Headache Disorders /These patients may also complain of shoulder or neck muscle tightness as well as sleep disturbances. Symptoms of nausea, vomiting, photophobia or phonophobia are typically absent or are very mild. These features, when present, easily differentiate TTH from migraines. Sometimes the symptoms are overlapping, and confirmation of an exact diagnosis may only occur over time. Medication history is also critical. The type, frequency, and response to analgesic drugs require evaluation in all the patients.

Primary headache disorders

Migraine headache

Tension-type headache

Trigeminal autonomic cephalalgias

Other primary headache disorder

  • Primary cough headache
  • Primary exercise headache
  • Primary headache associated with sexual activity
  • Primary thunderclap headache
  • Cold-stimulus headache
  • Hypnic headache
  • New daily persistent headache (NDPH)
  • Nummular headache
  • Primary stabbing headache
  • Idiopathic trochleitis
  • Supraorbital neuralgia
  • External compression headache
  • Nasociliary neuralgia
  • Occipital neuralgia
  • Auriculotemporal neuralgia

Secondary Headache disorders:

  • Trauma and Injury headache
  • Vascular headache
  • Headache secondary to intracranial disorders
  • Chemical or substance abuse-related headache
  • Headache related to infectious causes in the head and neck regions
  • Headache related to disorders of homeostasis
  • Headache related to hypoxia and hypercapnia
    • High altitude
    • Airplane travel
    • Diving
    • Sleep apnea
  • Dialysis headache

  • Hypertension headache

    • Autonomic dysreflexia
    • Preeclampsia and eclampsia
    • Pheochromocytoma
    • Hypertensive crisis and encephalopathy
  • Fasting headache
  • Cardiac cephalgia
  • Hypothyroidism headache
  • Other disorders of homeostasis

Causes Of Headache Disorders

The International Classification of Headache Disorders (ICHD-III) classifies headaches as either :

  • Primary headache, including tension, migraine, and cluster
  • Secondary headache, including potentially life-threatening etiologies such as traumatic brain injury and vascular disorders
  • Cranial neuropathies, such as trigeminal neuralgia

Headache can be a symptom of many underlying pathologies, some of which can lead to severe disability and mortality. The emergency clinician should be especially familiar with the following conditions:

  • Hypertensive emergencies
  • Idiopathic intracranial hypertension
  • Carotid or vertebrobasilar dissection
  • Space occupying lesions (tumors, abscesses, cysts)
  • Acute hydrocephalus
  • Dural sinus thrombosis
  • Intracranial hemorrhage
  • Giant cell (temporal) arteritis
  • Cerebrovascular accident or stroke
  • Meningitis and encephalitis
  • Carbon monoxide poisoning
  • Toxin exposure or withdrawal
  • Acute angle-closure glaucoma
  • Medication overuse headache

Symptoms Of Headache Disorders

Clinical features of primary headache subtypes

Migraine headache

  • Typically unilateral in adults, bilateral in children
  • Gradual onset, crescendo pattern, pulsating, moderate or severe, aggravated by routine activity
  • Duration 4 to 72 hours
  • Patient most comfortable resting in a dark, quiet room
  • May have associated nausea, vomiting, photophobia, phonophobia, aura (most often visual)

Tension headache

  • Typically bilateral
  • Pressure or tightness, waxing and waning intensity
  • Duration 30 minutes to 7 days
  • The patient may be active or desirous of rest
  • Usually no associated symptoms

Cluster headache

  • Always unilateral, usually beginning near the temple or eye
  • Pain begins quickly, reaching maximal intensity in minutes, quality is deep, constant, excruciating or explosive
  • Duration 15 minutes to 3 hours
  • Patient remains active
  • Associated symptoms include ipsilateral lacrimation and redness to the eye, nasal congestion or rhinorrhea, pallor, diaphoresis, horner syndrome, restlessness

Conversely, if patients have high-risk features or a history and physical not compatible with primary headache, the etiology of secondary headache must be investigated. As is often the case in clinical medicine, pattern recognition is useful.

The following are several of the most important critical diagnoses of secondary headaches to consider and their key clinical features:

Subarachnoid Hemorrhage

  • “Thunderclap” headache that is sudden, with maximal pain at onset and often described as the “worst headache of my life.”
  • Associated with nausea or vomiting, neck pain and/or stiffness, and focal neurological deficits.
  • History may include age greater than 50, loss of consciousness, known vascular aneurysms, connective tissue diseases, polycystic kidney disease, family members with SAH, or history of poorly controlled hypertension.
  • Physical exam findings may include hemotympanum, focal neurological deficits, or nuchal rigidity.

