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Cerebral Hemiplegia occurs when hemiplegia is caused by cerebral palsy (or other conditions affecting the brain), it can be referred to as cerebral hemiplegia. Cerebral hemiplegia symptoms are often similar to other forms of hemiplegia but may vary in severity and duration depending on the condition causing the paralysis.

Hemiplegia is a neurological condition that affects paralysis is on one vertical half of the body. Its most obvious result is a varying degree of weakness and lack of control on one side of the body. It affects everyone differently but its most obvious result is a varying degree of weakness and lack of control in one side of the body. You may be reading this because your child or someone you know has hemiplegia.

Hemiplegia, paralysis of the muscles of the lower face, arm, and leg on one side of the body. The most common cause of hemiplegia is a stroke, which damages the corticospinal tracts in one hemisphere of the brain. The corticospinal tracts extend from the lower spinal cord to the cerebral cortex. They decussate, or cross, in the brainstem; therefore, damage to the right cerebral hemisphere results in paralysis of the left side of the body. Damage to the left hemisphere of a right-handed person may also result in aphasia. Other causes of hemiplegia include trauma, such as spinal cord injury; brain tumors; and brain infections.

Hemiplegia is a condition where half of the body is paralyzed due to damage to the parts of the brain responsible for movement. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke, etc.

Types of Hemiplegia

• Alternate hemiplegia –  paralysis of one side of the face and the opposite side of the body.
• Cerebral hemiplegia –  that due to a brain lesion.
• Crossed hemiplegia – alternate hemiplegia. It affects the alter side of the body instated of the affected side.
• Facial hemiplegia paralysis – of one side of the face.
• Spastic hemiplegia – with spasticity of the affected muscles and increased tendon reflexes.
• Spinal hemiplegia – due to a lesion of the spinal cord.

While hemiplegia is typically characterized as paralysis on one side of the body, there are multiple types of hemiplegia—some of which may be more limited in scope than others. A few different types of hemiplegia include:

• Facial Hemiplegia – Also referred to as partial facial paralysis, this is a form of partial hemiplegia where the muscles on one side of the face are paralyzed. Often caused by a stroke or similar brain injury. This may or may not be associated with complete/incomplete hemiplegia in other areas of the body.
• Cerebral Hemiplegia  – When hemiplegia is caused by cerebral palsy (or other conditions affecting the brain), it can be referred to as cerebral hemiplegia. Cerebral hemiplegia symptoms are often similar to other forms of hemiplegia but may vary in severity and duration depending on the condition causing the paralysis.
• Spastic Hemiplegia – A variation of hemiplegia where the muscles on one side of the body are in a state of constant contraction. This type of hemiplegia may result in muscle pain, deformities in affected limbs (in extreme cases), and difficulty walking or maintaining motor control. Closely linked to cerebral palsy, and the severity (as well as the duration) of spastic hemiplegia symptoms may vary from case to case.
• Spinal Hemiplegia – Often the result of an incomplete injury to the spinal cord or lesions on spinal nerves (especially at the C6 vertebra or higher). Spinal cord injury hemiplegia is often a long-term condition.

Causes of Cerebral Hemiplegia

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Some common causes of hemiplegia include

Stroke is the commonest cause of hemiplegia. Insufficient blood supply to the brain leads to loss of brain functions. The stroke may be caused by:

• A clot formed within the blood vessel blocking the blood supply -> a thrombus
• A thrombus breaks away from its site of origin and forms a block elsewhere in the circulation -> an emboli
• A bleed from a blood vessel supplying the brain -> a hemorrhage
• A thrombus breaks away from its site of origin and forms a block elsewhere in the circulation. -> an emboli
• A bleed from a blood vessel supplying the brain -> a hemorrhage
• Traumatic brain injuries to one side of the brain only. These may be caused by car accidents, falls, acts of violence, and other factors.
• Cardiovascular problems, particularly aneurysms and hemorrhages in the brain.
• Infections, particularly encephalitis and meningitis. Some serious infections, particularly sepsis and abscesses in the neck, may spread to the brain if left untreated.
• Migraine syndrome -> recurrent headaches of severe intensity occasionally accompanied by sensations of numbness and tingling in one half of the body.
• Conditions that cause demyelination of the brain, including multiple sclerosis and some other autoimmune diseases.
• Reactions to surgery, medication, or anesthesia.
• Loss of oxygen to the brain due to choking or anaphylactic shock.
• Brain cancers.
• Lesions in the brain, even if non-cancerous, since these lesions can impede function on one side of the brain.
• Congenital abnormalities, including cerebral palsy and neonatal-onset multi-inflammatory disease.
• Rarely, psychological causes; some states of catatonia can cause hemiplegia, and people with parasomnia—a sleep disorder leading to unusual nighttime behavior—may experience nighttime episodes of hemiplegia.
• Head injury
• Diabetes
• Brain tumor
• Infections –> meningitis, encephalitis, meningitis, brain abscess
• Migraine syndrome -> recurrent headaches of severe intensity occasionally accompanied by sensations of numbness and tingling in one half of the body.
• Inflammation of the blood vessels -> vasculitis
• Diseases affecting the nerves -> like Multiple Sclerosis; acute necrotizing myelitis.
• Conditions presenting from birth -> cerebral palsy. Lack of blood supply damages nerve cells in the brain. Birth trauma, difficult labor, perinatal strokes in infants within 3 days of birth can all cause cerebral palsy.
• Hereditary diseases –> leukodystrophies. This is a rare disorder affecting the myelin sheath which covers and protects nerve cells in the brain. The condition usually appears in infancy or childhood.
• Vascular – cerebral hemorrhage
• Neoplastic – glioma-meningioma
• Demyelination – disseminated sclerosis, lesions to the internal capsule
• Traumatic – cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
• Congenital – cerebral palsy, Neonatal-Onset Multisystem Inflammatory Disease (NOMID)
• Disseminated – multiple sclerosis
• Psychological – parasomnia (nocturnal hemiplegia)
• Severe headache
• Impairment or loss of vision
• Memory loss
• Confusion
• Loss of balance or co-ordination
• Poor balance and dizziness
• Sudden numbness, paralysis or weakness of an arm, leg or side of the face.
• Slurred or abnormal speech
• Loss of consciousness
• Incontinence

Symptoms of Cerebral Hemiplegia

Rx

The main symptom of hemiplegia is weakness or paralysis on one side of the child’s body. The condition can vary in severity and affects each child differently. It will only affect one side of the child’s body. General symptoms include

• Total or partial loss of sensation on just one side.
• Changes in cognition, mood, or perception.
• Difficulty speaking.
• Changes on the other side of the body, since those muscles, may begin to atrophy or become painful due to chronic muscle spasms.
• Spastic attacks during which the muscles move without your conscious control.
• Seizures.
• Pusher syndrome – With this symptom, hemiplegics shift their weight to the paralyzed side of the body, resulting in significant loss of motor control.
• Severe, throbbing pain, often on one side of your head
• A pins-and-needles feeling, often moving from your hand up your arm
• Numbness on one side of your body, which can include your arm, leg, and half of your face
• Weakness or paralysis on one side of your body
• Loss of balance and coordination
• Dizziness or vertigo
• Nausea and vomiting

You may also have problems with your senses, communication, and drowsiness

• Seeing zigzag lines, double vision, or blind spots
• Extreme sensitivity to light, sound, and smell
• Language difficulties, such as mixing words or trouble remembering a word
• Slurred speech
• Confusion
• Loss of consciousness or coma
• Difficulty walking
• Poor balance
• Little or no use of one hand or leg
• Speech problems
• Visual problems
• Behavioral problems
• Learning difficulties
• Epilepsy
• Developmental delay, for example learning to walk later than other children

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Diagnosis of Cerebral Hemiplegia

To diagnose a stroke doctor hemiplegia will usually make an assessment using several of the following

• Examination of current signs and symptoms
• Review of medical history
• Electrocardiogram (ECG) – measures electrical activity in the heart
• Echocardiogram – to assess for any abnormalities in heart function and structure
• Electroencephalogram (EEG) – measures electrical activity in the brain
• Ultrasound scanning – of the neck arteries (carotids)
• Computerized tomography (CT) scan – specialized x-rays that can provide detailed cross-sectional images of the brain
• Magnetic resonance imaging (MRI) – a specialized scan that produces a detailed image of the brain
• Blood tests
• Chest x-rays.

Treatment of Cerebral Hemiplegia

Some potential hemiplegia exercises to consider include

• Strength Training Exercises – Some strength training exercises can prove to be beneficial for hemiplegics. The training recommended may vary depending on the type of hemiplegia, but common exercises include knee rolling, single-leg dropouts, and single-leg bridges, among others. In some cerebral hemiplegia patients, this can help improve range of motion and functionality in the affected limbs—though this isn’t certain.
• Muscle Stretches – Stretching specific muscle groups helps hemiplegics stave off some of the side effects of hemiplegia, such as joint/muscle pain from not moving limbs for too long and muscular atrophy. Spastic hemiplegics may need assistance in safely moving their contracted muscles without injury.
• Seated Aerobics – Seated aerobics provide a relatively safe way to burn calories and improve health from virtually anywhere. This form of exercise is recommended for hemiplegics recovering from a spinal cord injury.
• Water Aerobics – This hemiplegia exercise allows hemiplegics to relax their muscles and support the full weight of their bodies relatively easily as they stretch and work on their range of motion. Some rehabilitation programs use water aerobics as a chance to help people with paralysis to get out of the chair and experience some freedom of movement as they work muscles that are often neglected during in-chair exercises.
• Muscle relaxant – that help to increase muscle strength. It can be done either by any drugs or manually applying heat and electromagnetic radiation.
• Physical therapy – designed to help the brain work around the injuries. Physical therapy can also strengthen the unaffected side and help you reduce the loss of muscle control and tone.
• Support groups – family education, and advocacy by family support, friend circle, etc.
• Psychotherapy – to help you deal with the psychological effects of the disease.
• Exercise therapy – to help you remain healthy in spite of your disability.

Initial Treatment of Hemiplegia

Immediate treatment is aimed at limiting the size of the stroke and preventing further stroke. Acute stroke therapies try to stop a stroke while it is happening by quickly dissolving the blood clot causing an ischaemic stroke or by stopping the bleeding of a hemorrhagic stroke.  This will involve administering medications and may involve surgery in some cases.

Medications

RX

• Thrombolytic therapy – These medications dissolve blood clots allowing blood flow to be re-established
• Anticoagulants (eg: heparin) or aspirin – These medications help to prevent blot clots from getting bigger and prevent new blood clots from forming
• Antihypertensives –  In cases of hemorrhagic stroke these medications may be prescribed to help lower high blood pressure
• Medications– to reduce swelling in the brain and medications to treat underlying causes for the stroke eg: heart rhythm disorders may also be given.
• Blood thinners – to reduce cardiovascular blockages and decrease the chances of future strokes.
• Antibiotics – usually delivered intravenously, to combat brain infections.
• Muscle relaxant drugs – Tolperisone or eperisone hcl
• Surgery to address secondary issues-particularly involuntary muscle contractions, spinal damage, or damage to the ligaments or tendons on the unaffected side of the body.
• Physical therapy – designed to help the brain work around the injuries. Physical therapy can also strengthen the unaffected side and help you reduce the loss of muscle control and tone.
• Support groups – family education, and advocacy.
• Psychotherapy to help you deal with the psychological effects of the disease.
• Exercise therapy to help you remain healthy in spite of your disability.

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Treatment of Cerebral Hemiplegia

Brain cells do not generally regenerate. Following a stroke, surviving brain cells can take over the function of areas that are dead or damaged, but only to a certain degree. The adaptive ability of the brain requires the relearning of various skills. As each person who suffers a stroke is affected differently, individual rehabilitation plans are developed in conjunction with the patient, family, and healthcare team. These aim to teach skills and maximize function so that the person can achieve maximum independence.

Physiotherapy

Treatment of hemiplegia requires coordination of several health professionals. A physiotherapist, occupational therapist, a physician, a surgeon and support from family, etc.

• Treatment is focused – to find the causative factor and check its further progression. Secondly, after a few days, rehabilitation therapy helps to minimize disability.
• Several medicines – are prescribed to control the primary cause such as antihypertensive, anti-thrombolytic agents to dissolve the clot, drugs to control cerebral edema, etc.
• Intensive physical therapy – is begun after a few days. Activities such as walking, standing are done repeatedly under the guidance of a physiotherapist. It helps to improve the muscular functions which have become rigid. It is aimed to make the patient self-sufficient to perform his daily activities.
• The patient is taught – to move his affected arm with his strong arm. With exercise, it is possible to maintain the flexibility of joints and it also prevents tightening and shortening of muscles. Speech therapy is simultaneously begun to improve communication and speaking skills.
• Speech therapy – to improve communication
• Occupational therapy – to improve daily functions such as eating, cooking, toileting, and washing.

Recovery can take months and it may be several days or weeks after the stroke before doctors are able to give an accurate prediction for recovery.

