Migraine Headache

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Original Editors - Katie Elder from Bellarmine University's Pathophysiology of Complex Patient Problems project.

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Definition/Description

Migraine is a chronic, episodic primary headache.  Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brainstem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater).

Symptoms typically last 4 to 72 hours and may be severe. Pain is often but not always unilateral, throbbing, worse with exertion, and accompanied by autonomic symptoms (eg, nausea; sensitivity to light, sound, or odors).  Fortification spectra and other transient focal neurologic deficits occur in a few patients, usually just before the headache, also known as aura. Diagnosis of migraine can usually be made by history alone.  Treatment includes lifestyle changes (diet, exercise, sleeping habits), medications including NSAIDs, analgesics, serotonin receptor agonists, beta blockers, calcium channel blockers, and antiemetics.

Prevalence

Migraine headaches are the second most common type of primary headache. An estimated 28 million people in the United States (about 12% of the population) will experience migraine headaches at some point. Lifetime prevalence is 18% for women and 6% for men in the US.  It most commonly begins during puberty or young adulthood, waxing and waning in frequency and severity over the ensuing years and usually diminishing after age 50. In 90% of migraineurs, the first attack generally develops before the age of 40 years.  In women the frequency of headaches is highest during their reproductive years, when estrogen levels are higher, and decreases to some extent after menopause. About 45% of cases of migraine emerge during childhood or adolescence. Migraine with aura is more likely to develop at an earlier age than migraine without aura.

Characteristics/Clinical Presentation

     Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brain stem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater).Migraine headache occurs via intracranial vasoconstriction and extracranial vasodilation. This results in cerebral hypoxia and may be responsible for the neurologic defects that characterize the aura. Acetylcholine and vasoactive intestinal poly peptide in the cranial arteries as well as dilation of the middle cerebral artery and the superficial temporal artery on the pain side during migraine cause relaxation of the vessels.

     The pain associated with migraine can occur from the trigeminal complex, which supplies the head and face region via cranial nerve V. Surrounding the large cerebral vessels, peal vessels, large venous sinuses, and dura mater is a plexus of largely unmyelinated fibers that arise from the ophthalmic division of the trigeminal ganlion and the upper cervical dorsal roots. The stimulation of these vessels cause the pain associated with migraine via the release of substance P and calcitonin gene-related peptide when the trigeminal ganglion is stimulated. Migraineurs may have a sensitization to the mechanoreceptors in these structures enhancing the responses to mechanical stimuli and can result in allodynia (painful response to non-noxious stimuli).

     There may be an aberrant mechanism in the stimulation of sensory fibers that excite GABA receptors, and the inhibition that reduces the excitability of pain neurons in the dorsal horn of the spine in order to modulate pain response to stimulation. Low levels of serotonin has been found in migrainers. Platelets contain virtually all the serotonin present in the blood and release serotonin during aggregation. Migraineurs also tend to show hyperaggregability of platelets when free from headache. Aggregated platelets release catecholamines and serotonin that may cause the initial stage of vasoconstriction.  Platelet aggregation is increased during the prodromal stage of migraine and a decrease of aggregation during the headache. The nuclei raphes also appear to increase blood flow in the brain and can respond to changes in serotonin transmission. The serotonin neurons located in the brainstem nuclei raphes change their firing rate during the sleep-wake cycle and may explain why sleep is often the best antidote to a migraine.

     Cortical spreading depression is a mechanism that starts with a small excitatory response that begins to spread through the brain and then causes a suppression of electroencephalographic (EEG) activity that moves through the cortex and can disturb the extracellular environment.  Potassium levels increase, extracellular glutamate increases, and extracellular calcium level decreases. Abnormal ion channel function is believed to be the mechanism in the rare form of familial hemiplegic migraine (FHM). Cortical spreading depression is accompanied by local vascular responsiveness.  Cortical hyperemia may be responsible for the flashing jagged light that sometimes occurs just before the pain begins.  Cervical musculature can fire the neurons and cause pain and can be taut and tender during a migraine. Lastly, hormone levels, specifically estrogen can contribute to a migraine due to the falling levels of estrogen during menstruation.