Cervical artery dissection

  • Symptoms include headache, neck pain, dizziness or unsteadiness, double vision, focal weakness, confusion, and stroke-like symptoms in a younger patient.
  • History may include trauma to the head or neck.
  • Physical exam findings may include a carotid bruit, cerebellar deficits, visual field deficits, bulbar deficits, and asymmetric strength or motor findings.

Meningitis and encephalitis

  • Symptoms may include fever, headache, nuchal rigidity, altered mental status, non-specific flu-like prodrome, nausea, vomiting, focal neurological deficits, photophobia, and seizures.
  • History may include non-vaccination, immunocompromised state, close-quarter living, recent travel, tick or mosquito bite,  and sick contacts.
  • Physical exam findings may include Kernig sign (painful knee extension on hip flexion), Brudzinski sign (passive hip flexion on active neck flexion), papilledema, or petechial rash.

Dural sinus thrombosis

  • Symptoms include headache, blurry vision or visual field deficits, nausea, and vomiting. The history may include infection, head trauma, inherited or acquired hypercoagulable disorders of the patient or family members, or other causes of hypercoagulability such as systemic lupus erythematosus (SLE), sickle cell anemia, OCP use, cancer, pregnancy, estrogen use, previous thromboembolic events, antiphospholipid syndrome, and dehydration.
  • The physical exam may reveal papilledema and focal neurological and/or cranial nerve deficits.

Ischemic or hemorrhagic stroke/cerebrovascular accident

  • Symptoms correspond to the anatomic area of the brain affected. Focal neurological deficits are the most common and specific findings. Other symptoms may include headache, nausea, vomiting, vertigo, aphasia, confusion, and visual deficits.
  • History may include previous ischemic or hemorrhagic events, tobacco use, diabetes, hyperlipidemia,  hypertension, and other vascular risk factors.
  • The physical exam may include neurological deficits, altered mental status, and facial droop.

Carbon monoxide poisoning

  • Symptoms may include headache, dizziness, ataxia, confusion, nausea, and vomiting.
  • History may include the use of indoor heaters, house fires, and exposure to car exhaust.
  • The physical exam may reveal pink-tinged skin, wheezing, hyperventilation, singed nares, and an edematous oropharynx.

Acute angle-closure glaucoma

  • Symptoms may include unilateral or bilateral eye pain, photophobia, changes in or loss of vision, and sudden onset of headache.
  • The history may include older age, exacerbation of symptoms in a dark room, and family history.
  • Physical exam findings may include decreased visual acuity, conjunctival injection, increased intraocular pressure (60 to 90 mmHg is diagnostic), a shallow anterior chamber, and a fixed and mid-dilated pupil.

Idiopathic intracranial hypertension

  • Symptoms may include headache not responding to analgesia, changes in vision, nausea, and vomiting, and headache worse when supine.
  • History may include female gender, childbearing age, obesity, and new medication use. Specific medications implicated in IIH include oral contraceptives and tetracycline antibiotics, as well as lithium and vitamin A.
  • Physical exam findings may include papilledema, bradycardia, and visual field deficits.

 Hypertensive emergencies

  • Symptoms include headache, changes in vision, nausea and vomiting, confusion, seizure, and oliguria or anuria.
  • History may include pregnancy (preeclampsia/eclampsia), history of hypertension, and medication noncompliance, Autonomic dysregulation syndromes, including secondary to stroke, pheochromocytoma, and neuromuscular diseases.
  • Physical exam findings may include altered mental status, symptoms of heart failure, bradycardia, papilledema, jaundice, and a renal vein bruit.

Temporal (giant cell) arteritis

  • Symptoms may include unilateral headache, painless monocular vision loss, jaw claudication, and proximal muscle weakness.
  • History may include older age (greater than 65), polymyalgia rheumatic, and female gender.
  • Physical exam findings may include tenderness along the temporal bone, papilledema, and decreased strength of proximal muscle groups.

Diagnosis of Headache Disorders

Physical examination is normal in primary headache disorders, including the TTH. Although the transient trigeminal cranial features of ptosis, conjunctivitis, or orbital swelling may occur with the trigeminal autonomic cephalgias (TACs). Physical examination is vital in excluding the secondary causes, such as nuchal rigidity seen in meningitis and subarachnoid hemorrhage, focal neurological deficits seen in the space-occupying lesion, and/or papilledema in idiopathic intracranial hypertension, etc.

