blocker therapy is recommended within 12 hours of MI symptoms and is continued indefinitely. Treatment with a beta blocker decreases the incidence of ventricular arrhythmias, recurrent ischemia, reinfarction, and, if given early enough, infarct size and short-term mortality. Beta blockade decreases the rate and force of myocardial contraction and decreases overall myocardial oxygen demand. In the setting of reduced oxygen supply in MI, the reduction in oxygen demand provided by beta-blockade can minimize myocardial injury and death (Table 2).

Table 2: Beta-Blocker Therapy

Agent Dosing Original Trial
Metoprolol 15 mg IV × 1 then 200 mg/day PO in divided doses MIAMI
Atenolol 5-10 mg IV × 1, then 100 mg/day PO ISIS-1
Carvedilol 6.25 mg bid titrated to 25 mg BID CAPRICORN

ISIS-1, International Studies of Infarct Survival-1; MIAMI, Metoprolol in Acute Myocardial Infarction.

Beta-blockers is a slows heart rate, thus lowering blood pressure. These drugs include:

  • Acebutolol (Sectral)
  • Atenolol (Tenormin)
  • Bisoprolol (Zebeta)
  • Carteolol (Cartrol)
  • Metoprolol (Toprol XL)
  • Nadolol (Corgard)
  • Propranolol (Inderal)

The use of a beta blocker has a number of recognized adverse effects. The most serious are heart failure, bradycardia, and bronchospasm. During the acute phase of an MI, beta blocker therapy may be initiated intravenously; later, patients can switch to oral therapy for long-term treatment. The COMMIT-CCS 2 trial raised safety concerns about the use of early intravenous beta blockers in high-risk patients. In some patients who are considered high risk due to age or hemodynamic instability, it may be reasonable to hold off on early intravenous therapy.

According to the 2007 guideline updates, anticoagulation should be added to standard medical therapy for most patients after myocardial infarction.

Unfractionated Heparin

  • Unfractionated heparin is beneficial until the inciting thrombotic cause (ruptured plaque) has completely resolved or healed. Unfractionated heparin has been shown to be effective when administered intravenously or subcutaneously according to specific guidelines.
  • The minimum duration of heparin therapy after MI is generally 48 hours, but it may be longer, depending on the individual clinical scenario. Heparin has the added benefit of preventing thrombus through a different mechanism than aspirin (Box 1).

Box 1: Unfractionated Heparin Dosing
Loading Dose
  • 60 U/kg IV bolus
  • Max 5000 U if >65 kg or 4000 U if <65 kg
Maintenance Dose
  • 12 U/kg/hr IV
  • Max 1000 U/hr if >65 kg or 800 U/hr if <65 kg
Titration Goal
  • PTT 50-70 sec

PTT, prothrombin time.

Low-Molecular-Weight Heparin

  • Low-molecular-weight heparin (LMWH) can be administered to MI patients who are not treated with fibrinolytic therapy and who have no contraindications to heparin. The LMWH class of drugs includes several agents that have distinctly different anticoagulant effects. LMWHs are proved to be effective for treating acute coronary syndromes characterized by unstable angina and NSTEMI.Their fixed doses are easy to administer, and laboratory testing to measure their therapeutic effect is usually not necessary (Table 3).

Table 3: Low-Molecular-Weight Heparin

Generic name t1/2
(after SC dosing)
Dosing in ACS FDA Approved Indications
Dalteparin 3-5 hr 120 U/kg SC bid Prevention of ischemic complications in UA and NSTEMI
Enoxaparin 4.5 hr 100 U/kg (1 mg/kg) SC q12h Prophylaxis of ischemic complications of UA and NSTEMI when administered with aspirin

UA, unstable angina; NSTEMI, non−ST segment elevation myocardial infarction.

Warfarin

  • Warfarin is not routinely used after MI, but it does have a role in selected clinical settings. The latest guidelines recommend the use of warfarin for at least 3 months in patients with left ventricular aneurysm or thrombus, a left ventricular ejection fraction less than 30%, or chronic atrial fibrillation.

Fibrinolytics

  • Restoration of coronary blood flow in MI patients can be accomplished pharmacologically with the use of a fibrinolytic agent. Fibrinolytic therapy is indicated for patients who present with a STEMI within 12 hours of symptom onset without a contraindication.
  • Absolute contraindications to fibrinolytic therapy include the history of intracranial hemorrhage, ischemic stroke or closed head injury within the past 3 months, the presence of an intracranial malignancy, signs of an aortic dissection, or active bleeding. Fibrinolytic therapy is primarily used at facilities without access to an experienced interventionalist within 90 minutes of presentation.
  • As a class, the plasminogen activators have been shown to restore normal coronary blood flow in 50% to 60% of STEMI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years.
  • The most critical variable in achieving successful fibrinolysis is the time from symptom onset to drug administration. A fibrinolytic is most effective within the first hour of symptom onset and when the door-to-needle time is 30 minutes or less.

Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers

  • Angiotensin-converting enzyme (ACE) inhibitors should be used in all patients with a STEMI without contraindications. ACE inhibitors are also recommended in patients with NSTEMI who have diabetes, heart failure, hypertension, or an ejection fraction less than 40%.
  • In such patients, an ACE inhibitor should be administered within 24 hours of admission and continued indefinitely. Further evidence has shown that the benefit of ACE inhibitor therapy can likely be extended to all patients with an MI and should be started before discharge. Contraindications to ACE inhibitor use include hypotension and declining renal function.

ACE inhibitors  – is widen blood vessels and make it easier for your heart to pump blood. Side effects can include a chronic cough. ACE inhibitors include:

  • Benazepril (Lotensin)
  • Captopril (Capoten)
  • Fosinopril (Monopril)
  • Lisinopril (Zestril)
  • Enlapril (Vasotec)

The most commonly used ACE inhibitors are summarized in table 4.

Table 4: ACE Inhibitors

Agent Dosing (PO) Original Trial
Captopril 6.25 mg tid titrated to 50 mg tid SAVE: 3-16 days post-MI in asymptomatic patients with EF <40%
Ramipril 1.25 mg bid titrated to 5 mg bid AIRE: 3-10 days post-MI with symptoms of heart failure
Captopril 6.25 mg bid titrated to 50 mg bid ISIS-4: started within 24 hr of MI
Lisinopril 5 mg/day titrated to 10 mg/day GISSI-3: started within 24 hr of MI

AIRE, Acute Infarction Ramipril Efficacy; EF, ejection fraction; GISSI-3, Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico; ISIS-4, International Studies of Infarct Survival-1; MI, myocardial infarction; SAVE, Survival and Ventricular Enlargement.

Bile acid sequestrants. Lowers cholesterol; people who have high levels of triglycerides (fats in the blood) should not take bile acid sequestrants. These drugs include:

  • Cholestyramine (Questran)
  • Colestipol (Colestid)
  • Colesevelam (Welchol)

Fabric acid derivatives. Lower triglycerides and moderately lower LDL cholesterol. They include Gemfibrozil (Lopid).

Anticoagulants (blood thinners). Help keep clots from forming. Your doctor may prescribe aspirin, warfarin (Coumadin), or Clopidogrel (Plavix).

  • ACE inhibitors decrease myocardial afterload through vasodilatation. One effective strategy for instituting an ACE inhibitor is to start with a low-dose, short-acting agent and titrate the dose upward toward a stable target maintenance dose at 24 to 48 hours after symptom onset. Once a stable maintenance dose has been achieved, the short-acting agent can be continued or converted to an equivalent-dose long-acting agent to simplify dosing and encourage patient compliance. For patients intolerant of ACE inhibitors, angiotensin receptor blocker (ARB) therapy may be considered.

Glycoprotein IIb/IIIa Antagonists

  • Glycoprotein IIb/IIIa receptors on platelets bind to fibrinogen in the final common pathway of platelet aggregation. Antagonists to glycoprotein IIb/IIIa receptors are potent inhibitors of platelet aggregation.
  • The use of glycoprotein IIb/IIIa inhibitors during the percutaneous coronary intervention (PCI) and in patients with MI and acute coronary syndromes has been shown to reduce the composite endpoint of death, reinfarction, and the need to revascularize the target lesion at follow-up.
  • The current guidelines recommend the use of a IIb/IIIa inhibitor for patients in whom PCI is planned. For high-risk patients with NSTEMI who do not undergo PCI, a IIb/IIIa inhibitor may be used for 48 to 72 hours (Table 5).

Table 5: Glycoprotein IIb/IIIa Inhibitors

Agent Loading Dose (IV) Maintenance Dose (IV) Duration of Infusion FDA Approved Indications
Abciximab 0.25 mg/kg 0.125 µg/kg/min
max 10 µg/min
12-24 hr Coronary intervention
Eptifibatide 180 µg/kg 2 µg/kg/min Up to 72 hr Acute coronary syndrome
Coronary intervention
Tirofiban 0.4 µg/kg/min for 30 min 0.1 µg/kg/min 12-24 hr Acute coronary syndrome
Coronary intervention

  • The evidence is less well established for the direct thrombin inhibitor, bivalirudin. The 2007 American College of Cardiology (ACC) and the American Heart Association (AHA) guidelines recommend bivalirudin as an alternative to heparin therapy for patients who cannot receive heparin for a variety of reasons (e.g., heparin-induced thrombocytopenia).

Statin Therapy

  • A statin should be started in all patients with myocardial infarction without known intolerance or adverse reaction prior to hospital discharge. Preferably, a statin would be started as soon as a patient is stabilized after the presentation.
  • The Pravastatin or Atorvastatin Evaluation and Infection—Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) trial suggested a benefit of starting patients on high-dose therapy from the start (e.g., atorvastatin 80 mg/day).

Aldosterone Antagonists

  • In the Epleronone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) trial, a mortality benefit was seen with eplerenone administration in all post-MI patients, provided multiple criteria were met.
  • The criteria included concomitant use of an ACE inhibitor, ejection fraction less than 40%, symptomatic heart failure or diabetes, a creatinine clearance greater than 30 mL/min, and a potassium level less than 5 mEq/dL. In patients that meet these criteria, the use of eplerenone has a Class I indication.

Surgical Treatments

  • Percutaneous coronary intervention (PCI). In primary PCI, the doctor performs a coronary angiogram (injecting dye into the arteries) to see where the artery is blocked. The doctor then performs balloon angioplasty (widening an artery with a balloon), often with stent placement, to keep the artery open.

Primary PCI

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  • PCI (or percutaneous transluminal coronary angioplasty – PTCA) is regarded as superior to fibrinolysis in the management of AMI and is becoming increasingly available for initial patient care.
  • Primary angioplasty provides an early assessment of the extent of the underlying disease.
  • Any delay in primary PCI after a patient arrives at hospital is associated with higher mortality in hospital. Time to treatment should therefore be as short as possible. Door (or diagnosis) to treatment time should be less than 90 minutes, or less than 60 minutes if the hospital is PCI ready and symptoms started within 120 minutes.
  • There is general agreement that PCI should be considered if there is an ST-elevation ACS, if symptoms started up to 12 hours previously. There is no consensus whether PCI is also beneficial in patients presenting more than 12 hours from the onset of symptoms in the absence of clinical and/or ECG evidence of ongoing ischaemia.
  • Patients should receive a glycoprotein IIb/IIIa inhibitor to reduce the risk of immediate vascular occlusion and should also receive either unfractionated heparin, a low molecular weight heparin (eg, enoxaparin), or bivalirudin.
  • Prasugrel in combination with aspirin is recommended as an option for preventing atherothrombotic events in adults with unstable angina, non-ST-elevation myocardial infarction (NSTEMI) or ST-elevation myocardial infarction (STEMI) having primary or delayed PCI.
  • Balloon angioplasty following myocardial infarction reduces death, non-fatal myocardial infarction, and stroke compared with thrombolytic reperfusion. However, up to 50% of patients experience re-stenosis and 3-5% recurrent myocardial infarction.
  • There is no evidence to suggest that primary stenting reduces mortality when compared with balloon angioplasty but stenting seems to be associated with a reduced risk of re-infarction and target vessel revascularisation.
  • NICE, therefore, recommends that intracoronary stent implantation should be used in patients undergoing primary PCI.

Facilitated PCI

  • Facilitated PCI is the use of pharmacological reperfusion treatment delivered prior to a planned PCI.
  • There is no evidence of a significant clinical benefit and so facilitated PCI is currently not recommended.

Rescue PCI

  • Rescue PCI is defined as PCI performed on a coronary artery which remains occluded despite fibrinolytic therapy.
  • Rescue PCI is associated with a significant reduction in heart failure and re-infarction and a lower all-cause mortality and so should be considered when there is evidence of failed fibrinolysis based on clinical signs and insufficient ST-segment resolution, if there is clinical or ECG evidence of a large infarct and if the procedure can be performed less than 12 hours after the onset of symptoms.

Fibrinolytic drugs

For patients who cannot be offered PCI within 90 minutes of diagnosis, a thrombolytic drug should be administered along with either unfractionated heparin (for maximum two days), a low molecular weight heparin (eg, enoxaparin) or fondaparinux. Thrombolytic drugs break down the thrombus so that the blood flow to the heart muscle can be restored to prevent further damage and assist healing.

Reperfusion by thrombolysis is often gradual and incomplete and may be inadequate. There is a risk of early or late reocclusion and a 1-2% risk of intracranial hemorrhage.

  • Fibrinolytic drugs act as thrombolytics by activating plasminogen to form plasmin, which degrades fibrin and so breaks up the thrombi.
  • Streptokinase and alteplase have been shown to reduce mortality. Reteplase and tenecteplase are also licensed for AMI.
  • Streptokinase and alteplase are given by intravenous infusion. Reteplase and tenecteplase can be given by rapid bolus injection.
  • The benefit is greatest in those with ECG changes that include ST-segment elevation (especially in those with anterior infarction) and in patients with bundle branch block.
  • The earlier the treatment is given, the greater the absolute benefit. Alteplase, reteplase, and streptokinase need to be given within 12 hours of symptom onset, ideally within one hour. Tenecteplase should be given as early as possible and usually within six hours of symptom onset.
  • Bleeding complications are the main risks associated with thrombolysis. Contra-indications for thrombolysis include patients with bleeding disorders, or a history of recent haemorrhage, trauma, surgery or acute cerebrovascular event.
  • Persistence of antibodies to streptokinase can reduce the effectiveness of subsequent treatment and so streptokinase should not be used again after the first administration.

Antithrombotic therapy without reperfusion therapy

  • In patients presenting within 12 hours after the onset of symptoms but reperfusion therapy is not given, or in patients presenting after 12 hours, aspirin, clopidogrel and an antithrombin agent (heparin, enoxaparin or fondaparinux) should be given as soon as possible.
  • For patients who do not receive reperfusion therapy, angiography before hospital discharge is recommended (as for patients after successful fibrinolysis) if no contraindications are present.

Coronary bypass surgery

Only a few patients need a coronary artery bypass graft (CABG) in the acute phase but CABG may be indicated:

  • After failed PCI, coronary occlusion not amenable for PCI, or the presence of refractory symptoms after PCI.
  • Cardiogenic shock, or mechanical complications – eg, ventricular rupture, acute mitral regurgitation, or ventricular septal defect.
  • Multivessel disease.
  • In patients with a non-emergency indication for CABG (eg, multisystem disease), it is recommended to treat the infarct-related lesion by PCI and to perform CABG later in more stable conditions if possible.

Coronary artery bypass graft (CABG)

  • This surgery bypasses the blocked arteries by using a graft of another blood vessel (usually from your arm or leg) to restore blood flow to the heart.

Nutrition and Dietary Supplements

  • Healthy eating habits can help reduce high cholesterol, high blood pressure, and excess weight, three of the major risk factors for heart disease. The American Heart Association (AHA) has developed dietary guidelines that help lower fat and cholesterol intake and reduce the risk of heart disease and heart attack. The AHA does not recommend very low fat diets, because new research shows that “good” fats, such as those found in olive oil and avocadoes, are good for your heart.
  • Fad diets are popular, but they may not help you lose weight and keep it off. In some cases, they may not even be healthy. Any healthy diet will include a variety of foods. If a diet bans an entire food group (such as carbohydrates), it is probably not healthy.

The AHA recommends the following for healthy eating:

  • Grains: 6 to 8 servings per day (half of those servings should be whole grains)
  • Vegetables: 3 to 5 servings per day
  • Fruits: 4 to 5 servings per day
  • Fat-free or low-fat dairy: 2 to 3 servings per day
  • Lean meat, poultry, and seafood: 3 to 6 oz. per day (about the size of a deck of cards)
  • Fats and oils: 2 to 3 tbsp. per day (use unsaturated fats such as olive oil or canola oil)
  • Nuts, seeds, legumes: 3 to 5 servings per week
  • Sweets, sugars: 5 or fewer servings per week (the fewer, the better)

In addition, the AHA also recommends eating 2 servings of fatty fish (such as salmon or lake trout) per week; holding sodium (salt, including salt already added to food) to 2,400 mg per day or less; and limiting alcohol intake to one drink a day for women and two for men.

Diets for People with High Blood Pressure

  • People with high blood pressure especially need to lower the amount of sodium in their diet. The DASH diet (Dietary Approaches to Stop Hypertension) emphasizes a diet rich in fruits, vegetables, and low-fat or nonfat dairy products that provide high intake of potassium, magnesium, and calcium sources.
  • Sodium intake should be between 1,500 to 2,400 mg per day (the lower, the better). Weight loss, regular exercise, and limiting alcohol are also very important factors for lowering blood pressure.

Mediterranean Diet

  • The Mediterranean Style Diet concentrates on whole grains, fresh fruits and vegetables, fish, olive oil, and moderate wine consumption. The Mediterranean Style Diet is not low fat; it is low in saturated fat, but high in monounsaturated fat.
  • It appears to be heart healthy – In a long-term study of 423 people who had a heart attack, those who followed a Mediterranean Style Diet had a 50 to 70% lower risk of recurrent heart disease compared with people who received no special dietary counseling.

Vitamins and Supplements

  • Some supplements –  may help lower your risk factors for heart attacks, such as high blood pressure or high cholesterol. Most do not work as well as prescription medications. But some can be used along with prescription medications in your treatment. If you have had a heart attack, or are at high risk of having one, ask your doctor before taking any supplements. Your physician should manage your heart disease, and you should not take supplements without your physician’s approval. Many supplements can have negative interactions with medications used to treat heart disease.
  • B vitamins – Folic acid, vitamin B6, and vitamin B12 help the body break down homocysteine, an amino acid that has been linked to increased risk of heart disease and stroke. Researchers believe that homocysteine may also contribute to atherosclerosis by damaging artery walls, making it easier for blood clots to form, but so far they haven’t found a definite link. Researchers also do not yet know whether taking B vitamins reduces the risk of atherosclerosis or heart attack, nor do they know how much might have an effect. Talk to your doctor about checking your homocysteine levels and whether you should take a B complex vitamin supplement. In the meantime, be sure to get enough B vitamins through your diet by eating fruits and leafy green vegetables every day.
  • Vitamin D – Studies show that lower levels of vitamin D are associated with higher risk of myocardial infarction and premature death. Dose recommendations for vitamin D vary greatly between physicians. Your physician may do blood work to monitor your vitamin D levels and determine the appropriate dose for your needs.
  • Omega-3 fatty acids – There is good evidence that omega-3 fatty acids (known as EPA and DHA) found in fish oil can help treat atherosclerosis by preventing the development of plaque and blood clots. Omega-3s can also help prevent heart disease, lower blood pressure, and reduce the level of triglycerides (fats) in the blood. The AHA recommends that people eat at least 2 servings of fatty fish (such as salmon) per week. For people who have had a heart attack, several studies show that eating fish or taking fish oil reduces the risk of both fatal and nonfatal heart attacks, as well as lowers your risk of death from any cause. Because fish oil at high doses can increase the risk of bleeding, talk to your doctor before taking a high dose (more than 1 g per day), especially if you already take blood-thinning medication.
  • Beta-sitosterol – A plant sterol, a chemical found in plants that can stop cholesterol from being absorbed by the intestines. A number of well-designed scientific studies have shown that beta-sitosterol does lower LDL (bad) cholesterol levels in the body. Beta-sitosterol may lower the amount of vitamin E and beta-carotene absorbed by the body, so you may want to ask your doctor if you need to take extra E or carotene.
  • Policosanol – A mix of waxy alcohols usually derived from sugar cane and yams. Several studies have indicated it may lower LDL (bad) cholesterol and possibly even raise HDL (good) cholesterol. One study found that policosanol was equivalent to fluvastatin (Lescol) and simvastatin (Zocor) in lowering cholesterol levels. It may also help stop blood clots from forming. However, almost all the studies have been conducted in Cuba by a research group that uses a proprietary form of policosanol and is funded by the manufacturer. So it is hard to evaluate the evidence. Policosanol may increase the risk of bleeding, and it should not be taken by people who also take blood-thinning medications.
  • Coenzyme Q10 (CoQ10) – Researchers believe that CoQ10 may help stop blood clots from forming and boost levels of antioxidants. One study found that people who received daily CoQ10 supplements within 3 days of a heart attack were much less likely to experience another heart attack and chest pain. They were also less likely to die from heart disease than those who did not receive the supplements. Statins, drugs that lower cholesterol, can actually interfere with the body’s natural ability to make CoQ10, so your doctor may recommend taking a CoQ10 supplement. Still, more research is needed to say whether CoQ10 has any role in preventing or treating atherosclerosis. CoQ10 may interact with blood-thinning medications, such as warfarin (Coumadin), and others since CoQ10 helps blood clot it may make these medications less effective.
  • Psyllium – This fiber helps lower cholesterol levels and blood sugar levels. If you take medicine for diabetes or have digestive problems, talk to your health care provider before taking psyllium. Always take your medications at least a few hours away fro when you take psyllium.
  • L-carnitine – Studies suggest that people who take L-carnitine (an amino acid) soon after a heart attack may be less likely to have a subsequent heart attack, die of heart disease, experience chest pain and abnormal heart rhythms, or develop heart failure. (Heart failure occurs when the heart can’t pump blood properly and blood backs up into the lungs and legs.) Studies also suggest that people with heart disease who take carnitine may be better able to exercise. Most studies used a special form of carnitine called propionyl-L-carnitine. L-carnitine can interact with certain medications, including thyroid and blood-thinning medications such as warfarin (Coumadin). Talk to your provider about whether L-carnitine is right for you.

Herbal Remedies

Herbs should not be used in place of emergency medical attention for a heart attack, nor should they be used by themselves to lower your risk of heart attack after you have had one. However, certain herbs can be used along with prescription medications in your treatment, although many can interact with a variety of medications. The herbs below have the potential to interact with several different medications. It is critical that you consult your physician before adding any herbs to your regimen. If you have had a heart attack, or are at high risk of having one, ask your doctor before taking any herbs.

