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MIGRAINE
Do I suffer from Migraine?

Broadly there are two types of migraine headaches, episodicmigraine and chronic migraine. Episodic migraines are of two types. Episodic migraine without aura and with aura.

If you have the following symptoms, then you probably suffer from migraine:

Migraine without Aura (previously called Common migraine; hemicrania simplex):
  • At least five attacks fulfilling criteria B, C and D

  • Headache attacks lasting 4 – 72 hours (untreated or unsuccessfully treated)

  • Headache has at least two of the following :

    • Unilateral headache

    • Pulsating quality

    • Moderate to severe pain

    • Worsened by routine physical activities (walking or climbing stairs)

  • During headache at least one of the following :

    • Associated with nausea and or vomiting

    • Intolerance to Light and Sound


Migraine with Aura :

Synonyms: Classic or classical migraine; ophthalmic, hemiparaesthetic, hemiplegic or aphasic migraine; migraine accompagnee; complicated migraine.

Aura is a complex neurological symptom that occurs before headache. It may also start after the headache started or continue during headache.During aura abnormal neuronal activity occurs (cortical spreading depression). Cortical Spreading depression (CSD) is a severe but transient disruption of neural activity in the brain, which spreads like waves in a pond in which a stone has been cast. It propagates to normal tissues and is accompanied by flux of Na+, Ca++, and Cl- ions into the cells, resulting in a brief burst of action potentials followed by electrical silence. Its rate of spread correlates almost exactly with the observed spread of the aura of classical migraine.Lancet.1985 Oct 5;2(8458):763-6. It is also called Leao’s spreading depression. Ref: Is migraine explained by Leao's spreading depression?Pearce JM.

Before or simultaneously with the onset of aura symptoms, regional cerebral blood flow is decreased in the cortex corresponding to the clinically affected area and often over a wider area. Blood flow reduction usually starts posteriorly and spreads anteriorly, and is usually above the ischemic threshold. 1 to646 Cephalalgia 33(9). After several hours, gradual transition into hyperemia occurs in the same region. Cortical spreading depression of Lea˜o is the likely underlying mechanism.

Diagnosis of Migraine with Aura:
  • At least two attacks fulfilling criteria B and C

  • One or more of the following fully reversible aura symptoms given below.

    1. Visual (commonest)

    2. Sensory

    3. Speech or language

    4. Motor

    5. Brainstem

    6. Retinal

    The aura symptomsusually follow one another in succession, beginning with visual, then sensory, then aphasic; but the reverse and other orders have been noted. The accepted duration for most aura symptoms is 1 hour, but motor symptoms are often longer lasting (up to 72 hours).

  • At least two of the following four characteristics :

    1. At least one aura symptom spreads gradually over more than or equal to 5 minutes, and / or two or more symptoms occur in succession.

    2. Each individual aura symptom lasts 5 – 60 minutes

    3. At least one aura symptom is unilateral

    4. The aura is accompanied or followed within 60 minutes, by headache.

Most common aura is visual (90%). It is present as zigzag figure near the point of fixation (when one is looking at an object using both eyes) that may gradually spread right or left and assume convex shape with scintillating edge. Next common symptom of aura is sensory disturbance. Patients feel pins and needle moving slowly from the point of origin and affecting a greater or smaller part of one side of body, face and / or tongue. Numbness may occur n its wake, but numbness may also be the only symptom, less frequently speech disturbances is seen, usually aphasia (lack of ability to speak). Motor weakness is also known as hemiplegic migraine is less frequent.

So, the subtypes in this category are:
  • Migraine with typical aura (visual, sensory or speech, each lasting maximum 60 minutes and fully reversible).

  • Migraine with Brainstem aura. Brain stem aura symptoms are

    • Dysarthria (difficulty with speech)

    • Vertigo

    • Tinnitus (ringing in the ear)

    • Hypacusis (hearing defect; conductive or neurosensory)

    • Diplopia (double vision)

    • Ataxia (poor coordination and unsteadiness)

    • Decreased level of consciousness

  • Hemiplegic Migraine with aura (motor weakness) – motor symptoms may last < 72 hours but sometime can last up to weeks.

  • Familial hemiplegic migraine (aura, and history of first degree relative having the same problem.A causative mutation on the CACNA1A (type 1), ATP1A2 (type 2) or SCN1A (type 3)gene has been demonstrated respectively. Present in first or second degree relative. May become

  • Typical aura without headache(associated with mainly negative symptoms such as hemianopia with too short or too long aura, may be confused with Transient Ischemic attach – mild stroke).

  • Sporadic hemiplegic Migraine – no first of second degree relatives are affected with this disease as seen in Familial Hemiplegic migraine.

  • Retinal Migraine - Repeated attacks of monocular visual disturbance,including scintillations, scotomata or blindness, associated with migraine headache.

Premonitory symptomsmay begin hours or a day or two before the other symptoms of a migraine attack (with or without aura). They include various combinations of
  • Fatigue

  • Difficulty in concentrating

  • Neck stiffness

  • Sensitivity to light and/or sound

  • Nausea

  • Blurred vision

  • Yawning and

  • Pallor

Chronic Migraine:

Headache occurring on 15 or more days per month for more than 3 months, which has the features of migraine headache on at least 8 days per month. Need to be differentiated from Tension type headache and Medication overuse headache.