Occupational therapy

• Occupational therapy – Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening the hand, shoulder, and torso, and participating in activities of daily living (ADLs), such as eating and dressing.
• Therapists – may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual – which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Rehabilitation & Therapy for Hemiplegia

1. Improving motor control

a. Neurofacilitatory Techniques

In Stroke Physical Therapy these therapeutic interventions use sensory stimuli (e.g. quick stretch, brushing, reflex stimulation, and associated reactions), which are based on neurological theories, to facilitate movement in patients following stroke. The following are the different approaches

• Bobath Concept- Berta & Karel Bobath’s approach focuses to control responses from the damaged postural reflex mechanisms. Emphasis is placed on affected inputs facilitation and normal movement patterns (Bobath, 1990).
• ii.Brunnstrom – Brunnstrom approach is one form of neurological exercise therapy in the rehabilitation of stroke patients. The relative effectiveness of Neuro-developmental treatment versus the Brunnstrom method was studied by Wagenaar and colleagues from the perspective of the functional recovery of stroke patients. The result of this study showed no clear differences in the effectiveness of the two methods within the framework of functional recovery.
• iii.Rood – Emphasise the use of activities in developmental sequences, sensation stimulation, and muscle work classification. Cutaneous stimuli such as icing, tapping, and brushing are employed to facilitate activities.
• iv. Proprioceptive neuromuscular facilitation (PNF) – Developed by Knott and Voss, they advocated the use of peripheral inputs as stretch and resisted movement to reinforce existing motor response. Total patterns of movement are used in the treatment and are followed in a developmental sequence.

b. Learning theory approach

• i. Conductive education – In Stroke Physical Therapy, Conductive education is one of the methods in treating neurological conditions including hemiplegic patients. Cotton and Kinsman (1984) demonstrated a neuropsychological approach using the concept of CE for adult hemiplegia. The patient is taught how to guide his movements towards each task-part of the task by using his own speech – rhythmical intention.
• ii. Motor relearning theory – Carr & Shepherd, both are Australian physiotherapists, developed this approach in 1980. It emphasizes the practice of functional tasks and the importance of relearning real-life activities for patients. Principles of learning and biomechanical analysis of movements and tasks are important. There is no evidence adequately supporting the superiority of one type of exercise approach over another. However, the aim of the therapeutic approach is to increase physical independence and to facilitate the motor control of skill acquisition and there is strong evidence to support the effect of rehabilitation in terms of improved functional independence and reduced mortality.

c. Functional electrical stimulation (FES) 

• FES is a modality that applied a short burst of electrical current to the hemiplegic muscle or nerve. In Stroke Physical Therapy, FES has been demonstrated to be beneficial to restore motor control, spasticity, and reduction of hemiplegic shoulder pain and subluxation.  A recent meta-analysis of the randomized controlled trial study showed that FES improves motor strength. A study by Faghri has identified that FES can significantly improve arm function, electromyographic activity of posterior deltoid, the range of motion and reduction of severity of subluxation and pain of the hemiplegic shoulder.

d. Biofeedback

• Biofeedback is a modality that facilitates the cognizant of electromyographic activity in selected muscle or awareness of joint position sense via visual or auditory cues. In Stroke Physical Therapy the result of studies in biofeedback is controversial. A meta-analysis of 8 randomized controlled trials of biofeedback therapy demonstrated that electromyographic biofeedback could improve motor function in stroke patients.
• A conflicting meta-analysis study by showing that biofeedback was not efficacious in improving the range of motion in the ankle and shoulder in a stroke patient. Moreland conducted another meta-analysis that concluded that EMG biofeedback alone or with conventional therapy did not superior to conventional physical therapy in improving upper- extremity function in the adult stroke patient.

2. Hemiplegic shoulder management

Shoulder subluxation and pain of the affected arm is not uncommon in at least 30% of all patient after stroke, whereas subluxation is found in 80% of stroke patients. It is associated with the severity of the disability and is common in patients in rehabilitation settings. Suggested interventions are as follows:

• a. Exercise – Active weight-bearing exercise can be used as a means of improving motor control of the affected arm; introducing and grading tactile, proprioceptive, and kinesthetic stimulation; and preventing edema and pain. In Stroke Physical Therapy, Upper extremity weight bearing can be used to lengthen or inhibit tight or spastic muscles while simultaneously facilitating muscles that are not active (Donatelli, 1991). According to Robert (1992), the amount of shoulder pain in hemiplegia was related most to loss of motion. He advocated that the provision of ROM exercise (caution to avoid improvement) as treatment as early as possible.
• b. Functional electrical stimulation – Functional electrical stimulation (FES) is an increasingly popular treatment for hemiplegic stroke patients. It has been applied in stroke physical therapy for the treatment of shoulder subluxation spasticity and functionally, for the restoration of function in the upper and lower limb. In Stroke Physical Therapy, Electrical stimulation is effective in reducing pain and severity of subluxation, and possibly in facilitating recovery of arm function c. Positioning & proper handling – In Stroke Physical Therapy, proper positioning and handling of the hemiplegic shoulder, whenever in bed, sitting and standing or during lifting, can prevent shoulder injury is recommended in the AHCPR & SIGN guidelines for stroke rehabilitation. In Stroke Physical Therapy, positioning can be therapeutic for tone control and neuro-facilitation of stroke patients (Davies, 1991). Braus et al 94 found shoulder hand syndrome reduced from 27% to 8% by the instruction to everyone including family on handling technique.
• d. Neuro-facilitation
• e. Passive limb physiotherapy – Maintenance of a full pain-free range of movement without traumatizing the joint and the structures can be carried out. In Stroke Physical Therapy, at no time should pain in or around the shoulder joint be produced during treatment.
• f. Pain relief physiotherapy – Passive mobilization as described by Maitland can be useful in gaining relief of pain and range of movement. In Stroke Physical Therapy other treatment modalities such as thermal, electrical, cryotherapy, etc. can be applied for shoulder pains or musculoskeletal in nature.
• g. Reciprocal pulley – The use of reciprocal pulley appears to increase the risk of developing shoulder pain in stroke patients. It is not related to the presence of subluxation or to muscle strength.
• h. Sling – In Stroke Physical Therapy the use of a sling is controversial. No shoulder support will correct a glenohumeral joint subluxation. However, it may prevent the flaccid arm from hanging against the body during functional activities, thus decreasing shoulder joint pain. They also help to relieve downward traction on the shoulder capsule caused by the weight of the arm.

3. Limb physiotherapy

• Limb physiotherapy/Stroke Physical Therapy includes passive, assisted-active and active range-of-motion exercise for the hemiplegic limbs. This can be effective management for the prevention of limb contractures and spasticity and is recommended within AHCPR. Self-assisted limb exercise is effective for reducing spasticity and shoulder protection. Adams and coworkers recommended passive full-range-of-motion exercise for a paralyzed limb for potential reduction of complication for stroke patients

4. Chest physiotherapy

• In Stroke Physical Therapy, evidence shows that both cough and forced expiratory technique (FET) can eliminate induced radio aerosol particles in the lung field. Directed coughing and FET can be used as a technique for bronchial hygiene clearance in stroke patients.

5. Positioning

• In Stroke, Physical Therapy consistent “reflex-inhibitory” patterns of posture in resting is encouraged to discourage physical complication of stroke and to improve recovery (Bobath, 1990).
• Meanwhile, therapeutic positioning is a widely advocated strategy to discourage the development of abnormal tone, contractures, pain, and respiratory complications. It is an important element in maximizing the patient’s functional gains and quality of life.

6. Tone management

• A goal of Stroke Physical Therapy interventions has been to “normalize tone to normalize movement.” Therapy modalities for reducing tone include stretching, prolonged stretching, passive manipulation by therapists, weight-bearing, ice, contraction of muscles antagonistic to spastic muscles, splinting, and casting.
• Research on tone-reducing techniques has been hampered by the inadequacies of methods to measure spasticity and the uncertainty about the relationship between spasticity and volitional motor control.
• The manual stretch of finger muscles, pressure splints, and dantrolene sodium do not produce apparent long-term improvement in motor control. Dorsal resting hand splints reduced spasticity more than volar splints, but the effect on motor control is uncertain while TENS stimulation showed improvement for chronic spasticity of lower extremities.

7. Sensory re-education

• Bobath and other therapy approaches recommend the use of sensory stimulation to promote the sensory recovery of stroke patients.

8. Balance retraining

• Re-establishment of balance function in patients following stroke has been advocated as an essential component in the practice of stroke physical therapy. Some studies of patients with hemiparesis revealed that these patients have a greater amount of postural sway, the asymmetry with greater weight on the non-paretic leg, and a decreased ability to move within a weight-bearing posture. Meanwhile, research has demonstrated moderate relationships between balance function and parameters such as gait speed, independence, wheelchair mobility, reaching, as well as dressing. Some tenable support on the effectiveness of treatment of disturbed balance can be found in studies comparing the effects of balance retraining plus physiotherapy treatment and physiotherapy treatment alone.

9. Fall prevention

• In Stroke Physical Therapy, falls are one of the most frequent complications and the consequences of which are likely to have a negative effect on the rehabilitation process and its outcome.
• According to the systematic review of the Cochrane Library, which evaluated the effectiveness of several fall prevention interventions in the elderly, there was significant protection against falling from interventions that targeted multiple, identified, risk factors in individual patients. The same is true for interventions which focused on behavioral interventions targeting environmental hazards plus other risk factors

10. Gait re-education

• Recovery of independent mobility is an important goal for the immobile patient, and much therapy is devoted to gait-reeducation. Bobath assumes abnormal postural reflex activity is caused by dysfunction so gait training involved tone normalization and preparatory activity for gait activity.
• In contrast, Carr and Shepherd advocate task-related training with methods to increase strength, coordination and flexible MS system to develop skill in walking while Treadmill training combined with the use of a suspension tube. Some patient’s body weight can effective in regaining walking ability when used as an adjunct to convention therapy 3 months after active training.

11. Functional Mobility Training

• To handle the functional limitations of stroke patients, functional tasks are taught to them based on movement analysis principles. In Stroke Physical Therapy these tasks include bridging, rolling to sit to stand and vice versa, transfer skills, walking and staring, etc.
• Published studies report that many patients improve during rehabilitation. The strongest evidence of benefit is from studies that have enrolled patients with chronic deficits or have included a no-treatment control group.
• Meanwhile, early mobilization helps prevent compilations e.g. DVT, skin breakdown contracture and pneumonia. Evidence has shown better orthostatic tolerance and earlier ambulation.

12. Upper limb training

By 3 months poststroke, approximately 37% of the individuals continue to have decreased upper extremities (UE) function. Recovery of UE function lags behind that of the lower extremities because of the more complex motor skill required of the UE in daily life tasks. That means many individuals who have a stroke are at risk for a lowered quality of life. Many approaches to the physical rehabilitation of adults post-stroke exist that attempt to maximize motor skill recovery. However, the literature does not support the efficacy of any single approach. The followings are the current approaches to motor rehabilitation of the UE.

• a. Facilitation models – They are the most common methods of intervention for the deficits in UE motor skills including Bobath, proprioceptive neuromuscular facilitation, Brunnstrom’s movement therapy, and Rood’s sensorimotor approach. There is some evidence that practice based on the facilitation models can result in improved motor control of UE. However, an intervention based on the facilitation models has not been effective in restoring the fine hand coordination required for the performance of actions.
• b. Functional electric stimulation – In Stroke Physical Therapy, Functional electric stimulation (FES) can be effective in increasing the electric activity of muscles or increased active range of motion in individuals with stroke. Some evidence showed that FES may be more effective than facilitation approaches.
• c. Electromyographic biofeedback – In Stroke Physical Therapy, biofeedback can contribute to improvements in motor control at the neuromuscular and movement levels. Some studies have shown improvements in the ability to perform actions during post-testing after biofeedback training. However, the ability to generalize these skills and incorporate them into daily life is not measured.
• d. Constraint-induced therapy – Constraint-Induced (CI) therapy was designed to overcome the learned nonuse of the affected UE. In the most extreme form of CI therapy, individual post-stroke is prevented from using the less affected UE by keeping it in a splint and sling for at least 90% of their waking hours. Studies have found that the most extreme of CI therapy can effect rapid improvement in UE motor skill and that is retained for at least as long as 2 years. However, CI therapy currently is effective only in those with distal voluntary movement.

13. Mobility appliances and equipment

• Small changes in an individual’s local ‘environment’ can greatly increase independence, use of a wheelchair or walking stick. However, little research has been done for these ‘treatments’. It is acknowledged that walking aids and mobility appliances may benefit selected patients.

14. Acupuncture 

• The World Health Organisation (WHO) has listed acupuncture as a possible treatment for pariesis after stroke. Studies had sown its beneficial effects on stroke rehabilitation.
• Hua had reported a significant difference in changes of neurological score between the acupuncture group and the control group after 4 weeks of treatment in an RCT and no adverse effects were observed in patients treated with acupuncture.

15. Vasomotor training 

• Early stimulation of the muscle pump can reduce the venous stasis and enhance the general circulation of the body. It then hastens the recovery process.

16. Edema management

• Use of intermittent pneumatic pump, elastic stocking or bandages and massage can facilitate the venous return of the oedematous limbs. Therefore, the elasticity and flexibility of the musculoskeletal system can be maintained and enhance the recovery process and prevent complications like pressure ulcers.

Homeopathic Medicines for Hemiplegia

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What Is Spastic Hemiplegia/Spastic Hemiplegia a variation of hemiplegia where the muscles on one side of the body are in a state of constant contraction. This type of hemiplegia may result in muscle pain, deformities in affected limbs (in extreme cases), and difficulty walking or maintaining motor control. Closely linked to cerebral palsy, and the severity (as well as the duration) of spastic hemiplegia symptoms may vary from case to case.

Hemiplegia is a neurological condition that affects paralysis is on one vertical half of the body. Its most obvious result is a varying degree of weakness and lack of control on one side of the body. It affects everyone differently but its most obvious result is a varying degree of weakness and lack of control in one side of the body. You may be reading this because your child or someone you know has hemiplegia.

Hemiplegia, paralysis of the muscles of the lower face, arm, and leg on one side of the body. The most common cause of hemiplegia is a stroke, which damages the corticospinal tracts in one hemisphere of the brain. The corticospinal tracts extend from the lower spinal cord to the cerebral cortex. They decussate, or cross, in the brainstem; therefore, damage to the right cerebral hemisphere results in paralysis of the left side of the body. Damage to the left hemisphere of a right-handed person may also result in aphasia. Other causes of hemiplegia include trauma, such as spinal cord injury; brain tumors; and brain infections.

Hemiplegia is a condition where half of the body is paralyzed due to damage to the parts of the brain responsible for movement. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke, etc.

Types of Hemiplegia

• Alternate hemiplegia –  paralysis of one side of the face and the opposite side of the body.
• Cerebral hemiplegia –  that due to a brain lesion.
• Crossed hemiplegia – alternate hemiplegia. It affects the alter side of the body instated of the affected side.
• Facial hemiplegia paralysis – of one side of the face.
• Spastic hemiplegia – with spasticity of the affected muscles and increased tendon reflexes.
• Spinal hemiplegia – due to a lesion of the spinal cord.