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“Red flags” for secondary disorders should always be ruled out during the history and physical examination. These include:

  • Sudden onset of headache
  • Age of onset of headache after 50 years of age
  • Very severe headache
  • New onset of headache with an underlying medical condition
  • Headache with concomitant systemic illness
  • Focal neurologic signs or symptoms
  • Papilledema, and
  • History of head trauma

Secondary headache disorders can also have an evaluation using the acronym: “SNOOP4”.

  • “S” stands for systemic symptoms, fevers, chills, myalgias, and weight loss.
  • “N” is the neurological symptoms, especially the focal neurologic deficits.
  • The first “O” is for older onset, meaning the age of 50 years or greater.
  • The second “O” is onset, particularly that of a sudden onset headache like a subarachnoid hemorrhage.
  • “P1” is papilledema.
  • “P2” is positional.
  • “P3” is precipitated by the Valsalva maneuver or exertion.
  • “P4” is a progressive headache or substantial pattern change.

Evaluation

TTH is a clinical diagnosis using the IHS diagnostic criteria. No laboratory testing or imaging studies are usually necessary for the diagnosis of TTH. However, if one or more red-flags are present, then appropriate investigations, including but not limited to brain imaging, should be performed to rule out secondary causes. A magnetic resonance imaging (MRI) with gadolinium contrast is the recommended imaging study in these patients.

IHS Diagnostic criteria for TTH

IHS has proposed the diagnostic criteria in the third edition of the International Classification of Headache Disorders (ICHD-3). The criteria are as follows:

  • At least ten episodes of headache fulfilling criteria B-D
  • Lasting from 30 minutes to as long as seven days

  • Minimally two of the following four characteristics:

    • Bilaterally located
    • Pressing or tightening (non-pulsating) quality
    • Mild or moderate in intensity
    • Not exacerbated by routine physical activity, e.g., walking or climbing stairs.

  • Both of the following:

    • No nausea or vomiting
    • No more than one of photophobia or homophobia
  • They are not better explained by another ICHD-3 diagnosis.

The above is a general ICHD-3 diagnostic criterion for the TTH. If one of the above ICHD-3 features for TTH is missing and not fulfilling the criteria for another headache disorder, a diagnosis of probable tension-type headache is possible. These patients with probable TTH should undergo evaluation over time, and the clinician usually makes a diagnosis of TTH in these patients. TVs further subdivided into three subtypes based on the frequency of headache episodes.

  • Infrequent episodic TTH: At least ten episodes of headache occurring on <1 day/month on average (<12 days/year).
  • Frequent episodic TTH: At least ten episodes of headache occurring on 1 to 14 days/month on average for over 3 months (≥12 and <180 days/year).
  • Chronic TTH: Headache occurring on ≥15 days/month on average for >3 months (≥180 days/year).

Treatment of Headache Disorders

Treatment of Episodic TTH

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstay treatment options to abort episodes of TTH. Recent metanalysis studies suggest that ibuprofen 400 mg and acetaminophen 1000 mg are the best pharmacological agents for acute treatment of TTH. There appears to be a synergistic effect of these two drugs together, as the NNT to treat with ibuprofen alone was greater than that of both aforementioned in combination treatment. While ASA alone is used frequently over the counter for treatment, a 500 mg dose showed to be equivalent to a placebo. Other NSAIDs (e.g. naproxen sodium [375 to 550 mg], ketoprofen [25 to 50 mg], and diclofenac [50 to 100 mg] etc.) are also more effective than placebo in acute TTH. Patients should avoid the overuse of analgesic medicines as it may, ironically, lead to medication overuse headache. Evidence for the efficacy of muscle relaxants in TTH is weak, and there is a risk for habituation.

Treatment of Chronic TTH

Pharmacological Treatment: The goal of chronic TTH therapy is to reduce the frequency of headaches through the use of preventive medications. Among pharmacologic agents, amitriptyline (a tricyclic antidepressant [TCA]), is the most efficacious and well-studied drug in the management of chronic TTH. Amitriptyline should be started on a low dose (10 to 25 mg daily) and slowly titrated (10 to 25 mg weekly) till achieving an appropriate therapeutic response, or the adverse effects appear. The therapeutic response usually occurs in 3 to 4 weeks. In responsive patients, amitriptyline usually continues for at least six months, and then withdrawal may be attempted. In case of recurrence of chronic TTH on withdrawal, amitriptyline may be continued long term.  Adverse effects are common and include dry mouth, drowsiness, urinary retention, cardiac arrhythmias, and glaucoma.