Image of cortical spreading depression from:  http://3.bp.blogspot.com/_uc7mjKjM578/SqtEMSNISiI/AAAAAAAAAbY/BHC8UB3LOWU/s400/depresi%C3%B3n+cortical+propagada+migra%C3%B1a.jpg

      There are several different forms of migraine and it's clinical presentation. The following are the various types of migraine:

1. Migraine Without Aura
2. Migraine With Aura
3. Typical Aura Without Headache
4. Sporadic and Familial Hemiplegic Migraine
5. Basilar-Type Migraine
6. Vestibular Migraine
7. Ophthalmoplegic Migraine
8. Retinal Migraine
9. Status Migrainosus
10. Migraine Aura Status
11. Chronic Migraine

Clinical Presentation: 

1. Migraine Without Aura:

     Migraine headaches may be dull or throbbing, may last for 4 to 72 hours and may/may not present with photophobia (sensitivity to light), phonophobia (sensitivity to sound), and may be aggravated by physical activity.  This type of migraine is most commonly seen in clinical practice and is usually bilateral and periorbital. Vomiting  may occasionally terminate the headache. There are often various combinations of fatigue, difficulty in concentrating, neck stiffness, blurred vision, yawning, and pallor. When the headache resolves, there is commonly a feeling of heaviness and aching in the head, the scalp may be tender, and there may be considerable fatigue. The trigeminal brainstem nuclear complex has a somatotopic representation of the trigeminal dermatome that is continuous with the representation of the posterior head and neck region in the upper cervical dorsal horn. Pain patterns representing increased neuronal activity in the trigeminal nucleus caudalis and dorsal horn include upper cervical pain, usually on one side only.

2. Migraine With Aura:

     This type of headache is typically preceded by depression, irritability, loss of appetite, which can be a result of the spreading cortical depression. Paresthesias can also be present and are second in frequency to visual symptoms. Paresthesias of the hand and face are the most common, specifically the tongue, which can help differentiate from a transient ischemic attack (TIA). Speech difficulty during an aura reflects the involvement of the dominant hemisphere. Vertigo and dizziness may be related to brainstem activity or changes in blood flow around the vestibular mechanism.

     The aura consists of fully reversible symptoms that precede or accompany the headache (HA). The aura is commonly described as changes in the visual field. Visual images change, and there can be loss of focus, spots of darkness, and zigzag flashing lights.  It often begins with a hazy spot close to the center of vision and can form into a star shape that further develops into a shape known as fortification (semicircular with angles). This scintillating visoin consists of luminous, bright, flickering colors of the spectrum, like a prism catching light. It can be combined with a scotoma (an area of vision that appears to be obstructed, or missing).  The visual image fades as the headache begins. The headache is intense, throbbing, and usually contralateral to the visual field changes.

Image:Disstress_s.jpg 

Disstress

http://www.migraineartwork.com/distress_artwork.html

3. Typical Aura Without Headache: 

     In some cases, the aura symptoms are not followed by headache. This becomes very important in differential diagnosis if these symptoms begin after the age of 40. Aura without headache is seen primarily in men and in advancing age. 

4. Sporadic and Familial Hemiplegic Migraine:

     The presentation is migraine with aura, including motor weakness and impaired coordination. Prodromal symptoms include numbness of the face and arm that may spread to involve one side of the body. Basilar symptoms may present with dysphasia or aphasia causing difficulty with speech. Pain may be ipsilateral or contralateral to symptoms and on rare occasions there is a loss of consciousness. Although the symptoms appear to resemble a TIA, migrainous infarction is rare. Age of onset is 10-15 years usually accompanied by a family history via chromosome 19 or 1. This type of migraine is considered sporadic if there is no 1st or 2nd degree relative with hemiplegic migraine.

5. Basilar-Type Migraine:

     Basilar migraine have a symptom profile that suggests posterior fossa involvement localizing to the vascular territory of the basilar artery--the brainstem, cerebellum, and occipital lobes.  The prodromal symptoms reflect brainstem dysfunction: altered level of consciousness, dysarthria, tinnitus, ataxia, diplopia, symptoms in both the temporal and nasal fields of both eyes, and peripheral dysesthesias, followed by occipital headache. These symptoms complicate differential diagnosis and can be confused with hydrops or vertebrobasilar TIA. 

6.Vestibular Migraine: 

     When dizziness is the primary complaint or is the predominant component of the aura, then it may be considered as vestibular migraine. Vertigo occurring as an aura may arise from teh same transient inhibition of neuronal function responsible for the visual aura. Episodic vertigo from vestibular migraine can be thought of as a subset of basilar migraine. Spells usually last approximately an hour but can last up to several hours or days.  Nausea, vomiting, hypersensitivity to motion, and postural instability are cardinal signs. The dizziness can also be associated with benign paroxysmal positional vertigo.