While hemiplegia is typically characterized as paralysis on one side of the body, there are multiple types of hemiplegia—some of which may be more limited in scope than others. A few different types of hemiplegia include:

• Facial Hemiplegia – Also referred to as partial facial paralysis, this is a form of partial hemiplegia where the muscles on one side of the face are paralyzed. Often caused by a stroke or similar brain injury. This may or may not be associated with complete/incomplete hemiplegia in other areas of the body.
• Cerebral Hemiplegia  – When hemiplegia is caused by cerebral palsy (or other conditions affecting the brain), it can be referred to as cerebral hemiplegia. Cerebral hemiplegia symptoms are often similar to other forms of hemiplegia but may vary in severity and duration depending on the condition causing the paralysis.
• Spastic Hemiplegia – A variation of hemiplegia where the muscles on one side of the body are in a state of constant contraction. This type of hemiplegia may result in muscle pain, deformities in affected limbs (in extreme cases), and difficulty walking or maintaining motor control. Closely linked to cerebral palsy, and the severity (as well as the duration) of spastic hemiplegia symptoms may vary from case to case.
• Spinal Hemiplegia – Often the result of an incomplete injury to the spinal cord or lesions on spinal nerves (especially at the C6 vertebra or higher). Spinal cord injury hemiplegia is often a long-term condition.

Causes of Spastic Hemiplegia

Rx

Some common causes of hemiplegia include

Stroke is the commonest cause of hemiplegia. Insufficient blood supply to the brain leads to loss of brain functions. The stroke may be caused by:

• A clot formed within the blood vessel blocking the blood supply -> a thrombus
• A thrombus breaks away from its site of origin and forms a block elsewhere in the circulation -> an emboli
• A bleed from a blood vessel supplying the brain -> a hemorrhage
• A thrombus breaks away from its site of origin and forms a block elsewhere in the circulation. -> an emboli
• A bleed from a blood vessel supplying the brain -> a hemorrhage
• Traumatic brain injuries to one side of the brain only. These may be caused by car accidents, falls, acts of violence, and other factors.
• Cardiovascular problems, particularly aneurysms and hemorrhages in the brain.
• Infections, particularly encephalitis and meningitis. Some serious infections, particularly sepsis and abscesses in the neck, may spread to the brain if left untreated.
• Migraine syndrome -> recurrent headaches of severe intensity occasionally accompanied by sensations of numbness and tingling in one half of the body.
• Conditions that cause demyelination of the brain, including multiple sclerosis and some other autoimmune diseases.
• Reactions to surgery, medication, or anesthesia.
• Loss of oxygen to the brain due to choking or anaphylactic shock.
• Brain cancers.
• Lesions in the brain, even if non-cancerous, since these lesions can impede function on one side of the brain.
• Congenital abnormalities, including cerebral palsy and neonatal-onset multi-inflammatory disease.
• Rarely, psychological causes; some states of catatonia can cause hemiplegia, and people with parasomnia—a sleep disorder leading to unusual nighttime behavior—may experience nighttime episodes of hemiplegia.
• Head injury
• Diabetes
• Brain tumor
• Infections –> meningitis, encephalitis, meningitis, brain abscess
• Migraine syndrome -> recurrent headaches of severe intensity occasionally accompanied by sensations of numbness and tingling in one half of the body.
• Inflammation of the blood vessels -> vasculitis
• Diseases affecting the nerves -> like Multiple Sclerosis; acute necrotizing myelitis.
• Conditions presenting from birth -> cerebral palsy. Lack of blood supply damages nerve cells in the brain. Birth trauma, difficult labor, perinatal strokes in infants within 3 days of birth can all cause cerebral palsy.
• Hereditary diseases –> leukodystrophies. This is a rare disorder affecting the myelin sheath which covers and protects nerve cells in the brain. The condition usually appears in infancy or childhood.
• Vascular – cerebral hemorrhage
• Neoplastic – glioma-meningioma
• Demyelination – disseminated sclerosis, lesions to the internal capsule
• Traumatic – cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
• Congenital – cerebral palsy, Neonatal-Onset Multisystem Inflammatory Disease (NOMID)
• Disseminated – multiple sclerosis
• Psychological – parasomnia (nocturnal hemiplegia)
• Severe headache
• Impairment or loss of vision
• Memory loss
• Confusion
• Loss of balance or co-ordination
• Poor balance and dizziness
• Sudden numbness, paralysis or weakness of an arm, leg or side of the face.
• Slurred or abnormal speech
• Loss of consciousness
• Incontinence

Symptoms of Spastic Hemiplegia

Rx

The main symptom of hemiplegia is weakness or paralysis on one side of the child’s body. The condition can vary in severity and affects each child differently. It will only affect one side of the child’s body. General symptoms include

• Total or partial loss of sensation on just one side.
• Changes in cognition, mood, or perception.
• Difficulty speaking.
• Changes on the other side of the body, since those muscles, may begin to atrophy or become painful due to chronic muscle spasms.
• Spastic attacks during which the muscles move without your conscious control.
• Seizures.
• Pusher syndrome – With this symptom, hemiplegics shift their weight to the paralyzed side of the body, resulting in significant loss of motor control.
• Severe, throbbing pain, often on one side of your head
• A pins-and-needles feeling, often moving from your hand up your arm
• Numbness on one side of your body, which can include your arm, leg, and half of your face
• Weakness or paralysis on one side of your body
• Loss of balance and coordination
• Dizziness or vertigo
• Nausea and vomiting

You may also have problems with your senses, communication, and drowsiness

• Seeing zigzag lines, double vision, or blind spots
• Extreme sensitivity to light, sound, and smell
• Language difficulties, such as mixing words or trouble remembering a word
• Slurred speech
• Confusion
• Loss of consciousness or coma
• Difficulty walking
• Poor balance
• Little or no use of one hand or leg
• Speech problems
• Visual problems
• Behavioral problems
• Learning difficulties
• Epilepsy
• Developmental delay, for example learning to walk later than other children

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Diagnosis of Spastic Hemiplegia

To diagnose a stroke doctor hemiplegia will usually make an assessment using several of the following

• Examination of current signs and symptoms
• Review of medical history
• Electrocardiogram (ECG) – measures electrical activity in the heart
• Echocardiogram – to assess for any abnormalities in heart function and structure
• Electroencephalogram (EEG) – measures electrical activity in the brain
• Ultrasound scanning – of the neck arteries (carotids)
• Computerized tomography (CT) scan – specialized x-rays that can provide detailed cross-sectional images of the brain
• Magnetic resonance imaging (MRI) – a specialized scan that produces a detailed image of the brain
• Blood tests
• Chest x-rays.

Treatment of Spastic Hemiplegia

Some potential hemiplegia exercises to consider include

• Strength Training Exercises – Some strength training exercises can prove to be beneficial for hemiplegics. The training recommended may vary depending on the type of hemiplegia, but common exercises include knee rolling, single-leg dropouts, and single-leg bridges, among others. In some cerebral hemiplegia patients, this can help improve range of motion and functionality in the affected limbs—though this isn’t certain.
• Muscle Stretches – Stretching specific muscle groups helps hemiplegics stave off some of the side effects of hemiplegia, such as joint/muscle pain from not moving limbs for too long and muscular atrophy. Spastic hemiplegics may need assistance in safely moving their contracted muscles without injury.
• Seated Aerobics – Seated aerobics provide a relatively safe way to burn calories and improve health from virtually anywhere. This form of exercise is recommended for hemiplegics recovering from a spinal cord injury.
• Water Aerobics – This hemiplegia exercise allows hemiplegics to relax their muscles and support the full weight of their bodies relatively easily as they stretch and work on their range of motion. Some rehabilitation programs use water aerobics as a chance to help people with paralysis to get out of the chair and experience some freedom of movement as they work muscles that are often neglected during in-chair exercises.
• Muscle relaxant – that help to increase muscle strength. It can be done either by any drugs or manually applying heat and electromagnetic radiation.
• Physical therapy – designed to help the brain work around the injuries. Physical therapy can also strengthen the unaffected side and help you reduce the loss of muscle control and tone.
• Support groups – family education, and advocacy by family support, friend circle, etc.
• Psychotherapy – to help you deal with the psychological effects of the disease.
• Exercise therapy – to help you remain healthy in spite of your disability.

Initial Treatment of Hemiplegia

Immediate treatment is aimed at limiting the size of the stroke and preventing further stroke. Acute stroke therapies try to stop a stroke while it is happening by quickly dissolving the blood clot causing an ischaemic stroke or by stopping the bleeding of a hemorrhagic stroke.  This will involve administering medications and may involve surgery in some cases.

Medications

RX

• Thrombolytic therapy – These medications dissolve blood clots allowing blood flow to be re-established
• Anticoagulants (eg: heparin) or aspirin – These medications help to prevent blot clots from getting bigger and prevent new blood clots from forming
• Antihypertensives –  In cases of hemorrhagic stroke these medications may be prescribed to help lower high blood pressure
• Medications– to reduce swelling in the brain and medications to treat underlying causes for the stroke eg: heart rhythm disorders may also be given.
• Blood thinners – to reduce cardiovascular blockages and decrease the chances of future strokes.
• Antibiotics – usually delivered intravenously, to combat brain infections.
• Muscle relaxant drugs – Tolperisone or eperisone hcl
• Surgery to address secondary issues-particularly involuntary muscle contractions, spinal damage, or damage to the ligaments or tendons on the unaffected side of the body.
• Physical therapy – designed to help the brain work around the injuries. Physical therapy can also strengthen the unaffected side and help you reduce the loss of muscle control and tone.
• Support groups – family education, and advocacy.
• Psychotherapy to help you deal with the psychological effects of the disease.
• Exercise therapy to help you remain healthy in spite of your disability.

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Treatment of Spastic Hemiplegia

Brain cells do not generally regenerate. Following a stroke, surviving brain cells can take over the function of areas that are dead or damaged, but only to a certain degree. The adaptive ability of the brain requires the relearning of various skills. As each person who suffers a stroke is affected differently, individual rehabilitation plans are developed in conjunction with the patient, family, and healthcare team. These aim to teach skills and maximize function so that the person can achieve maximum independence.

Physiotherapy

Treatment of hemiplegia requires coordination of several health professionals. A physiotherapist, occupational therapist, a physician, a surgeon and support from family, etc.

• Treatment is focused – to find the causative factor and check its further progression. Secondly, after a few days, rehabilitation therapy helps to minimize disability.
• Several medicines – are prescribed to control the primary cause such as antihypertensive, anti-thrombolytic agents to dissolve the clot, drugs to control cerebral edema, etc.
• Intensive physical therapy – is begun after a few days. Activities such as walking, standing are done repeatedly under the guidance of a physiotherapist. It helps to improve the muscular functions which have become rigid. It is aimed to make the patient self-sufficient to perform his daily activities.
• The patient is taught – to move his affected arm with his strong arm. With exercise, it is possible to maintain the flexibility of joints and it also prevents tightening and shortening of muscles. Speech therapy is simultaneously begun to improve communication and speaking skills.
• Speech therapy – to improve communication
• Occupational therapy – to improve daily functions such as eating, cooking, toileting, and washing.

Recovery can take months and it may be several days or weeks after the stroke before doctors are able to give an accurate prediction for recovery.

Occupational therapy

• Occupational therapy – Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening the hand, shoulder, and torso, and participating in activities of daily living (ADLs), such as eating and dressing.
• Therapists – may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual – which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Rehabilitation & Therapy for Hemiplegia

1. Improving motor control

a. Neurofacilitatory Techniques

In Stroke Physical Therapy these therapeutic interventions use sensory stimuli (e.g. quick stretch, brushing, reflex stimulation, and associated reactions), which are based on neurological theories, to facilitate movement in patients following stroke. The following are the different approaches

• Bobath Concept- Berta & Karel Bobath’s approach focuses to control responses from the damaged postural reflex mechanisms. Emphasis is placed on affected inputs facilitation and normal movement patterns (Bobath, 1990).
• ii.Brunnstrom – Brunnstrom approach is one form of neurological exercise therapy in the rehabilitation of stroke patients. The relative effectiveness of Neuro-developmental treatment versus the Brunnstrom method was studied by Wagenaar and colleagues from the perspective of the functional recovery of stroke patients. The result of this study showed no clear differences in the effectiveness of the two methods within the framework of functional recovery.
• iii.Rood – Emphasise the use of activities in developmental sequences, sensation stimulation, and muscle work classification. Cutaneous stimuli such as icing, tapping, and brushing are employed to facilitate activities.
• iv. Proprioceptive neuromuscular facilitation (PNF) – Developed by Knott and Voss, they advocated the use of peripheral inputs as stretch and resisted movement to reinforce existing motor response. Total patterns of movement are used in the treatment and are followed in a developmental sequence.

b. Learning theory approach

• i. Conductive education – In Stroke Physical Therapy, Conductive education is one of the methods in treating neurological conditions including hemiplegic patients. Cotton and Kinsman (1984) demonstrated a neuropsychological approach using the concept of CE for adult hemiplegia. The patient is taught how to guide his movements towards each task-part of the task by using his own speech – rhythmical intention.
• ii. Motor relearning theory – Carr & Shepherd, both are Australian physiotherapists, developed this approach in 1980. It emphasizes the practice of functional tasks and the importance of relearning real-life activities for patients. Principles of learning and biomechanical analysis of movements and tasks are important. There is no evidence adequately supporting the superiority of one type of exercise approach over another. However, the aim of the therapeutic approach is to increase physical independence and to facilitate the motor control of skill acquisition and there is strong evidence to support the effect of rehabilitation in terms of improved functional independence and reduced mortality.

c. Functional electrical stimulation (FES) 

• FES is a modality that applied a short burst of electrical current to the hemiplegic muscle or nerve. In Stroke Physical Therapy, FES has been demonstrated to be beneficial to restore motor control, spasticity, and reduction of hemiplegic shoulder pain and subluxation.  A recent meta-analysis of the randomized controlled trial study showed that FES improves motor strength. A study by Faghri has identified that FES can significantly improve arm function, electromyographic activity of posterior deltoid, the range of motion and reduction of severity of subluxation and pain of the hemiplegic shoulder.

d. Biofeedback

• Biofeedback is a modality that facilitates the cognizant of electromyographic activity in selected muscle or awareness of joint position sense via visual or auditory cues. In Stroke Physical Therapy the result of studies in biofeedback is controversial. A meta-analysis of 8 randomized controlled trials of biofeedback therapy demonstrated that electromyographic biofeedback could improve motor function in stroke patients.
• A conflicting meta-analysis study by showing that biofeedback was not efficacious in improving the range of motion in the ankle and shoulder in a stroke patient. Moreland conducted another meta-analysis that concluded that EMG biofeedback alone or with conventional therapy did not superior to conventional physical therapy in improving upper- extremity function in the adult stroke patient.

