Migraine occurs in two forms. The first type is a migraine with an aura called classic migraine and the second form is a migraine without an aura called common migraine.

In the classic form of migraine, there is a phase of aura just before the headache appears. The most common aura observed is a visual aura. Patient reports of a temporary loss of vision partly or completely, flashes of light, objects appear to move, or shake. The other forms include difficulty in speaking, food cravings, getting an odd smell. Sometimes there is numbness starting from the hands and spreading upwards towards arms and gradually involving face, lips and tongue. These auras last for a few minutes before the headache appears.

The migraine without an aura presents with a unilateral or bilateral pain in head, usually beginning on the frontal or temporal side and spreading throughout the head [5]. The pain is usually pulsating or throbbing. The pain starts gradually and then becomes worse within 2 to 12 hours. Along with the head pain, symptoms such as severe nausea, vomiting, photosensitivity, blurriness of vision and sweating are also accompanied [6].

Migraine is diagnosed clinically [9]. Blood tests are not usually helpful. An MRI is only advised in cases where the auras are prolonged and persistent or in cases of post traumatic migraine. MRI detects white mater abnormalities.

Acute attacks are treated with drugs such as aspirin, acetaminophen or NSAIDs such as ibuprofen. Other sets of drugs include class of triptans like zolmitriptan, almotriptan and frovatriptan. Certain ergot derivatives such as ergotamine and tartrate also help in treating migraine. They are contraindicated in patients with underlying heart disease or high blood pressure.

The acute treatment lasts for maximum 2 to 3 days per week. For nausea or vomiting, nasal sprays, rectal or parenteral forms of medications are used. In case of rebound headaches, opioid combinations, butalbital and butorphanol nasal sprays and combinations are used [4] [6].

The prognosis of migraine is variable and is poorly studied. The long term prognosis studied of a recent population showed 10% complete remission and 84% of partial remission. It was also found that the remission occurs as the age progresses and psychological makeup of the individual highly influences the persistence of the migraine with regards to its frequency and intensity [4].

Though the exact cause for migraine remains unknown, there are certain theories postulated as its probable causes. The most common factor thought to initiate migraine is a complex dysfunction within the central nervous system. The neurotransmitter called serotonin is an important factor causing this dysfunction. It was observed that patients with migraine have significantly low levels of serotonin in their brains. Also, studies confirm that people on antidepressants tend to have a rise in serotonin levels which reduces the frequency of migraine.

Another factor is melatonin. Melatonin is an active metabolite of serotonin. Deficiency of this metabolite triggers migraines. A genetic link confirms the inheritance of the disease. It has been confirmed that individuals having a DNA variant on chromosome 8 between genes called PGCP and MTDH/AEG-1 has been related to carry a greater risk of migraine. The estimated theory for the pathogenesis is that a neurotransmitter called glutamate regulated by the DNA variant gets accumulated in the brain resulting into migraine.

Finally, the trigger factors which contribute to the cause of these attacks are dietary factors which include irregular meals, fasting for long hours, having cheese, chocolates, caffeine, foods containing an ingredient called tyramine, and certain citrus fruits.

Environmental factors include loud noises, strong smell exposure, direct exposure to glaring lights or VDU screens, red wine, head trauma, motion sickness, weather changes, cold stimulus such as ice creams and smoke. Psychological factors include excess stress, anxiety, depression, and lack of sleep. Certain medications linked with migraine triggers include oral contraceptive pills [1].

Migraine also affects women in large proportion suggesting a hormonal link. The drop in estrogen level at the luteal phase of the menstrual cycle appears to be the likely trigger to migraine.

The average prevalence of migraine in a year is about 18% in women and 6% in males. Statistics reveal that the age in which migraine attacks are commonly observed is between 25 to 50 years. Attacks before the age of 20 years are accounted to be 50% and that above 50 years are barely 2%.

Individuals with a positive family history are at a greater risk of suffering from migraine, its incidence being 70%. Lifetime prevalence accounts to 20% in females and 8% in males. In the United States, the prevalence among the low income groups is more than those with a high income. It is common amongst the Canadians, fair among the African Americans and lowest among the Asian Americans [2].

During the twentieth century, vascular dysregulation was believed to result in migraine. According to this hypothesis, transient vasoconstriction of the blood vessels resulted into aura, preceding migraine and the actual pain resulted due to rebound vasodilatation. This hypothesis had evidence based on certain vasodilating drugs such as nitroglycerin, which caused pain and vasoconstrictor drugs like ergotamine which relieved the attack.