  • Hawthorn (Cras monogynataegu) – Hawthorn contains the polyphenols rutin and quercetin, and was used traditionally to treat cardiovascular diseases. Animal and laboratory studies show that hawthorn has antioxidant properties that help protect against the formation of plaques and may help lower high cholesterol and high blood pressure. Talk to your doctor before taking hawthorn, as it can interact with other drugs taken for heart disease and high blood pressure.
  • Garlic (Allium sativum) – Studies show that fresh garlic and garlic supplements may lower cholesterol levels, prevent blood clots, and destroy plaque. However, other studies show mixed evidence. In one study, people who had a previous heart attack and then took a garlic oil extract for 3 years had fewer second heart attacks and a 50% reduction in death rate than those who did not take garlic. Garlic can increase the risk of bleeding. Garlic can interact with a number of medications, including some of those used to treat HIV/AIDS. You should not take garlic if you are also taking blood-thinning medication.
  • Bilberry (Vaccinium myrtillus) – and other flavonoids. A close relative of the cranberry, bilberry fruits contain flavonoid compounds called anthocyanidins. Flavonoids are plant pigments that have antioxidant properties. Researchers think they may help prevent several illnesses, including heart disease and diabetes. Bilberry has been used traditionally to treat heart disease. But only animal and test tube studies have been done. Animal studies have found that anthocyanidins and other flavonoids may strengthen blood vessels, improve circulation, and prevent LDL (bad) cholesterol from being damaged (which may cause blood clots to form in arteries). Bilberry may have a blood-thinning effect and therefore can increase the risk of bleeding in people taking blood-thinning medications such as warfarin (Coumadin) and others. Talk to your health care provider.
  • Green tea (Camellia sinensis) – Population studies suggest that regularly drinking green tea may reduce the risk of heart attack from atherosclerosis. It also may help you lower lose weight and your cholesterol levels. More research is needed to know for sure. Avoid caffeinated varieties.
  • Kudzu (Pueraria lobata) – Kudzu has been used traditionally to treat heart disease, including heart attack and congestive heart failure. A few studies suggest it may help relieve angina, but the studies were of poor quality. More research is needed to know whether kudzu has any benefit for heart disease. Kudzu might slow blood clotting, so people with bleeding disorders or who take blood-thinning medications, such as warfarin (Coumadin), should use caution. Talk to your doctor.

Homeopathy

  • Homeopathy should not be used instead of immediate medical attention for a heart attack. However, homeopathy may be used to help reduce the risk of heart disease. Although few studies have examined the effectiveness of specific homeopathic remedies, professional homeopaths would recommend appropriate therapy to lower high blood pressure and cholesterol.
  • Before prescribing a remedy, homeopaths take into account your constitutional type. In homeopathic terms, a person’s constitution is their physical, emotional, and intellectual makeup. An experienced homeopath assesses all of these factors when determining the most appropriate remedy for you as an individual.

Acupuncture

  • Acupuncture may be helpful in reducing some risk factors for heart disease. Some studies show that it can help people who want to stop smoking, and it may help some people lose weight and lower their blood pressure.

Massage and Physical Therapy

  • Although few studies have examined the effectiveness of massage therapy for heart disease, massage has a relaxing effect and can reduce stress-related hormone levels. Lowering stress hormone levels can lower cholesterol and blood pressure, reducing your risk of heart disease.
  • In addition, relaxation techniques may help you make lifestyle changes such as eating healthy, quitting smoking and exercising. At least one study found that massage can lower blood pressure.

Prevention

Risk factors for heart attack include cigarette smoking, high blood pressure, high blood cholesterol levels, diabetes, excess weight, lack of physical exercise, and a family history of heart disease. Hence, the following lifestyle changes can help to prevent a heart attack occurring as well as recovery from a heart attack:

  • stop smoking and avoid second-hand smoke
  • control high blood pressure or high blood cholesterol levels
  • get regular medical check-ups and take medication as prescribed
  • exercise regularly, especially healthy heart exercise
  • maintain a healthy weight
  • eat a healthy heart diet
  • manage diabetes
  • avoid drinking alcohol or do so in moderation.

Additionally, ‘blood-thinning’ medications, beta blockers, ACE inhibitors, and cholesterol-lowering drugs may be prescribed long-term to reduce the risk of a future heart attack.

Other statistics from the American Heart Association:

  • Over 500,000 American women die of cardiovascular disease each year. This twice the number of deaths from all cancers combined (lung cancer, the leading cause of cancer deaths, claims approximately 65,000 deaths per year, and breast cancer kills around 40,000 women per year).
  • One in three women have some form of cardiovascular disease.
  • 38% of women who have heart attacks die within the first year compared to 25% of men.
  • 35% of women have a second heart attack within six years of the first attack compared to 18% of men.
  • Over 60,000 women die of stroke each year; approximately 60% of stroke deaths occur in women.

Reference

Magnesium Deficiency

ByRx Harun

Muscle Cramp – Causes, Symptoms, Diagnosis, Treatment

A muscle cramp is a sudden and involuntary contraction of one or more of your muscles. If you’ve ever been awakened in the night or stopped in your tracks by a sudden charley horse, you know that muscle cramps can cause severe pain.

Muscle cramps are a common problem characterized by a sudden, painful, involuntary contraction of the muscle. These true cramps, which originate from peripheral nerves, may be distinguished from other muscle pain or spasm. Medical history, physical examination, and a limited laboratory screen help to determine the various causes of muscle cramps. Despite the “benign” nature of cramps, many patients find the symptom very uncomfortable. Treatment options are guided both by experience and by a limited number of therapeutic trials. Quinine sulfate is an effective medication, but the side-effect profile is worrisome, and other membrane-stabilizing drugs are probably just as effective. Patients will benefit from further studies to better define the pathophysiology of muscle cramps and to find more effective medications with fewer side-effects.

A muscle  cramp is a sudden, involuntary muscle contraction or over-shortening; while generally temporary and non-damaging, they can cause mild-to-excruciating pain, and a paralysis-like immobility of the affected muscle(s). Onset is usually sudden, and it resolves on its own over a period of several seconds, minutes, or hours. Cramps may occur in a skeletal muscle or smooth muscle. Skeletal muscle cramps may be caused by muscle fatigue or a lack of electrolytes (e.g., low sodium, low potassium, or low magnesium, although the evidence has been mixed). Cramps of smooth muscle may be due to menstruation or gastroenteritis.

Types of Muscle Cramps

 Praphysiologic muscle cramps

Paraphysiologic muscle cramps are commonly experienced, but they have no underlying medical condition. This includes cramps associated with:

  • Pregnancy – Up to 30% of pregnant women will experience leg cramps during their pregnancy, most frequently during the last trimester;
  • Exercise – The cause of exercise-associated muscle cramps (EAMC) is still largely unknown. It is believed to be highly related to physiological stress such as

Most people at some time of their life will experience an idiopathic muscle cramp. These cramps usually occur at night in the leg and foot muscles and can be triggered by even the slightest shortening of skeletal muscle.

Idiopathic muscle cramps can be classified into the following

  • Nocturnal cramps – Cramps that occur at night when in bed;
  • Autosomal dominant cramping disease – An inherited disease involving recurrent muscle cramping;
  • Continuous muscle fiber activity syndromes – Including Isaac’s syndrome, Stiff-man syndrome and cramp fasciculation syndrome (the uncontrollable twitching of muscles beneath the skin);
  • Sathoyoshi’s syndrome – Syndrome of progressive muscle spasm which includes diarrhea and alopecia;
  • Myokymia – Spontaneous muscle quivering;
  • Myokymia-hyperhidrosis syndrome – Myokymia paired with excessive perspiration;
  • Familial insulin resistance with acanthocytosis (spiky red blood cells) and acral hypertrophy – A rare syndrome characterized by enlarged hands and feet, velvety skin and muscle cramps;
  • Cancer-induced cramps 
  • Natural muscle atrophy – (muscle wasting): that occurs in people over 65 predisposes them to muscle cramps. 

Symptomatic muscle cramps

Symptomatic muscle cramps constitute the majority of muscle cramps and are related to underlying disease in a number of different body systems.

Central and peripheral nervous system

  • Motor neuron disease including amyotrophic lateral scoliosis;
  • Parkinson’s disease;
  • Multiple sclerosis (MS);
  • Tetanus (lockjaw);
  • Radiculopathy; and
  • Peripheral neuropathies.

Muscular system

  • Some myopathies (diseases that affect skeletal muscles); and
  • Myotonia (temporary muscle stiffness or contraction).

Cardiovascular system

  • Venous disease (disease of the veins);
  • Peripheral arterial disease (arteriosclerosis); and
  • Hypertension (high blood pressure).

Diseases of the endocrine-metabolic system

  • Hypothyroidism (under-activity of the thyroid gland) and hyperthyroidism (over-activity of the thyroid gland);
  • Hyperparathyroidism (disease of the parathyroid gland); and
  • Deficiency of corticotropin (a hormone secreted by the pituitary gland).

Muscle cramps are also associated with

  • Liver cirrhosis and other liver dysfunction;
  • Bartter syndrome (disorder defect in the loop of Henle of the kidney);
  • Gitelman’s syndrome (an inherited defect in the distal convoluted tubule of the kidney);
  • Conn’s syndrome (disease of the adrenal gland);
  • Addison’s disease (disease of the adrenal gland);
  • Uraemia (illness that accompanies kidney failure) and dialysis;
  • Heat cramps (cramps due to dehydration and electrolyte depletion);
  • Toxic .

Risk factors for muscle cramp

The exact cause of muscle cramp is not known, but risk factors may include:

  • Tight, inflexible muscles
  • Poor physical condition
  • Poor muscle tone
  • Inadequate diet
  • Physical overexertion
  • The physical exertion of cold muscles
  • Muscle injury
  • Muscle fatigue
  • Excessive perspiration
  • Dehydration – caused by, for example, about of gastroenteritis
  • Reduced blood supply (ischemia)
  • Wearing high-heeled shoes for lengthy periods.

Causes  of Muscle Cramps

The cause of muscle cramps isn’t always known. Muscle cramps may be brought on by many conditions or activities, such as:

  • Exercising – injury, or overuse of muscles.
  • Pregnancy – Cramps may occur because of decreased amounts of minerals, such as calcium and magnesium, especially in the later months of pregnancy.
  • Exposure to cold temperatures – especially to cold water.
  • Other medical conditions – such as blood flow problems (peripheral arterial disease), kidney disease, thyroid disease, and multiple sclerosis.
  • Standing on a hard surface for a long time – sitting for a long time, or putting your legs in awkward positions while you sleep.
  • Not having enough potassium – calcium, and other minerals in your blood.
  • Being dehydrated – which means that your body has lost too much fluid.
  • Taking certain medicines – such as antipsychotics, birth control pills, diuretics, statins, and steroids.
  • Straining or overusing a muscle – This is the most common cause.
  • Compression of your nerves – from problems such as a spinal cord injury or a pinched nerve in the neck or back
  • Dehydration
  • Low levels of electrolytes such as magnesium, potassium, or calcium
  • Not enough blood getting to your muscles
  • Pregnancy
  • Certain medicines
  • Getting dialysis

Possible Causes of Muscle Cramps

Muscle cramps can have many possible causes. They include

  • Poor blood circulation in the legs
  • Overexertion of the calf muscles while exercising
  • Insufficient stretching before exercise
  • Exercising in the heat
  • Muscle fatigue
  • Dehydration
  • Magnesium and/or potassium deficiency
  • Calcium deficiency in pregnant women
  • Malfunctioning nerves, which could be caused by a problem such as a spinal cord injury or pinched nerve in the neck or back
  • Calcium deficiency (in expectant mothers)
  • Dehydration
  • Inadequate/insufficient stretching before starting your workout
  • Malfunctioning nerves as a result of such problems as pinched nerves in the back or the neck, or spinal cord injury
  • Muscle fatigue

Drugs causing cramps

Always exclude a medicine-related cause. Implicated drugs include

  • Salbutamol and terbutaline
  • Raloxifene
  • Opiate withdrawal
  • Diuretics cause electrolyte loss
  • Nifedipine
  • Phenothiazines
  • Penicillamine
  • Nicotinic acid
  • Statin

Medications that can cause muscle cramps include

  • Lasix (furosemide), Microzide (hydrochlorothiazide), and other diuretics (“water pills”) used to remove fluid from the body
  • Aricept (donepezil), used to treat Alzheimer’s disease
  • Prostigmine (neostigmine), used for myasthenia gravis
  • Procardia (nifedipine), a treatment for angina and high blood pressure
  • Evista (raloxifene), an osteoporosis treatment
  • Brethine (terbutaline), Proventil and Ventolin (albuterol), asthma medications
  • Tasmar (tolcapone), a medication used to treat Parkinson’s disease
  • Statin medications for cholesterol such as Crestor (rosuvastatin), Lescol (fluvastatin), Lipitor (atorvastatin), Mevacor (lovastatin), Pravachol (pravastatin), or Zocor (simvastatin)

Cramps may also occur in association with metabolic disturbance, including:

  • Hyponatremia
  • Hypokalemia and hyperkalemia
  • Hypocalcemia
  • Hypomagnesaemia
  • Hypoglycemia

One or more of these may be the underlying etiology in many of the causes listed below. Blood tests measure the extracellular environment but do not reflect the intracellular fluid which is probably more important.

  • Arterial insufficiency.
  • Acute or chronic diarrhea.
  • Excessive heat and sweating causing Na+ depletion.
  • Hypothyroidism (associated with weakness, enlarged muscles, and painful muscle spasms).
  • Hyperthyroidism (associated with myopathy).
  • Lead poisoning.
  • Sarcoidosis.
  • Hyperparathyroidism (hypercalcemia).
  • Heavy alcohol ingestion and cirrhosis.
  • Hyperventilation-induced respiratory alkalosis.
  • Haemodialysis.
  • Parenteral nutrition.
  • Lower motor neuron disorders including amyotrophic lateral sclerosis, polyneuropathies, recovered poliomyelitis, peripheral nerve injury, and nerve root compression.

Many patients who complain of “cramps” actually have some other related phenomenon. What characteristics, then, can be helpful in making the correct diagnosis?

  • Quality – It is useful to find out about onset (abrupt or slow?), sensation (painful? stiff?), and appearance (if an abnormal posture is described, have the patient demonstrate it). With true cramps, the onset is sudden, the muscle feels taut and painful, and usually, it is visibly and palpably knotted (although this may not be readily apparent if only part of the muscle is involved).
  • Location – Determine if muscles are involved singly or in groups if certain muscles are consistently involved, and if the cramps remain limited or spread. While ordinary cramps often affect the leg (especially calf) muscles, other locations may point to a specific syndrome such as carpopedal spasms in tetany or unilateral facial involvement in hemifacial spasms.
  • Duration  Ordinary cramps last from seconds to several minutes if severe. Fleeting twitches or prolonged contractions suggest another type of disorder.
  • Precipitating or relieving maneuvers –  Attempt to uncover any relation to exercise; specifically, find out not only if the occurrence is at rest or during or after exercise but also the duration and intensity of exercise that may initiate cramps. Moreover, clarify if the cramps appear only sporadically or can be predictably expected at a certain level of exertion. One may also want to ask about other potential triggers such as movement, sensory or emotional stimuli, hyperventilation, cold, or fasting. Assess if anything alleviates the cramps.
  • The course of symptoms  A relatively recent onset suggests the possibility of acquired intercurrent illness, whereas affliction since youth may point to an inherited disorder.

Includes

  • Restless legs (Ekbom’s syndrome).
  • Intermittent claudication and ischaemic rest pain.
  • Muscle injury or strain.
  • Hypnagogic muscle jerking (when falling asleep).
  • Lumbar nerve root entrapment.
  • Ruptured Baker’s cyst.
  • Deep vein thrombosis or thrombophlebitis.
  • Peripheral neuropathy.
  • Occupational cramps – eg, writer’s cramp or musician’s cramp (focal dystonias, usually affecting the upper limb).
  • Causes of generalised muscle pain – eg, polymyositis, toxoplasmosis, alcohol-related myopathy, Guillain-Barré syndrome, polymyalgia rheumatic, Parkinsonism, fibromyalgia.

Potential investigations include

  • U&Es
  • LFTs
  • TFTs
  • Serum calcium or magnesium
  • Creatine kinase
  • Lead levels

Limited evidence supports treating nocturnal leg cramps with exercise and stretching, or with medications such as magnesium, calcium-channel blockers, vitamin B or vitamin C. Quinine is no longer recommended to treat leg cramps.

General

  • In most cases the aetiology is benign and the patient needs to be reassured of this whilst steps are taken to help alleviate the problem. Exclude known causes of muscle cramps without excessive and unnecessary investigation.
  • Management depends upon the cause of the problem. Review drugs. Address any correctable problems – eg, use of diuretics and electrolyte imbalance.
  • The severity of symptoms and their impact on sleep, mood and quality of life will determine whether treatment is required. Asking patients to keep a sleep and cramp diary may be helpful to assess progress.
  • The evidence base for management of this common but usually benign condition is not strong.

Drug for Muscle Cramp

Types of prescription medications include:

  • Analgesics – Prescription-strength drugs that relieve pain but not inflammation.
  • Anti-depressants – Drugs that block pain messages from your brain and boost the effects of endorphins (your body’s natural painkillers).
  • Corticosteroids – Also known as oral steroids, these medications reduce inflammation.
  • Muscle Relaxants – These medications provide relief from spinal muscle spasms.
  • Neuropathic Agents – Drugs that address neuropathic—or nerve-related—pain. This includes burning, numbness, and tingling.
  • NSAIDs – Prescription-strength drugs that reduce both pain and inflammation.
  • Opoid  – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
  • Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.

Non-drug

There is only limited evidence for the use of non-drug therapies for the treatment of lower-limb muscle cramps.

  • Passive stretching and massage of the affected muscle. This will help ease the pain of an acute attack – eg, for calf cramping, straighten the leg with dorsiflexion of the ankle or heel walk until the acute pain resolves.
  • Regular stretching of the calf muscles throughout the day. This may help to prevent acute attacks. Some people recommend stretching three times daily whilst others advocate stretching before going to bed.
  • Using a pillow to raise the feet through the night or raising the foot of the bed. This may help to prevent attacks in some people.
  • Note that whilst stretching exercises are unlikely to do harm, evidence for their efficacy is contradictory. In sport, stretching is widely advocated as likely to reduce injury and cramp but the quality of evidence tends to be poor, with failure to distinguish benefit from that due to improvement in physical fitness from training.
  • Avoiding over-training and risky conditions (eg, hot and humid environmental conditions) can be useful in preventing cramps

Quinine

  • some preliminary studies have found that a number of people benefit from taking quinine. There is no information yet about quinine’s safety and long-term effectiveness. Some doctors may recommend quinine if the stretching has not helped, attacks are frequent, and/or the patient’s quality of life is being undermined by the leg cramps. A course of treatment usually lasts from four to six weeks – the patient takes the medication just before going to bed.
  • Pregnant women should not take quinine. Individuals who had a previous reaction to quinine, those with previous hemolytic anemia, optic neuritis, and/or glucose 6-phosphate dehydrogenase deficiency should not take quinine.
  • As the quinine dosage is very low, side effects are rare. In rare cases the patient may develop a blood disorder. Some patients may develop cinchonism after long-term quinine therapy, which may cause vomiting, nausea, vision and/or hearing problems and dizziness.

How do I Avoid Muscle Cramp

In looking at the above risk factors, you can reduce your risk of cramping by trying the following tips:

  • Maintain your fitness.
  • Stretch regularly. 5 minutes of gentle stretching on the floor during a TV ad break each evening can be sufficient to drastically improve flexibility. Hold each stretch so that you are straining but not feeling pain, and release after 30 seconds.
  • Ensure you are getting the right minerals to maintain proper muscle function. Eating a varied diet is the best way to get a range of minerals. Cacao is a rich natural source of magnesium.
  • Try a supplement. Getting your RDI of some minerals is tough to do from food alone (adult women, for example, need 1300mg of calcium each day. That’s more than 4 glasses of milk). If you think you are struggling to get enough nutrients into your diet to stop cramping, you may benefit from taking a multivitamin that contains magnesium and nutrients to aid muscle relaxation or:
  •  Incorporate a Magnesium powder sourced from wholefoods (more readily absorbed by the body than tablets) OR Cacao Powder (cacao is rich in magnesium and potassium). It is possible to have too much magnesium, yet the side effects at the upper limit of recommended daily magnesium intake have not been shown to produce toxic effects when ingested as naturally occurring magnesium in food (according to nrv.gov.au) as contrasted against magnesium tablets.
  • Try a Calcium Supplement or Chia Seeds (chia seeds are incredibly rich in calcium, critical for muscles).
  • Ensure you are drinking enough fluids throughout the day, especially before, during and after periods of physical exertion. Drink a glass of water first thing when you wake up in the morning to top up any fluids lost during sleep.
  • Know your exercise boundaries. In hot/humid conditions, take it easy to avoid excessive perspiration.
  • If muscle cramps persist despite trying the above, see your doctor. Genetic factors, diseases such as atherosclerosis or sciatica or some prescription medications may be contributing.

Natural remedies for muscle cramps

  • Mix 1 part oil of wintergreen – (available from pharmacies or essential oils suppliers) with 4 parts vegetable oil and massage it into the cramp. Wintergreen contains methyl salicylate (related to aspirin), which relieves pain and stimulates blood flow. You can use this mixture several times a day, but not with a heating pad–it could burn your skin. (Caution: Note that wintergreen is highly toxic when swallowed.)
  • Cramp bark has long been used as a muscle relaxant – A medical herbalist can make up both a tonic to be taken internally and a rubbing lotion from this herb.
  • Take a long, warm shower or soak in the bath – For added relief, pour in half a cup of Epsom salts. The magnesium in Epsom salts promotes muscle relaxation.
  • Place an electric heating pad or a hot face washer – on the troublesome muscle to relax the cramp and increase blood flow to the affected tissue. Set the pad on low, apply for 20 minutes, then remove it for at least 20 minutes before reapplying.
  • Find the central point of the cramp – Press this spot with your thumb, the heel of your hand or a loosely clenched fist. Hold the pressure for 10 seconds, ease off for 10 seconds, then press again. You should feel some discomfort but not excruciating pain. After repeating this action several times, the pain should start to diminish.
  • Muscle cramps from dehydration – Cramps are often caused by dehydration, so if you get cramps frequently, drink more water.

If you tend to get cramps during exercise, drink at least 2 cups of water 2 hours before each work-out. Then stop and drink 100–250ml every 10 to 20 minutes during your exercise sessions. If you sweat a lot, consider a sports drink, such as Lucozade Sport, that replaces lost sodium and other electrolytes.

Minerals that prevent muscle cramps

  • Low levels of minerals known as electrolytes – which include potassium, sodium, calcium and magnesium, can contribute to cramps. You probably don’t need more sodium (salt) in your diet, but you may need other minerals. Good food sources of magnesium are wholegrain breads and cereals, nuts and beans. Potassium is in most fruits and vegetables, especially bananas, oranges and apricot. And dairy foods supply calcium. If you change your diet and you still get cramps, take 500mg of calcium and 500mg of magnesium twice a day, adding up to 1000mg of each supplement, or as professionally prescribed. Some people who get leg cramps due to a magnesium deficiency obtain rapid relief from supplements. Don’t take magnesium without calcium; the 2 minerals work as a pair.
  • If you take diuretics for high blood pressure – your increased need to urinate may be robbing you of potassium. The result is a condition called hypokalemia, which can cause fatigue, muscle weakness and muscle cramps. Ask your doctor if you can switch to a blood-pressure medication that isn’t a diuretic.

Muscle cramps at night

  • Drink a glass of tonic water – which contains quinine, before bedtime. Research supports the use of quinine for nocturnal leg cramps, but don’t take it as tablets; they can have serious side effects, such as ringing in the ears and disturbed vision.
  • To prevent night-time calf cramps – try not to sleep with your toes pointed. And don’t tuck in your sheets too tightly as this tends to bend your toes downwards, causing cramp.
  • Take 250mg of vitamin E a day –  to improve arterial blood flow, thus potentially preventing night-time leg cramps. Muscle cramps are usually temporary and don’t cause permanent damage, but contact your doctor if the cramp or spasm lasts for more than a day, or if it continues to bother you despite trying these home remedies. And call immediately if the spasm occurs in the lower back or neck, accompanied by pain that radiates down your leg or into your arm. Finally, if abdominal cramps occur in the lower right hand part of your belly, it could signal appendicitis.

References

Muscle cramp

ByRx Harun

Insomnia; Causes, Symptoms, Diagnosis, Treatment

Insomnia is a common sleep disorder that can make it hard to fall asleep, hard to stay asleep or cause you to wake up too early and not be able to get back to sleep. You may still feel tired when you wake up. Insomnia can sap not only your energy level and mood but also your health, work performance and quality of life.