2. Hemiplegic shoulder management

Shoulder subluxation and pain of the affected arm is not uncommon in at least 30% of all patient after stroke, whereas subluxation is found in 80% of stroke patients. It is associated with the severity of the disability and is common in patients in rehabilitation settings. Suggested interventions are as follows:

• a. Exercise – Active weight-bearing exercise can be used as a means of improving motor control of the affected arm; introducing and grading tactile, proprioceptive, and kinesthetic stimulation; and preventing edema and pain. In Stroke Physical Therapy, Upper extremity weight bearing can be used to lengthen or inhibit tight or spastic muscles while simultaneously facilitating muscles that are not active (Donatelli, 1991). According to Robert (1992), the amount of shoulder pain in hemiplegia was related most to loss of motion. He advocated that the provision of ROM exercise (caution to avoid improvement) as treatment as early as possible.
• b. Functional electrical stimulation – Functional electrical stimulation (FES) is an increasingly popular treatment for hemiplegic stroke patients. It has been applied in stroke physical therapy for the treatment of shoulder subluxation spasticity and functionally, for the restoration of function in the upper and lower limb. In Stroke Physical Therapy, Electrical stimulation is effective in reducing pain and severity of subluxation, and possibly in facilitating recovery of arm function c. Positioning & proper handling – In Stroke Physical Therapy, proper positioning and handling of the hemiplegic shoulder, whenever in bed, sitting and standing or during lifting, can prevent shoulder injury is recommended in the AHCPR & SIGN guidelines for stroke rehabilitation. In Stroke Physical Therapy, positioning can be therapeutic for tone control and neuro-facilitation of stroke patients (Davies, 1991). Braus et al 94 found shoulder hand syndrome reduced from 27% to 8% by the instruction to everyone including family on handling technique.
• d. Neuro-facilitation
• e. Passive limb physiotherapy – Maintenance of a full pain-free range of movement without traumatizing the joint and the structures can be carried out. In Stroke Physical Therapy, at no time should pain in or around the shoulder joint be produced during treatment.
• f. Pain relief physiotherapy – Passive mobilization as described by Maitland can be useful in gaining relief of pain and range of movement. In Stroke Physical Therapy other treatment modalities such as thermal, electrical, cryotherapy, etc. can be applied for shoulder pains or musculoskeletal in nature.
• g. Reciprocal pulley – The use of reciprocal pulley appears to increase the risk of developing shoulder pain in stroke patients. It is not related to the presence of subluxation or to muscle strength.
• h. Sling – In Stroke Physical Therapy the use of a sling is controversial. No shoulder support will correct a glenohumeral joint subluxation. However, it may prevent the flaccid arm from hanging against the body during functional activities, thus decreasing shoulder joint pain. They also help to relieve downward traction on the shoulder capsule caused by the weight of the arm.

3. Limb physiotherapy

• Limb physiotherapy/Stroke Physical Therapy includes passive, assisted-active and active range-of-motion exercise for the hemiplegic limbs. This can be effective management for the prevention of limb contractures and spasticity and is recommended within AHCPR. Self-assisted limb exercise is effective for reducing spasticity and shoulder protection. Adams and coworkers recommended passive full-range-of-motion exercise for a paralyzed limb for potential reduction of complication for stroke patients

4. Chest physiotherapy

• In Stroke Physical Therapy, evidence shows that both cough and forced expiratory technique (FET) can eliminate induced radio aerosol particles in the lung field. Directed coughing and FET can be used as a technique for bronchial hygiene clearance in stroke patients.

5. Positioning

• In Stroke, Physical Therapy consistent “reflex-inhibitory” patterns of posture in resting is encouraged to discourage physical complication of stroke and to improve recovery (Bobath, 1990).
• Meanwhile, therapeutic positioning is a widely advocated strategy to discourage the development of abnormal tone, contractures, pain, and respiratory complications. It is an important element in maximizing the patient’s functional gains and quality of life.

6. Tone management

• A goal of Stroke Physical Therapy interventions has been to “normalize tone to normalize movement.” Therapy modalities for reducing tone include stretching, prolonged stretching, passive manipulation by therapists, weight-bearing, ice, contraction of muscles antagonistic to spastic muscles, splinting, and casting.
• Research on tone-reducing techniques has been hampered by the inadequacies of methods to measure spasticity and the uncertainty about the relationship between spasticity and volitional motor control.
• The manual stretch of finger muscles, pressure splints, and dantrolene sodium do not produce apparent long-term improvement in motor control. Dorsal resting hand splints reduced spasticity more than volar splints, but the effect on motor control is uncertain while TENS stimulation showed improvement for chronic spasticity of lower extremities.

7. Sensory re-education

• Bobath and other therapy approaches recommend the use of sensory stimulation to promote the sensory recovery of stroke patients.

8. Balance retraining

• Re-establishment of balance function in patients following stroke has been advocated as an essential component in the practice of stroke physical therapy. Some studies of patients with hemiparesis revealed that these patients have a greater amount of postural sway, the asymmetry with greater weight on the non-paretic leg, and a decreased ability to move within a weight-bearing posture. Meanwhile, research has demonstrated moderate relationships between balance function and parameters such as gait speed, independence, wheelchair mobility, reaching, as well as dressing. Some tenable support on the effectiveness of treatment of disturbed balance can be found in studies comparing the effects of balance retraining plus physiotherapy treatment and physiotherapy treatment alone.

9. Fall prevention

• In Stroke Physical Therapy, falls are one of the most frequent complications and the consequences of which are likely to have a negative effect on the rehabilitation process and its outcome.
• According to the systematic review of the Cochrane Library, which evaluated the effectiveness of several fall prevention interventions in the elderly, there was significant protection against falling from interventions that targeted multiple, identified, risk factors in individual patients. The same is true for interventions which focused on behavioral interventions targeting environmental hazards plus other risk factors

10. Gait re-education

• Recovery of independent mobility is an important goal for the immobile patient, and much therapy is devoted to gait-reeducation. Bobath assumes abnormal postural reflex activity is caused by dysfunction so gait training involved tone normalization and preparatory activity for gait activity.
• In contrast, Carr and Shepherd advocate task-related training with methods to increase strength, coordination and flexible MS system to develop skill in walking while Treadmill training combined with the use of a suspension tube. Some patient’s body weight can effective in regaining walking ability when used as an adjunct to convention therapy 3 months after active training.

11. Functional Mobility Training

• To handle the functional limitations of stroke patients, functional tasks are taught to them based on movement analysis principles. In Stroke Physical Therapy these tasks include bridging, rolling to sit to stand and vice versa, transfer skills, walking and staring, etc.
• Published studies report that many patients improve during rehabilitation. The strongest evidence of benefit is from studies that have enrolled patients with chronic deficits or have included a no-treatment control group.
• Meanwhile, early mobilization helps prevent compilations e.g. DVT, skin breakdown contracture and pneumonia. Evidence has shown better orthostatic tolerance and earlier ambulation.

12. Upper limb training

By 3 months poststroke, approximately 37% of the individuals continue to have decreased upper extremities (UE) function. Recovery of UE function lags behind that of the lower extremities because of the more complex motor skill required of the UE in daily life tasks. That means many individuals who have a stroke are at risk for a lowered quality of life. Many approaches to the physical rehabilitation of adults post-stroke exist that attempt to maximize motor skill recovery. However, the literature does not support the efficacy of any single approach. The followings are the current approaches to motor rehabilitation of the UE.

• a. Facilitation models – They are the most common methods of intervention for the deficits in UE motor skills including Bobath, proprioceptive neuromuscular facilitation, Brunnstrom’s movement therapy, and Rood’s sensorimotor approach. There is some evidence that practice based on the facilitation models can result in improved motor control of UE. However, an intervention based on the facilitation models has not been effective in restoring the fine hand coordination required for the performance of actions.
• b. Functional electric stimulation – In Stroke Physical Therapy, Functional electric stimulation (FES) can be effective in increasing the electric activity of muscles or increased active range of motion in individuals with stroke. Some evidence showed that FES may be more effective than facilitation approaches.
• c. Electromyographic biofeedback – In Stroke Physical Therapy, biofeedback can contribute to improvements in motor control at the neuromuscular and movement levels. Some studies have shown improvements in the ability to perform actions during post-testing after biofeedback training. However, the ability to generalize these skills and incorporate them into daily life is not measured.
• d. Constraint-induced therapy – Constraint-Induced (CI) therapy was designed to overcome the learned nonuse of the affected UE. In the most extreme form of CI therapy, individual post-stroke is prevented from using the less affected UE by keeping it in a splint and sling for at least 90% of their waking hours. Studies have found that the most extreme of CI therapy can effect rapid improvement in UE motor skill and that is retained for at least as long as 2 years. However, CI therapy currently is effective only in those with distal voluntary movement.

13. Mobility appliances and equipment

• Small changes in an individual’s local ‘environment’ can greatly increase independence, use of a wheelchair or walking stick. However, little research has been done for these ‘treatments’. It is acknowledged that walking aids and mobility appliances may benefit selected patients.

14. Acupuncture 

• The World Health Organisation (WHO) has listed acupuncture as a possible treatment for pariesis after stroke. Studies had sown its beneficial effects on stroke rehabilitation.
• Hua had reported a significant difference in changes of neurological score between the acupuncture group and the control group after 4 weeks of treatment in an RCT and no adverse effects were observed in patients treated with acupuncture.

15. Vasomotor training 

• Early stimulation of the muscle pump can reduce the venous stasis and enhance the general circulation of the body. It then hastens the recovery process.

16. Edema management

• Use of intermittent pneumatic pump, elastic stocking or bandages and massage can facilitate the venous return of the oedematous limbs. Therefore, the elasticity and flexibility of the musculoskeletal system can be maintained and enhance the recovery process and prevent complications like pressure ulcers.

Homeopathic Medicines for Hemiplegia

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What Is The Latest Treatment of Tumor Lysis Syndrome/Tumor lysis syndrome (TLS) is characterized by a massive tumor cell death leading to the development of metabolic derangements and target organ dysfunction? TLS can occur as a result of cancer treatment or spontaneously. Blood cancers constitute the vast majority of TLS cases because of the sensitivity to therapy and rapid division rates.

Tumor lysis syndrome (TLS) is a potentially life-threatening condition that occurs in oncologic and hematologic patients with large tumor burden, either due to cytotoxic therapy or, less commonly, spontaneously because of massive tumor cell lysis. TLS is clinically characterized by acute renal failure, hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. While limited options are available for treating TLS, identifying patients at high risk for developing TLS and prevention in high-risk patients remain an important aspect in the treatment of cancer patients. In general, treatment of TLS consists of intensive hydration, stimulation of diuresis, and, more specifically, in the use of allopurinol and rasburicase.

Tumor lysis syndrome (TLS) describes the pathological sequela of the rapid lysis of tumor cells. The shift of potassium, phosphorus, and nucleic acid material into the extracellular space can rapidly overcome existing homeostatic mechanisms, leading to acute kidney failure, arrhythmia, and death. TLS is the most common oncologic emergency, and although commonly seen in the context of initial chemotherapeutic treatment of hematologic malignancies, increasing recognition is being paid to the occurrence of spontaneous TLS and TLS secondary to treatment of bulky solid tumors.^[rx,rx]

Tumor lysis syndrome is a group of metabolic abnormalities that can occur as a complication during the treatment of cancer,^[rx] where large amounts of tumor cells are killed off (lysed) at the same time by the treatment, releasing their contents into the bloodstream. This occurs most commonly after the treatment of lymphomas and leukemias. In oncology and hematology, this is a potentially fatal complication, and patients at increased risk for TLS should be closely monitored before, during, and after their course of chemotherapy.

Pathophysiology

The pathophysiology of tumor lysis syndrome is complicated. Tumor lysis syndrome is caused by the massive release of intracellular ions such as potassium, phosphorus, and nucleic acids that have been metabolized to uric acid. The main organ is responsible for the excretions of these substances in the kidney. When the compensatory response of the kidney is exhausted as a result of the massive release of intracellular ions, uric acid obstructive uropathy develops which can then progress to acute kidney injury.

Molecules called nucleotides comprise DNA. These nucleotides are units made of a phosphate group, a sugar group, and a nitrogen base. The nitrogen base is adenine, thymine, guanine or cytosine. Adenine and guanine are purines while thymine and cytosine are pyrimidines. Ribonucleic acid, however, is made up of a ribose sugar and a nitrogen base adenine, thymine, and uracil.

The metabolism of the purines adenine and guanine in a stepwise process leads to the production of xanthine. Adenine is metabolized to hypoxanthine whereas guanine is metabolized to xanthine. Xanthine is then further metabolized into uric acid in a reaction that is catalyzed by xanthine oxidase. Most mammals have the enzyme urate oxidase that can transform uric acid to allantoin which is a more soluble substance that can be easily excreted by the kidney. Human beings lack this enzyme.

Due to the rapid turnover of tumor cells, there is an overwhelming production of uric acid which then crystallizes in the renal tubules causing obstructive uropathy from and decreased glomerular filtration rate. In rat models, urate nephropathy causes an increase in both proximal and distal tubule pressure. Peritubular capillary pressure and vascular resistance also increase. Uric acid scavenges nitric oxide which is a potent vasodilator. The scavenging of nitric oxide produces vasoconstriction and kidney ischemia. Uric acid is also a potential pro-inflammatory agent and can cause the release of other cytokine-like tumor necrosis factor-alpha, protein I. These cytokines attract white blood cells and facilitate further injury to the kidney.

