Pathophysiology of Migraine

Vascular Theory 

       Intracranial vasoconstriction in the outer cortex plays a role in the occurrence of migraine with aura. This opinion is reinforced by the presence of headache accompanied with the same heart rate. Blood vessels constrict primarily located in the brain due to activation of peripheral nociceptive nerve locals. This theory was initiated above observation that the extracranial veins that will undergo vasodilation palpable heartbeat. This vasodilation will stimulate people to experience headaches. In such conditions, vasoconstrictor drugs, such as ergotamine will reduce headaches, while vasodilators such as nitroglycerin will worsen headaches.

Neurovascular Theory and Neurochemistry 

         Vascular theory evolved into the neurovascular theory espoused by the neurologist in the world. At the time of the migraine attack occurs, the trigeminal nerve secrete CGRP (Calcitonin Gene-related Peptide) in large quantities. This has resulted in multiple vessel vasodilatation, causing headache.

      CGRP is a peptide belonging to the calcitonin family members consisting of calcitonin, adrenomedullin, and amylin. Such as calcitonin, CGRP present in large quantities in the C cells of the thyroid gland. However, CGRP is also widely distributed in the central and peripheral nervous system, cardiovascular system, gastrointestinal system, and the system urologenital. When CGRP is injected into the nervous system, CGRP can cause various effects such as hypertension and nutrition emphasis. However, if injected into the systemic circulation that will happen is hypotension and tachycardia. CGRP is a peptide that has a working action as a potent vasodilator. Employment action CGRP 2 receptors is mediated by CGRP 1 and CGRP 2.

        In principle, patients who are not experiencing migraine attacks, suffered hyperexcitability of neurons in the cerebral cortex, especially in the occipital cortex, which is known from studies of MRI recordings and transcranial magnetic stimulation. This hyperexcitability causes migraine sufferers become vulnerable to attack, a situation similar to people with epilepsy. This opinion was reinforced the fact that at the time of migraine attacks, frequent allodynia (pain hypersensitivity) of the skin, due to the current path sensitized trigeminotalamus participate migraine episodes. Mechanisms of migraine tangible as trigeminal vascular reflex unstable with segmental defects in the pain pathway. The segmental defects that include excessive afferent that will happen later on cortibular excessive boost. With the absence of afferent stimulation on blood vessels, the cause throbbing pain.

Theory of cortical spreading depression (CSD)

       Pathophysiology of migraine with aura is known as the theory of cortical spreading depression (CSD). Aura occurs because there is excitation of neurons in the substantia nigra that spreads with speed of 2-6 mm / min. This spreading was followed by a wave of suppression of neurons with a similar pattern to form a rhythm vasodilation followed by vasoconstriction. CSD is the principle of neurochemical release of potassium or glutamate as excitatory amino acid of neural networks resulting in depolarization and releasing of neurotransmitters again.

      CSD on aura episode, will stimulate the caudate nucleus of the trigeminal nerve, initiates a migraine. In migraine without aura, small events in neurons may also stimulate the caudate nucleus and then initiate a migraine. Activated Trigeminal nerve, will stimulate the cranial vessels to dilate. As a result, the neurochemical compounds such as calcitonin gene-related peptide (CGRP) and substance P will be issued, there was extravasation of plasma. This incident eventually led to greater vasodilation , there was a sterile neurogenic inflammation in the trigeminovascular complex.

       In addition, migraine also occur due to some other mechanisms , including activation of the rostral part of the brain stem , dopaminergic stimulation, and magnesium deficiency in the brain. This mechanism manifests release hydroxytryptamine (5-HT), which is a vasoconstrictor. Giving dopamine antagonists, such as prochlorperazine, and 5-HT antagonists, such as sumatriptan can effectively eliminate migraine.

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