7. Ophthalmoplegic Migraine:

     Results in pain around the eye and paralysis in the distribution of the third, fourth, and sixth cranial nerve and can produce diplopia (double vision). The headache always precedes the oculomotor deficit by several days. The paralysis can progress from being transient to lasting several days, and in some persons it becomes permanent. People with ophthalmoplegic migraine typically have a long history of migraine prior to oculomotor involvement.

8. Retinal Migraine:

     Retinal migraine is repeated attacks of monocular visual disturbance, including scintillations, scotomata, or blindness, associated with migraine headache. Visual changes are strictly unilateral. There may be neuronal spreading depression or involvement of the posterior ciliary vasculature. TIA must be ruled out, as emboli from the carotid artery can cause similar symptoms.

File:Ocular-migraine-step3.jpg

Ocular Migraine-Step 3

http://oaklandvisioncenter.blogspot.com/2009/01/aura-am-i-going-blind-or-going-crazy.html

9. Status Migrainosus:

     This type of headache lasts more than 72 hours and a usual trigger will set it off. This resembles a person's typical migraine, but the pain may spread as well as the allodynia. The premenstrual part of the femal cycle is a time of particular risk for SM, and changes in hormone status, pregnancy, miscarriage, or chagne in birth control pills can be factors. Upper respiratory or urinary tract infections can also be the trigger for SM. Overuse of analgesics and rebound withdrawal-type headache, the headache that dcomes when not taking medication, can trigger SM. Prolonged vomiting to the point of dehydration is common. Severe pain and fatigue limit activity, and hospital admission may be appropriate. Comorbid depression is frequently seen.

10. Migraine Aura Status:

     This is a rare subtype with persistent aura without infarction. One or more symptoms that the individual usually experiences as part of his/her typical migraine aura persist for more than 1 week. Visual symptoms are most common, but it can be any symptom. Most typical treatment is ineffective, and the problem often must run its course.

11. Chronic Migraine:

     Most cases start without aura. The criterion for chronic migraine is headache for 15 or more days a month for more than 3 months. Medication overuse is the most common cause of chronic migraine, and they report a change in symptoms over time, with decreasing photophobia, and nausea and a headache that resembles a mixture of tension-type headache and migraine.

Associated Co-morbidities

• Allergies
• Meniere's disease
• Systemic lupus erythematosus
• Epilepsy
  • Although studies vary, individuals with either migraine or epilepsy are more than twice as likely to have the other disorder. 5 Possible causes for comorbidity: (1) Migraine could cause epilepsy by inducing brain ischaemia and injury. (2) Epilepsy could cause migraine by activating the trigeminovascular system, in which we would expect an excess risk of migraine after, but not before, the onset of epilepsy. (3) Shared environmental risk factors because the risk of migraine is significantly increased in people with idiopathic or cryptogenic epilepsy, known environmental risk factors cannot account for all of the comorbidity. (4) Shared genetic risk factors might account for comorbidity. (5) Ottman and Lipton proposed that an altered brain state (increased excitability) might increase the risk of both migraine and epilepsy and account for comorbidity, a hypothesis that draws support from therapeutic similarities.
• Stroke
  • The migraine-stroke association is mostly apparent for young women with migraine with aura. Although there are several hypotheses about the biologic link between migraine with aura and ischemic stroke, the precise mechanisms remain unclear. However, because the absolute risk of stroke is low in patients with migraine with aura, and migraine without aura is likely not associated with ischemic stroke, most migraine patients will not experience a stroke event..
  • According to large series, migrainous infarcts account for 0.5-1.5% of all ischaemic strokes and 10-14% in young patients. Migraine itself might cause spasm or even hyperplasia, it is unlikely to be the cause of embolism or among other disorders. dissection. Migrainous infarcts, due to severe hypoperfusion during an attack are rare and mostly involve the posterior-cerebral-artery territory and are more common during attacks of migraine with aura than without aura. The precise mechanism of this severe hypoperfusion is unknown. Increased risk due to treatments used in migraine, particularly vasoconstrictors, is supported by the increase in white-matter abnormalities and in mortality found in patients taking ergotamine, but two recent studies found no increase in severe vascular events with triptans. Drugs widely used in migraine, such as aspirin and non-steroidal antiinflammatory drugs, decrease the risk of cerebral ischaemic events.
  • Migraine headache can occur as a comorbidity of ischaemic stroke, carotid or vertebral artery dissection, arteriovenous malformations, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL syndrome), or platelet disorders (eg, thrombocytosis).