Electrolyte Imbalance

Hyperkalemia

The concentration of potassium within the cell is about 120 to 130 meq/L. The lysis of tumorous cells leads to a massive release of intracellular potassium. The excess potassium is usually taken up by the liver and skeletal muscle. The rest is excreted via the gastrointestinal system or the kidney. The obstructive uropathy from uric acid salts can limit the excretion of potassium. Sometimes the hyperkalemia from the solid tumor can reach a potentially life-threatening level. The risk of hyperkalemia is cardiac arrest from arrhythmia.

Hyperphosphatemia

Hyperphosphatemia is another electrolyte imbalance associated with tumor lysis syndrome. The nucleic acid has a phosphate group, and the breakdown of the tumorous cell will lead to the release of a significant amount of phosphorus into the bloodstream. Most of the phosphorus is really excreted. This ability of the kidney to handle a high load of phosphorus is inhibited by acute kidney injury or chronic kidney disease.

Hyperphosphatemia is less common in spontaneous tumor lysis syndrome than those induced by chemotherapy. It leads to the chelation of calcium causing hypocalcemia. Deposition of calcium and phosphorus salts in the kidney and soft tissues can also occur.

Hypocalcemia

Hypocalcemia in tumor lysis syndrome is mostly secondary to the chelation of phosphorus. This condition is more potentially life-threatening than hyperphosphatemia. Possible complications from hypocalcemia include arrhythmia, tetany, seizure, and death. The calcium level might still be relatively low even after the normalization of the phosphorus level because of a deficiency of 1, 25 Vitamin D.

Causes of Tumor Lysis Syndrome

Symptoms of Tumor Lysis Syndrome

Hyperkalemia – Potassium is mainly an intracellular ion. High turnover of tumor cells leads to a spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 7 mmol/L) [normal 3.5–5.0 mmol/L] and they include

• cardiac conduction abnormalities (can be fatal)
• severe muscle weakness or paralysis

Hyperphosphatemia – Like potassium, phosphates are also predominantly intracellular. Hyperphosphatemia causes acute kidney failure in tumor lysis syndrome, because of deposition of calcium phosphate crystals in the kidney parenchyma.

Hypocalcemia – Because of the hyperphosphatemia, calcium is precipitated to form calcium phosphate, leading to hypocalcemia. Symptoms of hypocalcemia include (but are not limited to):

• Tetany
• Sudden mental incapacity, including emotional lability
• Parkinsonian (extrapyramidal) movement disorders
• Papilledema
• Myopathy

Hyperuricemia^[rx] and hyperuricosuria. Massive cell death and nuclear breakdown generate large quantities of nucleic acids. Of these, the purines (adenine and guanine) are converted to uric acid via the purine degradation pathway and excreted in the urine. However, at the high concentrations of uric acid generated by tumor lysis, uric acid is apt to precipitate as monosodium urate crystals.

• Acute uric acid nephropathy (AUAN) – due to hyperuricosuria has been a dominant cause of acute kidney failure but with the advent of effective treatments for hyperuricosuria, AUAN has become a less common cause than hyperphosphatemia. Two common conditions related to excess uric acid, gout and uric acid nephrolithiasis, are not features of tumor lysis syndrome.
• Lactic acidosis.^[rx][rx]
• Pretreatment spontaneous tumor lysis syndrome. This entity is associated with acute kidney failure due to uric acid nephropathy prior to the institution of chemotherapy and is largely associated with lymphoma and leukemia. The important distinction between this syndrome and the post-chemotherapy syndrome is that spontaneous TLS is not associated with hyperphosphatemia.
• One suggestion for the reason for this is that the high cell turnover rate leads to high uric acid levels through nucleobase turnover but the tumor reuses the released phosphate for the growth of new tumor cells. In post-chemotherapy TLS, tumor cells are destroyed and no new tumor cells are being synthesized

TLS is most common during cytotoxic treatment of hematologic neoplasms.^[rx]

• Dark urine reduced urine output or flank pain
• Lack of appetite and fatigue
• Numbness, seizures, or hallucinations
• Muscle cramps and spasms
• Heart palpitations symptoms are generally nonspecific and can include:
• Kidney failure and death can occur, especially if TLS is left untreated.
• TLS is diagnosed based on blood tests, along with signs and symptoms. Its onset may be subtle, with only a few abnormal laboratory values, but it can also present with frank kidney and organ failure.
• Nausea with or without vomiting

Diagnosis of Tumor Lysis Syndrome

[stextbox id=’warning’]

[/stextbox]

Laboratory tumor lysis syndrome: abnormality in two or more of the following, occurring within three days before or seven days after chemotherapy.

Alkalinization of urine

References

People Also Reading

Tumor Lysis Syndrome; Causes, Symptoms, Treatment How Can I Insure Tumor Lysis Syndrome Not Going Doctor How is tumor lysis syndrome treated? What Is The Main Causes of Tumor Lysis Syndrome Before Going To Doctor I Must Know Tumor lysis syndrome How is tumor lysis syndrome diagnosed? Tests What are the signs and symptoms of tumor lysis syndrome? How does allopurinol prevent tumor lysis syndrome? Allopurinol; Uses, Dosage, Side Effects, Interaction, Pregnancy Wilms Tumor- Causes, Symptoms, Treatment Tumor – Types, Classification, Treatment Mirizzi Syndrome – Causes, Symptoms, Treatment

How Can I Insure Tumor Lysis Syndrome Not Going Doctor/Tumor lysis syndrome (TLS) is characterized by a massive tumor cell death leading to the development of metabolic derangements and target organ dysfunction? TLS can occur as a result of cancer treatment or spontaneously. Blood cancers constitute the vast majority of TLS cases because of the sensitivity to therapy and rapid division rates.

Tumor lysis syndrome (TLS) is a potentially life-threatening condition that occurs in oncologic and hematologic patients with large tumor burden, either due to cytotoxic therapy or, less commonly, spontaneously because of massive tumor cell lysis. TLS is clinically characterized by acute renal failure, hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. While limited options are available for treating TLS, identifying patients at high risk for developing TLS and prevention in high-risk patients remain an important aspect in the treatment of cancer patients. In general, treatment of TLS consists of intensive hydration, stimulation of diuresis, and, more specifically, in the use of allopurinol and rasburicase.

Tumor lysis syndrome (TLS) describes the pathological sequela of the rapid lysis of tumor cells. The shift of potassium, phosphorus, and nucleic acid material into the extracellular space can rapidly overcome existing homeostatic mechanisms, leading to acute kidney failure, arrhythmia, and death. TLS is the most common oncologic emergency, and although commonly seen in the context of initial chemotherapeutic treatment of hematologic malignancies, increasing recognition is being paid to the occurrence of spontaneous TLS and TLS secondary to treatment of bulky solid tumors.^[rx,rx]

Tumor lysis syndrome is a group of metabolic abnormalities that can occur as a complication during the treatment of cancer,^[rx] where large amounts of tumor cells are killed off (lysed) at the same time by the treatment, releasing their contents into the bloodstream. This occurs most commonly after the treatment of lymphomas and leukemias. In oncology and hematology, this is a potentially fatal complication, and patients at increased risk for TLS should be closely monitored before, during, and after their course of chemotherapy.

Pathophysiology

The pathophysiology of tumor lysis syndrome is complicated. Tumor lysis syndrome is caused by the massive release of intracellular ions such as potassium, phosphorus, and nucleic acids that have been metabolized to uric acid. The main organ is responsible for the excretions of these substances in the kidney. When the compensatory response of the kidney is exhausted as a result of the massive release of intracellular ions, uric acid obstructive uropathy develops which can then progress to acute kidney injury.

Molecules called nucleotides comprise DNA. These nucleotides are units made of a phosphate group, a sugar group, and a nitrogen base. The nitrogen base is adenine, thymine, guanine or cytosine. Adenine and guanine are purines while thymine and cytosine are pyrimidines. Ribonucleic acid, however, is made up of a ribose sugar and a nitrogen base adenine, thymine, and uracil.

The metabolism of the purines adenine and guanine in a stepwise process leads to the production of xanthine. Adenine is metabolized to hypoxanthine whereas guanine is metabolized to xanthine. Xanthine is then further metabolized into uric acid in a reaction that is catalyzed by xanthine oxidase. Most mammals have the enzyme urate oxidase that can transform uric acid to allantoin which is a more soluble substance that can be easily excreted by the kidney. Human beings lack this enzyme.

Due to the rapid turnover of tumor cells, there is an overwhelming production of uric acid which then crystallizes in the renal tubules causing obstructive uropathy from and decreased glomerular filtration rate. In rat models, urate nephropathy causes an increase in both proximal and distal tubule pressure. Peritubular capillary pressure and vascular resistance also increase. Uric acid scavenges nitric oxide which is a potent vasodilator. The scavenging of nitric oxide produces vasoconstriction and kidney ischemia. Uric acid is also a potential pro-inflammatory agent and can cause the release of other cytokine-like tumor necrosis factor-alpha, protein I. These cytokines attract white blood cells and facilitate further injury to the kidney.

Electrolyte Imbalance

Hyperkalemia

The concentration of potassium within the cell is about 120 to 130 meq/L. The lysis of tumorous cells leads to a massive release of intracellular potassium. The excess potassium is usually taken up by the liver and skeletal muscle. The rest is excreted via the gastrointestinal system or the kidney. The obstructive uropathy from uric acid salts can limit the excretion of potassium. Sometimes the hyperkalemia from the solid tumor can reach a potentially life-threatening level. The risk of hyperkalemia is cardiac arrest from arrhythmia.

Hyperphosphatemia

Hyperphosphatemia is another electrolyte imbalance associated with tumor lysis syndrome. The nucleic acid has a phosphate group, and the breakdown of the tumorous cell will lead to the release of a significant amount of phosphorus into the bloodstream. Most of the phosphorus is really excreted. This ability of the kidney to handle a high load of phosphorus is inhibited by acute kidney injury or chronic kidney disease.

Hyperphosphatemia is less common in spontaneous tumor lysis syndrome than those induced by chemotherapy. It leads to the chelation of calcium causing hypocalcemia. Deposition of calcium and phosphorus salts in the kidney and soft tissues can also occur.

Hypocalcemia

Hypocalcemia in tumor lysis syndrome is mostly secondary to the chelation of phosphorus. This condition is more potentially life-threatening than hyperphosphatemia. Possible complications from hypocalcemia include arrhythmia, tetany, seizure, and death. The calcium level might still be relatively low even after the normalization of the phosphorus level because of a deficiency of 1, 25 Vitamin D.

Causes of Tumor Lysis Syndrome

Symptoms of Tumor Lysis Syndrome

Hyperkalemia – Potassium is mainly an intracellular ion. High turnover of tumor cells leads to a spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 7 mmol/L) [normal 3.5–5.0 mmol/L] and they include

• cardiac conduction abnormalities (can be fatal)
• severe muscle weakness or paralysis

Hyperphosphatemia – Like potassium, phosphates are also predominantly intracellular. Hyperphosphatemia causes acute kidney failure in tumor lysis syndrome, because of deposition of calcium phosphate crystals in the kidney parenchyma.

Hypocalcemia – Because of the hyperphosphatemia, calcium is precipitated to form calcium phosphate, leading to hypocalcemia. Symptoms of hypocalcemia include (but are not limited to):

• Tetany
• Sudden mental incapacity, including emotional lability
• Parkinsonian (extrapyramidal) movement disorders
• Papilledema
• Myopathy

Hyperuricemia^[rx] and hyperuricosuria. Massive cell death and nuclear breakdown generate large quantities of nucleic acids. Of these, the purines (adenine and guanine) are converted to uric acid via the purine degradation pathway and excreted in the urine. However, at the high concentrations of uric acid generated by tumor lysis, uric acid is apt to precipitate as monosodium urate crystals.

• Acute uric acid nephropathy (AUAN) – due to hyperuricosuria has been a dominant cause of acute kidney failure but with the advent of effective treatments for hyperuricosuria, AUAN has become a less common cause than hyperphosphatemia. Two common conditions related to excess uric acid, gout and uric acid nephrolithiasis, are not features of tumor lysis syndrome.
• Lactic acidosis.^[rx][rx]
• Pretreatment spontaneous tumor lysis syndrome. This entity is associated with acute kidney failure due to uric acid nephropathy prior to the institution of chemotherapy and is largely associated with lymphoma and leukemia. The important distinction between this syndrome and the post-chemotherapy syndrome is that spontaneous TLS is not associated with hyperphosphatemia.
• One suggestion for the reason for this is that the high cell turnover rate leads to high uric acid levels through nucleobase turnover but the tumor reuses the released phosphate for the growth of new tumor cells. In post-chemotherapy TLS, tumor cells are destroyed and no new tumor cells are being synthesized

TLS is most common during cytotoxic treatment of hematologic neoplasms.^[rx]

• Dark urine reduced urine output or flank pain
• Lack of appetite and fatigue
• Numbness, seizures, or hallucinations
• Muscle cramps and spasms
• Heart palpitations symptoms are generally nonspecific and can include:
• Kidney failure and death can occur, especially if TLS is left untreated.
• TLS is diagnosed based on blood tests, along with signs and symptoms. Its onset may be subtle, with only a few abnormal laboratory values, but it can also present with frank kidney and organ failure.
• Nausea with or without vomiting

Diagnosis of Tumor Lysis Syndrome

[stextbox id=’warning’]

[/stextbox]

Laboratory tumor lysis syndrome: abnormality in two or more of the following, occurring within three days before or seven days after chemotherapy.