Insomnia disorder is characterized by chronic dissatisfaction with sleep quantity or quality that is associated with difficulty falling asleep, frequent nighttime awakenings with difficulty returning to sleep, and/or awakening earlier in the morning than desired. Although progress has been made in our understanding of the nature, etiology, and pathophysiology of insomnia, there is still no universally accepted model. Greater understanding of the pathophysiology of insomnia may provide important information regarding how, and under what conditions, the disorder develops and is maintained as well as potential targets for prevention and treatment. most every night.

Insomnia is the most common sleep disorder affecting millions of people as either a primary or comorbid condition. Insomnia has been defined as both a symptom and a disorder, and this distinction may affect its conceptualization from both research and clinical perspectives. However, whether insomnia is viewed as a symptom or a disorder, it nevertheless has a profound effect on the individual and society. The burden of medical, psychiatric, interpersonal, and societal consequences that can be attributed to insomnia underscores the importance of understanding, diagnosing, and treating the disorder[Rx]

Insomnia includes a wide range of sleeping disorders, from lack of sleep quality to lack of sleep quantity.

The International Classification of Sleep Disorders 2[] codes insomnia under the broad heading of dyssomnias, either intrinsic or extrinsic sleep disorders. Based on the severity, it classifies insomnia into three types as follows.

  • Mild insomnia – This term describes an almost nightly complaint of an insufficient amount of sleep or not feeling rested after the habitual sleep episode. It is accompanied by little or no evidence of impairment of social or occupational functioning. Mild insomnia is often associated with feelings of restlessness, irritability, mild anxiety, daytime fatigue, and tiredness.
  • Moderate insomnia – This term describes a nightly complaint of an insufficient amount of sleep or not feeling rested after the habitual sleep episode. It is accompanied by mild or moderate impairment of social or occupational functioning. Moderate insomnia is always associated with feelings of restlessness, irritability, anxiety, daytime fatigue, and tiredness.
  • Severe insomnia –  This term describes a nightly complaint of an insufficient amount of sleep or not feeling rested after the habitual sleep episode. It is accompanied by severe impairment of social or occupational functioning. Severe insomnia is associated with feelings of restlessness, irritability, anxiety, daytime fatigue, and tiredness.

According to Severity

  • Transient insomnia – occurs when symptoms last from a few days to a few weeks.
  • Acute insomnia – also called short-term insomnia. Symptoms persist for several weeks.
  • Chronic insomnia – this type lasts for months, and sometimes years. According to the National Institutes of Health, the majority of chronic insomnia cases are secondary, meaning they are side effects or symptoms resulting from another primary problem.

Although insomnia can affect people of any age, it is more common in adult females than adult males. The sleeping disorder can undermine school and work performance, as well as contributing to obesity, anxiety, depression, irritability, concentration problems, memory problems, poor immune system function, and reduced reaction time.

Insomnia has also been associated with a higher risk of developing chronic diseases.

According to the National Sleep Foundation, 30-40 percent of American adults report that they have had symptoms of insomnia within the last 12 months, and 10-15 percent of adults claim to have chronic insomnia.

Normal Sleep 

Before thinking about disturbed sleep, it’s important to understand what normal sleep really is. Normal slumber involves falling asleep relatively easily once you’re in bed, Silberman said. “People have a range of how quickly they go to sleep,” she said, but typically they can drift off to sleep anywhere from a few minutes to 15 minutes.

Normal sleepers will also go through four stages of sleep several times a night, she said. According to The Insomnia Workbook, the stages are:

  • Stage N1 –  the lightest stage, which usually makes up 10 percent of your total sleep time.
  • Stage N2 –  unlike stage N1, you lose awareness of external stimuli, and people spend most of their sleep time in this stage.
  • Stage N3 – known as slow-wave sleep, and believed to be the most restorative.
  • Stage R – known as REM sleep, or rapid eye movement. It’s the most active of the stages for your brain and body functions, such as breathing and heart rate. Your muscles relax, however, so you don’t act out your dreams.It’s also normal for it to take about 20 to 30 minutes to feel truly awake in the morning.

Causes of Insomnia

Symptoms of insomnia can be caused by or be associated with:

  • Use of psychoactive drugs (such as stimulants), including certain medications, herbs, caffeine, nicotine, cocaine, amphetamines, methylphenidate, aripiprazole, MDMA, modafinil, or excessive alcohol intake.
  • Use of or withdrawal from alcohol and other sedatives, such as anti-anxiety and sleep drugs like benzodiazepines.
  • Use of or withdrawal from pain-relievers such as opioids.
  • Previous thoracic surgery.
  • Heart disease.
  • Deviated nasal septum and nocturnal breathing disorders.
  • Restless legs syndrome, which can cause sleep onset insomnia due to the discomforting sensations felt and the need to move the legs or other body parts to relieve these sensations.
  • Periodic limb movement disorder (PLMD), which occurs during sleep and can cause arousals of which the sleeper is unaware.
  • Pain, an injury or condition that causes pain can preclude an individual from finding a comfortable position in which to fall asleep and can in addition cause awakening.
  • Hormone shifts such as those that precede menstruation and those during menopause.
  • Life events such as fear, stress, anxiety, emotional or mental tension, work problems, financial stress, the birth of a child, and bereavement.
  • Gastrointestinal issues such as heartburn or constipation.
  • Mental disorders such as bipolar disorder, clinical depression, generalized anxiety disorder, post traumatic stress disorder, schizophrenia, obsessive compulsive disorder, dementia, and ADHD.
  • Disturbances of the circadian rhythm, such as shift work and jet lag, can cause an inability to sleep at some times of the day and excessive sleepiness at other times of the day. Chronic circadian rhythm disorders are characterized by similar symptoms.
  • Certain neurological disorders, brain lesions, or a history of traumatic brain injury.
  • Medical conditions such as hyperthyroidism and rheumatoid arthritis.
  • Abuse of over-the-counter or prescription sleep aids (sedative or depressant drugs) can produce rebound insomnia.
  • Poor sleep hygiene, e.g., noise or over-consumption of caffeine.
  • A rare genetic condition can cause a prison-based, permanent and eventually fatal form of insomnia called fatal familial insomnia.
  • Physical exercise. Exercise-induced insomnia is common in athletes in the form of prolonged sleep onset latency.

Sleep studies using polysomnography have suggested that people who have sleep disruption have elevated nighttime levels of circulating cortisol and adrenocorticotropic hormone. They also have an elevated metabolic rate, which does not occur in people who do not have insomnia but whose sleep is intentionally disrupted during a sleep study. Studies of brain me

  • Disruptions in circadian rhythm – jet lag, job shift changes, high altitudes, environmental noise, heat, or cold.
  • Psychological issues – people with mood disorders such as bipolar disorder, depression, anxiety disorders, or psychotic disorders are more likely to have insomnia.
  • Medical conditions – brain lesions and tumors, stroke, chronic pain, chronic fatigue syndrome, congestive heart failure, angina, acid-reflux disease (GERD), chronic obstructive pulmonary disease, asthma, sleep apnea, Parkinson’s and Alzheimer’s diseases, hyperthyroidism, arthritis.
  • Hormones – estrogen, hormone shifts during menstruation.
  • Other factors – sleeping next to a snoring partner, parasites, genetic conditions, overactive mind, pregnancy.
  • Media technology in the bedroom – researchers from the University of Helsinki, Finland, reported in the journal BMC Public Health that media technology in the bedroom disrupts sleep patterns in children. They found that children with TVs, computers, video games, DVD players, and mobile phones in their bedrooms slept considerably less than kids without these devices in their bedrooms. In addition, a study conducted by Rensselaer Polytechnic Institute found that back-lit tablet computers can affect sleep patterns.

Medications – according to the American Association of Retired Persons (AARP), the following medications can cause insomnia in some patients

  • Corticosteroids – used for treating patients with allergic reactions, gout, Sjögren’s syndrome, lupus, rheumatoid arthritis, and inflammation of the muscles and blood vessels. Examples include prednisone, triamcinolone, methylprednisolone, and cortisone.
  • Statins – medications used for treating high cholesterol levels. Examples include simvastatin, rosuvastatin, lovastatin, and atorvastatin.
  • Alpha blockers – used for treating hypertension (high blood pressure), Raynaud’s disease and BPH (benign prostatic hyperplasia). Examples include terazosin, silodosin, alfuzosin, prazosin, doxazosin, and tamsulosin.
  • Beta blockers – used for treating hypertension and irregular heartbeat (arrhythmias). Examples include carvedilol, propranolol, atenolol, metoprolol, and sotalol.
  • SSRI antidepressants – used for treating depression. Examples include fluoxetine, citalopram, paroxetine, escitalopram, and sertraline.
  • ACE inhibitors – used for the treatment of hypertension and other heart conditions. Examples include ramipril, fosinopril, benazepril, enalapril, lisinopril, and captopril.
  • ARBs (Angiotensin II-receptor blockers) – used for treatment of hypertension (generally when patient cannot tolerate ACE inhibitors). Examples include candesartan, valsartan, and losartan.
  • Cholinesterase inhibitors – used for treating memory loss and other symptoms in patients with dementia, including Alzheimer’s disease. Examples include rivastigmine, donepezil, and galantamine.
  • Second generation (non-sedating) H1 agonists – used for treating allergic reactions. Examples include loratadine, levocetirizine, desloratadine, and cetirizine.
  • Glucosamine/chondroitin – dietary supplements used for relieving the symptoms of joint pain and to reduce inflammation.

Who gets insomnia?

Insomnia

Shift workers commonly suffer from insomnia because of inconsistent sleep routines.

Some people are more likely to suffer from insomnia than others; these include:

  • Travelers
  • Shift workers with frequent changes in shifts (day vs. night)
  • The elderly
  • Drug users
  • Adolescent or young adult students
  • Pregnant women
  • Menopausal women
  • Those with mental health disorders


Symptoms of insomnia

Insomnia itself may be a symptom of an underlying medical condition. However, there are several signs and symptoms that are associated with insomnia:

  • Difficulty falling asleep at night
  • Waking during the night
  • Waking earlier than desired
  • Still feeling tired after a night’s sleep
  • Daytime fatigue or sleepiness
  • Irritability, depression, or anxiety
  • Poor concentration and focus
  • Being uncoordinated, an increase in errors or accidents
  • Tension headaches (feels like a tight band around head)
  • Difficulty socializing
  • Gastrointestinal symptoms
  • Worrying about sleeping

Sleep deprivation can cause other symptoms. The afflicted person may wake up not feeling fully awake and refreshed and may have a sensation of tiredness and sleepiness throughout the day. Having problems concentrating and focusing on tasks is common for people with insomnia.

According to the National Heart, Lung, and Blood Institute, 20 percent of non-alcohol related car crash injuries are caused by driver sleepiness.

General Criteria for Insomnia

  • A complaint of difficulty initiating sleep, difficulty maintaining sleep, or waking up too early or sleep that is chronically nonrestorative or poor in quality. In children, the sleep difficulty is often reported by the caretaker and may consist of observed bedtime resistance or inability to sleep independently.
  • The above sleep difficulty often occurs despite adequate opportunity and circumstances for sleep.

At least one of the following forms of daytime impairment related to the nighttime sleep difficulty is reported by the patient:

  • Fatigue or malaise
  • Attention, concentration, or memory impairment
  • Social or vocational dysfunction or poor school performance
  • Mood disturbance or irritability
  • Daytime sleepiness
  • Motivation, energy, or initiative reduction
  • Proneness for errors or accidents at work or while driving
  • Tension, headaches, or gastrointestinal symptoms in response to sleep loss
  • Concerns or worries about sleep
adapted from the International Classification of Sleep Disorders, Second Edition ().

Diagnosis of Insomnia

Insomnia Differential Diagnosis and Common Comorbidities

(References: Buysse(); Sateia et al. ())
Medical Conditions:
  Cardiovascular congestive heart failure, arrythmia, coronary artery disease
  Pulmonary COPD, asthma
  Neurologic stroke, Parkinson’s disease, neuropathy traumatic brain injury
  Gastrointestinal gastroesophageal reflux
  Renal chronic renal failure
  Endocrine diabetes, hyperthyroidism
  Rheumatologic rheumatoid arthritis, osteoarthritis, fibromyalgia, headaches
Sleep Disorders:
  Restless legs syndrome
  Periodic limb movement disorder
  Sleep apnea
  Circadian rhythm disorder
  Parasomnias
  Nocturnal panic attacks
  Nightmares
  REM behavior disorder
Psychiatric Conditions:
  Depression
  Anxiety
  Panic disorder
  Post-traumatic stress disorder
Medications:
  Decongestants
  Antidepressants
  Corticosteroids
  Beta-agonists
  Beta-antagonists
  Stimulants
  Statins
Substances:
  Caffeine
  Alcohol
  Nicotine
  Cocaine

Diagnosis of primary insomnia

DSM IV TR criteria of primary insomnia
These include any of the following:
  • The predominant complaint is difficulty initiating or maintaining sleep, or non-restorative sleep, for at least 1 month.
  • The sleep disturbance (or associated daytime fatigue) causes clinically significant distress or impairment in social, occupational, or other important areas of functioning
  • The sleep disturbance does not occur exclusively during the course of narcolepsy, breathing-related sleep disorder, a circadian rhythm sleep disorder or a parasomnia.
  • The disturbance does not occur exclusively during the course of another mental disorder (e.g., major depressive disorder, generalized anxiety disorder, a delirium).
  • The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.

 

A sleep specialist will usually begin a diagnostic session by asking a battery of questions about the individual’s medical history and sleep patterns. A physical exam may be conducted to look for conditions that could be causing insomnia. Similarly, doctors might screen for psychiatric disorders and drug and alcohol use.

The Stanford Center for Sleep Sciences and Medicine explains that the term “insomnia” is often used colloquially in reference to “disturbed sleep.”

  • For somebody to be diagnosed with an insomnia disorder, their disturbed sleep should have persisted for more than 1 month. It should also negatively impact the patient’s wellbeing, either through the distress that results or the disturbance in mood or performance.
  • A sleep specialist is trained to determine whether the symptoms are being caused by an underlying condition. The patient may be asked to keep a sleep diary to help understand their sleeping patterns.
  • More sophisticated tests may be employed, such as a polysomnograph, which is an overnight sleeping test that records sleep patterns. In addition, actigraphy may be conducted, which uses a small, wrist-worn device called an actigraph to measure movement and sleep-wake patterns.

DSM-5 criteria

The DSM-5 criteria for insomnia include the following

Predominant complaint of dissatisfaction with sleep quantity or quality, associated with one (or more) of the following symptoms:

  • Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep without caregiver intervention.)
  • Difficulty maintaining sleep, characterized by frequent awakenings or problems returning to sleep after awakenings. (In children, this may manifest as difficulty returning to sleep without caregiver intervention.)
  • Early-morning awakening with inability to return to sleep.

In addition,

  • The sleep disturbance causes clinically significant distress or impairment in social, occupational, educational, academic, behavioral, or other important areas of functioning.
  • The sleep difficulty occurs at least 3 nights per week.
  • The sleep difficulty is present for at least 3 months.
  • The sleep difficulty occurs despite adequate opportunity for sleep.
  • The insomnia is not better explained by and does not occur exclusively during the course of another sleep-wake disorder (e.g., narcolepsy, a breathing-related sleep disorder, a circadian rhythm sleep-wake disorder, a parasomnia).
  • The insomnia is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication).
  • Coexisting mental disorders and medical conditions do not adequately explain the predominant complaint of insomnia.

Use of prescription drugs

  • Various prescription drugs may be responsible for chronic insomnia. Such a use should be asked for specifically and ruled out. The drugs may include anticonvulsants such as phenytoin and lamotrigine, beta-blockers like acebutolol, atenolol, metoprolol, oxprenolol, propranolol, and sotalol, antipsychotics like sulpiride, antidepressants such as Selective Serotonin Reuptake Inhibitors (SSRIs) or Monoamine oxidase inhibitors (MAOIs) and non-steroidal anti-inflammatory drugs (NSAIDs) such as indomethacin, diclofenac, naproxen, and sulindac.

Sleep diary or sleep log

  • A sleep diary helps in specifically estimating the severity of the problem, the night to night variability, and presence of maladaptive habits such as taking naps or spending excessive time in bed (more than 8 hours). Sleep diary also keeps track of compliance with behavioral interventions and response to treatment.

Sleep and psychological rating scale

  • Epworth Sleepiness Scale (ESS) rates the chance of dozing in the following situations[] which may be during sitting and reading, watching television, sitting inactively in a public place, being a passenger in a car for an hour without a break, during lying down to rest in the afternoon, sitting and talking to someone, sitting quietly after lunch without alcohol or while waiting at a traffic signal in a car.

The ESS is rated on a 4-point scale for each of the above factors based on the following scores:

  • 0 – no chances of dozing;
  • 1 – slight chances of dozing;
  • 2 – moderate chances of dozing; and
  • 3 – high chances of dozing.

A score of more than 16 indicates daytime somnolence, while a cutoff of 11 is often employed to indicate a possible disorder associated with excessive sleepiness.

Focused physical examination

  • A general physical examination may help assess certain organic pathologies such as chronic obstructive pulmonary diseases (COPD), asthma, or restless leg syndrome which may disturb sleep.

Blood tests

  • Blood tests may help to rule out subtle manifestations of thyroid diseases, iron deficiency anemia, and vitamin B12 deficiency (restless leg syndrome).

Polysomnography

  • It is considered the gold standard for measuring sleep. electroencephalogram (EEG), electrooculography (EOG), electromyography (EMG), electrocardiography (ECG), pulse oximetry, and air flow are used to reveal a variety of findings like periodic limb movement disorder, sleep apnea, and narcolepsy.[]

Actigraphy

  • Actigraphy measures physical activity with a portable device (usually including an accelerometer) worn on the wrist. Data recorded can be stored for weeks and then downloaded into a computer. Sleep and wake time can be analyzed by analyzing the movement data. This approach to estimating sleep and wake time has been shown to correlate with polysomnographic measures in normal sleepers, with reduced values noted in patients with insomnia.[,]

Summary of investigations

  • Investigations do not always correlate well with the patient’s experience of insomnia and cannot replace a thorough clinical evaluation. Hence, it is important to recognize that insomnia is a subjective clinical diagnosis, and therefore, a patient’s subjective report of sleep difficulties should play the most important role in directing management in most cases.
  • It is also important to ask questions about the range of symptoms experienced and changes over time. Because insomnia is a patient-reported symptom, rather than a polysomnographically defined disorder, referral to a sleep laboratory for polysomnographic diagnosis should be reserved for cases in which another primary sleep disorder, such as obstructive sleep apnea or periodic movement disorder, is suspected, because these may require greater expertise in sleep medicine.[] Other measures that can be used are evaluation of mental status, subjective sleep quality, psychological assessment scales, daytime function, quality of life, and dysfunctional beliefs and attitudes.

Treatment of Insomnia

Studies have suggested that electronic devices with self-luminous “backlit” displays can affect evening melatonin, which might result in delayed sleep.

Some types of insomnia resolve when the underlying cause is treated or wears off. In general, insomnia treatment focuses on determining the cause.

Once identified, this underlying cause can be properly treated or corrected. In addition to treating the underlying cause of insomnia, both medical and non-pharmacological (behavioral) treatments may be used as therapies.

Non-pharmacological approaches and home remedies for insomnia include:

  • Improving “sleep hygiene” – not sleeping too much or too little, exercising daily, not forcing sleep, maintaining a regular sleep schedule, avoiding caffeine at night, avoiding smoking, avoiding going to bed hungry, and ensuring a comfortable sleeping environment
  • Using relaxation techniques – such as meditation and muscle relaxation
  • Cognitive therapy – one-on-one counseling or group therapy
  • Stimulus control therapy – only go to bed when sleepy, avoid watching TV/ reading/ eating/ worrying in bed, set an alarm for the same time every morning (even weekends), avoid long daytime naps
  • Sleep restriction – decrease the time spent in bed and partially deprive the body of sleep, this increases tiredness ready for the next night.
  • Relaxation training – aims to reduce tension or minimise intrusive thoughts that may be interfering with sleep
  • Paradoxical intention – you try to stay awake and avoid any intention of falling asleep; it’s used if you have trouble getting to sleep, but not maintaining sleep
  • Biofeedback – sensors connected to a machine are placed on your body to measure your body’s functions, such as muscle tension and heart rate; the machine produces pictures or sounds to help you recognise when you’re not relaxed

Sleeping tablets

Sleeping tablets (hypnotics) are medications that encourage sleep. In the past, they were frequently used to help with insomnia, but they’re used much less often nowadays.

They will generally only be considered:

  • if your insomnia is severe
  • as a temporary measure to help ease short-term insomnia
  • if the good sleep habits and cognitive and behavioural treatments mentioned above don’t help

Doctors are usually reluctant to recommend sleeping tablets in the long-term because they just mask the symptoms without treating the underlying cause.They can also cause potentially dangerous side effects, such as drowsiness the following morning, and some people become dependent on them.

If they are recommended, you should have the smallest effective dose possible for the shortest time (usually no more than two to four weeks).

Over-the-counter sleeping pills

  • A number of sleeping tablets are available to buy over the counter (OTC) from pharmacies. These are usually a type of antihistamine medicine that causes you to feel drowsy.
  • Taking OTC sleeping tablets regularly isn’t usually recommended if you have insomnia, because it’s not clear how effective they are, they don’t tackle the underlying cause of your sleeping difficulties and they can cause side effects.
  • In particular, they can cause you to feel drowsy the next morning, which can make activities such as driving and operating machinery dangerous.
  • Speak to your GP for advice if you find yourself needing to take OTC sleeping tablets regularly.

Benzodiazepines

  • Benzodiazepines are prescription medicines that can reduce anxiety and promote calmness, relaxation and sleep. Your GP may prescribe them for a short time if you have severe insomnia or it’s causing extreme distress.

Examples of benzodiazepines include temazepam, loprazolam, lormetazepam, diazepam and nitrazepam.

Long-term treatment with benzodiazepines isn’t usually recommended because they can become less effective over time and some people become dependent upon them.

They can also cause a number of side effects, including:

  • drowsiness and dizziness, which can persist into the next day
  • finding it difficult to concentrate or make decisions
  • depression
  • feeling emotionally numb
  • irritability

You should avoid driving if you feel drowsy, dizzy, or unable to concentrate or make decisions, as you may not be able to do so safely.

  • Z-drugs

Z–drugs are a newer type of medicine that work in a similar way to benzodiazepines and are similarly effective. They include zaleplon, zolpidem and zopiclone.

As with benzodiazepines, long-term treatment with Z–drugs isn’t normally recommended because they can become less effective over time and some people become dependent on them.

They’re usually only prescribed for a maximum of two to four weeks.

Side effects of Z-drugs can include:

  • drowsiness and dizziness, which can persist into the next day
  • feeling and being sick
  • diarrhoea
  • increased snoring and breathing problems during sleep
  • dry mouth
  • confusion

Z–drugs can also sometimes cause psychiatric reactions, such as delusions, nightmares and hallucinations. Contact your GP if you experience any of these effects.

Antihistamines

  • As an alternative to taking prescription drugs, some evidence shows that an average person seeking short-term help may find relief by taking over-the-counter antihistamines such as diphenhydramine or doxylamine.
  • Diphenhydramine and doxylamine are widely used in nonprescription sleep aids. They are the most effective over-the-counter sedatives currently available, at least in much of Europe, Canada, Australia, and the United States, and are more sedating than some prescription hypnotics.
  • Antihistamine effectiveness for sleep may decrease over time, and anticholinergic side-effects (such as dry mouth) may also be a drawback with these particular drugs. While addiction does not seem to be an issue with this class of drugs, they can induce dependence and rebound effects upon abrupt cessation of use. However, people whose insomnia is caused by restless legs syndrome may have worsened symptoms with antihistamines.