Medications

According to Clinical Neurology (6th ed), the following medications are generally used:

For more information regarding medicine used for treating Migraine Headaches: http://www.rxlist.com/script/main/hp.asp https://online.epocrates.com/home http://www.drugs.com/
For further information and research regarding medical management for Migraines: http://www.medscape.com/viewarticle/704767 http://www.medscape.com/viewarticle/715399 http://www.headaches.org/education/Headache_Topic_Sheets/Migraine

Diagnostic Tests/Lab Tests/Lab Values

Diagnosis is based on characteristic symptoms and a normal physical (including neurologic) examination. Typical cases without worrisome findings do not require CNS imaging. Patients requiring very urgent CT or MRI to look for hemorrhage, increased intracranial pressure, and other structural causes of headache include those with:

• Sudden-onset thunderclap headache: an abrupt severe headache that may be a sign of bleeding in the brain and requires immediate medical attention.
• Altered mental status, including seizure
• Focal neurologic deficits
• Papilledema: an optic disc swelling that is secondary to elevated intracranial pressure.
• Severe hypertension

Causes

Common causes include: 

• Vasodilators (eg, Nitroglycerin)
• Skipping meals
• Weather changes
• Sleep deprivation
• Stress
  
• Excessive afferent stimuli (eg, flashing lights, strong odors)
• Head trauma, neck pain, or temporomandibular joint dysfunction can trigger or exacerbate a migraine
• Hormonal factors: fluctuating estrogen levels are a potent migraine trigger. Many women have onset of migraine at menarche, severe attacks during menstruation (menstrual migraine: appear to be more frequently in migraine with aura) and worsening migraine during menopause. Oral contraceptives and other hormone therapy occasionally trigger or worsen migraine and have been associated with stroke in women who have migraine with aura. Pregnancy can either exacerbate or relieve migraine attacks.
• Certain foods can precipitate a migraine attack (including, but not limited to):
  
  • Tyramine-containing chesses
  • Meat, such as hot dogs or bacon, with nitrate preservatives
  • Chocolate containing phenylethylamine but not chocolate alone
  • Food additives such as monosodium glutamate, a commonly used flavor enhancer
  • Coffee and alcohol (especially red wine)
  • Sugar (in vulnerable individuals)
• Genetics: There is a positive family history of migraine in about 60% of cases, which suggests a hereditary factor. All twin studies done so far (comparison of concordance rates between monozygotic and dizygotic twins) show that migraine has a genetic component in addition to environmental factors. Familial hemiplegic migraine (FHM), a rare type of migraine with aura, is the only form in which a monogenic mendelian ode of inheritance has been clearly established.

Systemic Involvement

     Migraines can affect various other systems of the body aside from the headache itself.  As mentioned previously, migraines produce extracranial vasodilation and intracranial vasoconstriction. This vasoconstriction along with the cortical spreading depression can have various affects on vision, and hearing.  The most common effect of migraine with aura is the scintillating scotoma and many migraineurs with or without aura have a hypersensitivity to light and sound.  This is why they generally seek a quiet, dark environment to lie down. The extracranial vasodilation can affect functions within the migraine, specifically the locus ceruleus and nucleus raphe. The locus ceruleus is responsible for attention and the nucleus raphe produces serotonin. Also mentioned in the clinical presentation, serotonin production can affect aggregability of platelets.  However, serotonin levels also affect mood.  The medullary raphe nucei send axons into the spinal cord to modulate sensory, autonomic, and motor activity. The medullary raphe nuclei have an affect on pain by releasing serotonin onto interneurons in the dorsal horn that inhibit the transmission of pain information. Raphespinal endings in the lateral horn influence the cardiovascular system. This vasodilation and imbalance of serotonin during the migraine can have profound affects on mood, sensory, autonomic, and motor activity as well as pain. Familial hemiplegic migraine has an affect on sensory and motor activity on one side of the body.  There is also a small percentage of patients that may cardiovascular events during a migraine including a myocardial infarction or an obstruction of blood flow to the brain causing a transient ischemic attack or cerebrovascular accident. This is why differential diagnosis is critical and referral back to the physician or emergency room is pertinent if the the therapist suspects the patient is experiencing a stroke or a cardiovascular event.

http://1.bp.blogspot.com/_YdAacBURVXE/R1RQd5hDJkI/AAAAAAAACE0/lqq-yDdO7Zk/s1600-R/stroke.jpg

     The ascending reticular activating system (ARAS) is located in the brainstem and is responsible for regulating consciousness and is located in the reticular formation of the brainstem. Generally, the migraineur will lie down and rest and sleep can resolve the symptoms of the migraine.  The vestibular nuclei are located in the brainstem at the cerebellopontine angle. Migraineurs that have vestibular effects may have problems with balance, coordination, head movements, postural control, motor planning, and eye movements.  Migraineurs may also have difficulty concentrating. 