Alkalinization of urine

References

People Also Reading

Before Going To Doctor I Must Know Tumor lysis syndrome What Is The Latest Treatment of Tumor Lysis Syndrome How is tumor lysis syndrome treated? What Is The Main Causes of Tumor Lysis Syndrome How is tumor lysis syndrome diagnosed? Tests Tumor Lysis Syndrome; Causes, Symptoms, Treatment What are the signs and symptoms of tumor lysis syndrome? How does allopurinol prevent tumor lysis syndrome? Allopurinol; Uses, Dosage, Side Effects, Interaction, Pregnancy How Can I Insure Blau Syndrome How Can I Insure H. Pylori Infection Not Going Doctor How Can You Insure Pneumothorax Not Going to Doctor

How Can I Enlarge My Panis Not Going To Doctor/Penis Enlargement or male enhancement is any technique aimed to increase the size of a human penis. Some methods aim to increase total length, others the shaft’s girth, and yet others the glans size. Techniques include surgery, supplements, ointments, patches, and physical methods like pumping, jelqing, and traction.

Inflatable penile prosthetic (IPP) devices have been available and used for more than four decades. Often times, medical conditions causing erectile dysfunction also cause penis shortening, causing the decreased patient quality of life. To identify and review all available penis lengthening procedures that can be performed at the time of IPP insertion. An extensive, systematic literature review was performed using PubMed searching for key terms penis lengthening, inflatable penis prosthesis, penile girth, clitoroplasty, glans augmentation, and penis enhancement; all articles with subjective or objective penis length outcomes were reviewed.

Anatomy of Penis Enlargement

Parts

• The root of the penis (radix): It is the attached part, consisting of the bulb of the penis in the middle and the crus of the penis, one on either side of the bulb. It lies within the superficial perineal pouch.
• Body of the penis (corpus): It has two surfaces: dorsal (posterosuperior in the erect penis), and ventral or urethral (facing downwards and backward in the flaccid penis). The ventral surface is marked by a groove in a lateral direction.
• Epithelium of the penis consists of the shaft skin, the foreskin, and the preputial mucosa on the inside of the foreskin and covering the glans penis. The epithelium is not attached to the underlying shaft so it is free to glide to and fro.^[rx]

Structure

The human penis is made up of three columns of tissue –  two corpora cavernosa lie next to each other on the dorsal side and one corpus spongiosum lies between them on the ventral side.^[rx]

The enlarged and bulbous-shaped end of the corpus spongiosum forms the glans penis with two specific types of sinusoids, which supports the foreskin, or prepuce, a loose fold of skin that in adults can retract to expose the glans.^[rx] The area on the underside of the penis, where the foreskin is attached, is called the frenum, or frenulum. The rounded base of the glans is called the corona. The perineal raphe is the noticeable line along the underside of the penis.

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Comparison of mean body weight, mean testicular weight, mean plasma testosterone and mean IGF-1 among experimental groups.

[/stextbox]

Disorders of Penis Enlargement

• Paraphimosis – is an inability to move the foreskin forward over the glans. It can result from fluid trapped in a foreskin left retracted, perhaps following a medical procedure, or accumulation of fluid in the foreskin because of friction during vigorous sexual activity.
• In Peyronie’s disease – anomalous scar tissue grows in the soft tissue of the penis, causing curvature. Severe cases can be improved by surgical correction.
• A thrombosis can occur during periods of frequent and prolonged sexual activity – especially fellatio. It is usually harmless and self-corrects within a few weeks.
• Infection with the herpes virus can occur after sexual contact with an infected carrier –  this may lead to the development of herpes sores.
• Pudendal nerve entrapment – is a condition characterized by pain on sitting and the loss of penile sensation and orgasm. Occasionally there is a total loss of sensation and orgasm. The pudendal nerve can be damaged by narrow, hard bicycle seats and accidents. This can also occur in the clitoris of females.
• Penile fracture – can occur if the erect penis is bent excessively. A popping or cracking sound and pain is normally associated with this event. Emergency medical assistance should be obtained as soon as possible. Prompt medical attention lowers the likelihood of permanent penile curvature.
• In diabetes – peripheral neuropathy can cause tingling in the penile skin and possibly reduced or completely absent sensation. The reduced sensations can lead to injuries for either partner and their absence can make it impossible to have sexual pleasure through stimulation of the penis. Since the problems are caused by permanent nerve damage, preventive treatment through good control of diabetes is the primary treatment. Some limited recovery may be possible through improved diabetes control.
• Erectile dysfunction – is the inability to develop and maintain an erection sufficiently firm for satisfactory sexual performance. Diabetes is a leading cause, as is natural aging. A variety of treatments exist, most notably including the phosphodiesterase type 5 inhibitor drugs (such as sildenafil citrate, marketed as Viagra), which work by vasodilation.
• Priapism – is a painful and potentially harmful medical condition in which the erect penis does not return to its flaccid state. Priapism lasting over four hours is a medical emergency. The causative mechanisms are poorly understood but involve complex neurological and vascular factors. Potential complications include ischemia, thrombosis, and impotence. In serious cases, the condition may result in gangrene, which may result in amputation. However, that is usually only the case if the organ is broke out and injured because of it. The condition has been associated with a variety of drugs including prostaglandin. Contrary to common knowledge, sildenafil (Viagra) will not cause it.^[rx]
• Lymphangiosclerosis – is a hardened lymph vessel, although it can feel like a hardened, almost calcified or fibrous, vein. It tends not to share the common blue tint with a vein, however. It can be felt as a hardened lump or “vein” even when the penis is flaccid and is even more prominent during an erection. It is considered a benign physical condition. It is fairly common and can follow a particularly vigorous sexual activity for men, and tends to go away if given rest and more gentle care, for example by use of lubricants.
• Carcinoma of the penis – is rare with a reported rate of 1 person in 100,000 in developed countries. Some sources state that circumcision can protect against this disease, but this notion remains controversial among medical circles.^[rx]

Developmental Disorders

• Hypospadias is a developmental disorder where the meatus is positioned wrongly at birth. Hypospadias can also occur iatrogenically by the downward pressure of an indwelling urethral catheter.^[rx] It is usually corrected by surgery.
• A micropenis is a very small penis caused by developmental or congenital problems.
• Diphallia, or penile duplication (PD), is the condition of having two penises. However, this disorder is extremely rare.

Alleged and observed psychological disorders

• Penis panic (koro in Malaysian/Indonesian) – delusion of shrinkage of the penis and retraction into the body. This appears to be culturally conditioned and largely limited to Ghana, Sudan, China, Japan, Southeast Asia, and West Africa.
• In April 2008, the Kinshasa Democratic Republic of Congo, West Africa’s ‘Police arrested 14 suspected victims (of penis snatching) and sorcerers accused of using black magic or witchcraft to steal (make disappear) or shrink men’s penises to extort cash for cure, amid a wave of panic. Arrests were made in an effort to avoid bloodshed seen in Ghana a decade before when 12 penis snatchers were beaten to death by mobs.^[rx]
• Penis envy—the contested Freudian belief of all women inherently envying men for having penises.

The technique of Penis Enlargement

Physical Techniques

• Physical techniques involve extension devices, hanging weights, and vacuum pressure. There is also significant overlap between techniques intended to enlarge the penis and techniques intended to achieve other, related objectives, such as reversing impotence, extending the duration of erections, or enhancing sexual climax.

Pumping

Jelqing

• Performed on the halfway tumescent penis, jelqing is a manual manipulation of simultaneous squeezing and stroking the shaft from base to corona. Also called “milking”,^[rx] the technique has ancient Arab origins.^[rx] Despite many anecdotal reports of success, medical evidence is absent.^[rx]
• Journalists have dismissed the method as biologically implausible,^[rx] or even impossible, albeit unlikely to seriously damage the penis.^[rx] Still, if done excessively or harshly, jelqing could conceivably cause ruptures, scarring, disfigurement, and desensitization.^[rx][rx]

Traction

• Traction is a nonsurgical method to lengthen the penis by employing devices that pull at the glans of the penis for extended periods of time. As of 2013, the majority of research investigating the use of penile traction focuses on treating the curvature and shrinkage of the penis as a result of Peyronie’s disease, although some literature exists on the impact on men with short penises.^[rx] Scientific evidence supports some elongation by prolonged traction.^[rx]

Jelqing exercises

• Jelqing is an exercise that some people use to try to naturally increase the size of their penis. It involves using a hand-over-hand rolling motion to move blood to the head of your penis and stretch it. It’s sometimes called “milking.”
• There aren’t enough medical studies to suggest that jelqing can actually increase your penis size. It’s a fairly safe practice, but it may lead to pain, irritation, or scar tissue formation if you do it too often or aggressively.

Clamps and rings

• Some people use a clamp or ring to try to stretch and elongate their penis. To use one of these devices, you place it around the base of your penis after you’ve developed an erection. It’s meant to prevent blood from flowing out of your penis.
• Wearing one of these devices may temporarily enlarge your penis. But wearing it for more than 30 minutes can cut off blood flow and cause damage to your penile tissue.

Diet, Exercise, and Lifestyle

• The sad truth is that in a significant number of cases, erectile dysfunction is a condition we bring upon ourselves. Even when these things aren’t the outright cause of ED, they’re almost certain to be contributing factors that make your condition worse. This is a big, expansive category that covers a lot of ground, but in a nutshell, here’s what you need to know.
• Eating lots of leafy greens, whole grains, oysters, watermelon, and blueberries (most any fruit will work, really) will help you give your body all that it needs to improve the quality of your erections while cutting out processed foods, cigarettes and alcohol will provide further benefits. Add in a healthy dose of exercise at least three times per week, and you’re well on your way to better sexual health!

References

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Ischemic heart disease, structural disorders, various forms of cardiomyopathy associated with myocardial fibrosis, cardiac channelopathies, myocarditis, congenital heart diseases, and other genetic rare disorders are associated with ventricular arrhythmias[rx].

Even though treatment for heart failure lowers mortality and SCD, it was unsuccessful in lessening ventricular tachycardia (VT) recurrences[rx]. Implantable cardioverter defibrillators (ICD) are very effective in eliminating VT episodes and in lowering the possibility of SCD, but they are not useful for arrhythmia prevention[rx]. When the VT substrate manifests, anti-arrhythmic drug treatment or catheter ablation are the current choices to reduce VT episodes[rx]. Catheter ablation and antiarrhythmic drug therapy though, are also limited by incomplete efficacy, unfavorable side effects, and procedural risk[rx]. In this review, we outline the current advances in VT treatment options and describe the imaging modalities, progress, and novel strategies.

Epicardial catheter ablation

Endocardial catheter ablation and antiarrhythmic drug treatment are currently the mainstays of VT treatment[rx,rx]. However, the procedural success rates of VT are quite variable due to the heterogeneous substrates that reflect the variety of pathophysiological processes[rx,rx]. The success rate of endocardial ablation in patients with outflow tract VT is 84%, in patients with papillary muscle VT is 60%, and in patients with idiopathic left ventricular VT is 70%[rx]. Moreover, the VT recurrence rates of endocardial ablation in ischemic cardiomyopathy patients are between 23% and 49% and in dilated cardiomyopathy patients between 46% and 61%[rx]. Non-ischemic cardiomyopathy patients have worse outcomes than ischemic cardiomyopathy patients due to scar patterns with epicardial and intramural sites[rx].

Epicardial ablation has emerged as a potential alternative ablation strategy in order to increase the success rate in complex substrates and to eliminate VT in patients with different cardiomyopathies and more recently in patients with Brugada syndrome[rx–rx]. Percutaneous approach to the pericardial area facilitates epicardial ablation when the VT substrate is situated in the subepicardium[rx] (Figure ​[rx]. Adjacency to coronary circulation and the phrenic nerve may hinder the procedure in certain situations[rx]. In patients with previous heart surgery or previous epicardial ablation attempts, percutaneous access may not be possible and as such, video-assisted thoracoscopy may be a good and minimally invasive alternative to open surgery[rx].

Arrhythmia substrate is deep (blue arrow), but the radiofrequency ablation lesions are not that deep. RF: Radiofrequency.

Epicardial ablation is a safe procedure with low complication rates[rx]. Pericardial effusion is the most common complication[rx]. Damage to subdiaphragmatic organs and hemorrhage from diaphragmatic vessels have also been reported[rx].

Della Bella et al[rx] evaluated the possible benefit of endo-epicardial catheter ablation for the management of VT in 528 patients with any form of the structural cardiac disorder (Figure ​[rx]. Endo-epicardial catheter ablation resulted in a VT recurrence rate of 34.1%, in comparison to a rate of up to 50% with the standard endocardial approach[rx].

Endocardial and epicardial voltage mapping. A: The voltage map of the endocardium shows an area of the scar. The map is color-coded to represent bipolar electro-gram voltage (red: Dense scar, 0.5 mV; purple: Normal tissue, 1.5 mV, intervening colors represent voltage values in between); B: The voltage map of the epicardium shows a larger area of scar.

Intramyocardial infusion-needle catheter ablation

Transcoronary alcohol ablation has emerged to approach deep intramyocardial substrate in patients not amenable to endo-epicardial catheter ablation (mechanical valve, thrombus, significant comorbidities)[rx,rx]. Transcoronary alcohol ablation requires the injected dose of sterile pure ethanol with proximal balloon expansion to a culprit vessel with a target of abolishing perfusion[rx,rx] . This method can prevent recurrent VT, VT storm and can control incessant VT[rx,rx]. The exact recognition of the target vessel and the existence of collaterals may hinder the adoption of the method[rx–rx].

Transcoronary alcohol ablation. Coronary angiography of the left anterior descending artery shows a septal perforator with a course to the site of the earliest activity. A balloon catheter occludes this branch and ethanol is infused (blue arrows). The ablation catheter is placed in the region of the earliest activity (red circle).

Kim et al[rx] introduced the novel use of cardioplegia as a mapping technique in order to identify the critical VT isthmus to facilitate effective transcoronary ethanol ablation and avoid irreversible myocardial injury. Furthermore, Sapp et al[rx] showed that intramyocardial needle mapping and ablation with saline infusion could create deep injuries and is a practical and efficient method. Intracoronary wire mapping and coil embolization have also been utilized just as alcohol ablation to target VT arising from intraventricular septum[rx]. After intracoronary wire mapping and recognition of a culprit’s vessel, coils are directed to embolize the branch, eliminating the desired target perfusion[rx].