Melatonin

  • The evidence for melatonin in treating insomnia is generally poor. There is low quality evidence that it may speed the onset of sleep by 6 minutes. Ramelteon, a melatonin receptor agonist, does not appear to speed the onset of sleep or the amount of sleep a person gets.
  • Most melatonin drugs have not been tested for longitudinal side effects. Prolonged-release melatonin may improve quality of sleep in older people with minimal side effects.
  • Studies have also shown that children who are on the Autism spectrum or have learning disabilities, Attention-Deficit Hyperactivity Disorder (ADHD) or related neurological diseases can benefit from the use of melatonin. This is because they often have trouble sleeping due to their disorders.
  • For example, children with ADHD tend to have trouble falling asleep because of their hyperactivity and, as a result, tend to be tired during most of the day. Another cause of insomnia in children with ADHD is the use of stimulants used to treat their disorder.
  • Children who have ADHD then, as well as the other disorders mentioned, may be given melatonin before bedtime in order to help them sleep.

Antidepressants

  • While insomnia –  is a common symptom of depression, antidepressants are effective in treating sleep problems whether or not they are associated with depression. While all antidepressants help regulate sleep, some antidepressants such as amitriptyline, doxepin, mirtazapine, and trazodone can have an immediate sedative effect and are prescribed to treat insomnia.
  • Amitriptyline –  and doxepin both have anti histaminergic, anticholinergic, and antiadrenergic properties, which contribute to both their therapeutic effects and side effect profiles, while mirtazapine’s side effects are primarily anti histaminergic, and trazodone’s side-effects are primarily antiadrenergic.
  • Mirtazapine – is known to decrease sleep latency (i.e., the time it takes to fall asleep), promoting sleep efficiency and increasing the total amount of sleeping time in people with both depression and insomnia.

Cognitive-Behavioral Interventions for Insomnia

Intervention General description Specific techniques
Sleep hygiene
education
Recommendations
promoting behaviors that
help sleep, discouraging
behaviors that interfere with
sleep
  • Don’t try to sleep
  • Avoid stimulants (caffeine, nicotine)
  • Limit alcohol intake
  • Maintain a regular sleep schedule 7 nights a week
  • Avoid naps
  • Get regular exercise, at least 6 hours before sleep
  • Keep the bedroom dark and quiet
Stimulus control Based on operant and
classical conditioning
principles: Non-sleep
activities and the bedroom
environment can serve as
stimuli that interfere with
sleep. Treatment prescribes
behaviors that strengthen
associations between the
environment and sleep.
  • Go to bed only when sleepy.
  • Use the bed and bedroom for sleep only. Do not read, watch television, talk on the phone, worry, or plan activities in the bedroom.
  • If unable to fall asleep within 10-20 minutes, leave the bed and the bedroom. Return only when felling sleepy again.
  • Set the alarm and wake up at a regular time every day.
  • Do not snooze. Do not nap during the day.
Sleep restriction
therapy
Based on experimental
evidence that sleep is
regulated by circadian and
homeostatic processes.
Treatment increases
homeostatic sleep drive by
reducing time in bed, and
maintaining a consistent
wake time in the morning to
reinforce circadian rhythms.
  • Restrict time awake in bed using by setting strict bedtime and rising schedules limited to the average number of hours of actual sleep reported in one night.
  • Increase time in bed by advancing bedtime by 15-30 minutes when the time spent asleep is >85% of time in bed.
  • Keep a fixed wake-up time, regardless of actual sleep duration.
  • If after 10 days, sleep efficiency is lower that 85%, further restrict bedtime by 15-30 minutes.
Relaxation training Muscular tension and
cognitive arousal are
incompatible with sleep.
Relaxation decreases waking
arousal, and facilitates sleep
at night.
Specific techniques may include:

  • Progressive muscle relaxation
  • Guided imagery
  • Paced breathing
Cognitive therapy Identify, challenge, and
replace dysfunctional beliefs
and attitudes regarding sleep
and sleep loss. These beliefs
increase arousal and tension,
which impede sleep and
further reinforce the
dysfunctional beliefs.
  • Challenge unhelpful beliefs and fears about sleep, e.g.:

    • ○ Overestimation of numbers of hours of sleep necessary to be rested.
    • ○ Apprehensive expectation that sleep cannot be controlled.
    • ○ Fear of missing opportunities for sleep.
  • Thought journaling to reduce rumination
  • Design behavioral ―experiments‖ to test beliefs about sleep
Cognitive
Behavioral
Treatment of
Insomnia (CBT-I)
Multi-modal treatment
combining elements of above
techniques
  • Sleep education
  • Stimulus control techniques
  • Sleep restriction techniques
  • Cognitive therapy techniques
  • May include relaxation training
Brief Behavioral
Treatment of
Insomnia
Core techniques from
Stimulus Control, Sleep
Restriction therapies
  • Limit time in bed to actual sleep time + 30 minutes
  • Establish regular wake time every day, regardless of prior night’s sleep duration
  • Do not go to bed until sleepy
  • Do not stay in bed if awake

Good Sleep Habits for Beating Insomnia

Good sleep habits, also called sleep hygiene, can help you get a good night’s sleep and beat insomnia. Here are some tips:

  • Try to go to sleep at the same time each night and get up at the same time each morning. Try not to take naps during the day, because naps may make you less sleepy at night.
  • Avoid prolonged use of phones or reading devices (“e-books”) that give off light before bed. This can make it harder to fall asleep.
  • Avoid caffeine, nicotine, and alcohol late in the day. Caffeine and nicotine are stimulants and can keep you from falling asleep. Alcohol can cause waking in the night and interferes with sleep quality.
  • Get regular exercise. Try not to exercise close to bedtime, because it may stimulate you and make it hard to fall asleep. Experts suggest not exercising for at least three to four hours before the time you go to sleep.
  • Don’t eat a heavy meal late in the day. A light snack before bedtime, however, may help you sleep.
  • Make your bedroom comfortable. Be sure that it is dark, quiet, and not too warm or too cold. If light is a problem, try a sleeping mask. If noise is a problem, try earplugs, a fan, or a “white noise” machine to cover up the sounds.
  • Follow a routine to help you relax before sleep. Read a book, listen to music, or take a bath.
  • Avoid using your bed for anything other than sleep or sex.
  • If you can’t fall asleep and don’t feel drowsy, get up and read or do something that is not overly stimulating until you feel sleepy.
  • If you find yourself lying awake worrying about things, try making a to-do list before you go to bed. This may help you to not focus on those worries overnight.

Home Remedies to overcome Insomnia

Milk

A glass of lukewarm milk before bedtime gives soporific effect on your body that helps you doze off easily. Additionally, it contains amino acid- tryptophan, which stimulates serotonin production that ultimately provides you with a better sleep.

  • You can mix honey in the milk.
  • Alternatively, along with honey, mix a dash of cinnamon powder in it.
  • Massaging your toes with milk can induce sleep.

Bottle Gourd  

  • Bottle gourd is one of the excellent remedies to induce sleep. Take out the bottle gourd juice and add sesame oil in same proportion. Massage with this on your scalp, before going to bed. Alternatively, include bottle gourd in your diet.

Poppy Seeds

  • Poppy seeds are a good source of minerals, calcium, carbohydrates and B-complex vitamins. Taking 1 teaspoon of poppy seed/oil before going to bed can actually solve the problem of insomnia.
  • Alternatively, get 1 teaspoon each of white poppy seeds and coconut powder and adds a small amount of water, in order to make a thick paste. Now, take a frying pan and melt some clarified butter in it. Then, add a pinch of cumin and turmeric and remove immediately from heat. After a minute, mix that paste in it and add salt to taste. Chomp this mixture one hour before you sack out.
  • Or else, consume 30 grams of poppy seeds’ milk flavored with a little sugar.

Nutmeg

  • Nutmeg effectually heals insomnia. It is loaded with myristicin which works as a tranquilizer and helps you get natural sleep. You can mix a pinch of nutmeg powder with one teaspoon of fresh Indian gooseberry juice. Consume it 3 times a day. Apart from insomnia, it also resolves the problem of indigestion and depression.
  • Alternatively, blend ½ teaspoon of powdered nutmeg with a pinch of cinnamon powder, 1 teaspoon each of raw honey and water to form a paste. Now, boil a cup of milk and pour all the mixture in it. Stir well and sip it before you hit the hay.
  • Take a one-eighth teaspoon of nutmeg powder and mix it with one cup of lukewarm milk.
  • Take a quarter teaspoon of nutmeg powder. Add it in a cup of warm water or any of your favorite juice.

Note:

  • Don’t consume it more than a pinch, at one time.
  • Over doses of nutmeg may cause hallucination and some other psychiatric turmoil.

Green Tea

  • Green tea is full of theanine and amino acid that helps combat anxiety and de-stress a person. Drink a cup of green tea 1-2 hours before bedtime.

Bananas

  • Banana contains melatonin, tryptophan, magnesium and serotonin, which work as body relaxants. The high amount of carbohydrate in bananas will make you sleepy. Simply eat a banana before going to bed.
  • A blend of mashed banana and roasted cumin seeds can be consumed after dinner.
  • Alternatively, you can also have a banana smoothie one hour before your bedtime.
  • You can also try banana with some toast and peanut butter.

Aniseed

  • Take one teaspoon of aniseeds and add it to 375ml of boiling water. Simmer this concoction for 15 minutes.  Filter this solution and add honey and milk to it. Sip this tea every day before bedtime.

Oatmeal

  • Oats are rich in melatonin which makes it a sleep inducing meal. Simply eat oatmeal regularly to get rid of this problem. You can also sprinkle two tablespoons of flaxseeds in your oatmeal. Chomp it at night.

Curd

  • Curd enables the body to absorb essential minerals and nutrients and improves the digestive system as well. A person suffering from insomnia should consume 3 cups of curd daily, in order to get a sound sleep. Besides eating curd, its massage on head is also beneficial.

Cumin Tea

  • Heat 1 teaspoon of cumin seeds for about 5 seconds. Then, add 1 cup of water in it and simmer it to the boiling point. Remove it from heat and cover it with a lid. Strain the solution after 5 minutes. Drink this tea before you hit the sack.

Saffron

  • Saffron contains mild sedative properties that help treat the problem of insomnia. Take 3-4 strands of saffron and soak them in a cup of warm milk. Sip this warm drink every day before you sack out.

Apple Cider Vinegar and Honey

  • Apple cider vinegar is loaded with amino acids that relieve body from fatigue, thereby help you get natural sleep. On the other side, honey raises the insulin levels that release serotonin, thus, promotes sleep. Take a glass of warm water and mix two tsp each of honey and organic apple cider vinegar to it. Drink it before you hit the hay.
  • Otherwise, blend 2 tsp of apple cider vinegar in a cup of honey. Take one tbsp of this mixture with or without water.

Hot Bath

  • Have a hot shower about two hours before going to sleep. It will soothe the nerves and relax your body. You can also add a few drops of essential oils like chamomile, lemon balm, lavender or rosemary to the bathwater, as it soothes your body in an effective way.

Acupuncture

  • Acupuncture is somewhat similar to acupressure. It heals the problem by putting a thin needle in your skin, at some specific points. It works wonders for insomnia.

Note- Get this therapy done from an experienced practitioner.

Almonds

  • Almonds relax your muscles, as it contains magnesium as well as tryptophan. Simply eat a handful of almonds throughout the day, in order to treat the problem of insomnia.

Honey

  • Honey works tremendously great for treating insomnia. Due to its hypnotic and sedative effects, it induces sound sleep. It also promotes relaxation. Simply mix 2 tbsp of honey in a cup of water. Stir well and drink it before you sack out.
  • Alternatively, intake a spoon full of honey before you hit the hayThis is one of the best remedies, for children suffering from insomnia.

Sesame Oil

  • Sesame seeds are affluent in polyunsaturated fat that helps relieve the nervous and muscular tension and gives sound sleep. Regular consumption of sesame oil improves blood circulation, prevents digestive disorders and reduces anxiety. Massage your feet with this oil daily before you hit the sack.

Celery

  • Celery is rich in phthalides that decreases the secretion of stress-inducing hormones and, ultimately, relax the muscular and nervous systems. This feature of celery makes it an excellent home cure for insomnia. Crush celery leaves along with their stalk, in order to extract their juice. Mix a tablespoon of honey with it. One should consume it at night before catching some zzz’s.

Note- Honey and celery should be taken in equal proportion.

Herbal Remedies to Cure Insomnia

  • Indian Sorrel – Juice of Indian sorrel leaves is very useful in healing insomnia. Extract some juice of these leaves and mix it with castor oil, in equal amount. Now, boil down the water content. Store it in a bottle when it cools down. Massage the scalp with this oil before bedtime. It gives cool sensation near the eyes which induces sound sleep.
  • Lavender Oil – This oil works as a tranquilizer and helps you get a good sleep. Take a few drops of this herbal oil and apply it on the forehead and temple. The fragrance of this oil induces sleep. So, use it before catching some zzz’s.
  • Jasmine Essential Oil – Take a few drops of this oil and apply it on your wrist. Perform this before you hit the sack and you will certainly have a better sleep.
  • Rauwolfia – Rauwolfia is loaded with sedative properties, which cures insomnia. Take around 0.25 to 0.5 grams of its root powder and mix it with cardamom. A patient of chronic insomnia can take it two times a day- in the morning and at night.
  • Basil – A person suffering from sleep disorder should be given a leaf of basil for chomping. Alternatively, spread some basil leaves beneath the patient’s pillow and around the corners of the bed throw.  The aroma of the leaves will strike the person’s nostril which will make him/her feel sleepy.
  • Fenugreek Juice – Fenugreek juice acts as a tranquilizer that induces sleep and effectively prevents insomnia. Extract 2 tsp of fresh fenugreek juice from its leaves. Add one tsp of honey to it. Take it on a daily basis before catching some zzz’s.
  • Valerian – Valerian is a very popular herb that is commonly used to treat sleep disorders. It gives sedative effect and relaxes body muscles. Combine ½ teaspoon of grated valerian root and nutmeg. Add this mixture in 2 cups of hot water. After 15 minutes, strain the solution and drink it.
  • Alternatively, boil a cup of water and remove it from heat. Add one tsp of valerian herb to it. Stir well. After a few minutes, strain this decoction and then, drink.
  • Or else, use valerian tincture. Dilute half tsp of its tincture in a glass of water. Drink it two times a day.

Note- This herb should not be consumed by children and pregnant or breastfeeding women.

  • Chamomile Tea – Chamomile tea is a good herbal remedy to get a sound sleep. It contains apigenin that gives sedative effect to the body. Brew 1 tsp of chamomile herb in one cup of water for a few minutes. Stir well and filter this solution. You can add a dash of cinnamon and a little bit of honey to it.
  • Lemon Balm – Mix 2-3 teaspoons of lemon balm to a cup of boiling water. Steep it for a few minutes. For effective results, drink this herbal tea before bedtime.
  • Lettuce – Lettuce contains a sleep stimulating substance called lectucarium, which has tranquilizing properties and give effects similar to the opium poppy. Take 2 lettuce leaves and boil them in two cups of water for 5 minutes. Add either honey or sugar to the solution. Wait until it cools down. Then, strain it. Drink a cup of lettuce tea at least half an hour before you sack out. It will definitely give you a sound sleep.
  • Alternatively, lettuce juice can also be consumed.
  • Moreover, take one tsp of lettuce seeds and boil them in half liter water until it reduces to 1/3. Strain this infusion and drink it throughout the day.


Homeopathic 

  • Acidum phos.(tds) – Sleeplessness after depressing events, sorrow or loss and death of a friend or a relative.
  • Ambra grisea (tds) – Sleeplessness due to worries or business troubles.
  • Ammonium val.3x(tds) Insomnia especially during pregnancy and menopause, with a neuralgic headache.
  • Arnica mont.(tds) Sleeplessness caused by over-exertion. Mental or physical. Bed appears too hard. Tosses about to find a soft portion of the bed.
  • Avena saliva Q 10 (bd) 10 drops in !A cup of water: Sleeplessness in alcoholics and those with morphine habits.
  • Cataria nep Q (od) 5 drops in ‘A cup of water. It relieves sleeplessness Of children who cannot sleep due to colic. It cures colic and produces sleep.
  • Chloralum 200 (od) It is a powerful sleep producing remedy in patients with mental diseases, with asthma, hallucinations and night terrors. Insomnia from over-fatigue.
  • Cimicifuga (tds)  Sleeplessness in children during the period of dentition.
  • Conium mac (tds) Sleeplessness due to neuralgic pains.
  • Helonias  Sleeplessness on account of tiring hard labor with aching of muscles.
  • Kalium phos A great remedy for. sleeplessness. The patient is weak and nervous. Sleeplessness due to business worries and due to mental disturbances.
  • Magnesium phos (tds) Sleeplessness on account of indigestion.
  • Nux vomica (tds) – Sleeplessness is due to over-excitement exhaustion and stress.
  • Pulsatilla nig.(tds) – falls asleep but cannot sleep. Bed feels hot. Moves about in vain in bed to find a cool spot. Even the ticking of a clock disturbs.
  • Antinionium crud.(Ids) Continuous drowsiness in old people.
  • Baptisia.(Ids) –  Falls asleep while being spoken to.
  • Causticum.(bd)   Very drowsy. Can hardly keep awake. Suited to old people.
  • Chloralosum.(tds) – A useful remedy for prolonged drowsiness, which may continue for number of days. It is also useful for drowsiness and sleep of drunkards, whose faculties are only partially depressed.
  • Cimex lect.(tds)  Irresistible sleepiness.
  • Gelsemium (tds) Patient is sluggish and always feels sleepy. He does not like to discuss matters but likes to be alone and undisturbed.
  • Hydrocyanicum acidum (tds) – Irresistible drowsiness.
  • Hypericum 3x (tds) The patient constantly feels drowsy.
  • Indolum (tds)  Wants to sleep all time. Aversion to work .
  • Lupulus (tds)  Drowsy during the day.
  • Lycopodium (tds) – Feels sleepy soon after taking dinner.
  • Natrium sulp.(tds)  Sleepy while reading.
  • Nux mosch (tds) – Great drowsiness.
  • Opium (tds)  Great drowsiness. Falls asleep at work.
  • Paullinia sorb (tds)  Feels sleepy after eating. Patient cannot control sleep. Head becomes heavy if he does not sleep.
  • Staphysagria (tds) – Feels sleepy after eating.

Simple Tips (Home Remedies) to cure Insomnia

  • Maintaining regular sleep schedule and getting up the same time everyday morning. This helps synchronize the body’s biological clock
  • Do not mix activities like watching TV or mobile chatting from the Bed. Keep it reserved for sleeping activity only
  • If you do not fall asleep within 20 minutes of getting into bed, try and use a body massager, listen to slow music or try a warm oil head massage
  • Limit daytime sleep (cat naps)
  • Having a hot bath or a glass of warm milk before bed abets sleep better
  • Don’t drink caffeinated beverages & chocolate in the evening
  • Keeping hands & feet warm in a cold bedroom induces sleep quickly ( as per researchers at the Psychiatric university, clinic of chronobiology & sleep Laboratory, Switzerland)

Do’s

  • Perform deep breathing exercises, meditation, and yoga.
  • Sleep in a peaceful, dark, comfortable room.
  • Have dinner at least 2-3 hours before bedtime.
  • If you need to stay up late at night, then snack only on those stuffs that are low in protein and high in carbohydrates.
  • Listen to soft music around 45 minutes before catching some zzz’s.
  • Consume raw onion salad.
  • Take ample calcium, potassium and iron to cope up with sleep disorders.
  • Blue wavelengths of your phones reduce the secretion of melatonin which, in turn, affects your sleep. So, stay away from laptop, iPod, and smart phones at night.

Don’ts

  • Avoid watching TV before bedtime.
  • Reduce the consumption of alcohol and caffeine.
  • Avoid naps during the day time.
  • Don’t take excessive liquids half an hour before you hit the sack, in order to avoid urination.


References

Insomnia


By

Magnesium Health Benefit; Rich Foods, Deficiency Symptoms

Magnesium health benefit are important minerals needed for all cells in the body to function properly . It is an antidote to stress, the most powerful relaxation mineral available, and it can help improve your sleep. So health benefit of magnesium and potassium are important elements to maintain our healthy life. In our every day  eating list must have it.

Magnesium Health Benefit; Magnesium Rich Foods, Deficiency Symptoms

Interesting Facts & Magnesium Health Benefit

Still feeling estranged from your body’s friend magnesium?

Here are 15 fun facts about this particular mineral:

  • Magnesium is one of the most common mineral deficiencies.
  • The chemical element symbol for magnesium is Mg.
  • The atomic number for magnesium is 12.
  • Magnesium is essential for photosynthesis to take place.
  • Magnesium has a boiling point of 1,091F. To put this into perspective, water has a boiling point of 212F.
  • Aside from sodium, magnesium is the most plentiful metal found in seawater.
  • Magnesium is essential for life; not only for our bodies, but for our planet as well.
  • More than 10% of the Earth’s mass is made up from magnesium.
  • The human body absorbs anywhere from 10-50% of magnesium intake.
  • Magnesium is essential for sleep.
  • There is enough magnesium in the Earth to make another planet roughly the size of Mars, plus three moons on the side.
  • This element burns both pure carbon dioxide and nitrogen. This means that if you tried to use a carbon dioxide fire-extinguisher to put out a magnesium fire, you would only end up adding to the flames.
  • Magnesium is one of the three most commonly used metals.
  • The first suggested name from Sir Humphrey Davy was Magnium, but it soon evolved into the name Magnesium.
  • Of all the magnesium found in the human body, 60% can be found in the skeleton.

If pregnant women came in with pre-term labor, or high blood pressure of pregnancy (pre-eclampsia) or seizures, we gave them continuous high doses of intravenous magnesium.

But you don’t have to be in the hospital to benefit from getting more magnesium. You can start taking regular magnesium supplementation today and see results.

The Relaxation Mineral with Magnesium Health Tips

  • Think of magnesium as the relaxation mineral. Anything that is tight, irritable, crampy, and stiff — whether it is a body part or an even a mood — is a sign of magnesium deficiency.
  • This critical mineral is actually responsible for over 300 enzyme reactions and is found in all of your tissues — but mainly in your bones, muscles, and brain. You must have it for your cells to make energy, for many different chemical pumps to work, to stabilize membranes, and to help muscles relax.
  • When was the last time you had a good dose of seaweed, nuts, greens, and beans? If you are like most Americans, your nut consumption mostly comes from peanut butter.
  • That is why the list of conditions that are found related to magnesium deficiency is so long. In fact, there are over 3,500 medical references on magnesium deficiency!

Even so, this mineral is mostly ignored because it is not a drug, even though it is MORE powerful than drugs in many cases. That’s why we use it in the hospital for life-threatening and emergency situations like seizures and heart failure.

You might be magnesium deficient if you have any of the following symptoms:

  • Muscle cramps or twitches
  • Insomnia
  • Irritability
  • Sensitivity to loud noises
  • Anxiety
  • Autism
  • ADD
  • Palpitations
  • Angina
  • Constipation
  • Anal spasms
  • Headaches
  • Migraines
  • Fibromyalgia
  • Chronic fatigue
  • Asthma
  • Kidney stones
  • Diabetes
  • Obesity
  • Osteoporosis
  • High blood pressure
  • PMS
  • Menstrual cramps
  • Irritable bladder
  • Irritable bowel syndrome
  • Reflux
  • Trouble swallowing

Magnesium deficiency has even has been linked to inflammation in the body and higher CRP levels.

In our society, magnesium deficiency is a huge problem. By conservative standards of measurement (blood, or serum, magnesium levels), 65 percent of people admitted to the intensive care unit — and about 15 percent of the general population — have magnesium deficiency.