Adapted from Cephalalgia 33(9) 629–808, International Headache Society 2013

Why migraine causes throbbing headache?

Migraine was known to be the effect of vasodilatation of cranial blood vessels after being triggered by typical triggers (MSG, loud sound, bright light etc.) in a susceptible individual. Recent understanding of the cause of migraine indicates that the vasodilatation of the cranial blood vessels is secondary to activation of the trigeminal nociceptive pathway (Goadsby et al, 2002) from any migraine trigger in migraine prone individuals.

The headache associated with migraine is from abnormal nerve and blood vessel interaction caused by a primary brain dysfunction, leading to activation of the trigeminovascular system* and the release of vasoactive neuropeptides (small proteins used for communication between neurons or nerve cells) such as Calcitonin Gene relate peptide (CGRP),pituitary adenylate cyclase-activating polypeptide (PACAP) etc. The pain during a migraine attack is associated with the release of the CGRP which has a key role in migraine pathophysiology. CGRP is a 37 amino acid neuropeptide.

The activation of trigeminal CORTICAL SPREADING DEPRESSION originating in the occipital region is thought to represent the neurobiological underpinning of visual aura. Somjen GG. Aristides Leão's discovery of cortical spreading depression. J Neurophysiol 2005; 94:2-4.

Activation of trigeminal nociceptive terminals will stimulate the release of CGRP. CGRP stimulates the pain receptors (nociceptors) present around the blood vessels and dilates the blood vessel. Multiple Clinical studies have fully established the importance of CGRP in causation of migraines. CGRP levels have been reported to be elevated during an attack of migraine and reduced when the symptoms of migraine subsides. IV administration of CGRP induces migraine mainly in migraineurs where as in non migrainures only mild headache or fullness of head sensation was noted.

References:

Ho TW, Edvinsson L, Goadsby PJ. CGRP and its receptors provide new insights into migraine pathophysiology. Nat Rev Neurol 2010;6:573-82. Villalón CM, Olesen J. The role of CGRP in the pathophysiology of migraine and efficacy of CGRP receptor antagonists as acute antimigraine drugs. PharmacolTher 2009;124:309-23. Russo AF. Calcitonin gene-related peptide (CGRP): a new target for migraine. Annu Rev PharmacolToxicol 2015;55:533-52. Hansen JM, Hauge AW, Olesen J, et al. Calcitonin generelated peptide triggers migraine-like attacks in patients with migraine with aura. Cephalalgia 2010;30:1179-86.

WHY RESEARCH MIGRAINE?

The American Migraine Prevalence and Prevention (AMPP) study found an overall prevalence of migraine of 16.2% (11.7% + 4.5% (probable migraine). It is the fifth leading cause of ED visits overall in the U.S. and accounted for 1.2% of outpatient visits. Among females 18-44 age group, the incidence of migraine or severe headache was as high as 26.1% and head pain was the third leading cause of ED visits. Even in age group of 75 or older, 4.6% reported experiencing severe headache or migraine in the previous 3 months.
Triptans accounted for 80% of antimigraine treatment (sumatriptan). Chronic migraine is associated with other psychiatric comorbidities such as anxiety etc.

  • Smitherman TA1, Burch R, Sheikh H, Loder E. The prevalence, impact, and treatment of migraine and severe headaches in the United States: a review of statistics from national surveillance studies.Headache. 2013 Mar; 53(3):427-36
In the Global Burden of Disease Survey 2010, Migraine was ranked as the third most prevalent disorder and seventh-highest specific cause of disability worldwide. Migraine has been ranked as the 6th disabling condition by World Health Organization (WHO) with domestic prevalence of 9.3% and the global prevalence of around 10%.

  • Cephalgia 33(9) 629-808, International Headache Society 2013.

  • Global Burden of Disease Study 2013 Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet 2015;386:743-800.

  • Yu S, Liu R, Zhao G, et al. The prevalence and burden of primary headaches in China: a population-based door-to –door survey. Headache 2012; 52:582-91.

In a study conducted by Bigal ME et al, 24,000 headache sufferers drawn from more than 165,000 US populations were surveyed using validated questionnaires for the diagnosis of episodic migraine and chronic migraine and were asked to report the specific medications used for headaches as well as level of satisfaction with treatment. Over a three month period more than half of the individuals with chronic headache (520 patients) missed at least 5 days of household work, reduced productivity, missing family activities etc. 87.6% of chronic migraineurs consulted health professionals. Migraine specific acute treatments were used only by 31.6% of chronic migraineurs and only 24.8% suffering from episodic migraine. 48% of individuals with CM were satisfied with the acute therapies. Only 33.3% of those with CM were currently using preventive medications.


Based on the above facts, we feel that there is an urgent need for finding more effective treatment of episodic migraine. Since the CGRP is the main mediator of pain in migraine, antibodies to CGRP is being studied to see if it reduces the intensity and frequency of episodic migraine attacks and eventually reduce the incidence of chronic migraine.
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