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Tachycardia Treatment/Tachycardia conventionally but arbitrarily defined as an atrial and/or ventricular rate of >100 beats per minute, is encountered commonly and can be physiological or pathological in origin. Various adverse consequences from tachycardia have been recognized, and an important one is an association between persistent tachycardia and cardiomyopathy.

Tachycardia also called tachyarrhythmia, is a heart rate that exceeds the normal resting rate.^[rx] In general, a resting heart rate over 100 beats per minute is accepted as tachycardia in adults.^[rx] Heart rates above the resting rate may be normal (such as with exercise) or abnormal (such as with electrical problems within the heart). The upper threshold of a normal human resting heart rate is based on age.

Cutoff values for tachycardia in different age groups are fairly well standardized; typical cutoffs are listed below:^[rx]

• 1–2 days – Tachycardia > 159 beats per minute (bpm)
• 3–6 days – Tachycardia >166 bpm
• 1–3 weeks – Tachycardia >182 bpm
• 1–2 months – Tachycardia >179 bpm
• 3–5 months – Tachycardia >186 bpm
• 6–11 months – Tachycardia >169 bpm
• 1–2 years – Tachycardia >151 bpm
• 3–4 years – Tachycardia >137 bpm
• 5–7 years – Tachycardia >133 bpm
• 8–11 years – Tachycardia >130 bpm
• 12–15 years – Tachycardia >119 bpm
• >15 years – adult – Tachycardia >100 bpm

Heart rate is considered in the context of the prevailing clinical picture. For example: in sepsis >90 bpm is considered tachycardia.

Types of Tachycardia

Supraventricular

• Atrial fibrillation
• Atrial flutter
• Atrial tachycardia
  
• AV nodal reentrant tachycardia
  
• AV reentrant tachycardia
  
• Permanent junctional reciprocating tachycardia (PJRT)

Ventricular

• Idiopathic ventricular tachycardia
• Fascicular tachycardia (left septal ventricular tachycardia)

Ectopy

• Frequent premature ventricular contractions
• Frequent premature atrial contractions

Pacing 

• High-rate atrial pacing
• Persistent rapid ventricular pacing

Atrial tachycardia tends to occur in individuals with structural heart disease, with or without heart failure, and ischemic coronary artery disease. However, focal atrial tachycardia often occurs in healthy individuals without structural heart disease. Other possible etiologies are listed below:

Causes of Tachycardia

Etiological causes

• Hypoxia
• Pulmonary disease
• Ischemic heart disease
• Stimulants: cocaine, caffeine, chocolate, ephedra
• Alcohol
• Metabolic disturbances
• Digoxin toxicity
• Heightened sympathetic tone

Some other causes of tachycardia include

EKG can aid the diagnosis of focal atrial tachycardia. EKG features may also inform the origin of focal atrial tachycardias.[rx] Electrocardiographic features include:

• Atrial rate: 100 to 250 BPM
• Ventricular conduction can be variable
  • Irregular or irregularly irregular in the setting of variable AV block
  • Regular if 1 to 1, 2 to 1, or 4 to 1 AV block
• P wave morphology
• Unifocal, but similar in morphology to each other
• Might be inverted
• Differs from normal sinus P wave
• May exhibit either long RP or short PR intervals
• Rhythm may be paroxysmal or sustained
  • May demonstrate an increase in the rate at initiation (i.e., “warm-up,” or “rev up”)
  • May demonstrate a decrease in the rate at termination (i.e., “cool down”)

Below is a differential of similar appearing arrhythmias with their identifying features.

Narrow complex, regular tachycardias

Narrow complex, irregular tachycardia

Treatment of Tachycardia

But if the episodes are prolonged, or recur often, your doctor may recommend treatment, including

• Carotid sinus massage – A healthcare professional can apply gentle pressure on the neck, where the carotid artery splits into two branches.
• Pressing gently on the eyeballs with eyes closed. Caution – This procedure should be supervised carefully by a healthcare physician.
• Valsalva maneuver – This consists of holding your nostrils closed while blowing air through your nose.
• Using the dive reflex – The dive reflex is the body’s response to sudden immersion in water, especially cold water.
• Sedation
• Cutting down on coffee or caffeinated substances
• Cutting down on alcohol
• Quitting tobacco use
• Getting more rest

Pharmacologic Treatment

• If vagal maneuvers fail – a trial of intravenous adenosine may be given at an initial dose of 6 mg and a subsequent dose of 12 mg.^[rx,rx] Its use may serve as a diagnostic and therapeutic tool because it will terminate almost all AVNRTs and AVRTs by breaking the AV-nodal dependent circuit. In patients with non–AV-nodal dependent circuits (i.e., focal atrial tachycardia and atrial flutter), intravenous use of adenosine may prove to be a valuable diagnostic tool because the transient AV block may unmask ectopic atrial P waves or flutter waves.^[rx] Patients should always be monitored by ECG during adenosine administration.
• Adenosine – may induce a wide range of transient bradycardias (including sinus arrest and asystole) as well as atrial fibrillation, SVT and ventricular tachycardia. Albeit very rare, cases of sustained ventricular tachycardia, ventricular fibrillation, and Torsades de pointes have been reported.^[rx] In patients with underlying coronary disease, adenosine may lead to coronary steal syndrome and subsequent myocardial ischemia. ^[rx] Adenosine should therefore always be administered with an external pacemaker or defibrillator nearby.^[rx]
• When vagal maneuvers and adenosine – fail to terminate a narrow-complex tachycardia, intravenous treatment with a nondihydropiridine calcium-channel blocker (e.g., diltiazem and verapamil) or β-blocker may be used. Calcium-channel blockers terminate 64%–98% of SVTs in hemodynamically stable patients. Administering a calcium-channel blocker intravenously over 20 minutes has been shown to reduce the rate of hypotension.^[rx] There are fewer data supporting the use of β-blockers in the acute treatment of SVT; however, they are considered reasonable choices because of their safety profile.^[rx,rx]
• If all aforementioned pharmacologic therapies fail – synchronized cardioversion is recommended, even in hemodynamically stable patients.^[rx]
• In patients presenting in atrial fibrillation who have known Wolff–Parkinson – White or new pre-excitation pattern on ECG, the use of potent AV-nodal blockers (i.e., β-blockers, diltiazem, verapamil, and digoxin) should be avoided because these medications may potentiate conduction over the accessory pathway and lead to potentially life-threatening ventricular arrhythmias. In these cases, intravenous use of procainamide is the preferred approach in the acute setting.^[rx]
• Adenosine is rapidly metabolized in the periphery – and therefore must be given as a rapid push through a large, ideally peripheral, intravenous route. The initial dose is 6 mg intravenously (IV) (pediatric dose 0.1 mg/kg, maximum dose of 6 mg). If the initial dose is ineffective, adenosine may be dosed again at 12 mg IVP (pediatric dose 0.2 mg/kg, maximum dose 12 mg). The second dose of adenosine 12 mg IVP may be repeated one additional time if there is no effect. Each dose of adenosine needs to be flushed rapidly with 10 mL to 20 mL normal saline. Often two-person administration, with one person administering the adenosine at a proximal IV port, and a second person flushing the IV line via a distal port immediately after adenosine administration, is required to adequate flush in the adenosine.
• Consider reducing the adenosine dose to 3 mg – IVP if the patient is currently receiving carbamazepine or dipyridamole, is the recipient of a heart transplant, or adenosine is being given through a central line.
• If adenosine fails – second line medications include diltiazem (0.25 mg/kg IV loading dose followed by 5mg/hr to 15 mg/hr infusion), esmolol (0.5 mg/kg IV loading dose, then 0.5 mg/kg/min up to 0.2 mg/kg/min, will need to repeat bolus for every up-titration), or metoprolol (2.5 mg to 5 mg IV every two to five minutes, not to exceed 15 mg over 10 to 15 minutes).

Acute treatment

• Vagal maneuvers are recommended for acute treatment in patients with regular SVT (class I recommendation, level B-R evidence)
• Intravenous administration of adenosine is recommended for acute treatment in patients with regular SVT (class I recommendation, level B-R evidence)
• Synchronized cardioversion is recommended for acute treatment in patients with hemodynamically stable SVT when pharmacologic treatment is ineffective or contraindicated (class I recommendation, level B-NR evidence)
• Intravenous administration of diltiazem or verapamil can be effective for acute treatment in patients with hemodynamically stable SVT (class IIa recommendation, level B-R evidence)
• Intravenous use of β-blockers is reasonable for acute treatment in patients with hemodynamically stable SVT (class IIa recommendation, level C-LD evidence)

Ongoing management

• Oral β-blocker – diltiazem or verapamil treatment is useful for ongoing management in patients with symptomatic SVT who do not have ventricular pre-excitation during sinus rhythm (class I recommendation, level B-R evidence)
• Electrophysiologic study – with the option of radiofrequency catheter ablation is useful for the diagnosis and potential treatment of SVT (class I recommendation, level B-NR evidence)
• Patients with SVT – should be educated on how to perform vagal maneuvers for ongoing management of SVT (class I recommendation, level C-LD evidence)

Referral for radiofrequency catheter ablation

• Catheter ablation of the slow pathway is recommended in patients with AVNRT (class I recommendation, level B-NR evidence)
• Catheter ablation is recommended in patients with symptomatic focal atrial tachycardia as an alternative to pharmacologic treatment (class I recommendation, level B-NR evidence)
• Catheter ablation of the accessory pathway is recommended in patients with AVRT or pre-excited atrial fibrillation (class I recommendation, level B-NR evidence)
• An electrophysiologic study is reasonable in asymptomatic patients with pre-excitation to stratify risk for arrhythmic events (class IIa recommendation, level B-NR evidence)
• Catheter ablation of the cavotricuspid isthmus is useful in patients with atrial flutter that is either symptomatic or refractory to pharmacologic rate control (class I recommendation, level B-R evidence)

Note: AVNRT = atrioventricular nodal re-entrant tachycardia, AVRT = atrioventricular re-entrant tachycardia.

• Class I = strong recommendation where benefits > risks; class IIa = moderate-strength recommendation where benefits >> risks.
• Level B-R = moderate-quality evidence from one or more randomized controlled trials (RCTs) or meta-analyses of moderate-quality RCTs;
• Level B-NR = moderate-quality evidence from one or more nonrandomized or observational or registry studies;
• Level C-LD = limited data from RCTs or nonrandomized observational or registry studies with limitations of design or execution.

Complications

Complications are either related to the medications or radiofrequency ablation. Since the latter is an invasive procedure the following complications may occur:

• Hematoma
• Pseudoaneurysm of the artery
• Bleeding
• Myocardial infarction
• Heart block and the need for a pacemaker
• Stroke
• Death
• Overall, focal atrial tachycardia is a benign arrhythmia.
• Focal atrial tachycardia typically occurs secondary to an underlying disease process or acute illness.
• Focal atrial tachycardia is one form of atrial tachycardia. Atrial activation patterns in focal atrial tachycardia will be similar during the tachycardia, yet distinct from the normal sinus P wave. Focal atrial tachycardia can be regular or irregular if variable block exists. A “warm-up” and “cool down” pattern can occur during initiation and termination, respectively.
• Patients can be asymptomatic or present with palpitations, chest pain, lightheadedness, dizziness, or presyncope. Focal atrial tachycardia often presents on telemetry on asymptomatic or sleeping patients.
• Ventricular rate control is achievable with calcium channel or beta-blockers. If the patient remains persistently tachycardic or has uncontrolled symptoms, the patient may benefit from antiarrhythmic therapy with class IC or III antiarrhythmics.
• A possible significant cardiac sequella of prolonged atrial tachycardia (or any tachycardia) is tachycardia-induced cardiomyopathy. If there are concerns for high tachycardia burden, outpatient monitoring may be necessary.

Prevention

The most effective way to prevent tachycardia is to maintain a healthy heart and reduce your risk of developing heart disease. If you already have heart disease, monitor it and follow your treatment plan to lower your tachycardia risk.

Prevent Heart Disease

Treat or eliminate risk factors that may lead to heart disease. Take the following steps:

• Exercise and eat a healthy diet – Live a heart-healthy lifestyle by exercising regularly and eating a healthy, low-fat diet that’s rich in fruits, vegetables, and whole grains.
• Maintain a healthy weight – Being overweight increases your risk of developing heart disease.
• Keep blood pressure and cholesterol levels under control – Make lifestyle changes and take medications as prescribed to correct high blood pressure (hypertension) or high cholesterol.
• Stop smoking – If you smoke and can’t quit on your own, talk to your doctor about strategies or programs to help you break a smoking habit.
• Drink in moderation – If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women of all ages and men older than age 65, and up to two drinks a day for men age 65 and younger. For some conditions, it’s recommended that you completely avoid alcohol. Ask your doctor for advice specific to your condition.
• Don’t use recreational drugs – Don’t use stimulants, such as cocaine. Talk to your doctor about an appropriate program for you if you need help ending recreational drug use.
• Use over-the-counter medications with caution – Some cold and cough medications contain stimulants that may trigger a rapid heartbeat. Ask your doctor which medications you need to avoid.
• Limit caffeine – If you drink caffeinated beverages, do so in moderation (no more than one to two beverages daily).
• Control stress – Avoid unnecessary stress and learn coping techniques to handle normal stress in a healthy way.
• Go to scheduled checkups – Have regular physical exams and report any signs or symptoms to your doctor.

Monitor and treat existing heart disease

If you already have heart disease, you can take steps to lower your risk of developing tachycardia or another arrhythmia:

• Follow the plan – Be sure you understand your treatment plan and take all medications as prescribed.
• Report changes immediately – If your symptoms change or get worse or you develop new symptoms, tell your doctor immediately.

References

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Which Test May Help To Confirm Diagnosis Tachycardia/Tachycardia conventionally but arbitrarily defined as an atrial and/or ventricular rate of >100 beats per minute, is encountered commonly and can be physiological or pathological in origin. Various adverse consequences from tachycardia have been recognized, and an important one is an association between persistent tachycardia and cardiomyopathy.