  • But this seriously underestimates the problem, because a serum magnesium level is the LEAST sensitive way to detect a drop in your total body magnesium level. So rates of magnesium deficiency could be even higher!
  • The reason we are so deficient is simple: Many of us eat a diet that contains practically no magnesium — a highly-processed, refined diet that is based mostly on white flour, meat, and dairy (all of which have no magnesium).
  • When was the last time you had a good dose of sea vegetables (seaweed), nuts, greens, and beans? If you are like most Americans, your nut consumption mostly comes from peanut butter, and mostly in chocolate peanut butter cups.
  • Much of modern life conspires to help us lose what little magnesium we do get in our diet. Magnesium levels are decreased by excess alcohol, salt, coffee, phosphoric acid in colas, profuse sweating, prolonged or intense stress, chronic diarrhea, excessive menstruation, diuretics (water pills), antibiotics and other drugs, and some intestinal parasites. In fact, in one study in Kosovo, people under chronic war stress lost large amounts of magnesium in their urine.

Magnesium-Rich-Food

This is all further complicated by the fact that magnesium is often poorly absorbed and easily lost from our bodies. To properly absorb magnesium we need a lot of it in our diet, plus enough vitamin B6, vitamin D, and selenium to get the job done.

A recent scientific review of magnesium concluded, “It is highly regrettable that the deficiency of such an inexpensive, low-toxicity nutrient results in diseases that cause incalculable suffering and expense throughout the world.” (ii) I couldn’t’ have said it better myself.

Stop Draining Your Body of Magnesium

  • Limit coffee, colas, salt, sugar, and alcohol
  • Learn how to practice active relaxation
  • Check with your doctor if your medication is causing magnesium loss (many high blood pressure drugs or diuretics cause loss of magnesium)

Eat Foods High in Magnesium

Include the following in your diet as often as you can

  • Kelp, wheat bran, wheat germ, almonds, cashews, buckwheat, brazil nuts, dulse, filberts, millet, pecans, walnuts, rye, tofu, soybeans, brown rice, figs, dates, collard greens, shrimp, avocado, parsley, beans, barley, dandelion greens, and garlic.

Here are two recipes to help you include magnesium in your daily diet – Coconut Peach Crumble and Grilled Salmon with Avocado & Garlic Salsa.

Take Magnesium Supplements

  • The RDA (the minimum amount needed) for magnesium is about 300 mg a day. Most of us get far less than 200 mg.
  • Some may need much more depending on their condition.
  • Most people benefit from 400 to 1,000 mg a day.
  • The most absorbable forms are magnesium citrate, glycinate taurate, or aspartate, although magnesium bound to Kreb cycle chelates (malate, succinate, fumarate) are also good.
  • Avoid magnesium carbonate, sulfate, gluconate, and oxide. They are poorly absorbed (and the cheapest and most common forms found in supplements).
  • Side effects from too much magnesium include diarrhea, which can be avoided if you switch to magnesium glycinate.
  • Most minerals are best taken as a team with other minerals in a multi-mineral formula.
  • Taking a hot bath with Epsom salts (magnesium sulfate) is a good way to absorb and get much needed magnesium.

People with kidney disease or severe heart disease should take magnesium only under a doctor’s supervision. So if you’re coping with the symptoms here, relax! Magnesium is truly a miracle mineral. It is essential for lifelong vibrant health.

Food Sources

Magnesium-Rich-Food

The following foods are good to excellent sources of magnesium:

  • Pumpkin seeds: 46% of the RDI in a quarter cup (16 grams).
  • Spinach boiled: 39% of the RDI in a cup (180 grams).
  • Swiss chard boiled: 38% of the RDI in a cup (175 grams).
  • Dark chocolate (70–85% cocoa): 33% of the RDI in 3.5 ounces (100 grams).
  • Black beans: 30% of the RDI in a cup (172 grams).
  • Quinoa, cooked: 33% of RDI the in a cup (185 grams).
  • Halibut: 27% of the RDI in 3.5 ounces (100 grams).
  • Almonds: 25% of the RDI in a quarter cup (24 grams).
  • Cashews: 25% of the RDI in a quarter cup (30 grams).
  • Mackerel: 19% of the RDI in 3.5 ounces (100 grams).
  • Avocado: 15% of the RDI in one medium avocado (200 grams).
  • Salmon: 9% of the RDI in 3.5 ounces (100 grams).

Supplements

If you have a medical condition, then check with your doctor before taking a supplement.

Although these supplements are generally well-tolerated, they may not be safe for people who take certain diuretics, heart medications or antibiotics.

Magnesium supplements that are absorbed well include:

  • Magnesium citrate.
  • Magnesium glycinate.
  • Magnesium orotate.
  • Magnesium carbonate.

The recommended daily amount is 300–400 mg, taken with food. However, for some people, this amount may cause loose stools

Health Benefits of Magnesium

Constipation

  • If you are suffering from Irritable Bowel Syndrome (IBS) or constipation you would do well to turn your attention to magnesium for help.
  • Getting the proper amount of magnesium helps negate the acids found within your stomach, thereby allowing digested food to run smoothly through your intestines.

This is a natural way to ease the suffering associated with digestive issues.

Magnesium and Bone Health

  • The bones are one of the main elements of your body that benefit most from magnesium.
  • Magnesium regulates the levels of calcium absorbed by your body, along with zinc, copper, and vitamin D.
  • Not only will these minerals help keep your bones healthy and strong, but they may also prevent or lower the chance of developing osteoporosis later in life.

Helps Treat Asthma

  • Those suffering from chronic asthma have benefited from using magnesium to treat their symptoms.
  • This is due to the fact that many who suffer from asthma are shown to have lower levels of magnesium than normal.
  • The intake of magnesium supplements may regulate breathing, ease wheezing, and relax the bronchial muscles to promote easier breathing.

Protein Molecules and Enzymes

  • Enzymes, or protein molecules, work inside the body to stimulate chemical reactions. Magnesium is one of the key factors in assisting these molecules.

Contributes to Muscle Building

  • Magnesium contributes to building muscle. When it comes to toning and exercise, the body requires plenty of iron, zinc, calcium, chromium, and magnesium to build muscle.
  • Research indicates that even minuscule magnesium deficiencies may hinder muscle growth and performance in athletes.
  • Magnesium also plays a vital role in your body’s energy production, or ATP (Adenosine Triphosphate).

Studies also show that proper magnesium intake for athletes results in increased peak oxygen intake.

Chronic Pain

  • A 2010 study done by the Journal of Physiology tested a theory that magnesium is found to reduce nerve pain in patients. N-methyl-D-aspartate or NMDA  is a brain chemical that triggers nerve pain when overstimulated. Magnesium will help settle the NMDA and ease chronic pain.

Eases Muscle Pain

  • Proper magnesium intake is great for easing sore muscles.
  • Magnesium causes muscles to relax and can, therefore, decrease pain associated with overworked muscles.

Maintains Excellent Heart Health

  • Those who have a magnesium deficiency may experience negative impacts on their heart health. A lack of adequate magnesium can lead to heart disease.
  • A study in the Circulation Journal tested the effectiveness of magnesium supplements on patients with heart disease and found that those who took the supplement twice a day for half a year had better physical stamina and improved blood vessels.

Insulin and Diabetes

  • Studies show that those suffering from a magnesium deficiency are more at risk of developing diabetes in the future. On the other hand, those who are meeting the recommended daily intake of magnesium will have much healthier options ahead.
  • This is because magnesium aids in the activity and release of insulin and will get a better handle on maintaining a healthy blood glucose level.
  • While magnesium is said to be good for individuals with type-2 diabetes, it is always wise to consult your doctor before adding any supplements into your diet.

Keeps Your Teeth Healthy

  • Since the bones take in the majority of magnesium’s benefits, it’s no surprise that this mineral is fantastic for your teeth. Magnesium helps your body better absorb calcium, which leads to strengthened bones and well-formed teeth.

Pregnancy

  • Magnesium is essential for a baby’s growth and healthy pregnancy. Proper magnesium intake increases the pain threshold, reduces the risk of bone deficiencies, optimizes blood circulation, and may prevent eclampsia. Magnesium also contributes to a baby’s nutrition while in-utero, as well as tissue recovery and growth.

Migraines

  • Magnesium can operate as a muscle relaxant, making it an ideal mineral for those who suffer from migraines, muscle tension, or tension headaches. Chronic migraine sufferers often have low levels of magnesium in the body – in fact, this is often one of the prominent symptoms of a magnesium deficiency. Adding a magnesium supplement into your diet may reduce both the occurrence and severity of future migraines.

Premenstrual Syndrome

  • Due to the muscle relaxing qualities that magnesium has on the body, many women have been able to ease cramps and pains brought on by premenstrual syndrome, or PMS.
  • Not only will magnesium help combat aching brought on by PMS, some studies even suggest that women can find relief in mood changes brought on by that time of the month.

Collagen Production

  • Collagen is beneficial for your whole body. Not only does it keep your hair healthy and shiny, and your skin looking young and supple, it also aids in many other facets of bodily care.
  • For example, collagen helps balance hormones and benefits joint and bone health, and digestion. Magnesium helps aid the same proteins that turn into collagen.

Contributes to Bladder Control

  • People of all ages suffer from bladder control issues ranging from the frequent urge to urinate to problems spotting throughout the day.
  • Magnesium helps fight infections, interstitial cystitis, and nephritis, all of which can contribute to bladder control issues.

How to Add Magnesium into Your Diet

  • As you can see, there are many health benefits of magnesium in your daily diet.
  • Adding that recommended daily intake of magnesium doesn’t have to be a complicated process. The following foods are easy to find at your local grocery store and are rich in magnesium. It is recommended that men get at least 400 mg of magnesium in their diet per day and women should have at least 300.

References

Magnesium Deficiency

ByRx Harun

Trigeminal Neuralgia – Causes, Symptoms, Diagnosis, Treatment

Trigeminal neuralgia (TN or TGN) is a chronic pain uncommon disorder characterized by recurrent attacks of lancinating pain in the trigeminal nerve distribution that affects the trigeminal nerve. Typically, brief attacks are triggered by talking, chewing, teeth brushing, shaving, a light touch, or even a cool breeze. The pain is nearly always unilateral, and it may occur repeatedly throughout the day.[Rx]

Trigeminal neuralgia (TN), also called tic douloureux, is a chronic pain condition that affects the trigeminal or 5th cranial nerve, one of the most widely distributed nerves in the head. TN is a form of neuropathic pain (pain associated with nerve injury or nerve lesion.) The typical or “classic” form of the disorder (called “Type 1” or TN1) causes extreme, sporadic, sudden burning or shock-like facial pain that lasts anywhere from a few seconds to as long as two minutes per episode.  These attacks can occur in quick succession, in volleys lasting as long as two hours.  The “atypical” form of the disorder (called “Type 2” or TN2), is characterized by constant aching, burning, stabbing pain of somewhat lower intensity than Type 1.  Both forms of pain may occur in the same person, sometimes at the same time. The intensity of pain can be physically and mentally incapacitating.

Types of Trigeminal Neuralgia

There are two main types: typical and atypical trigeminal neuralgia.

  • The typical trigeminal neuralgia – form results in episodes of severe, sudden, shock-like pain in one side of the face that lasts for seconds to a few minutes. Groups of these episodes can occur over a few hours.
  • The atypical trigeminal neuralgia – form results in a constant burning pain that is less severe. Episodes may be triggered by any touch to the face. Both forms may occur in the same person. It is one of the most painful conditions and can result in depression.

 

Anatomy Trigeminal Neuralgia

The brain is connected to the body by the spinal cord with spinal nerves sending and receiving impulses and messages to and from the brain. However, there are twelve cranial nerves that directly connect to the body. These nerves are involved with the muscle and sensory function of the head and neck. (The exception is cranial nerve X or the vagus nerve, which is also responsible for the parasympathetic system of the chest and abdomen).

The nerve has three branches that conduct sensations from the upper, middle, and lower portions of the face, as well as the oral cavity, to the brain. The ophthalmic, or upper, branch supplies sensation to most of the scalp, forehead, and front of the head. The maxillary, or middle, branch stimulates the cheek, upper jaw, top lip, teeth and gums, and to the side of the nose. The mandibular, or lower, branch supplies nerves to the lower jaw, teeth and gums, and bottom lip.

Function I

12 Cranial Nerves
Cranial Nerve Name
functions Smell
II Optic Vision
III, IV, VI Oculomotor, Trochlear, Abducens Eye movement
V Trigeminal Facial sensation, chewing
VII Facial Facial movement
VIII Auditory Hearing
IX Glossopharyngeal Taste, swallowing
X Vagus Swallowing, voice modulation, the parasympathetic tone of the body
XI Accessory Neck muscles
XII Hypoglossal Swallowing, speech articulation

The trigeminal nerve (cranial nerve V) is so named because it has three (tri) branches responsible for face sensation; one branch also regulates chewing.

  • The ophthalmic branch (V1) – is responsible for sensation from the scalp, forehead, upper eyelid and tip of the nose.
  • The maxillary branch (V2) – sensation covers the lower eyelid, the side of the nose, the upper lip and cheek, and the upper teeth and gums.
  • The mandibular branch (V3) – is responsible for sensation than of the lower teeth and gums, lower lip, chin, jaw, and part of the ear. It is also responsible for supplying the muscles involved with chewing (mastication), those muscles involved with chewing.

rxharun.com/trigeminal-nerve-12-638-(1)

Causes of Trigeminal Neuralgia

TN is associated with a variety of conditions. TN can be caused by a blood vessel pressing on the trigeminal nerve as it exits the brain stem. This compression causes the wearing away or damage to the protective coating around the nerve (the myelin sheath). TN symptoms can also occur in people with multiple sclerosis, a disease that causes deterioration of the trigeminal nerve’s myelin sheath. Rarely, symptoms of TN may be caused by nerve compression from a tumor, or a tangle of arteries and veins called an arteriovenous malformation. Injury to the trigeminal nerve (perhaps the result of sinus surgery, oral surgery, stroke, or facial trauma) may also produce neuropathic facial pain.

  • In trigeminal neuralgia, also called tic douloureux, the trigeminal nerve’s function is disrupted. Usually, the problem is contact between a normal blood vessel in this case, an artery or a vein — and the trigeminal nerve at the base of your brain. This contact puts pressure on the nerve and causes it to malfunction.
  • Trigeminal neuralgia can occur as a result of aging, or it can be related to multiple sclerosis or a similar disorder that damages the myelin sheath protecting certain nerves. Less commonly, trigeminal neuralgia can be caused by a tumor compressing the trigeminal nerve.
  • Most cases of trigeminal neuralgia are believed to be caused by blood vessels pressing on the root of the trigeminal nerve. This is said to make the nerve transmit pain signals which are experienced as the stabbing pains of trigeminal neuralgia. However, experts are not completely sure of the cause. Pressure on the trigeminal nerve may also be caused by a tumor or multiple sclerosis.

Below is a list of known and suspected causes

  • A blood vessel presses – against the root of the trigeminal nerve.
  • Multiple sclerosis – due to demyelination of the nerve. Trigeminal neuralgia typically appears in the advanced stages of multiple sclerosis.
  • A tumor presses –  against the trigeminal nerve. This is a rare cause.
  • Physical damage to the nerve – this may be the result of injury, a dental or surgical procedure, or infection.
  • Family history (genes, inherited) – 4.1% of patients with unilateral trigeminal neuralgia (affects just one side of the face) and 17% of those with bilateral trigeminal neuralgia (affects both sides of the face) have close relatives with the disorder. Compared to a 1 in 15,000 risks in the general population, 4.1% and 17% indicate that inheritance is probably a factor

A variety of triggers may set off the pain of trigeminal neuralgia, including

  • Shaving
  • Touching your face
  • Eating
  • Drinking
  • Brushing your teeth
  • Talking
  • Putting on makeup
  • Encountering a breeze
  • Smiling
  • Washing your face

Symptoms of Trigeminal Neuralgia

TN presents as attacks of stabbing unilateral facial pain, most often on the right side of the face. The number of attacks may vary from less than 1 per day to 12 or more per hour and up to hundreds per day.

Pain varies, depending on the type of TN, and may range from sudden, severe, and stabbing to a more constant, aching, burning sensation. The intense flashes of pain can be triggered by vibration or contact with the cheek (such as when shaving, washing the face, or applying makeup), brushing teeth, eating, drinking, talking, or being exposed to the wind. The pain may affect a small area of the face or may spread. Bouts of pain rarely occur at night, when the affected individual is sleeping.[rx]

Triggers of pain attacks include the following

  • Chewing, talking or smiling
  • Drinking cold or hot fluids
  • Touching, shaving, brushing teeth, blowing the nose
  • Encountering cold air from an open automobile window

Pain localization is as follows

  • Patients can localize their pain precisely
  • The pain commonly runs along the line dividing either the mandibular and maxillary nerves or the maxillary and ophthalmic portions of the nerve
  • In 60% of cases, the pain shoots from the corner of the mouth to the angle of the jaw
  • In 30%, pain jolts from the upper lip or canine teeth to the eye and eyebrow, sparing the orbit itself
  • In less than 5% of cases, pain involves the ophthalmic branch of the facial nerve

The pain has the following qualities

  • Characteristically severe, paroxysmal, and lancinating
  • Commences with a sensation of electrical shocks in the affected area
  • Crescendos in less than 20 seconds to an excruciating discomfort felt deep in the face, often contorting the patient’s expression
  • Begins to fade within seconds, only to give way to a burning ache lasting seconds to minutes
  • Pain fully abates between attacks, even when they are severe and frequent
  • Attacks may provoke patients to grimace, wince, or make an aversive head movement, as if trying to escape the pain, thus producing an obvious movement, or tic; hence the term “tic douloureux”

Other diagnostic clues are as follows

  • Patients carefully avoid rubbing the face or shaving a trigger area, in contrast to other facial pain syndromes, in which they massage the face or apply heat or ice
  • Many patients try to hold their face still while talking, to avoid precipitating an attack
  • In contrast to migrainous pain, attacks of TN rarely occur during sleep

Diagnosis of Trigeminal Neuralgia

  • No laboratory, electrophysiologic, or radiologic testing is routinely indicated for the diagnosis of TN, as patients with a characteristic history and normal neurologic examination may be treated without further workup.

Strict criteria for TN as defined by the International Headache Society (IHS) are as follows :

  • A – Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting 1 or more divisions of the trigeminal nerve and fulfilling criteria B and C
  • B – Pain has at least 1 of the following characteristics: (1) intense, sharp, superficial or stabbing; or (2) precipitated from trigger areas or by trigger factors
  • C – Attacks stereotyped in the individual patient
  • D – No clinically evident neurologic deficit
  • E – Not attributed to another disorder

IHS criteria for symptomatic TN vary slightly from the strict criteria and include the following 

  • A – Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, with or without persistence of aching between paroxysms, affecting 1 or more divisions of the trigeminal nerve and fulfilling criteria B and C
  • B – Pain has at least 1 of the following characteristics: (1) intense, sharp, superficial or stabbing; or (2) precipitated from trigger areas or by trigger factors
  • C – Attacks stereotyped in the individual patient
  • D – A causative lesion, other than vascular compression, demonstrated by special investigations and/or posterior fossa exploration

A blood count and liver function tests are required if therapy with carbamazepine is contemplated. Oxcarbazepine can cause hyponatremia, so the serum sodium level should be measured after the institution of therapy.

Treatment of Trigeminal Neuralgia

Anticonvulsant medicines—used to block nerve firing—are generally effective in treating TN1 but often less effective in TN2. These drugs include carbamazepine, oxcarbazepine, topiramate, gabapentin, pregabalin, clonazepam, phenytoin, lamotrigine, and valproic acid.

Tricyclic antidepressants such as amitriptyline or nortriptyline can be used to treat pain. Common analgesics and opioids are not usually helpful in treating the sharp, recurring pain caused by TN1, although some individuals with TN2 do respond to opioids.

There are several effective ways to alleviate the pain, including a variety of medications.

  • Carbamazepine, an anticonvulsant drug, is the most common medication that doctors use to treat trigeminal neuralgia. In the early stages of the disease, carbamazepine controls pain for most people. When a patient shows no relief from this medication, a physician has cause to doubt whether trigeminal neuralgia is present. However, the effectiveness of carbamazepine decreases over time. Possible side effects include dizziness, double vision, drowsiness, and nausea.
  • Baclofen is a muscle relaxant. Its effectiveness may increase when it is used with either carbamazepine or phenytoin. Possible side effects include confusion, depression, and drowsiness.
  • Phenytoin, an anticonvulsant medication, was the first medication used to treat trigeminal neuralgia. Possible side effects include gum overgrowth, balance disturbances, and drowsiness.
  • Oxcarbazepine, a newer medication, has been used more recently as the first line of treatment. It is structurally related to carbamazepine and may be preferred because it generally has fewer side effects. Possible side effects include dizziness and double vision.
  • Other medications include gabapentin, clonazepam, sodium valporate, lamotrigine and topiramate.
  • Lamotrigine 200–400 mg –  as add-on therapy was shown to be an effective and safe treatment, in comparison with CBZ alone, for management of TN [] in 67 % of included patients with a mean age of 63 years (range 44–84). The reported side effects were a headache, dizziness, and a skin rash.
  • Tizanidine 12–18 mg  – showed no greater effectiveness than CBZ or placebo in 22 patients, with response rates of 56 % for tizanidine, 66 % for CBZ, and 40 % for placebo [].
  • Baclofen –  was superior to placebo in reducing the number of painful paroxysms, with a 70 % response rate in 10 patients with a mean age of 64 years (range 36–77) []. In a small group of 12 patients, tocainide was as effective as CBZ in reducing the frequency and severity of pain attacks on a Visual Analogue Scale (VAS), with a response rate of 75 % [].
  • Pimozide – was even more effective than CBZ in a single trial including 48 patients, with a response rate of 100 % for pimozide versus 56 % for CBZ []. The reported side effects were physical and mental retardation, hand tremors, and memory impairment in 83 % of the pimozide group. Drugs with local administration have been studied in single trials as well.
  • Topical ophthalmic anesthesia (proparacaine) –  was not effective in a single placebo-controlled trial in 47 patients [].
  • Botulinum toxin (BTX) type A – administered subcutaneously, proved to be effective (with a 50 % response rate, defined as a decrease in the VAS score of >50 %) in three placebo-controlled trials, which included a total of 102 patients with a mean age of 57 years (range 30–88) []. The reported side effects were transient, such as facial asymmetry, hematoma, or edema.
  • Sumatriptan – administered subcutaneously, was more effective than placebo (response rate 83 %) in a single trial in a small group of 24 patients []. Lidocaine 8 % applied on the mucosa or administered via the intranasal route was effective in 85 % of 49 patients in two placebo-controlled trials, but the effect diminished after approximately 3 h [].