     The musculoskeletal system can also be affected specifically in the cervical spine.  It is common for migraine headache sufferers to have increased muscular tone in the suboccipital and paraspinal musculature as well as an underlying cervical dysfunction that may occur at the same time as the migraine and must be addressed. With familial hemiplegic migraine, they may have weakness in their extremities and also can be addressed with physical therapy. Many migraineurs have an intolerance to a certain amount of physical activity. Again, this can also be addressed with physical therapy.  

     Other systems may be affected via the medication that is prescribed depending on dosage, how long the patient has been taking the medication and any interactions from taking multiple medications for various other conditions the patient may also have in addition to migraine.  The systems that may be affected from medications could include pulmonary, gastrointestinal, endocrine, hepatic, hematologic, genitourinary, and neurological systems.  It is recommended that these patients are monitored by their physician and/or pharmacist to monitor adverse side effects and potential serious drug interaction effects. 

Medical Management (current best evidence)

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Physical Therapy Management (current best evidence)

     Research regarding physical therapy for the treatment of migraine headache is limited. However, migraineurs can still benefit from physical therapy intervention of spinal manipulation (soft tissue mobilization, non-thrust, and thrust) if there is an underlying cervical dysfunction that occurs while the migraine is present. As mentioned in the clinical presentation, pericranial muscles can be the cause of a migraine and will be tender during a migraine.  This can be addressed through physical therapy using manual therapy, specific exercise training (including, stretching, strengthening, and self-distraction), education, and modalities to decrease the frequency/onset of the attack and duration/intensity of the attack. Migraineurs can also benefit from physical therapy for vestibular related dysfunction as seen in vestibular migraine. If the migraine is accompanied or caused by benign paroxysmal positional vertigo (BPPV), PT can assist in reducing the frequency of attacks especially if the is is the cause or exacerbation of the attack. See the case report section below for differential diagnosis of migrainous positional vertigo and horizontal BPPV.

     There is limited evidence regarding modalities used for the treatment of migraine including manual therapy, ice, cervical traction, exercise, and electrical stimulation. One aspect of physical therapy that could be beneficial to the migraine patient could be education on general health, exercise, sleep, diet (a more in depth look at diet needs to be addressed by a registered dietitian), and relaxation techniques.  There is controversial evidence on the effectiveness on migraine and relaxation techniques.  However, a considerable amount of the literature supports RT as an adjunct treatment to the patient's current medical management for their headaches.  More research needs to be done on physical therapy treatment for migraine headaches.  A multidisciplinary approach should be considered to coordinate care to improve the probability of long term success for the migraineur. Neurofeedback and biofeedback literature is increasing with positive outcomes for the treatment of migraine headache. 

Physical Therapy Management (Spinal Manipulation, Exercise, Modalities)

     This first article is a collection of systematic reviews regarding the efficacy of various forms of physical therapy (PT) for primary headaches. David M. Biondi, DO, found cervical manipulation to be successful for short term treatment of migraine headache, but does mention the possible risk for vertebral artery dissection, stroke, or transient ischemic attack. This review found that spinal manipulation was as effective as Amitriptyline for the treatment of migraine.  This review found that PT is most effective for the treatment of migraine when combined with other treatments such as thermal biofeedback, relaxation training, and exercise.

     A critical review conducted by Volker Busch, MD and Charly Gaul, MD found that exercise is effective in reducing the intensity of migraine headache, but did not find a significant reduction in frequency or duration of migraine attacks.  More research is needed regarding the value of exercise for the treatment of migraine headaches.