Selective serotonin reuptake inhibitors (SSRIs) and serotonin/norepinephrine reuptake inhibitors (SNRIs) were not as effective as TCAs.

Evidence for the efficacy of muscle relaxants in TTH is weak, and there is a risk for habituation.

Unlike chronic migraine, botulinum toxin type A has varying efficacy in different studies for chronic TTH prevention and is usually not recommended as a first-line treatment. However, in refractory chronic TTH cases, a trial of botulinum toxin A may be given.

Non-pharmacological Treatment 

The best non-pharmacological therapy for chronic TTH are physical therapy, biofeedback, and cognitive-behavioral therapy. Relaxation, exercise programs, and improvement of posture are critical components of physical therapy. Several other treatments, including massage, manipulation, acupuncture, and osteopathic manipulative medicine, have also shown improvement in both acute and chronic presentations, using measures such as increasing range of motion of the head.


Children and Headache

Headaches are common in children. Headaches that begin early in life can develop into migraines as the child grows older. Migraines in children or adolescents can develop into tension-type headaches at any time. In contrast to adults with migraines, young children often feel migraine pain on both sides of the head and have headaches that usually last less than 2 hours. Children may look pale and appear restless or irritable before and during an attack. Other children may become nauseous, lose their appetite, or feel pain elsewhere in the body during the headache.

Headaches in children can be caused by a number of triggers, including emotional problems such as the tension between family members, stress from school activities, weather changes, irregular eating and sleep, dehydration, and certain foods and drinks. Of special concern among children are headaches that occur after a head injury or those accompanied by rash, fever, or sleepiness.

It may be difficult to identify the type of headache because children often have problems describing where it hurts, how often the headaches occur, and how long they last. Asking a child with a headache to draw a picture of where the pain is and how it feels can make it easier for the doctor to determine the proper treatment.

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Migraine in particular is often misdiagnosed in children. Parents and caretakers sometimes have to be detectives to help determine that a child has a migraine. Clues to watch for include sensitivity to light and noise, which may be suspected when a child refuses to watch television or use the computer, or when the child stops playing to lie down in a dark room. Observe whether or not a child is able to eat during a headache. Very young children may seem cranky or irritable and complain of abdominal pain (abdominal migraine).

Headache treatment in children and teens usually includes rest, fluids, and over-the-counter pain relief medicines. Always consult with a physician before giving headache medicines to a child. Most tension-type headaches in children can be treated with over-the-counter medicines that are marked for children with usage guidelines based on the child’s age and weight. Headaches in some children may also be treated effectively using relaxation/behavioral therapy. Children with cluster headaches may be treated with oxygen therapy early in the initial phase of the attacks.

Headache and Sleep Disorders

Headaches are often a secondary symptom of a sleep disorder. For example, tension-type headache is regularly seen in persons with insomnia or sleep-wake cycle disorders. Nearly three-fourths of individuals who suffer from narcolepsy complain of either migraine or cluster headache. Migraines and cluster headaches appear to be related to the number of and transition between rapid eye movement (REM) and other sleep periods an individual has during sleep. Hypnic headache awakens individuals mainly at night but may also interrupt daytime naps. Reduced oxygen levels in people with sleep apnea may trigger early morning headaches.

Getting the proper amount of sleep can ease headache pain. Generally, too little or too much sleep can worsen headaches, as can the overuse of sleep medicines. Daytime naps often reduce deep sleep at night and can produce headaches in some adults. Some sleep disorders and secondary headaches are treated using antidepressants. Check with a doctor before using over-the-counter medicines to ease sleep-associated headaches.

Coping with Headache

Headache treatment is a partnership between you and your doctor, and honest communication is essential. Finding a quick fix to your headache may not be possible. It may take some time for your doctor or specialist to determine the best course of treatment. Avoid using over-the-counter medicines more than twice a week, as they may actually worsen headache pain and the frequency of attacks. Visit a local headache support group meeting (if available) to learn how others with headaches cope with their pain and discomfort. Relax whenever possible to ease stress and related symptoms, get enough sleep, regularly perform aerobic exercises, and eat a regularly scheduled and healthy diet that avoids food triggers. Gaining more control over your headache, stress, and emotions will make you feel better and let you embrace daily activities as much as possible.