Follow chart

Type Drug Brand Name Manufacturer
Anti-epileptic Carbamazepine Carbatrol, Equetro, Tegretol, Tegretol XR Shire Pharmaceuticals, Validus Pharmaceuticals, Novartis Pharmaceuticals
Anti-epileptic Felbamate Felbatol Meda Pharmaceuticals
Anti-epileptic Gabapentin Neurontin Pfizer
Anti-epileptic Lamotrigine Lamictal GlaxoSmithKline
Anti-epileptic Levetiracetam Keppra UCB
Anti-epileptic Oxcarbazepine Trileptal Novartis Pharmaceuticals
Anti-epileptic Pregabalin Lyrica Pfizer
Anti-epileptic Tiagabine Gabitril Cephalon
Anti-epileptic Topiramate Topamax Ortho-McNeil-Janssen Pharmaceuticals
Anti-epileptic Valproate Depakote, Depakote ER, Depakene, Depacon, Valproate, Valrelease Abbott Laboratories
Anti-epileptic Zonisamide Zonegran Dainippon
Anti-spasticity Baclofen Lioresal, Lioresal Intrathecal, Gablofen Various Drug Companies
Anti-epileptic Phenytoin Dilantin, Phenytek
Anti-epileptic Clonazepam Klonopin, Rivatril
Anti-depressant Amitriptyline Elavil
Anti-depressant Protriptyline Vivactil
Anti-depressant Nortriptyline Pamelor
Anti-depressant Fluoxetine Prozac, Seronil, Fontex
Anti-depressant Trazodone Desyrel
Opioids Morphine
Opioids Codeine
Opioids Fentanyl
Opioids Hydrocodone
Opioids Hydromorphone
Dermatologic Lidocaine
Dermatologic Lidoderm patch
Dermatologic Lidocaine cream
Dermatologic Capsaicin
Antianxiety SSRIs Paxil, Celexa
Antianxiety Benzodiazepines Ativan, Valium, Xanax, Klonopin
Analgesic Ultram Tramadol
Analgesic Ketamine
SNRIS Venlafaxine Effexor – serotonin/norepinephrine reuptake inhibitors
SNRIS Duloxetine Cymbalta – serotonin and noradrenaline reuptake inhibitor

Surgery of Trigeminal Neuralgia

If medications have proven ineffective in treating trigeminal neuralgia, there are several surgical procedures that may help control the pain. Surgical treatment is divided into two categories: percutaneous (through the skin) and open. In general, percutaneous approaches are preferred in older or medically frail patients, in patients with multiple sclerosis, or in individuals who have failed to attain pain relief from the open approach. The open approach is recommended for younger and healthier patients. All of the procedures have varying success rates and some side effects, such as recurrence of pain and facial numbness.

  • Microvascular decompression – involves microsurgical exposure of the trigeminal nerve root, identification of a blood vessel that may be compressing the nerve, and gentle movement of the blood vessel away from the point of compression. Decompression may reduce sensitivity and allow the trigeminal nerve to recover and return to a more normal, pain-free condition. While this generally is the most effective surgery, it also is the most invasive, because it requires opening the skull through a craniotomy. There is a small risk of decreased hearing, facial weakness, facial numbness, double vision, and stroke or death. The risk of facial numbness, however, is less likely with procedures that involve damaging the trigeminal nerve.
  • Percutaneous stereotactic rhizotomy – Treats trigeminal neuralgia through the use of electrocoagulation (heat). It can relieve nerve pain by destroying the part of the nerve that causes pain and suppressing the pain signal to the brain. The surgeon passes a hollow needle through the cheek into the trigeminal nerve. A heating current, which is passed through an electrode, destroys some of the nerve fibers.
  • Percutaneous glycerol rhizotomy – Utilizes glycerol injected through a needle into the area where the nerve divides into three main branches. The goal is to damage the nerve selectively in order to interfere with the transmission of the pain signals to the brain.
  • Percutaneous balloon compression – Utilizes a needle that is passed through the cheek to the trigeminal nerve. The neurosurgeon places a balloon in the trigeminal nerve through a catheter. The balloon is inflated where fibers produce pain. The balloon compresses the nerve, injuring the pain-causing fibers. After several minutes, the balloon and catheter are removed.

  • Stereotactic radiosurgery – (through such procedures as Gamma Knife, Cyberknife, LINAC) delivers a single highly concentrated dose of ionizing radiation to a small, precise target at the trigeminal nerve root. This treatment is non-invasive and avoids many of the risks and complications of open surgery and other treatments. Over a period of time and as a result of radiation exposure, the slow formation of a lesion in the nerve interrupts the transmission of pain signals to the brain.
  • Motor cortex stimulation – is another option, but often is considered a last resort because it can be very difficult to predict which patients may benefit. While about half of patients experience pain relief, it tends to be short-term. This is an open procedure with all of the risks of microvascular decompression, but without the high success rates. The benefits of surgery should always be weighed carefully against its risks. Although a large percentage of trigeminal neuralgia patients report pain relief after surgery, there is no guarantee that surgery will help every individual.
  • Percutaneous procedures on the Gasserian ganglion-gamma knife and microvascular decompression are recommended, efficacy-proven surgical treatment options for medical refractory TN. Surgery for TN is either destructive (ablative), where the trigeminal nerve sensory function is intentionally destroyed, or non-destructive, where the trigeminal nerve is decompressed preserving its normal function.
  • Gasserian ganglion percutaneous techniques –  are all destructive and include radiofrequency thermocoagulation (RFT), balloon compression (BC) and percutaneous glycerol rhizolysis (PGR). Ninety percent of patients report pain relief following these procedures. After 1 year, 68–85% of patients are still pain-free, after 3 years this is reduced to 54–64% and after 5 years only 50% of patients are still pain-free following RFT. The most common side effects are sensory loss (50%) which extremely decreases the quality of life [], dysesthesias (6%), anesthesia Dolorosa (4%), corneal numbness with the risk of keratitis (4%). Gasserian ganglion therapies require short-acting anesthetics, are primarily overnight minor procedures with extremely low mortality [].
  • In gamma knife surgery – a focused beam of radiation is aimed at the trigeminal root in the posterior fossa. One year after gamma knife surgery, 69% of patients are pain-free without additional medication. At 3 years, 52% are still pain-free. The development of pain relief can be delayed (mean 1 month). Side effects are sensory complications in 6% that may develop with a delay of up to 6 months, facial numbness in 9–37% which improves over time and paresthesias in 6–13% []. Quality of life improves by 88% []. The main disadvantage of gamma knife surgery is the treatment expense that limits widespread usage making it a reserve treatment option for patients that cannot undergo open surgery or have blood coagulation problems (e.g. are receiving warfarin).
  • Microvascular decompression – achieves the most sustained pain relief with 90% of patients reporting initial pain relief and over 80% still pain-free after 1 year, with 75% after 3 years and 73% after 5 years remaining pain-free. It is, however, a major surgical procedure that entails craniotomy to reach the trigeminal nerve in the posterior fossa. The average mortality rate ranges from 0.2% to 0.5%, and up to 4% of patients suffer from major problems such as cerebrospinal fluid (CSF) leakage, infarcts or hematomas. The most common complications are aseptic meningitis (11%), sensory loss (7%) and hearing loss (10%) as long-term complications [].

Surgery In Advance stage

A rhizotomy (rhizolysis) is a procedure in which nerve fibers are damaged to block pain. A rhizotomy for TN always causes some degree of sensory loss and facial numbness. Several forms of rhizotomy are available to treat trigeminal neuralgia:

  • Balloon compression – works by injuring the insulation on nerves that are involved with the sensation of light touch on the face. The procedure is performed in an operating room under general anesthesia. A tube called a cannula is inserted through the cheek and guided to where one branch of the trigeminal nerve passes through the base of the skull. A soft catheter with a balloon tip is threaded through the cannula and the balloon is inflated to squeeze part of the nerve against the hard edge of the brain covering (the dura) and the skull. After about a minute the balloon is deflated and removed, along with the catheter and cannula. Balloon compression is generally an outpatient procedure, although sometimes the patient may be kept in the hospital overnight. Pain relief usually lasts one to two years.
  • Glycerol injection – is also generally an outpatient procedure in which the individual is sedated with intravenous medication. A thin needle is passed through the cheek, next to the mouth, and guided through the opening in the base of the skull where the third division of the trigeminal nerve (mandibular) exits. The needle is moved into the pocket of spinal fluid (cistern) that surrounds the trigeminal nerve center (or ganglion, the central part of the nerve from which the nerve impulses are transmitted to the brain). The procedure is performed with the person sitting up, since glycerol is heavier than spinal fluid and will then remain in the spinal fluid around the ganglion. The glycerol injection bathes the ganglion and damages the insulation of trigeminal nerve fibers. This form of rhizotomy is likely to result in recurrence of pain within a year to two years. However, the procedure can be repeated multiple times.
  • Radiofrequency thermal lesioning – (also known as “RF Ablation” or “RF Lesion”) is most often performed on an outpatient basis. The individual is anesthetized and a hollow needle is passed through the cheek through the same opening at the base of the skull where the balloon compression and glycerol injections are performed. The individual is briefly awakened and a small electrical current is passed through the needle, causing tingling in the area of the nerve where the needle tips rests. When the needle is positioned so that the tingling occurs in the area of TN pain, the person is then sedated and the nerve area is gradually heated with an electrode, injuring the nerve fibers.  The electrode and needle are then removed and the person is awakened. The procedure can be repeated until the desired amount of sensory loss is obtained; usually a blunting of sharp sensation, with preservation of touch. Approximately half of the people have symptoms that reoccur three to four years following RF lesioning. Production of more numbness can extend the pain relief even longer, but the risks of anesthesia dolorosa also increase.
  • Stereotactic radiosurgery – (Gamma Knife, Cyber Knife) uses computer imaging to direct highly focused beams of radiation at the site where the trigeminal nerve exits the brain stem. This causes the slow formation of a lesion on the nerve that disrupts the transmission of sensory signals to the brain. People usually leave the hospital the same day or the next day following treatment but won’t typically experience relief from pain for several weeks (or sometimes several months) following the procedure.  The International RadioSurgery Association reports that between 50 and 78 percent of people with TN who are treated with Gamma Knife radiosurgery experience “excellent” pain relief within a few weeks following the procedure. For individuals who were treated successfully, almost half have recurrence of pain within three years.
  • Microvascular decompression (MVD) – is the most invasive of all surgeries for TN, but also offers the lowest probability that pain will return. About half of individuals undergoing MVD for TN will experience recurrent pain within 12 to 15 years.  This inpatient procedure, which is performed under general anesthesia, requires that a small opening be made through the mastoid bone behind the ear. While viewing the trigeminal nerve through a microscope or endoscope, the surgeon moves away the vessel (usually an artery) that is compressing the nerve and places a soft cushion between the nerve and the vessel. Unlike rhizotomies, the goal is not to produce numbness in the face after this surgery. Individuals generally recuperate for several days in the hospital following the procedure, and will generally need to recover for several weeks after the procedure.
  • A neurectomy (also called partial nerve section) – which involves cutting part of the nerve, may be performed near the entrance point of the nerve at the brain stem during an attempted microvascular decompression if no vessel is found to be pressing on the trigeminal nerve. Neurectomies also may be performed by cutting superficial branches of the trigeminal nerve in the face. When done during microvascular decompression, a neurectomy will cause more long-lasting numbness in the area of the face that is supplied by the nerve or nerve branch that is cut. However, when the operation is performed in the face, the nerve may grow back and in time sensation may return.  With neurectomy, there is risk of creating anesthesia dolorosa.

Surgical treatment for TN2 is usually more problematic than for TN1, particularly where vascular compression is not detected in brain imaging prior to a proposed procedure. Many neurosurgeons advise against the use of MVD or rhizotomy in individuals for whom TN2 symptoms predominate over TN1, unless vascular compression has been confirmed. MVD for TN2 is also less successful than for TN1.

Alternative Treatment of Trigeminal Neuralgia

  • Ignition hypothesis – According to the ignition hypothesis, based on recent advances in the understanding of the electrical behavior of injured sensory neurons and on findings from histopathologic observations obtained from patients undergoing MVD, injury of trigeminal afferent neurons in the trigeminal root or ganglion makes these axons and axotomized somata hyperexcitable, giving rise to pain paroxysms as a result of synchronized afterdischarge activity.
  • Transcranial magnetic stimulation – Repetitive transcranial magnetic stimulation (rTMS) is an emerging technology that introduces the possibility of assessing whether patients with trigeminal neuropathic pain will respond to direct epidural cortical stimulation by first measuring their response to a trial of non-invasive cortical stimulation. In a study of 24 TN patients given rTMS to the motor cortex at 20 Hz daily for 5 days, pain ratings decreased by approximately 45% for 2 weeks []. In a different study of 12 patients with chronic intractable TN who had failed surgical treatment, 58% experienced a greater than 30% reduction in pain after receiving repetitive TMS [].
  • Alternative Medicine – This section contains a wide variety of so-called “alternative” treatments. Some are medical treatments that are generally used for other purposes, but which have anecdotally been used to try to treat facial neuralgia pain. Most of this anecdotal information has been gathered from feedback with facial neuralgia sufferers. They may or may not be effective; the important point is that someone has tried them. Some of the treatments in this category are what is often known as “pseudo-scientific”. That is, there seems to be no rigorous scientific basis for them.
  • Anesthetics – There is some anecdotal evidence for the use of various anesthetic substances for treating acute attacks of facial neuralgias. Some of these substances should only be used under professional supervision. In general, any pain relief is likely to be short-lived. In addition, these treatments are probably more effective for cases of atypical TN than for classical TN.
  • Capsaicin – Has been anecdotally used, especially for atypical forms of TN and atypical facial pain. This is becoming more of a mainstream treatment and possibly should be included as a standard drug treatment instead of an alternative treatment.
  • Lidocaine cream/patch –  Again, relatively harmless if used properly.
  • Lidocaine nose sprays
  • Therapeutics – This group includes a variety of substances that have been suggested for facial neuralgia pain. Some of the substances may raise controversy, but an attempt has been made to avoid listing any substances that are directly harmful or poisonous.
  • Herbal remedies – various herbal regimes have been suggested for TN.
  • Homeopathy – a controversial treatment, but has been used by some.
  • Vitamin B12 –In her B12 study “DO TN patients have a B12 deficiency and Is there a role of Vitamin B12 in TN Management:  Irene Wood found those who used B12 supplements were able to lessen their pain, and some were also able to achieve “no pain no medication. Many in our Association are now using B12 supplements to help manage their pain. The hypothesis is repairing of the myelin (re-myelination). Low Vitamin B12 Syndrome in Trigeminal Neuralgia.
  • Musculoskeletal – These treatments treat the muscles rather than dealing with the nerve directly. At the very least, this relaxation can make it easier to deal with the pain. It is also possible that some cases of facial neuralgias are made worse by muscular strain, in which case these treatments could provide direct help. For classical TN, these treatments are likely to have little effect; however, they may well help those with more atypical symptoms.
  • ChiropracticAtlas Orthogonal Chiropractic focuses on aligning the C1, C2. Has helped others in achieving pain-free.
  • Myotherapy/myofascial release therapy
  • Cranial Osteopathy/Craniosacral therapy
  • Acupuncture – These treatments treat the nervous system directly (at least in theory). For lack of a better term, they can be classified under the term acupuncture-like. All have been reported to be used for facial neuralgia pain; as with all alternative treatments, the results have been inconclusive. It is used relatively common; however, reliable success rates are almost impossible to calculate.
  • Laser treatment – new, experimental treatment. The mechanism may be somewhat similar to acupuncture
  • Moxa therapy – similar to normal acupuncture.
  • TENS – electrical treatment; effects may be similar to acupuncture.
  • Psychological Hypnosis – This has been suggested for atypical as well as classical forms of TN. Only anecdotal evidence for it seems to exist so far. However, even some reputable textbooks do mention it as a reputable treatment.

Who is affected?

Trigeminal neuralgia occurs most often in people over age 50, although it can occur at any age, including infancy. The possibility of TN being caused by multiple sclerosis increases when it occurs in young adults. The incidence of new cases is approximately 12 per 100,000 people per year; the disorder is more common in women than in men.


References

By

Snoring; Causes, Symptoms, Diagnosis, Treatment

Snoring is the vibration of respiratory structures and the resulting sound due to obstructed air movement during breathing while sleeping. In some cases, the sound may be soft, but in most cases, it can be loud and unpleasant. Snoring during sleep may be a sign, or first alarm, of obstructive sleep apnea(OSA). Research suggests that snoring is one of the factors of sleep deprivation.

Snoring and OSA syndrome are prevalent and important causes of sleep disturbance. Snoring, historically considered to be only a habitual annoyance, has significant physical and social consequences. OSA is now considered to be a major public health concern with significant morbidity and mortality. CPAP is considered the treatment of choice for OSA syndrome, but poor patient acceptance and compliance remain problematic. Surgical procedures have been developed to alter the offending anatomic abnormalities responsible for OSA. Identification of the offending anatomic site with application of the most appropriate surgical procedure is essential for effective surgical treatment of OSA. When the region of the retropalate is correctly identified as the site of obstruction, UPPP can effectively treat OSA in a majority of patients. Surgical correction of nasal obstruction is advocated in conjunction with sleep apnea surgery when nasal obstruction exists. In OSA patients with retrolingual airway obstruction, a number of surgical procedures have been performed, with or without UPPP, with some improvement over UPPP alone. MMO has been effective in the treatment of OSA in patients with significant retrolingual airway obstruction with contributing skeletal abnormalities and in patients who have failed multiple other surgical procedures. MMO, however, is a procedure of considerable magnitude, requiring extensive oromaxillofacial surgical expertise. MMO is likely appropriate only in a limited number of patients. Tracheostomy is completely effective in the treatment of OSA syndrome but is undesirable to patients and is associated with significant physical and emotional morbidity.

snoring

Snoring occurs when the muscles of the airway relax too much during sleep and vibrate (creating noise) when air we breathe passes in and out. Most people will snore at some time, however loud or chronic snoring can disrupt sleep-quality and disturb others. Particularly when loud, it is often associated with other sleep-related breathing disorders, such as obstructive sleep apnoea (OSA).

Anatomy of Snoring

HOW you snore reveals WHY you snore
Type of snoring What it may indicate
Closed-mouth snoring May indicate a problem with your tongue
Open-mouth snoring May be related to the tissues in your throat
Snoring when sleeping on your back Probably mild snoring—improved sleep habits and lifestyle changes may be effective cures
Snoring in all sleep positions Can mean your snoring is more severe and may require a more comprehensive treatment

snoring-causes

Common Causes of Snoring

  • Allergies
  • Eating too much at night
  • Nasal congestion
  • Deformity of the nose
  • Consumption of alcohol close to bed-time, especially if the amount is large
  • Being overweight or obese
  • Pregnancy
  • Swelling of the muscular part of the roof of the mouth
  • Swollen adenoids or tonsils, especially in children
  • Medications, including sleeping tablets
  • Sleep position – sleeping on your back may cause your throat muscles and tongue to relax; the tongue is then more likely to fall back and compress the airway, causing snoring or making snoring louder.
  • Age – As you reach middle age and beyond, your throat becomes narrower, and the muscle tone in your throat decreases. While you can’t do anything about growing older, lifestyle changes, new bedtime routines, and throat exercises can all help to prevent snoring.
  • Being overweight or out of shape – Fatty tissue and poor muscle tone contribute to snoring. Even if you’re not overweight in general, carrying excess weight just around your neck or throat can cause snoring. Exercising and losing weight can sometimes be all it takes to end your snoring.
  • The way you’re built – Men have narrower air passages than women and are more likely to snore. A narrow throat, a cleft palate, enlarged adenoids, and other physical attributes that contribute to snoring are often hereditary. Again, while you have no control over your build or gender, you can control your snoring with the right lifestyle changes, bedtime routines, and throat exercises.
  • Nasal and sinus problems – Blocked airways or a stuffy nose make inhalation difficult and create a vacuum in the throat, leading to snoring.
  • Alcohol, smoking, and medications – Alcohol intake, smoking, and certain medications, such as tranquilizers like lorazepam (Ativan) and diazepam (Valium), can increase muscle relaxation leading to more snoring.
  • Sleep posture – Sleeping flat on your back causes the flesh of your throat to relax and block the airway. Changing your sleep position can help.

Structural factors related to craniofacial bony anatomy that predisposes patients with OSA to pharyngeal collapse during sleep, e.g

  • Retrognathia and micrognathia
  • Maxillo-Mandibular hypoplasia
  • Adenotonsillar hypertrophy, particularly in children and young adults
  • High, arched palate (particularly in women)

Nonstructural risk factors for OSA include

  • Central fat distribution
  • Male sex
  • Age
  • Postmenopausal state
  • Alcohol use
  • Sedative use
  • Other conditions associated with the development of OSA are as follows: Hypothyroidism, Stroke, and Acromegaly.

Smoking and alcohol consumption are often considered as risk factors for sleep apnea despite the limited evidence, especially in females.

It is well-known that alcohol consumption before going to bed worsens sleep apnea in males and that smoking is related to snoring in males and females.

snoring-causes

An overnight sleep study can be performed to assess the nature and severity of snoring, and to check for other sleep-disorders that often accompany snoring, especially obstructive sleep apnoea (OSA).

Symptoms of Snoring

Obstructive Sleep Apnea (OSA) symptoms begin insidiously and are often present for years before the patient is referred for evaluation.

Nocturnal symptoms may include:

  • Frequent loud snoring, witnessed apneas, restless sleep, nocturia and mouth breathing associated with the presence of obstructive SDB.
  • The hallmark of OSA are the witnessed apneas during sleep.

Daytime symptoms may include:

  • Nonrestorative sleep (e.g., “waking up as tired as when they went to bed”)
  • Morning headache, dry or a sore throat
  • Excessive daytime sleepiness (EDS) that usually begins during quiet activities
  • Daytime fatigue/tiredness
  • Cognitive deficits; memory and intellectual impairment
  • Sexual dysfunction, including impotence and decreased libido.
  • Disruptive snoring: A history of disruptive snoring has 71% sensitivity in predicting sleep-disordered breathing (SDB).
  • Disruptive snoring and witnessed apneas: These factors taken together have 94% specificity for SDB.

Physical exam findings may include:

  • Obesity – Body mass index (BMI) greater than 30 kg/m
  • Large neck circumference – Greater than 43 cm (17 in) in men and 37 cm (15 in) in women
  • Abnormal (increased) Mallampati score (Mallampati score assessment (originally designed for quantifying different intubation) is a simple and fast method for assessing upper airway dimensions)
  • Enlarged, or “kissing,” tonsils (3+ to 4+)
  • Retrognathia or micrognathia, macroglossia
  • Large degree of overjet
  • High-arched hard palate
  • Systemic arterial hypertension, present in approximately 50% of patients with OSA

Clinical assessment of tonsillar size (Brodsky score) is a weak predictor of presence or severity of obstructive SDB. During an evaluation, other differential diagnoses must be considered before labeling as sleep apnea.

Causes of nocturnal dyspnea include bronchial asthma, gastroesophageal reflux disease, and panic disorder. EDS might be a result of poor sleep hygiene, alcohol or drug abuse, atypical depression, and narcolepsy. Nocturia is prevalent and increases sharply with age. It might be caused by urological and other medical conditions such as hypertrophic benign prostate, diabetes mellitus, congestive heart failure, renal disease, diabetes insipidus and intake of diuretic medication.

Treatment of Snoring

All patients with OSA should be counseled about the potential benefits of therapy and the hazards of going without treatment.

Non Pharmacological Measure including Diet, Devices and Surgery.

Pharmacological

  • Treatment depends in part on the severity of the sleep-disordered breathing (SDB). People with mild apnea have a wider variety of options, while people with moderate-to-severe apnea should be treated with nasal continuous positive airway pressure (CPAP).
  • CPAP treatment is indicated for all OSA patients with an RDI of 30 or more events per hour, regardless of symptoms, based on the increased risk of hypertension.
  • Treatment with CPAP is indicated for patients with an RDI of five to 30 events per hour for documented cardiovascular diseases to include hypertension, ischemic heart disease or stroke.
  • A randomized clinical trial shows significant improvement in all sleep-related symptoms, including snoring, witnessed apnoeas, choking, nightmares, daytime hypersomnolence (all p<0.001) and nocturia (p=0.049), in the CPAP group. In elderly patients with severe sleep apnea, CPAP treatment achieves an improvement in all domains of quality of life measured by QSQ, including day-time and night-time symptoms and social and emotional domains.
  • Effective CPAP is defined as the pressure level at which all apneas, hypopneas, respiratory-effort related arousals and snoring events are abolished. This pressure level could be maintained constantly throughout the night (Standard CPAP) or it could be automatically adjusted by the CPAP-device according to the patient needs (Auto-CPAP).
  • In patients with mild-to-severe obstructive sleep apnea who refuse or reject nasal CPAP therapy or who cannot tolerate CPAP due to persistent massive nasal mask air leakage or discomfort, BiPAP therapy should be tried next. If this therapy fails or is rejected, Oral Appliances should be considered.
  • Adequate adherence to PAP is defined as more than 4.5 hours of PAP use per night on a routine basis. Maximal improvement in neurocognitive symptoms can require as long as two months of PAP treatment.