Thermal Biofeedback and Neurofeedback

     The following information is based upon a study using neurofeedback and thermal biofeedback for treatment of migraine headaches and can be found at the following website: http://www.behavioralandbrainfunctions.com/content/pdf/1744-9081-6-9.pdf
     Neurotherapy is a broad term referring to the many types of biofeedback used to deliver information about the central nervous system which involve blood flow, thermal output from the brain or electrical activity. Neurofeedback (also called neurobiofeedback or EEG biofeedback) usually refers to frequency-based biofeedback that uses an EEG to give clients information about their brainwaves and gradually and subtly teaches people how to alter their brainwave activity.
     This article explored neurobiofeedback in addition to thermal biofeedback on 37 migraineurs. Their research was based on prior success of grade A evidence on thermal biofeedback on patients with migraine. They conducted their study looking at the efficacy of neurobiofeedback for migraineurs.
     This research study was based on prior studies focusing on neurobiofeedback on the midline frontal and central areas of the forehead teaching them to control slow cortical potential activity representing cortical sensitivity and reactivity. Another study looked at a newer form of biofeedback called hemoencephalography (which targets the frontal lobe) and passive infrared hemoencephalography (utilizes forehead skin temperature). Patients using passive infrared hemoencephalography watch a movie and as their skin temperature on their forehead drops, the movie ceases. The goal is to keep the movie running by maintaining a raised forehead temperature. Both studies showed success with treatment of migraines.
     The patients nor the researcher were blinded in this study to the treatment given and the inclusion criteria required no less than one migraine or greater than twenty migraines per month. The study involved treatment using EEG biofeedback, pIR HEG biofeedback and handwarming biofeedback for an average total of 40 sessions. All clients, whether or not they were successful at reducing their migraines, demonstrated an ability to warm their hands and foreheads and decrease their elevated EEG amplitudes of both slow and fast-wave activity. Patients related during session interviews that these techniques have eventually enabled them to automatically learn to abort their headaches without having to use the actual devices. These patients described the biofeedback as helping them to acquire the ability to better self-regulate by learning to control their EEG and reducing muscle tension, slowing the rate of their breathing and warming their hands and forehead, all of which were necessary for the types of biofeedback they had undergone.

     The second article is a meta-analysis of various forms of biofeedback used in the treatment of Migraine and Tension-Type Headaches.  This study reviewed 94 articles from 1973-2007 that utilized the following forms of biofeedback for headaches: peripheral skin temperature feedback (TEMP-FB), blood-volume-pulse feedback (BVP-FB), electromyographic feedback (EMG-FB), electroencephalographic feedback (EEG-FB), and galvanic skin response training (GSR-FB). The latter two are seldom used in application to migraine headaches. In migraine, frequency, intensity, duration, and the headache index were all reduced with significant medium effect sizes. For medication consumption, a small-to-medium effect size resulted. This effect was significantly smaller than the reduction on headache frequency and duration. Significant stronger improvements were shown for self-efficacy. Here a significant medium-to-large effect size resulted. Depression and anxiety showed medium effects, with confidence intervals ranging from small to large.  In the biofeedback treatment of migraine, home training was shown to be an essential component of the efficacy and maintenance of treatment benefits. Treatment manuals incorporating home training led to nearly 20% higher treatment effects for headache reduction. 

Video on neurofeedback for migraine headache treatment: http://www.youtube.com/watch?v=SKY-TlAt4co

To view more articles regarding biofeedback and physical therapy intervention for the treatment of migraine, the following key words were used in this search: biofeedback, thermal biofeedback, neurobiofeedback, migraine, migraine headache, ice, cryotherapy, exercies, cervical manipulation, spinal manipulation, relaxation, relaxation techniques, manual therapy, electrical stimulation. 

Alternative/Holistic Management (current best evidence)

  Acupuncture

     A randomized controlled trial examined the efficacy of acupuncture for the prophylaxis of migraine.  This study randomly assigned 794 patients, 18-65 years of age to a treatment group (verum acupuncture, sham acupuncture and prophylactic treatment with beta blockers, flunarizine, or valproic acid).   The patients and the treatment centers that were used for treatment were blinded to the form of acupuncture treatment the patients received. Only body needle acupuncture, without electrical stimulation or oxibustion, was allowed.  Both verum and sham acupuncture was performed from a select list of treatment points and needling was bilateral. The sham acupuncture was performed on points of the body where no traditional Chinese medicine (verum) acupuncture points are known. The verum acupuncture points were selected based on diagnosis and channels related to the individual headache area. The physicians were not blinded to the subjects. All three treatments were effective in reducing the frequency of migraine attacks in all treatment groups.  This study demonstrated that after 26 weeks acupuncture treatment over 6 weeks had a similar efficacy compared with the 24 weeks of continuous treatment with standard drug therapy.