What Research is Being Done?

Several studies either conducted or supported by the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health, are revealing much about the headache process and may lead to new treatments or perhaps ways to block debilitating headache pain. Studies by other investigators are adding insight to headache etiology and treatment.

Understanding headache mechanisms and underlying causes

The molecular basis for migraine headaches and the aura associated with certain migraines is uncertain. One multi-faceted research study is examining how migraine with aura may affect metabolism and neurophysiological function. Investigators are also studying if particular regions of the visual cortex are unusually susceptible to the events in the brain that cause the aura. Another study component is investigating what happens at the beginning of a headache and how changes in the brain’s meninges may lead to vascular and trigeminal nerve stimulation associated with the painful part of a migraine headache. Results may provide a greater understanding of migraine and assist the development of new therapies.

Mast cells, which are part of the immune system and are involved in the inflammatory allergic response, are activated in some chronic pain conditions, including headache. Researchers are examining the possibility of a relationship between the mast cells’ anti-analgesic properties and their proximity to and enhanced activation of nerve fiber endings that receive and transmit pain signals (nociceptors). Mast cells may release substances that activate nociceptive nerve cells that transmit signals from the linings of the skull and its blood vessels. Findings that link mast cell activation to headache pain may identify drug targets that could lead to new analgesics for headache and other pain syndromes.

Cortical spreading depression (CSD) is a process in migraine with aura in which a wave of increased brain activity, followed by decreased activity, slowly spreads along the brain’s surface. The wave of brain activity often travels across the part of the brain that processes vision and corresponds to the typical visual aura of migraine. Research has shown that migraines with aura may be associated with tiny areas of stroke-like brain damage caused by a short-term drop in oxygen levels (associated with the CSD) which prevents normal cell function and swelling in the brain’s nerve cells. Animal studies have shown that CSD also irritates the trigeminal nerve, causing it to transmit pain signals and trigger inflammation in the membranes that surround the brain. CSD inhibiting drugs such as tonabersat are being tested in clinical trials for their usefulness in treating migraine and other neurological diseases. Other investigators hope to build on initial results showing that estrogen withdrawal makes it easier for CSD to occur in the brains of animals, which may explain the contribution of estrogen fluctuation to menstrual migraines. This research may result in a better understanding of how a migraine starts in the brain and offer new methods of treatment by interrupting this process and preventing the migraine.

Cutaneous allodynia is the feeling of pain or unpleasant sensations in response to normally nonpainful stimuli, such as light touch. Researchers are investigating why it is present on the head or face in people with cluster headaches, to better understand neurological changes that occur with these headaches. Similar research is looking at why some people with migraines have more than the typically restricted allodynia that affects a particular area of the head predicted by the headache (for example, on the same side of the face as the migraine pain). Individuals with extended allodynia may experience unpleasant sensations on the side of the face opposite the headache pain or even on their feet. Previous studies have shown that sensitized nociceptors in the brain’s coverings are involved in the throbbing pain of migraine and that other sensitized neurons found deeper in the brain are involved with restricted allodynia, but it is not certain which cells are responsible for extended allodynia. Future studies will explore whether nerve cells in the thalamus (which is involved in relaying signals between the brain and the body) become more sensitive a result of headache pain and cause extended allodynia. Findings may offer a better understanding of how the nervous system changes and becomes more sensitive after repeated stimulation, resulting in chronic pain.

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Social and other factors may impact headaches. Researchers are examining how race and psychiatric conditions are related to headache severity, quality of life, the ability to reliably follow a treatment program, and treatment response in people with migraines, tension-type headache, substance abuse headache, or cluster headache.

Genetics of headache

Genetics may contribute to a predisposition for migraines. Most migraine sufferers have a family member with migraine. Researchers are studying the activity of different genes to see if they make some people more likely to have migraines. One strategy is to test for a gene in several families having members with migraines and then determine if the gene is related to migraine in a broader population.

In April 2008, researchers at the University of Helsinki reported significant evidence for linkage between a gene variant on a specific site on chromosome 10q22-q23 and susceptibility to common types of migraine. The findings were from a study of 1,675 migraine sufferers or their close relatives from 210 Finnish and Australian migraine families. Another study replicated the findings in the two populations and also showed that the site was particularly linked to female migraine sufferers. Although it has been known for some time that genetic factors shared by family members make people more susceptible to migraines, this study is the first to identify convincingly a specific gene locus for common forms of migraine.