Tachycardia also called tachyarrhythmia, is a heart rate that exceeds the normal resting rate.^[rx] In general, a resting heart rate over 100 beats per minute is accepted as tachycardia in adults.^[rx] Heart rates above the resting rate may be normal (such as with exercise) or abnormal (such as with electrical problems within the heart). The upper threshold of a normal human resting heart rate is based on age.

Cutoff values for tachycardia in different age groups are fairly well standardized; typical cutoffs are listed below:^[rx]

• 1–2 days – Tachycardia > 159 beats per minute (bpm)
• 3–6 days – Tachycardia >166 bpm
• 1–3 weeks – Tachycardia >182 bpm
• 1–2 months – Tachycardia >179 bpm
• 3–5 months – Tachycardia >186 bpm
• 6–11 months – Tachycardia >169 bpm
• 1–2 years – Tachycardia >151 bpm
• 3–4 years – Tachycardia >137 bpm
• 5–7 years – Tachycardia >133 bpm
• 8–11 years – Tachycardia >130 bpm
• 12–15 years – Tachycardia >119 bpm
• >15 years – adult – Tachycardia >100 bpm

Heart rate is considered in the context of the prevailing clinical picture. For example: in sepsis >90 bpm is considered tachycardia.

Types of Tachycardia

Supraventricular

• Atrial fibrillation
• Atrial flutter
• Atrial tachycardia
  
• AV nodal reentrant tachycardia
  
• AV reentrant tachycardia
  
• Permanent junctional reciprocating tachycardia (PJRT)

Ventricular

• Idiopathic ventricular tachycardia
• Fascicular tachycardia (left septal ventricular tachycardia)

Ectopy

• Frequent premature ventricular contractions
• Frequent premature atrial contractions

Pacing 

• High-rate atrial pacing
• Persistent rapid ventricular pacing

Atrial tachycardia tends to occur in individuals with structural heart disease, with or without heart failure, and ischemic coronary artery disease. However, focal atrial tachycardia often occurs in healthy individuals without structural heart disease. Other possible etiologies are listed below:

Causes of Tachycardia

Etiological causes

• Hypoxia
• Pulmonary disease
• Ischemic heart disease
• Stimulants: cocaine, caffeine, chocolate, ephedra
• Alcohol
• Metabolic disturbances
• Digoxin toxicity
• Heightened sympathetic tone

Some other causes of tachycardia include

EKG can aid the diagnosis of focal atrial tachycardia. EKG features may also inform the origin of focal atrial tachycardias.[rx] Electrocardiographic features include:

• Atrial rate: 100 to 250 BPM
• Ventricular conduction can be variable
  • Irregular or irregularly irregular in the setting of variable AV block
  • Regular if 1 to 1, 2 to 1, or 4 to 1 AV block
• P wave morphology
• Unifocal, but similar in morphology to each other
• Might be inverted
• Differs from normal sinus P wave
• May exhibit either long RP or short PR intervals
• Rhythm may be paroxysmal or sustained
  • May demonstrate an increase in the rate at initiation (i.e., “warm-up,” or “rev up”)
  • May demonstrate a decrease in the rate at termination (i.e., “cool down”)

Below is a differential of similar appearing arrhythmias with their identifying features.

Narrow complex, regular tachycardias

Narrow complex, irregular tachycardia

Treatment of Tachycardia

But if the episodes are prolonged, or recur often, your doctor may recommend treatment, including

• Carotid sinus massage – A healthcare professional can apply gentle pressure on the neck, where the carotid artery splits into two branches.
• Pressing gently on the eyeballs with eyes closed. Caution – This procedure should be supervised carefully by a healthcare physician.
• Valsalva maneuver – This consists of holding your nostrils closed while blowing air through your nose.
• Using the dive reflex – The dive reflex is the body’s response to sudden immersion in water, especially cold water.
• Sedation
• Cutting down on coffee or caffeinated substances
• Cutting down on alcohol
• Quitting tobacco use
• Getting more rest

Pharmacologic Treatment

• If vagal maneuvers fail – a trial of intravenous adenosine may be given at an initial dose of 6 mg and a subsequent dose of 12 mg.^[rx,rx] Its use may serve as a diagnostic and therapeutic tool because it will terminate almost all AVNRTs and AVRTs by breaking the AV-nodal dependent circuit. In patients with non–AV-nodal dependent circuits (i.e., focal atrial tachycardia and atrial flutter), intravenous use of adenosine may prove to be a valuable diagnostic tool because the transient AV block may unmask ectopic atrial P waves or flutter waves.^[rx] Patients should always be monitored by ECG during adenosine administration.
• Adenosine – may induce a wide range of transient bradycardias (including sinus arrest and asystole) as well as atrial fibrillation, SVT and ventricular tachycardia. Albeit very rare, cases of sustained ventricular tachycardia, ventricular fibrillation, and Torsades de pointes have been reported.^[rx] In patients with underlying coronary disease, adenosine may lead to coronary steal syndrome and subsequent myocardial ischemia. ^[rx] Adenosine should therefore always be administered with an external pacemaker or defibrillator nearby.^[rx]
• When vagal maneuvers and adenosine – fail to terminate a narrow-complex tachycardia, intravenous treatment with a nondihydropiridine calcium-channel blocker (e.g., diltiazem and verapamil) or β-blocker may be used. Calcium-channel blockers terminate 64%–98% of SVTs in hemodynamically stable patients. Administering a calcium-channel blocker intravenously over 20 minutes has been shown to reduce the rate of hypotension.^[rx] There are fewer data supporting the use of β-blockers in the acute treatment of SVT; however, they are considered reasonable choices because of their safety profile.^[rx,rx]
• If all aforementioned pharmacologic therapies fail – synchronized cardioversion is recommended, even in hemodynamically stable patients.^[rx]
• In patients presenting in atrial fibrillation who have known Wolff–Parkinson – White or new pre-excitation pattern on ECG, the use of potent AV-nodal blockers (i.e., β-blockers, diltiazem, verapamil, and digoxin) should be avoided because these medications may potentiate conduction over the accessory pathway and lead to potentially life-threatening ventricular arrhythmias. In these cases, intravenous use of procainamide is the preferred approach in the acute setting.^[rx]
• Adenosine is rapidly metabolized in the periphery – and therefore must be given as a rapid push through a large, ideally peripheral, intravenous route. The initial dose is 6 mg intravenously (IV) (pediatric dose 0.1 mg/kg, maximum dose of 6 mg). If the initial dose is ineffective, adenosine may be dosed again at 12 mg IVP (pediatric dose 0.2 mg/kg, maximum dose 12 mg). The second dose of adenosine 12 mg IVP may be repeated one additional time if there is no effect. Each dose of adenosine needs to be flushed rapidly with 10 mL to 20 mL normal saline. Often two-person administration, with one person administering the adenosine at a proximal IV port, and a second person flushing the IV line via a distal port immediately after adenosine administration, is required to adequate flush in the adenosine.
• Consider reducing the adenosine dose to 3 mg – IVP if the patient is currently receiving carbamazepine or dipyridamole, is the recipient of a heart transplant, or adenosine is being given through a central line.
• If adenosine fails – second line medications include diltiazem (0.25 mg/kg IV loading dose followed by 5mg/hr to 15 mg/hr infusion), esmolol (0.5 mg/kg IV loading dose, then 0.5 mg/kg/min up to 0.2 mg/kg/min, will need to repeat bolus for every up-titration), or metoprolol (2.5 mg to 5 mg IV every two to five minutes, not to exceed 15 mg over 10 to 15 minutes).

Acute treatment

• Vagal maneuvers are recommended for acute treatment in patients with regular SVT (class I recommendation, level B-R evidence)
• Intravenous administration of adenosine is recommended for acute treatment in patients with regular SVT (class I recommendation, level B-R evidence)
• Synchronized cardioversion is recommended for acute treatment in patients with hemodynamically stable SVT when pharmacologic treatment is ineffective or contraindicated (class I recommendation, level B-NR evidence)
• Intravenous administration of diltiazem or verapamil can be effective for acute treatment in patients with hemodynamically stable SVT (class IIa recommendation, level B-R evidence)
• Intravenous use of β-blockers is reasonable for acute treatment in patients with hemodynamically stable SVT (class IIa recommendation, level C-LD evidence)

Ongoing management

• Oral β-blocker – diltiazem or verapamil treatment is useful for ongoing management in patients with symptomatic SVT who do not have ventricular pre-excitation during sinus rhythm (class I recommendation, level B-R evidence)
• Electrophysiologic study – with the option of radiofrequency catheter ablation is useful for the diagnosis and potential treatment of SVT (class I recommendation, level B-NR evidence)
• Patients with SVT – should be educated on how to perform vagal maneuvers for ongoing management of SVT (class I recommendation, level C-LD evidence)

Referral for radiofrequency catheter ablation

• Catheter ablation of the slow pathway is recommended in patients with AVNRT (class I recommendation, level B-NR evidence)
• Catheter ablation is recommended in patients with symptomatic focal atrial tachycardia as an alternative to pharmacologic treatment (class I recommendation, level B-NR evidence)
• Catheter ablation of the accessory pathway is recommended in patients with AVRT or pre-excited atrial fibrillation (class I recommendation, level B-NR evidence)
• An electrophysiologic study is reasonable in asymptomatic patients with pre-excitation to stratify risk for arrhythmic events (class IIa recommendation, level B-NR evidence)
• Catheter ablation of the cavotricuspid isthmus is useful in patients with atrial flutter that is either symptomatic or refractory to pharmacologic rate control (class I recommendation, level B-R evidence)

Note: AVNRT = atrioventricular nodal re-entrant tachycardia, AVRT = atrioventricular re-entrant tachycardia.

• Class I = strong recommendation where benefits > risks; class IIa = moderate-strength recommendation where benefits >> risks.
• Level B-R = moderate-quality evidence from one or more randomized controlled trials (RCTs) or meta-analyses of moderate-quality RCTs;
• Level B-NR = moderate-quality evidence from one or more nonrandomized or observational or registry studies;
• Level C-LD = limited data from RCTs or nonrandomized observational or registry studies with limitations of design or execution.

Complications

Complications are either related to the medications or radiofrequency ablation. Since the latter is an invasive procedure the following complications may occur:

• Hematoma
• Pseudoaneurysm of the artery
• Bleeding
• Myocardial infarction
• Heart block and the need for a pacemaker
• Stroke
• Death
• Overall, focal atrial tachycardia is a benign arrhythmia.
• Focal atrial tachycardia typically occurs secondary to an underlying disease process or acute illness.
• Focal atrial tachycardia is one form of atrial tachycardia. Atrial activation patterns in focal atrial tachycardia will be similar during the tachycardia, yet distinct from the normal sinus P wave. Focal atrial tachycardia can be regular or irregular if variable block exists. A “warm-up” and “cool down” pattern can occur during initiation and termination, respectively.
• Patients can be asymptomatic or present with palpitations, chest pain, lightheadedness, dizziness, or presyncope. Focal atrial tachycardia often presents on telemetry on asymptomatic or sleeping patients.
• Ventricular rate control is achievable with calcium channel or beta-blockers. If the patient remains persistently tachycardic or has uncontrolled symptoms, the patient may benefit from antiarrhythmic therapy with class IC or III antiarrhythmics.
• A possible significant cardiac sequella of prolonged atrial tachycardia (or any tachycardia) is tachycardia-induced cardiomyopathy. If there are concerns for high tachycardia burden, outpatient monitoring may be necessary.

Prevention

The most effective way to prevent tachycardia is to maintain a healthy heart and reduce your risk of developing heart disease. If you already have heart disease, monitor it and follow your treatment plan to lower your tachycardia risk.

Prevent Heart Disease

Treat or eliminate risk factors that may lead to heart disease. Take the following steps:

• Exercise and eat a healthy diet – Live a heart-healthy lifestyle by exercising regularly and eating a healthy, low-fat diet that’s rich in fruits, vegetables, and whole grains.
• Maintain a healthy weight – Being overweight increases your risk of developing heart disease.
• Keep blood pressure and cholesterol levels under control – Make lifestyle changes and take medications as prescribed to correct high blood pressure (hypertension) or high cholesterol.
• Stop smoking – If you smoke and can’t quit on your own, talk to your doctor about strategies or programs to help you break a smoking habit.
• Drink in moderation – If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women of all ages and men older than age 65, and up to two drinks a day for men age 65 and younger. For some conditions, it’s recommended that you completely avoid alcohol. Ask your doctor for advice specific to your condition.
• Don’t use recreational drugs – Don’t use stimulants, such as cocaine. Talk to your doctor about an appropriate program for you if you need help ending recreational drug use.
• Use over-the-counter medications with caution – Some cold and cough medications contain stimulants that may trigger a rapid heartbeat. Ask your doctor which medications you need to avoid.
• Limit caffeine – If you drink caffeinated beverages, do so in moderation (no more than one to two beverages daily).
• Control stress – Avoid unnecessary stress and learn coping techniques to handle normal stress in a healthy way.
• Go to scheduled checkups – Have regular physical exams and report any signs or symptoms to your doctor.

Monitor and treat existing heart disease

If you already have heart disease, you can take steps to lower your risk of developing tachycardia or another arrhythmia:

• Follow the plan – Be sure you understand your treatment plan and take all medications as prescribed.
• Report changes immediately – If your symptoms change or get worse or you develop new symptoms, tell your doctor immediately.

References

People Also Reading

Tachycardia; Causes, Symptoms, Diagnosis, Treatment What Is The Main Causes of Tachycardia, Diagnosis Tachycardia Causes, Symptoms, Diagnosis, Treatment Which Test Diagnosis Confirm Hemiplegia What Is The Latest Test /Diagnosis to Confirm H. Pylori Tachycardia Treatment, Complication, Prevention What Is The Main Sign Symptoms of Tachycardia Before Going To Doctor You Must Know Tachycardia How Can I Prevent Tachycardia, Treatment What Heart Rate is Considered Tachycardia Test Diagnosis of Ischemic Cardiomyopathy Which Test Confirm That It Is Cancerous Skin Mole