Oral appliances

  • Oral appliances are considered an alternative to CPAP for treating OSA. Mandibular advancement devices/tongue retaining devices reduce sleep-disordered breathing and subjective daytime sleepiness, improve the quality of life compared with control treatments and are recommended in the treatment of patients with mild to moderate OSA.
  • General and behavioral measures, such as weight loss, avoidance of alcohol for four to six hours before bedtime, and sleeping on one’s side rather than on the stomach or back, are elements of conservative nonsurgical treatment.
  • Because obesity is a major predictive factor for OSA, weight reduction reduces the risk of OSA. The best data suggest that a 10% reduction in weight leads to a 26% reduction in the respiratory disturbance index (RDI). Patients with sleep-disordered breathing should be advised to have sufficient sleep and appropriate sleep hygiene.

Sleep hygiene instructions

  • Restricting caffeine after lunch
  • Restriction of other drinks or foods with activating properties (e.g. coke, tea, chocolate)
  • No alcohol intake in the evening
  • Restriction of smoking especially close to bedtime
  • Regular physical activity
  • Reduction of noises in the bedroom
  • Instructions to make the bed comfortable and to keep the bedroom dark during the night
  • Proper ventilation of the bedroom

Positional treatment aims at avoiding the supine horizontal posture while sleeping. This method might be effective in patients with positional OSA. Tennis ball attached to the back of a night-shirt, a variety of straps and vests with foam attachments, auditory alarms aimed at training patients to refrain from sleeping in the supine posture are a number of devices used for postural therapy.

Surgery: Upper airway surgery and Barriatric Surgery for weight loss.

Medications

  • Dronabinol – Nonselective agonist of cannabinoids type I and type II receptor reduces central apneas and reduction in AHI index in small studies but still need further safety data to be estabilshed treatment.
  • Modafinil –  is approved by the US Food and Drug Administration (FDA) for use in patients who have residual daytime sleepiness despite optimal use of CPAP. The most improvement has been seen in patients who have taken modafinil at doses of 200-400 mg/d. The mechanism of action of modafinil in wakefulness is unknown. It has wake-promoting actions similar to sympathomimetic agents.
  • Armodafinil – the R-enantiomer of modafinil, is also now FDA approved for use in these patients. Patients in whom noninvasive medical therapy (e.g., CPAP, BiPAP, OAS) fails should be offered surgical options.

Surgery

  • Various surgical techniques are available for treatment of OSA. Their aim is to permanently increase upper airway patency and decrease pharyngeal resistance. Surgery may be applied as a first-line therapy in selected patients with mild OSA who have surgically correctible anatomical abnormalities contributing to upper airway collapse during sleep.
  • Nasal surgery, radiofrequency tonsil reduction, tongue base surgery, uvulopalatal flap, laser midline glossectomy, tongue suspension and genioglossus advancement cannot be recommended as single interventions. Uvulopalatopharyngoplasty, pillar implants, and hyoid suspension should only be considered in selected patients, and potential benefits should be weighed against the risk of long-term side-effects.
  • Hypoglossal nerve stimulation for the treatment of OSA may be a safe and effective alternative for improving OSA outcomes in individuals with moderate to severe OSA who have difficulties with CPAP therapy.
  • The most appropriate treatment for snoring varies according to the severity of snoring, presence of sleep apnoea, age, body-weight, degree of daytime sleepiness, alcohol-consumption, medical history and the anatomy of the upper airway. A Sleep Physician is a doctor who specialises in treating patients with snoring and other sleep-disorders, and who is qualified to help sufferers make an informed decision about which treatment is the most appropriate.

 Theravent

  • Theravent Snoring Therapy is available in Australia for patients with snoring (but no obstructive sleep apnoea).  The treatment involves small adhesive devices that cover the nostrils.  Similar to Provent Therapy, the unique valve system is designed to eliminate snoring by increasing the pressure inside the airway.
  • Theravent is an effective treatment for many patients with troublesome snoring, particularly when combined with other conservative snoring treatments (including lateral sleep and weight-reduction).

Exclusively Lateral Sleep

  • Exclusively lateral sleep can be an effective, non-invasive treatment of snoring and obstructive sleep apnoea.  It achieves this by preventing the tongue, soft palate and uvula from falling backward under the effect of gravity, thereby causing the pharyngeal airway to be restricted. This, in turn, results in an increased speed of air-flow through the narrowed airway, causing an increase in soft-tissue vibration and resultant snoring.  A variety of simple measures can be implemented to encourage exclusively lateral sleep, such as the use of a bolster pillow placed lengthwise in the bed (to lean against) or pinning tennis balls (or the like) to the back of a pajama top.  As the tennis ball causes discomfort to the wearer when supine, it typically causes the wearer to turn back to a lateral position.  Within a few weeks, most people learn the habit of sleeping laterally and will no longer require tennis balls or similar measures.  Exclusively lateral sleep is limited however in its effectiveness, particularly in sufferers with severe obstructive sleep apnoea.  In this case alternative treatments are required.

Night Shift Device

snoring-causes

  • Night Shift is a new lateral sleep position aid that assists patients to sleep exclusively on their side.  Many patients have obstructive sleep apnoea that is significantly worse (or only present) when sleeping on their back (the supine position).   The device accurately monitors sleep-position and vibrates when supine sleep is detected, helping many patients with position-related airway disorders to avoid other OSA treatments. It records positional data and snoring volumes that can be downloaded, either to provide you with information on your sleep, or to provide to your Sleep Physician to monitor the progress of your treatment.
  • Night Shift can also be used in conjunction with other OSA treatments, including Provent Therapy.  Patients who require CPAP can use Night Shift as well to lower their nightly CPAP setting.
  • For ethical reasons, we do not sell Night Shift or any other treatment device, but our doctors may recommend a trial based on the results of your sleep study.

Weight-loss

  • Weight loss will generally decrease the severity of snoring, although not all people who snore are overweight, but weight gain will typically make existing snoring even worse.  Losing even a little weight can reduce fatty tissue in the back of the throat and decrease snoring. In some patients, weight loss may not cure snoring, but can significantly reduce its loudness

Cessation of Tobacco Smoking

  • In addition to causing cancer and being a major health risk, tobacco smoke causes the walls of airways to retain fluid and swell (this is called oedema). This causes the airway to narrow, worsening snoring (and sleep apnoea). Smokers are 4 to 5 times more likely than non-smokers to suffer from snoring and obstructive sleep apnoea. Nicotine also contributes to insomnia and poor sleep-habits.

Mandibular Advancement Splint (MAS)

  • A Mandibular Advancement Splint is a small device (a type of dental splint) which is placed in the mouth during sleep, causing the lower jaw and tongue to be held more forward than usual. This in turn opens the pharyngeal airway, resulting in a lower rate of air-flow.
  • This minimises vibration of the tissues at the back of the pharynx, thereby reducing the volume of snoring. However, there are a number of problems which can occur for users of a MAS, including a build-up of excessive amounts of saliva, discomfort of jaws and teeth, problems with the gums and other oral tissues with certain types of MAS, particularly if fitted incorrectly and in a significant percentage of patients, permanent repositioning of the teeth and an altered bite over a period of years.

Continuous Positive Airway Pressure (CPAP)

  • As for obstructive sleep apnoea (OSA), CPAP is currently the most effective treatment for simple snoring. CPAP involves the use of a compact air pump to deliver a continuous flow of pressurized air (via a mask) to an individual’s airway. This pressurised air acts as a pneumatic splint and prevents the airway from collapsing, which in turn causes snoring to cease. Each individual’s pressure-requirement differs, depending on a variety of factors, including weight and severity of snoring. These and other details of

Nasal Steroids and Allergy Treatments

  • Naso-pharyngeal congestion from allergies can also contribute to a narrowing of the airways.  Nasal congestion limits the amount of air a person can breathe through their nose while asleep.  This can be caused by the presence of an allergen in an individual’s immediate environment, resulting in an inflammatory response and mucosal swelling, which blocks the nose.
  • Mouth-breathing is then the only available means to ensure that sufficient oxygen is delivered to the body. Nasal steroids can be an effective way to combat the underlying allergic reaction, eg, with prescription agents such as ‘Nasonex’.  Certain over-the-counter nasal steroids are also available from pharmacies.

Non-Steroidal Over-The-Counter Nasal Sprays and Other Anti-Allergy Treatments

  • Other over-the-counter treatments may also be beneficial in patients prone to nasal allergies or troublesome nasal congestion at night-time.  The most common cause of nasal congestion is temporary swelling of nasal passages due to colds or allergic reactions to pollen, dust, mould, animals or some foods.
  • These can cause the lining of the nasal membrane to become inflamed, and mucus to thicken and become acidic. There are a number of over-the-counter nasal sprays that can be helpful in the short term, eg, FESS Nasal Spray, a non-medicated saline nasal spray.
  • Nasal sprays like Afrin, Neo-Synephrine, NasalCrom (Cromyln) and anti-histamines can also be useful as decongestants. However the use of such sprays for more than 72 hours can cause a rebound, negative effect.  Allergy desensitization treatments will sometimes be recommended by a Sleep Physician, Allergist or General Practitioner.

snoring-causes

ENT Interventions and Surgery and Other Procedures on the Soft Palate

  • When narrowing is due to structural abnormality, ENT surgery can be very helpful as a means of opening the nasal passages, thereby improving nasal air-flow and eliminating the sufferer’s need for mouth-breathing.

Surgical procedures which have been used in the hope of reducing snoring include uvulopalatopharyngectomy (UPPP), radio frequency uvulopalatopharyngectomy (RFUPPP) and laser-assisted uvuloplasty (LUAP). These treatments tend to be painful and expensive, and they often fail to cure snoring, especially when this is loud.  They have no place as a treatment for snorers who also suffer from moderate or severe OSA (and in fact, can complicate later treatment of OSA with CPAP).

  • Injection snoreplasty is a nonsurgical treatment for snoring whereby the soft palate is injected in front of the uvula with a hardening agent. This creates an inflammatory reaction and results in scar tissue, which in turn stiffens the soft palate and ultimately reduces the amount of palatal tissue ‘flutter’.
  • When this is the cause of snoring, the treatment can result in reduced snoring volume. Unfortunately, a number of other pharyngeal tissues can vibrate and cause snoring and this technique cannot assist when this is the case. Also, this is presently a new treatment, with limited long-term evidence of its effectiveness.

External Nasal Strips

  • Nasal strips such as ‘Breathe Right’ appear to reduce snoring in some patients through opening the nasal passages, but there are no published scientific studies which definitely prove that these strips do in fact assist significantly with snoring.  These strips probably have their main place in the 5-10% of individuals whose nostrils collapse during inspiration.

Nocturnal Sedatives and Alcohol

  • Nocturnal sedatives (such as sleeping pills) and alcohol (especially in large quantities) can cause narrowing of the pharynx as a result of relaxation of pharyngeal muscles, with a resulting increase in soft-tissue vibration and snoring.  Reducing the intake of these agents commonly therefore helps to reduce snoring volume.

Bedtime remedies to help you stop snoring

  • Change your sleeping position – Elevating your head four inches may ease breathing and encourage your tongue and jaw to move forward. There are specifically designed pillows available to help prevent snoring by making sure your neck muscles are not crimped.
  • Sleep on your side instead of your back – Try attaching a tennis ball to the back of a pajama top or T-shirt (you can sew a sock to the back of your top then put a tennis ball inside). If you roll over onto your back, the discomfort of the tennis ball will cause you to turn back onto your side. Alternatively, wedge a pillow stuffed with tennis balls behind your back. After a while, sleeping on your side will become a habit and you can dispense with the tennis balls.
  • Try an anti-snoring mouth appliance – These devices, which resemble an athlete’s mouth guard, help open your airway by bringing your lower jaw and/or your tongue forward during sleep. While a dentist-made appliance can be expensive, cheaper do-it-yourself kits are also available.
  • Clear nasal passages – If you have a stuffy nose, rinse sinuses with saline before bed. Using a Neti pot, nasal decongestant, or nasal strips can also help you breathe more easily while sleeping. If you have allergies, reduce dust mites and pet dander in your bedroom or use an allergy medication.
  • Keep bedroom air moist – Dry air can irritate membranes in the nose and throat, so if swollen nasal tissues are the problem, a humidifier may help.

Self-help strategies for snoring

  • There are so many bizarre anti-snoring devices available on the market today, with more being added all the time, that finding the right solution for your snoring can seem like a daunting task.
  • Unfortunately, many of these devices are not backed up by research, or they work by simply keeping you awake at night. There are, however, plenty of proven techniques that can help eliminate snoring.
  • Not every remedy is right for every person, though, so putting a stop to your snoring may require patience, lifestyle changes, and a willingness to experiment with different solutions.

Bedtime remedies to help you stop snoring

  • Change your sleeping position – Elevating your head four inches may ease breathing and encourage your tongue and jaw to move forward. There are specifically designed pillows available to help prevent snoring by making sure your neck muscles are not crimped.
  • Sleep on your side instead of your back – Try attaching a tennis ball to the back of a pajama top or T-shirt (you can sew a sock to the back of your top then put a tennis ball inside). If you roll over onto your back, the discomfort of the tennis ball will cause you to turn back onto your side. Alternatively, wedge a pillow stuffed with tennis balls behind your back. After a while, sleeping on your side will become a habit and you can dispense with the tennis balls.
  • Try an anti-snoring mouth appliance – These devices, which resemble an athlete’s mouth guard, help open your airway by bringing your lower jaw and/or your tongue forward during sleep. While a dentist-made appliance can be expensive, cheaper do-it-yourself kits are also available.
  • Clear nasal passages – If you have a stuffy nose, rinse sinuses with saline before bed. Using a Neti pot, nasal decongestant, or nasal strips can also help you breathe more easily while sleeping. If you have allergies, reduce dust mites and pet dander in your bedroom or use an allergy medication.
  • Keep bedroom air moist – Dry air can irritate membranes in the nose and throat, so if swollen nasal tissues are the problem, a humidifier may help.

Lifestyle changes to help you stop snoring

  • Lose weight – Losing even a little bit of weight can reduce fatty tissue in the back of the throat and decrease, or even stop, snoring.
  • Quit smoking – If you smoke, your chances of snoring are high. Smoking irritates the membranes in the nose and throat which can block the airways and cause snoring. While quitting is easier said than done, it can bring quick snoring relief.
  • Avoid alcohol, sleeping pills, and sedatives – because they relax the muscles in the throat and interfere with breathing. Also talk to your doctor about any prescription medications you’re taking, as some encourage a deeper level of sleep which can make snoring worse.
  • Be careful what you eat before bed – Research shows that eating large meals or consuming certain foods such as dairy or soymilk right before bedtime can make snoring worse. Placing a household ban on the following snore-hazards right before bedtime can make for quieter nights.

Six anti-snoring throat exercises

  • Exercise in general can reduce snoring, even if it doesn’t lead to weight loss. That’s because when you tone various muscles in your body, such as your arms, legs, and abs, this leads to toning the muscles in your throat, which in turn can lead to less snoring. There are also specific exercises you can do to strengthen the muscles in your throat.

Studies show that by pronouncing certain vowel sounds and curling the tongue in specific ways, muscles in the upper respiratory tract are strengthened and therefore reduce snoring. The following exercises can help

  • Repeat each vowel (a-e-i-o-u) out loud for three minutes a few times a day.
  • Place the tip of your tongue behind your top front teeth. Slide your tongue backwards for three minutes a day.
  • Close your mouth and purse your lips. Hold for 30 seconds.
  • With your mouth open, move your jaw to the right and hold for 30 seconds. Repeat on the left side.
  • With your mouth open, contract the muscle at the back of your throat repeatedly for 30 seconds. Tip: Look in the mirror to see the uvula (“the hanging ball”) move up and down.
  • For a more fun exercise, simply spend some time singing. Singing can increase muscle control in the throat and soft palate, reducing snoring caused by lax muscles.

References

By

Tuberculosis; Types, Causes, Symptom, Diagnosis, Treatment

Tuberculosis is a potentially fatal contagious disease that can affect almost any part of the body but is mainly an infection of the lungs. It is caused by a bacterial microorganism, the tubercle bacillus or Mycobacterium tuberculosis. Although TB can be treated, cured, and can be prevented if persons at risk take certain drugs, scientists have never come close to wiping it out. Few diseases have caused so much distressing illness for centuries and claimed so many lives.
Description.
Tuberculosis (TB) is an infectious disease usually caused by Mycobacterium tuberculosis (MTB) bacteria.[Rx] Tuberculosis generally affects the lungs, but can also affect other parts of the body.[Rx] Most infections do not have symptoms, in which case it is known as latent tuberculosis.[Rx] About 10% of latent infections progress to active disease which, if left untreated, kills about half of those infected.[Rx] The classic symptoms of active TB are a chronic cough with blood-containing sputum, fever, night sweats, and weight loss.[Rx] It was historically called “consumption” due to weight loss.[Rx] Infection of other organs can cause a wide range of symptoms.[Rx]
Pott’s Disease, also known as tuberculosis spondylitis, is a rare infectious disease of the spine which is typically caused by an extraspinal infection. Pott’s Disease is a combination of osteomyelitis and arthritis which involves multiple vertebrae.

Types of Tuberculosis

Active TB Disease

  • Active TB is an illness in which the TB bacteria are rapidly multiplying and invading different organs of the body. The typical symptoms of active TB variably include a cough, phlegm, chest pain, weakness, weight loss, fever, chills and sweating at night. A person with active pulmonary TB disease may spread TB to others by airborne transmission of infectious particles coughed into the air. If you are diagnosed with an active TB disease, be prepared to give a careful, detailed history of every person with whom you have had to contact. Since the active form may be contagious, these people will need to be tested, as well.
  • Multi-drug treatment is employed to treat active TB disease. Depending on the state or local public health regulations, you may be asked to take your antibiotics under the supervision of your physician or other healthcare professional. This program is called “Directly Observed Therapy” and is designed to prevent abandonment or erratic treatment, which may result in “failure” with a continued risk of transmission or acquired resistance of the bacteria to the medications, including the infamous multi-drug resistant TB (MDR-TB).

Military TB

  • Military TB is a rare form of the active disease that occurs when TB bacteria find their way into the bloodstream. In this form, the bacteria quickly spread all over the body in tiny nodules and affect multiple organs at once. This form of TB can be rapidly fatal.

Latent TB Infection

  • Many of those who are infected with TB do not develop overt disease. They have no symptoms and their chest x-ray may be normal. The only manifestation of this encounter may be a reaction to the tuberculin skin test (TST) or interferon-gamma release assay (IGRA). However, there is an ongoing risk that the latent infection may escalate to active disease. The risk is increased by other illnesses such as HIV or medications which compromise the immune system. To protect against this, the United States employs a strategy of preventive therapy or treatment of latent TB infection.

Pathoanatomy/Causes of Tuberculosis

Early infection

  • begins in the metaphysics of the vertebral body
  • spreads under the anterior longitudinal ligament and leads to
  • contiguous multilevel involvement
  • skip lesion or non-contiguous segments (15%)
  • paraspinal abscess formation (50%) usually anterior and can be quite large (much more common in TB than pyogenic infections)
  • initially does not involve the disc space (distinguishes from pyogenic osteomyelitis, but can be misdiagnosed as a neoplastic lesion)

Chronic infection

Severe kyphosis

  • mean deformity in nonoperative cases is 15° in 5% of patients, the deformity is >60°
  • infection is often diagnosed late, there is often much more severe kyphosis in granulomatous spinal infections compared to pyogenic infections
  • in adults kyphosis stays static after healing of disease
  • in children, kyphosis progresses in 40% of cases because of a growth spurt

Classification of progression (Rajasekaran)

  • Type-I, increase in deformity until the cessation of growth should be treated with surgery
  • Type-II, decreasing progression with growth
  • Type-III, minimal change during either active / healed phases.

Symptoms of Tuberculosis

Symptoms and signs of tuberculosis

  • Cough—usually productive
  • Sputum—usually mucopurulent or purulent
  • Haemoptysis—not always a feature, volume variable
  • Breathlessness—gradual increase rather than sudden
  • Weight loss—gradual
  • Anorexia—variable
  • Fever—may be associated with night sweats
  • Malaise— the patient may realize only retrospectively when feeling better after treatment
  • Wasting and terminal cachexia—late, ominous signs

Although your body may harbor the bacteria that cause tuberculosis, your immune system usually can prevent you from becoming sick. For this reason, doctors make a distinction between:

  • Latent TB –  In this condition, you have a TB infection, but the bacteria remain in your body in an inactive state and cause no symptoms. Latent TB, also called inactive TB or TB infection, isn’t contagious. It can turn into active TB, so treatment is important for the person with latent TB and to help control the spread of TB. An estimated 2 billion people have latent TB.
  • Active TB. This condition makes you sick and can spread to others. It can occur in the first few weeks after infection with the TB bacteria, or it might occur years later.

Signs and symptoms of active TB include:

  • Coughing that lasts three or more weeks
  • Coughing up blood
  • Chest pain, or pain with breathing or coughing
  • Unintentional weight loss
  • Fatigue
  • Fever
  • Night Sweats
  • Chills
  • Loss of appetite

Tuberculosis can also affect other parts of your body, including your kidneys, spine or brain. When TB occurs outside your lungs, signs, and symptoms vary according to the organs involved. For example, tuberculosis of the spine may give you back pain, and tuberculosis in your kidneys might cause blood in your urine.

Tuberculous spinal infections should be suspected in patients with an insidious, progressive history of back pain and in individuals from an endemic area, especially when the thoracic vertebrae are affected and with a pattern of bone destruction with relative disc preservation and paravertebral and epidural soft tissue masses

  • The onset is gradual.
  • Back pain is localized.
  • Fever, night sweats, anorexia, and weight loss.
  • Signs may include kyphosis (common) and/or a paravertebral swelling.
  • Affected patients tend to assume a protective, upright, stiff position.
  • If there is neural involvement there will be neurological signs.

A psoas abscess may present as a lump in the groin and resemble a hernia

  • A psoas abscess most often originates from a tuberculous abscess of the lumbar vertebra that tracks from the spine inside the sheath of the psoas muscle.
  • Other causes include extension of renal sepsis and posterior perforation of the bowel.
  • There is a tender swelling below the inguinal ligament and they are usually apyrexial.
  • The condition may be confused with a femoral hernia or enlarged inguinal lymph nodes.

Screening Tests 

Tuberculin skin testing: Mantoux test (skin testing with PPD)

The Mantoux reaction following injection of a dose of PPD (purified protein derivative) is the traditional screening test for exposure to Tuberculosis. The result is interpreted taking into consideration the patient’s overall risk of exposure. Patients are classified into 3 groups based on the risk of exposure with three corresponding cut-off points. The 3 major groups used are discussed below.

Low Risk 

  • Individuals with minimal probability of exposure are considered to have a positive Mantoux test only if there is very significant induration following intradermal injection of PPD. The cut-off point for this group of people (with minimal risk of exposure) is taken to be 15 mm.

Intermediate Risk

  • Individuals with intermediate probability are considered positive if the induration is greater than 10 mm.

High Risk

  • Individuals with a high risk of a probability of exposure are considered positive if the induration is greater than 5 mm.

Examples of Patients in the Different Risk Categories

  • Low Risk/Low Probability: Patients with no known risk of exposure to TB. Example: No history of travel, military service, HIV-negative, no contact with a chronic cough patient, no occupational exposure, no history of steroids. Not a resident of a TB-endemic region.
  • Intermediate Risk/Probability: Residents of TB-endemic countries (Latin America, Sub -Sahara Africa, Asia), workers or residents of shelters, Medical or microbiology department personnel.
  • High Risk/Probability: HIV-positive patient, a patient with evidence of the previous TB such as the healed scar on an x-ray), contact with chronic cough patients.