Currently, neuronal dysfunction is considered as the most possible primary factor in the pathophysiology of migraine. This includes activation of trigeminovascular system, cortical spreading depression and neuronal sensitization.

Activation of trigeminovascular system: It involves sensory neurons from the trigeminal ganglion and upper cervical dorsal roots. These innervate the dural vascular structures such as the Dura mater and cerebral vessels [3]. These nerve fibers then ascend from the trigeminal nucleus to the sensory cortex via the thalamus. Thereafter, the pain occurs in the regions supplied by the trigeminal nerve.

Cortical spreading depression: This self-propagated wave spreads slowly across the entire span of the cerebral cortex reducing the bionueronal activity. It leads to inflammatory changes by activating the neurons in the trigeminal nucleus caudalis. This produces headache via the reflex actions of the central and peripheral nervous systems.

Neuronal sensitization: This is a process in which the neurons become responsive to both nociceptive and non-nociceptive stimulation. Pain is caused due to peripheral sensitization in the primary afferent neuron and central sensitization of the higher order neurons of the spinal cord [4].

There are some medicines which help prevent the attacks of migraine. These include beta blockers such as propanolol and timolol, calcium channel blockers like verapamil and antidepressants such as amitripyline or venlafaxine [7]. The general principle observed while giving a prophylactic is to start slow and increase the dose gradually and to get a trial of 2 to 3 months done before administration.

Certain lifestyle changes are highly recommended, in order to reduce and prevents the frequency and intensity of migraine attacks [8]. These include eating healthy foods, maintaining adequate amount of sleep daily without altering its timings, to avoid any conditions which are known to trigger migraine, reduce alcohol, meditation and limiting stress and worry [10] [11].

The word migraine is derived from a Greek word hemikrainia. This term was translated to French and called migraine.

Migraine is a chronic nervous system disorder characterized by recurrent headaches, intense in character. About 28 million people in United States suffer from migraine. About 25% of migraine sufferers experience a pre-migraine phenomenon called aura.

A migraine comprises of an intense unbearable headache which is throbbing and pulsating in character. This is usually accompanied by sensation of nausea, vomiting and a heightened sensitivity to light with or without audio-visual disturbances.

The migraine attacks can stay for few minutes to hours or even for days together. Some of these attacks are preceded by aura such as flashes of light before eyes, altered consciousness or numbness of limbs. Stress, fasting for long hours, lack of sleep are found to trigger migraine. Hence these lifestyle changes are advised to prevent migraine [11]. Diagnostic tests are of little use in diagnosing a migraine and prognosis is generally good.

1. Allais G, Gabellari IC, De Lorenzo C, Mana O, Benedetto C. Oral contraceptives in migraine. Expert Rev Neurother. Mar 2009;9(3):381-93.
2. Cutrer, FM. Pathophysiology of migraine. Semin Neurol. 2010 Apr; 30(2):120-30.
3. Spierings EL. Pathogenesis of the migraine attack. Clin J Pain. 2003 Jul-Aug;19(4):255-62.
4. Stewart WF, Lipton RB, Celentano DD, Reed ML. Prevalence of Migraine Headache in the United States Relation to Age, Income, Race, and Other Sociodemographic Factors. JAMA. 1992;267(1):64-69.
5. Pietrobon D, Striessnig J. Neurobiology of migraine. Nat Rev Neurosci. 2003 May 1; 4(5)386–398.
6. Skaer TL. Clinical presentation and treatment of migraine. Clin THer. 1996 Mar-Apr;18(2):229-45; discussion 228.
7. Silberstein SD, Holland S, Freitag F, Dodick DW, Argoff C, Ashman E. Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Evidence-based guideline update: pharmacologic treatment for episodic migraine prevention in adults. Neurology. 2012 Apr 24;78(17):1337-45.
8. Elrington G. Migraine: diagnosis and management. J Neurol Neurosurg Psychiatry. 2002 Jun; 72 Suppl 2:ii10-ii15.
9. Hildreth CJ, Lynm C, Glass RM. Migraine Headache. JAMA. 2009 June 24; 301(24).
10. Goadsby PJ. Stress and migraine: something expected, something unexpected. Neurology. 2014 April 22;82(16)1388-9.
11. Lipton RB, Buse DC, Hall CB, Tennen H. Reduction in perceived stress as a migraine trigger Testing the “let-down headache” hypothesis. Neurology. 2014 April 22; 82(16): 1395-1401.