    A second randomized controlled trial examined traditional acupuncture in migraine patients in addition to Rizatriptan (10mg).  The patients were divided into four groups: (1) group true acupuncture plus Rizatriptan; (2) group RMA, treated with ritualized mock acupuncture plus Rizatriptan; (3) group SMA, treated with standard mock acupuncture plus Rizatriptan; (4) group R, without prophylactic treatment with relief therapy only (Rizatriptan).  The results of this study revealed that all groups showed significant improvement in the MIDAS index score, but the true acupuncture group was the only group to show long term effects and decreased intake of Rizatriptan.

Massage

     Another randomized controlled trial explored the efficacy of massage on migraine with long term measures of stress and coping efficacy.  This study performed massage using the neuromuscular and trigger-point framework of the back, shoulders, neck, and head.  The massage included myofascial release, deep ischaemic compression, and cross-fiber work of the erector spinae, upper and lower trapezius, levator scapulae, lamina groove, suboccipital muscles, sternocleidomastoid, masseter, and temporalis muscles using scent-free almond oil on a standard massage table. This preliminary study provides evidence that massage therapy can have beneficial effects on migraine experience, stress arousal, and sleep for individuals with migraine. Most notably, massage therapy significantly reduced migraine frequency both during the 6 weeks of massage therapy as well as during the 3 weeks following the end of therapy. This is the first evidence that massage therapy may reduce migraine frequency beyond the end of treatment, and research is now needed to further evaluate the durability of these effects. This study did not show any significance of reducing migraine intensity or medication use. More research is needed to further evaluate the efficacy of massage therapy for the treatment and management of migraine.

Migraine Art

    Numerous artists are expressing the pain of migraine through their artwork. The following is some examples of artwork done by different artists with links to follow to view more artwork.

Image:Slaybaugh_hzoom1.jpg

Tiffany Slaybaugh
http://health.discovery.com/centers/headaches/migraineart/slide.html

Carole Stoiber
http://health.discovery.com/centers/headaches/migraineart/migraineart.html

                        

Origin                                                                               Laceration

http://www.migraineartwork.com/origin_artwork.html             http://www.migraineartwork.com/laceration_artwork.html

Blast of Light

http://www.migraineartwork.com/migraine_art1.html

Another site to visit more migraine art and to read more about migraine art: http://www.migraine-aura.org/content/e24966/index_en.html

Slideshow from the NY Times: http://www.nytimes.com/slideshow/2008/02/28/opinion/20080222_MIGRAINE_SLIDESHOW_index.html

YouTube: http://www.youtube.com/watch?v=lJRPThL7qa0

Differential Diagnosis

      Due to the complexity of the pathophysiology and signs and symptoms attributed to migraine headaches, differential diagnosis is crucial for determining whether the headache is a medical emergency or a non-life threatening headache from other causes.  The following is a criteria developed by the International Headache Society classifying each type of headache into either primary, secondary, or other causes of headache with subclasses for each category for specific diagnosis. 

IHS Classification of Headaches

      This classification is hierarchical and you must decide how detailed you want to make your diagnosis. This can range from the first-digit level to the fourth. First one gets a rough idea about which group the patient belongs to. Then one obtains information allowing a more detailed diagnosis. The desired detail depends on the purpose. In general practice only the first- or second-digit diagnoses are usually applied whilst in specialist practice and headache centres a diagnosis at the third- or fourth-digit levels is appropriate.

Part I: The Primary Headaches

1. Migraine 1.1. Migraine without aura 1.2. Migraine with aura In younger patients, several unusual disorders can mimic migraine with aura: Dissection of the carotid or vertebral artery Antiphospholipid antibody syndrome Cerebral vasculitis Moyamoya disease CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) MELAS (mitochondrial encephalopathy, lactic acidosis, and strokelike episodes) syndrome In older patients, migraine with aura can be mistaken for a transient ischemic attack, especially when the aura occurs without headache. 1.3. Childhood periodic syndromes that are commonly precursors of migraine 1.4. Retinal migraine 1.5. Complications of migraine 1.6. Probable migraine

2. Tension-Type Headache (TTH) 2.1. Infrequent episodic tension-type headache 2.2. Frequent episodic tension-type headache 2.3. Chronic tension-type headache 2.4. Probable tension-type headache

3. Cluster Headache and Other Trigeminal Autonomic Cephalgias 3.1. Cluster headache 3.2. Paroxysmal hemicrania 3.3. Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) 3.4. Probable trigeminal autonomic cephalgia

