Clinical Manifestation and Pathophysiology of Migraine

Clinical Manifestation of Migraine

Migraine is a chronic condition. Most of the migraine attacks are also accompanied with another headache. Migraine headache is often described as a severe headache, throbbing and attacking head on one side. Some pain is felt in the forehead, around the eyes and behind the head so obscure symptoms with another headache. Although most of the migraine attack on one side of the head, but often also found symptoms of migraine headaches on both sides of the head. Side of the head migraines too often turns on every time attack. Be careful when the affected side of the head is always the same, another possibility is the occurrence of a brain tumor. Patients with migraine often tormented in performing daily activities, especially when the attack occurred. Other accompanying symptoms of migraine include, nausea, vomiting, diarrhea, facial pallor, cold hands feet, and the patient will be sensitive to light and sound. Due to an increased sensitivity to light and sound then migraine sufferers had to lie in a quiet and dark room. Migraine attacks usually subside within 4 to 72 hours.

Nearly 70% had a family history of migraine. Most of the women. The first attack in the migraine usually starts during adolescence and young adulthood, and then tended to decrease at the age of 5 and 6 decades. Usually there is a triggering factor. Patients generally have a perfectionist personality, rigid, and impulsive.
The clinical features of migraine is usually a throbbing headache but unilateral and bilateral or switched sides. Migraine attacks typically 2-8 times per month, once the attack duration between 4-24 hours or longer isa, moderate-severe pain intensity, accompanying symptoms, among others,: nausea, vomiting, photophobia and / or phonophobia, pale face, vertigo , tinnitus, irritable. On migraine with aura, the symptoms prodromalnya is skotomata.teikopsia (fortification spectra), photophobia (light flashes) paresthesias and visual hallucinations exhausted, feeling tired, very hungry and feeling nervous / anxious.
Headaches often appear at the wake, but it can happen at any time.


Pathophysiology of Migraine

Signs and symptoms of migraine on the result of cerebral cortical ischemia varying degrees. Typical attack starts with a scalp artery vasoconstriction and retinal blood vessels and cerebral. Extracranial and intracranial blood vessels dilated, which causes pain and discomfort. Studies suggest that arterial dilatation hyperpermeable and cause local inflammation that sterilize, which causes pain in surrounding areas and arterial dilatation. The state aims to enable existing substances in the blood vessels (histamine, serotonin, plasmokinin) who participated in cleaning the inflammatory reaction.

Migraine attacks commonly activate the sympathetic nervous going. The meaning of the sympathetic nerve is the nerve that is part of the human nervous system is responsible for controlling the body's response to stress and pain. Increased sympathetic nervous activity in the intestine causes nausea , vomiting and diarrhea. Sympathetic activity will also lead to slow gastric emptying resulting in drug delivery to the small intestine to be absorbed will also be hampered. Barriers to drug absorption that is the problem for people with migraine when administered orally administered drug. Increased sympathetic activity also decreases the flow of blood so that the skin will appear pale and cold. Increased neural activity will also lead to increased sensitivity to light and sound.

There are various theories that explain the occurrence of migraine.

Vascular theory, disruptions vasospasm causing cerebral blood vessels constrict, causing brain hypoperfusion which began in the visual cortex and spread forward. Continued deployment of frontal headache and cause phase begins.

Theory of cortical spread depression, which in the migraine threshold value decreases neuronal excitation of neurons so easily happen, then apply shortlasting depolarization wave, by potassium - liberating depression ( decreased release of potassium ) that results in a prolonged period of depressed neurons. Furthermore, there will be deployment of depression that would suppress the activity of neurons as it passes through the cerebral cortex.

Theory of neovascular (trigeminovascular), the vasodilatory effect NOS activity and NO production would stimulate the trigeminal nerve endings in blood vessels, releasing CGRP (calcitonin gene related). CGRP binds to its receptor on mast cells and will stimulate spending meningens inflammatory mediators that lead to inflammation of neurons. CGRP is also working on the cerebral arteries and the smooth muscle that will lead to increased blood flow. In addition, CGRP will work on post junctional second order neurons site that acts as the transmission of pain impulses.