Note that a Mantoux test indicates exposure or latent tuberculosis. However, this test lacks specificity, and patients would require subsequent visits for interpreting the results as well as chest x-ray for confirmation. Although relatively sensitive, the Mantoux reaction is not very specific and may give false positive reactions in individuals who have been exposed to the BCG-vaccine.

Interferon release assays (IGRA, Quantiferon Assays)

  • This is a tuberculosis screening test that is more specific and equally as sensitive as the Mantoux test. This test assays for the level of the inflammatory cytokine, especially interferon gamma.
  • The advantages of Quantiferon, especially in those with prior vaccination with BCG vaccine, includes, the test requires a single blood draw, obviating the need for repeat visits to interpret results. Furthermore, additional investigations such as HIV screening could be performed (after patient consent) on the same blood draw.
  • Quantiferon’s disadvantages include cost and the technical expertise required to perform the test.

Screening in Immunocompromised Patients

  • Immunocompromised patients may show lower levels of reaction to PPD or false negative Mantoux because of cutaneous anergy.
  • A high level of suspicion should be entertained when reviewing negative screening tests for tuberculosis in HIV-positive individuals.

The Significance of Screening

  • A positive screening test indicates exposure to tuberculosis and a high chance of developing active tuberculosis in the future. Tuberculosis incidence in patients with positive Mantoux test averages between 2% to 10% without treatment.
  • Patients with a positive test should have a chest x-ray as a minimum diagnostic test. In some cases, these patients should have additional tests. Patients meeting the criteria for latent tuberculosis should receive prophylaxis with isoniazid.

Screening Questionnaires for Resource-Poor Settings

  • Several screening questionnaires have been validated to enable healthcare workers working in remote and resource-poor environments screen for tuberculosis.

These questionnaires make use of an algorithm that combines several clinical signs and symptoms of tuberculosis. Some of the commonly used symptoms are:

  • A chronic cough
  • Weight loss
  • Fever and night sweats
  • History of contact
  • HIV status
  • Blood in sputum

Several studies have confirmed the utility of using several criteria rather than a focus on only chronic cough or weight loss.

Confirmatory and Diagnostic Tests

  • A chest x-ray is indicated to rule out or rule in the presence of active disease in all screening test positive cases.
  • Acid Fast Staining-Ziehl-Neelsen
  • Culture
  • Nuclear Amplification and Gene-Based Tests: These represent a new generation of diagnostic tools for tuberculosis. These tests enable identification of the bacteria or bacteria particles making use of DNA-based molecular techniques. Examples are Genexpert and DR-MTB.

The new molecular-based techniques are faster and enable rapid diagnosis with high precision. Confirmation of TB could be made in hours rather than the days or weeks it takes to wait for a standard culture. This is very important, especially among immunocompromised host where there is a high rate of false negative results. Some molecular-based tests such as GeneXpert and DR-MTB also allow for identification of multi-drug resistant tuberculosis.

  • Pyogenic osteitis of the spine.
  • Spinal tumours.

Kyphotic deformity

  • neurologic deficits (present in 10-47% of patients with Pott’s Disease)
  • mechanical pressure on cord by abscess, granulation tissue, tubercular debris, caseous tissue
  • mechanical instability from subluxation/dislocation
  • paraplegia from healed disease can occur with severe deformity
  • stenosis from ossification of ligamentum flavum adjacent to severe kyphosis

CXR

  • 66% will have an abnormal CXR
  • should be ordered for any patients in which TB is a possibility

Spine radiographs

  • early infection shows involvement of anterior vertebral body with sparing of the disc space (this finding can differentiate from pyogenic infection)
  • late infection shows disk space destruction, lucency and compression of adjacent vertebral bodies, and development of severe kyphosis

Risk factors for buckling collapse (“spine at risk signs”)

  • retropulsion
  • subluxation
  • lateral translation
  • toppling

MRI with gadolinium contrast

  • indications >remains preferred imaging study for diagnosis and treatment diagnose adjacent levels ,multiple levels involved in 16-70%

Findings

  • low signal on T1-weighted images, bright signal on T2-weighted images
  • presence of a septate pre-/ paravertebral / intra-osseous smooth walled abscess with a subligamentous extension and breaching of the epidural space
  • end-plate disruption sensitivity 100%, specificity 81%
  • paravertebral soft tissue shadow sensitivity 97%, specificity 85%
  • high signal intensity of the disc on the T2-weighted image sensitivity 81%, specificity 82%

Spinal cord

  • edema
  • myelomalacia
  • atrophy
  • syringomyelia

CT Scan 

Indications

  • demonstrates lesions <1.5cm better than radiographs ,inaccurate for defining epidural extension
  • types of destruction ,fragmentary, osteolytic ,subperiosteal ,sclerotic
  • CT guided biopsy with cultures and staining effective at obtaining a diagnosis
  • should be tested for acid-fast bacilli (AFB) mycobacteria (acid-fast bacilli) may take 10 weeks to grow in culture
  • PCR allows for faster identification (95% sensitivity and 93% accuracy) , smear positive in 52% ,culture positive in 83%

Nuclear medicine studies

  • obtain with a combination of technetium and gallium
  • shown to have the highest sensitivity for detecting infection

CBC

  • relative lymphocytosis
  • low hemoglobin
  • Strongly positive Mantoux skin test.

ESR

  • usually elevated but may be normal in up to 25%
  • PPD (purified protein derivative of tuberculin)
    • positive in ~ 80%

Other etiologies of granulomatous infection may have a similar clinical picture as TB and include

atypical bacteria

  • Actinomyces israelii
  • Nocardia asteroids
  • Brucella

Fungi

  • Coccidioides immitis
  • Blastomyces dermatitidis
  • Cryptococcus neoformans
  • Aspergillosis
  • spirochetes
    • Treponema pallidum
  • Tuberculosis co-infection with HIV has become common. It is up to 11% in some areas of the UK and over 60% in countries such as Zambia, Zimbabwe and South Africa.
  • In the developed world, the disease is more common in certain sections of society, such as those with alcohol dependency, the undernourished, ethnic minority communities and the elderly.
  • The disease is also more common in patients after gastrectomy for peptic ulcer.
  • The most common area affected is T10 to L1.
  • The lower thoracic region is the most common area of involvement at 40-50%, with the lumbar spine in a close second place at 35-45%.
  • The cervical spine accounts for about 10%

Treatment of Tuberculosis

Dosages of first line antituberculosis drugs and major adverse effects

Drug Dosage Adverse effects
Daily Twice or thrice weekly
Isoniazid 5 mg/kg oral (maximum 300 mg) 900 mg twice weekly
600 mg thrice weekly
Hepatitis, peripheral neuritis, drug induced lupus, seizures, and hypersensitivity with rash and fever. Drug interactions with dilantin and disulfiram
Rifampicin 10 mg/kg oral (maximum 600 mg) 10 mg/kg
600 mg twice weekly
600 mg thrice weekly
Orange body secretions, flu-like syndrome, hepatitis, thrombocytopenia, nausea, anorexia, diarrhoea, renal failure, and multiple drug interactions
Pyrazinamide 25-30 mg/kg oral 30-35 mg/kg Hyperuricemia, hepatitis, rash, nausea, and anorexia
Ethambutol 25 mg/kg initial 2 months, then 15 mg/kg oral 50 mg/kg twice weekly
30 mg/kg thrice weekly
Optic neuritis and gastrointestinal discomfort
Streptomycin 15 mg/kg intravenously or intramuscularly (maximum 1.0 g) 5 days a week 15 mg/kg (maximum 1.5 g) twice weekly or thrice weekly Ototoxicity, vestibular dysfunction, nephrotoxicity, rash, and hypersensitivity reactions

First line

All first-line anti-tuberculous drug names have a standard three-letter and a single-letter abbreviation:

  • ethambutol is EMB or E,
  • isoniazid is INH or H,
  • pyrazinamide is PZA or Z,
  • rifampicin is RMP or R,
  • streptomycin is SM or S.

First-line anti-tuberculous drug names are often remembered with the mnemonic “RIPE,” referring to the use of a rifamycin (like rifampin), isoniazid, pyrazinamide, and ethambutol. The US uses abbreviations and names that are not internationally recognised: rifampicin is called rifampin and abbreviated RIF; streptomycin is abbreviated STM. In the US only, streptomycin is no longer considered a first line drug by ATS/IDSA/CDC because of high rates of resistance. The WHO have made no such recommendation.

Second line

The second line drugs (WHO groups 2, 3 and 4) are only used to treat disease that is resistant to first line therapy (i.e., for extensively drug-resistant tuberculosis (XDR-TB) or multidrug-resistant tuberculosis (MDR-TB)).A drug may be classed as second-line instead of first-line for one of three possible reasons: it may be less effective than the first-line drugs (e.g., p-aminosalicylic acid); or, it may have toxic side-effects (e.g., cycloserine); or it may be effective, but unavailable in many developing countries (e.g., fluoroquinolones):

  • aminoglycosides (WHO group 2): e.g., amikacin (AMK), kanamycin (KM);
  • polypeptides (WHO group 2): e.g., capreomycin, viomycin, enviomycin;
  • fluoroquinolones (WHO group 3): e.g., ciprofloxacin (CIP), levofloxacin, moxifloxacin (MXF);
  • thioamides (WHO group 4): e.g. ethionamide, prothionamide
  • cycloserine (WHO group 4)
  • terizidone (WHO group 5)

Third line

Third-line drugs (WHO group 5) include drugs that may be useful, but have doubtful or unproven efficacy:

  • rifabutin
  • macrolides: e.g., clarithromycin (CLR);
  • linezolid (LZD);
  • thioacetazone (T);
  • thioridazine;
  • arginine;
  • vitamin D;
  • bedaquiline.

These drugs are listed here either because they are not very effective (e.g., clarithromycin) or because their efficacy has not been proven (e.g., linezolid, R207910). Rifabutin is effective, but is not included on the WHO list because for most developing countries, it is impractically expensive.

Or

Latent Tuberculosis

Drug of choice is isoniazid. It is usually given with vitamin B6, pyridoxine (to prevent nerve damage). Isoniazid is recommended for Mantoux or quantiferon positive individuals and should be continued for 6 or 9 months.

The WHO recommends the following treatment regimen for treating latent tuberculosis:

  • 6-month or 9-month isoniazid daily
  • 3-month rifapentine plus isoniazid weekly
  • 3-month or 4-month isoniazid plus rifampicin daily
  • 3–month or 4-month rifampicin alone daily

Treatment of Active Infection

  • Treatment of confirmed TB requires a combination of drugs. Combination therapy is always indicated, and monotherapy should never be used for tuberculosis. The  most common regimen for TB includes the following anti-TB medications:

First-Line Medications, Group 1

  • Isoniazid
  • Rifampicin
  • Rifabutin
  • Rifapentine
  • Pyrazinamide
  • Ethambutol

Isoniazid and Rifampicin follow a 4-drug regimen (usually including Isoniazid, Rifampicin, Ethambutol, and Pyrazinamide) for 2 months or six months. Vitamin B6 is always given with Isoniazid to prevent neural damage (neuropathies).

Several other antimicrobials are effective against tuberculosis including the following categories:

Second-Line Anti-tuberculosis Drugs, Group 2

Injectables aminoglycosides and injectable polypeptides

Injectable aminoglycosides

  • Amikacin
  • Kanamycin
  • Streptomycin

Injectable polypeptides

  • Capreomycin
  • Viomycin

SecondLine Anti-Tuberculosis Drugs, Group 3, Oral and Injectable Fluoroquinolones

Fluoroquinolones

  • Levofloxacin
  • Moxifloxacin
  • Ofloxacin
  • Gatifloxacin

Second-Line Anti-tuberculosis Drugs, Group 4

  • Para-aminosalicylic acid
  • Cycloserine
  • Terizidone
  • Ethionamide
  • Prothionamide
  • Thioacetazone
  • Linezolid

Third-Line Anti-Tuberculosis Drugs, Group 5

These are medications with variable but unproven efficacy against TB. They are used for total drug-resistant TB as drugs of last resort.

  • Clofazimine
  • Linezolid
  • Amoxicillin/clavulanic acid
  • Imipenem/Cilastatin
  • Clarithromycin

MDR-TB, XDR-TB

  • Multi-drug resistant TB is becoming increasingly common.
  • The combination of first-line and second-line medications are used at high doses to treat this condition.

Bedaquiline

  • On December 28, 2012, the United States Food and Drug Administration Agency (FDA), approved Bedaquiline as a drug for treating MDR-TB. This is the first FDA approval for an anti-TB medication in 40 years. While showing remarkable promise in drug-resistant tuberculosis, cost remains a big obstacle to delivering this drug to the people most affected by MDR-TB.

Clinical and Laboratory Monitoring

  • Liver function test is required for all patients taking isoniazid. Other monitoring in TB includes monitoring for retinopathies for patients on ethambutol.

Steroids

  • The usefulness of corticosteroids (e.g., prednisolone or dexamethasone) in the treatment of TB is proven for TB meningitis and TB pericarditis. The dose for TB meningitis is dexamethasone 8 to 12 mg daily tapered off over six weeks (for those who prefer more precise dosing should refer to Thwaites et al., 2004). The dose for pericarditis is prednisolone 60 mg daily tapered off over four to eight weeks.

Steroids may be of temporary benefit in pleurisy, extremely advanced TB, and TB in children:

  • Pleurisy: prednisolone 20 to 40 mg daily tapered off over 4 to 8 weeks
  • Extremely advanced TB: 40 to 60 mg daily tapered off over 4 to 8 weeks
  • TB in children: 2 to 5 mg/kg/day for one week, 1 mg/kg/day the next week, then tapered off over 5 weeks

Steroids may be of benefit in peritonitis, miliary disease, tubercular osteomyelitis, TB osteomyelitis, laryngeal TB, lymphadenitis and genitourinary disease, but the evidence is scant and the routine use of steroids cannot be recommended. Steroid treatment in these patients should be considered on a case by case basis by the attending physician.

Thalidomide may be of benefit in TB meningitis and has been used in cases where patients have failed to respond to steroid treatment.

Some supplements may be useful as adjuncts in the treatment of tuberculosis, but for the purposes of counting drugs for MDR-TB, they count as zero (if you already have four drugs in the regimen, it may be beneficial to add arginine or vitamin D or both, but you still need another drug to make five).

  • arginine, some clinical evidence (peanuts are a good source)
  • Vitamin D, (some in-vitro evidence & see Vitamin D and tuberculosis treatment )

The drugs listed below have been used in desperation and it is uncertain whether they are effective at all. They are used when it is not possible to find five drugs from the list above.

  • imipenem
  • co-amoxiclav
  • clofazimine
  • prochlorperazine
  • metronidazole

On December 28, 2012, the U.S. Food and Drug Administration (FDA) approved bedaquiline (marketed as Sirturo by Johnson & Johnson) to treat multi-drug resistant tuberculosis, the first new treatment in 40 years. Sirturo is to be used in a combination therapy for patients who have failed standard treatment and have no other options. Sirturo is an adenosine triphosphate synthase (ATP synthase) inhibitor.

The follow drug is experimental compounds that are not commercially available, but which may be obtained from the manufacturer as part of a clinical trial or on a compassionate basis. Their efficacy and safety are unknown:

  • Pretomanid (manufactured by Novartis, developed in partnership with TB Alliance)

There is increasing evidence for the role of surgery (lobectomy or pneumonectomy) in the treatment of MDR-TB, although whether this is should be performed early or late is not yet clearly defined.

Surgical Technique

Anterior decompression/corpectomy, strut grafting ± posterior instrumented stabilization ± posterior column shortening

  • indications  for kyphosis with active disease

Techniques for single-stage transpedicular 2-stage

  • anterior decompression with bone grafting
  • posterior kyphosis correction and instrumentation
  • single-stage extrapleural anterolateral

Risk factors

Anyone can get tuberculosis, but certain factors can increase your risk of the disease. These factors include:

Weakened immune system

A healthy immune system often successfully fights TB bacteria, but your body can’t mount an effective defense if your resistance is low. A number of diseases and medications can weaken your immune system, including:

  • HIV/AIDS
  • Diabetes
  • Severe kidney disease
  • Certain Cancers
  • Cancer treatment, such as chemotherapy
  • Drugs to prevent rejection of transplanted organs
  • Some drugs used to treat rheumatoid arthritis, Crohn’s disease and psoriasis
  • Malnutrition
  • Very young or advanced age

Complications

Deformity (kyphosis/Gibbs)

  • the highest risk after anterior decompression and grafting alone slippage and breakage of the graft (especially if ≥ 2 levels)
  • the lowest risk after both anterior and posterior fusion
  • Retropharyngeal abscess affects swallowing/hoarseness
  • TB arteritis and pseudoaneurysm
  • Respiratory compromise if there is costopelvic impingement
  • Sinus formation
  • Pott’s paraplegia spinal cord injury can be caused by abscess/bony sequestra or meningomyelitis
  • abscess/bony sequestra have a better prognosis than meningomyelitis as the cause of spinal cord injury
  • definition of compressive myelopathy without visible spinal deformity, without the typical radiological appearance
  • etiology intraspinal granuloma, neural arch involvement, concertina collapse of vertebral body, sclerotic vertebra with bridging of the vertebral body

Laminectomy

  • indications extradural extraosseous granuloma & subdural granuloma

Decompression and myelotomy

  • indications intramedullary granuloma

Traveling or living in certain areas

The risk of contracting tuberculosis is higher for people who live in or travel to countries that have high rates of tuberculosis and drug-resistant tuberculosis, including:

  • Africa
  • Eastern Europe
  • Asia
  • Russia
  • Latin America
  • Caribbean Islands

Poverty and substance abuse

  • Lack of medical care – If you receive a low or fixed income, live in a remote area, have recently immigrated to the United States, or are homeless, you may lack access to the medical care needed to diagnose and treat TB.
  • Substance abuse – IV drug use or alcohol abuse weakens your immune system and makes you more vulnerable to tuberculosis.
  • Tobacco use – Using tobacco greatly increases the risk of getting TB and dying of it.

Where you work or live

  • Health care work – Regular contact with people who are ill increases your chances of exposure to TB bacteria. Wearing a mask and frequent hand-washing greatly reduce your risk.
  • Living or working in a residential care facility – People who live or work in prisons, immigration centers or nursing homes are all at a higher risk of tuberculosis. That’s because the risk of the disease is higher anywhere there is overcrowding and poor ventilation.
  • Living in a refugee camp or shelter – Weakened by poor nutrition and ill health and living in crowded, unsanitary conditions, refugees are at especially high risk of tuberculosis infection.

References

Magnesium Deficiency

By

Whiplash Injury; Causes, Symptoms, Diagnosis, Treatment

Whiplash injury is a hyperextension and flexion injury to the neck or sudden thrusting forwards due to forceful, rapid back-and-forth movement of the neck, like the cracking of a whip. Whiplash most often occurs during a rear-end auto accident, but the injury can also result from a sports accident, physical abuse or other trauma.

Whiplash is a common injury associated most often with motor vehicle accidents. It may present with a variety of clinical manifestations, collectively termed WAD. Whiplash is an important cause of chronic disability. Many controversies exist regarding the diagnosis and treatment of whiplash injuries. The multifactorial etiology believed to underly whiplash injuries, make management highly variable between patients. Radiographic evidence of injury often cannot be identified in the acute phase. Recent studies suggest early mobilization may lead to improved outcomes. Ligamentous and bony injuries may go undetected at initial presentation leading to delayed diagnosis and inappropriate therapies.

Whiplash is commonly associated with motor vehicle accidents, usually, when the vehicle has been hit in the rear;[Rx] however, the injury can be sustained in many other ways, including headbanging,[Rx] bungee jumping and falls.[Rx] It is one of the most frequently claimed injuries on vehicle insurance policies in certain countries; for example, in the UnitedKingdom 430,000 people made an insurance claim for whiplash in 2007, accounting for 14% of every driver’s premium.[Rx]

  • Trauma and sports injuries are more common in young adults.
  • Rates of whiplash are higher in persons using a seatbelt with shoulder restraint than with no restraint but seatbelts often prevent more serious injuries.
  • Poor posture.
  • Poorly-fitted head restraints.
  • Women sustain higher rates of whiplash, probably because their neck muscles are less well developed than men’s.
  • Narrowing of the cervical spinal canal due to acquired or congenital disorders predisposes to spinal cord damage with these types of injuries.

Types of Whiplash Injury

There are two types of injury

  • Typical cervical hyperextension injuries – occur in drivers/passengers of a stationary or slow-moving vehicle that is struck from behind. The person’s body is thrown forward but the head lags, resulting in hyperextension of the neck. When the head and neck have reached maximum extension, the neck then snaps into flexion.
  • A rapid deceleration injury throws – the head forwards and flexes the cervical spine. The chin limits forward flexion but the forward movement may be sufficient to cause longitudinal distraction and neurological damage. Hyperextension may occur in the subsequent recoil.

Whiplash-associated disorders (WAD) can be classified by the severity of signs and symptoms

  • Grade 0 – no complaints or physical signs.
  • Grade 1 –  indicates neck complaints but no physical signs.
  • Grade 2 –  indicates neck complaints and musculoskeletal signs.
  • Grade 3 –  neck complaints and neurological signs.
  • Grade 4 –  neck complaints and fracture/dislocation

or

QTF classification of whiplash-associated disorders

Grade Classification
0 No complaint about the neck. No physical signs
I Neck complain of pain, stiffness or tenderness only. No physical signs
II Neck complain and musculoskeletal signs. Musculoskeletal signs include decreased range of motion and point tenderness
III Neck complain and neurological signs. Neurological signs include decreased or absent deep tendon reflexes, weakness, and sensory deficits
IV Neck complain and fracture or dislocation

The Position of spine vertebra Affected most

  • Most cervical spine fractures occur predominantly at two levels – at the level of C2 or at C6 or C7.
  • Most fatal cervical spine injuries occur in upper cervical levels, either at the cranio-cervical junction C1 or at C2.

The Canadian cervical spine rule for risk of skeletal injury:

  • The Canadian cervical spine rule applies to trauma patients who are alert (Glasgow Coma Scale of 15) and stable.
  • It has been shown to be safe and reliable, missing only one unstable injury in a series of over 16,000 cases.

High-risk factors

  • Age 65 years or over.
  • Paraesthesia in extremities.

Dangerous mechanism of injury, which is considered to be

  • A fall from a height of at least a meter or five stairs.
  • An axial load to the head – eg, during diving.
  • A motor vehicle collision at high speed (>100 km/h) or with rollover or ejection.
  • A collision involving a motorized recreational vehicle.
  • A bicycle collision.
 Low-risk factors
  • Simple rear-end motor vehicle collision (excludes being pushed into oncoming traffic, being hit by a bus or a large truck, a rollover, and being hit by a high-speed vehicle).
  • Able to sit rather than lie down in the emergency department.
  • Ambulatory at any time.
  • The delayed (not immediate) onset of neck pain.
  • The absence of midline cervical spine tenderness

Causes of whiplash injuries

  • A whiplash injury may occur if the head is moved violently away from the body because of a sudden and powerful jerk or jolt. The neck moves beyond its normal range of movement, resulting in overstretched ligaments, muscles and tendons. The injury is often exacerbated because the muscles, in order to compensate for the sudden movement, pull the head back into position too hard, causing another overstretching in the opposite direction.
  • The jolt (or blow to the head) can come from behind, in front, and from the side. A slow-speed collision may also cause a whiplash injury.

Possible causes of whiplash

  • Automobile accidents
  • A sudden blow to the head from a contact sport, such as rugby, boxing, karate, or American football.
  • A horse riding or a cycling accident
  • Any fall which causes the head to violently jolt backward
  • Being hit on the head with a heavy object
  • Shaking a child/baby violently (possible child abuse)
  • Punching a child/baby (possible child abuse).

Symptoms of Whiplash Injury

Common symptoms related to whiplash may include