4. Other Primary Headache

Part II: The Secondary Headaches:

5. Headache attributed to head and/or neck trauma 5.1. Acute post-traumatic headache 5.2. Chronic post-traumatic headache 5.3. Acute headache attributed to whiplash injury (S13.4) 5.4. Chronic headache attributed to whiplash injury (S13.4) 5.5. Headache attributed to traumatic intracranial haematoma 5.6. Headache attributed to other head and/or neck trauma (S06) 5.7. Post-craniotomy headache

6. Headache attributed to Cranial or Cervical Vascular Disorder 6.1. Headache attributed to ischemic stroke or transient ischemic attack 6.2. Headache attributed to non-traumatic intracranial hemorrhage (I62) 6.3. Headache attributed to unruptured vascular malformation (Q28) 6.4. Headache attributed to arteritis (M31) 6.5. Carotid or vertebral artery pain (I63.0, I63.2, I65.0, I65.2 or I67.0) 6.6. Headache attributed to cerebral venous thrombosis (CVT) (I63.6) 6.7. Headache attributed to other intracranial vascular disorder

7. Headache attributed to non-vascular intracranial disorder

8. Headache attributed to a substance or its withdrawal

9. Headache attributed to infection

10. Headache attributed disorder of homeostasis

11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures

12. Headache attributed to psychiatric disorder

Part III: Cranial Neuralgias, Central and Primary Facial Pain and Other Headaches:

13. Cranial Neuralgias and Central Causes of Facial Pain

14. Other Headache, Cranial Neuralgia, Central or Primary Facial Pain

    

For the full classification, visit the International Headache Society website at: http://ihs-classification.org/en/02_klassifikation/01_inhalt/

Pathologic Conditions Causing Headache:

• Subdural Hematoma: Mild to severe, intermittent headache; neurologic symptoms include fluctuating consciousness
• Subarachnoid Hemorrhage: Sudden onset, severe and constant headache; elevated BP; can cause change in consciousness
• Increased Intracranial Pressure (ICP): Mild to severe headache; neurologic symptoms include hemiparesis, visual changes, and brainstem symptoms, such as vomiting, altered consciousness
• Meningitis, viral and bacterial: Severe headache with radiation down neck; acute illness and fever; positive Kernig's sign
• Brain abscess: Mild to severe headache; local or distant infection; fever may not be present; neurologic signs consistent with local site of infection
• Central nervous system: Localized headache and focal neurologic symptoms; cranial nerve symptoms often seen
• Central nervous system neoplasm: Localized headache and focal neurologic symptoms; cranial nerve symptoms often seen
• Toxicity: Generalized headache, pulsating; other signs of toxicity may be present
• Sinusitis: Frontal or dull headache, usually worse in the morning; increased pain in cold damp air; nasal discharge
• Otitis media, mastoiditis: Feeling of fullness in ear, stabbing pains in head, vertigo, and tinnitus

For further information regarding differential diagnosis of headaches, refer to the text: Pathology: Implications for the Physical Therapist (Goodman and Fuller), Clinical Neurology (Aminoff, Greenberg, and Simon), or The Merck Manual of Diagnosis and Therapy (18th ed.)  You can also visit the online version of The Merck Manual at: http://www.merck.com/mmpe/index.html

Case Reports

Vestibular Migraine:

http://web.ebscohost.com.libproxy.bellarmine.edu/ehost/pdf?vid=4&hid=13&sid=3ce3b6e3-cdf1-4d49-93f8-2cd5b33ad2d4@sessionmgr4

http://web.ebscohost.com.libproxy.bellarmine.edu/ehost/pdf?vid=5&hid=13&sid=809ff100-7b2d-42b8-b726-e5fc07598431@sessionmgr11

Pharmacology Case Reports:

Aripiprazole: http://www.medscape.com/viewarticle/559624

Eletriptan, Triptans, and Serotonin Syndrome: http://cep.sagepub.com/cgi/reprint/27/12/1421

Sumatriptan: http://cep.sagepub.com/cgi/reprint/14/5/374.pdf

Triptan and Troponin: http://www.ojrd.com/content/pdf/1750-1172-4-15.pdf

• May need to sign up for Biomed Central to review the articles listed above. 

Chronic migraine and chiropractic rehabilitation:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646959/

Resources

PDF's of the articles used in this page:

Recent Related Research (from Pubmed)

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References

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