Currently under investigation are gene expression patterns (signs of changes in gene activity) in the blood of individuals during migraine attacks and among individuals with chronic daily headaches. Preliminary studies show that children with acute migraines and chronic daily headaches have specific similar gene expression profiles in their blood that are different from healthy individuals and from children with other non-related neurological diseases. Researchers are exploring differences in gene expression profiles among individuals who respond to different types of headache drugs. Study results may indicate a molecular genomic approach using blood samples to detect genes that may be activated during headaches and identify which drugs are best used for each person with migraines.

Scientists are exploring the role of the calcitonin gene-related peptide (CGRP) in migraines. Levels of the CGRP molecule, which is involved in sending signals between neurons, increase during migraine attacks and revert to normal when the pain resolves. Researchers plan to use CGRP as a model and then to use functional magnetic resonance imaging to estimate the pain response in the central nervous system. Evidence from individuals with Familial Hemiplegic Migraine (FHM) with known mutations indicates that migraine pathways in FHM may be different from normal migraine. Investigators are also measuring levels of CGRP during the premonitory, mild, moderate, and severe phases of a single migraine compared to the baseline level when individuals are pain-free. The fluctuations of CGRP during the migraine process will help to define its role in migraine pain and may offer new opportunities for acute treatment.

Clinical studies in headache management

A major focus of headache research is the development of new drugs and other treatment options. Several drug studies seek to identify new drugs to treat various headache disorders and to find safer, more effective doses for medications already being used. Other research is aimed at identifying receptors or drug targets to stop the process of migraine aura in the brain.

Results of three randomized, placebo-controlled clinical trials show the drug topiramate is effective, safe, and generally well-tolerated for treating chronic migraine. Experts agree that treatment with combinations of preventive agents offers maximum relief for the majority of individuals with chronic migraines. An NINDS-funded clinical trial is examining the effectiveness and safety of the drug propranolol combined with topiramate in reducing the frequency of chronic migraine in 250 participants who will be randomly selected to receive treatment with both drugs or topiramate and placebo.

Sleep plays an important role in migraine. Migraine in older adults is sometimes triggered by sleep changes; regulating their sleep may lessen the frequency of migraines. Younger migraine sufferers often report migraine relief after sleep. Researchers are studying the use of the drug ramelteon, which is approved by the U.S. Food and Drug Administration for insomnia, in reducing the number of migraines over a 12-week period.

Headache is the most common symptom after a closed head injury, and it can last for more than 2 months in 60 percent of affected individuals. Unfortunately, individuals with chronic post-traumatic headaches also have cognitive and behavioral problems, and many drugs currently used to treat the headaches also have a negative influence on cognition. Scientists are testing different drugs, such as naratriptan (which acts as a neurotransmitter) and galantamine (used to treat Alzheimer’s disease), to treat both headache and cognitive disturbances in individuals with chronic post-traumatic headaches.

Non-pharmaceutical approaches to treatment and prevention

Historically, very little research has been done on children with headaches. A variety of headache education and drug and/or behavioral management techniques are aimed at improving headache treatment and prevention in children and adolescents. Scientists are testing the effectiveness of combined pain coping skills (including age-appropriate biofeedback, muscle relaxation techniques, imagery, activity pacing, and the use of calming techniques) and the drug amitriptyline in reducing headache frequency, intensity, and depressive symptoms in youth ages 10 to 17 years. Additional studies include the use of alternative approaches such as yoga to decrease headaches in adolescents, a modified diet to treat chronic daily headaches in teenagers, and programs designed to teach very young children how to understand and self-manage their headaches.


Craniosacral therapy (CST) involves gentle massaging of the neck, head, and spine to release constraints in tissue in the head and around the spine. Limited preliminary data shows significant, the sustained benefit of CST in a small group of individuals with migraines. Future research will gather data on the usefulness of CST in preventing migraines and examine the feasibility of a larger, randomized trial.

Electrical stimulation of the occipital nerve has effectively eased the symptoms of painful chronic headache conditions such as cluster headache as well as hard-to-treat migraine in small clinical studies. A tiny battery-powered rechargeable electrode, surgically implanted near the occipital nerve, sends continuous energy pulses to the nerve to ease pain. The use of this non-drug treatment in reducing migraine frequency, intensity, and effect on the quality of life is being tested in larger clinical trials.

References

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