Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brain neuronal dysfunction has been implicated in pathogenesis of migraine but direct evidence is lacking. Scintillating scotoma of migraine is generally believed to originate at the visual cortex. While cortical spreading depression is a relatively late physiological alteration in migraine, its protective role in neuronal ischaemia is increasingly being recognized. Atenolol, nadolol, or verapamil prevent migraine but do not readily cross the blood-brain barrier or critically influence any brain or peripheral neuronal function. Typical migraine headache, aura, or scintillating scotoma has not been reported following enucleation or evisceration of the eye. In humans, pain and temperature fibres from only the ophthalmic division of the trigeminal nerve reach the upper cervical spinal segments. Pain in migraine attacks including occipital and nuchal discomfort reflects selective involvement of the ophthalmic nerve. Photophobia is largely a retinal reflex involving the ophthalmic division of the trigeminal nerve. Key clinical features of the migrainous scintillating scotoma are consistent with retinal origin. Spreading depression in the retina is well-established. A subtle regional ocular sympathetic deficit prevails in migraine patients and possibly impairs regulation of intraocular choroidal blood volume and intraocular pressure. Several first-line migraine prophylactic agents lower the intraocular pressure. The neuro-ophthalmological basis for a monocular origin of migrainous scintillating scotomata due to mechanical deformation of the posterior segment of the corneo-scleral envelope consequent to choroidal venous congestion and rise in intraocular pressure is presented. Study of distribution and displaceability of the migrainous scintillating scotoma can settle its site of origin. Headache of migraine possibly arises from a similar mechanical deformation of the anterior eye segment followed by antidromic discharge in the trigeminovascular system. Lateralizing negative deficits such as homonymous hemianopia probably reflect vasospastic complications of migraine. A rational explanation for the most characteristic clinical features of migraine and a new template to elucidate the pharmacological basis of anti-migraine drugs is offered.
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PMID:Migrainous scintillating scotoma and headache is ocular in origin: A new hypothesis. 1635 54

The most frequent type of migraine aura is the typical one in which the most frequently occurring aura type are visual phenomena. Types of visual aura may be different. Scintillating scotoma, fortification zigzags (teichopsiae), fragmentation of the visual image are typical illusions in visual aura. The visual illusion of a typical corona phenomenon was represented as a visual migraine aura symptom. The extra edges of the corona phenomenon are commonly seen around the perceptual images of objects. The corona phenomenon is strongly associated with visual loss and the presence of elementary geometric illusions. It is surrounding a person's head, shoulders, hands, or body. Illusory splitting can be differentiated from the fragmentation of visual images and from the geometric illusion or mosaic illusion. The pathogenesis of migraine aura remains unclear. The probable cause of migraine aura may be cortical spreading depression (CSD) and cerebral hypoperfusion. Ionic changes, activation of trigeminal nerve and release of neuropeptides seem to be secondary to CSD during the attack of migraine aura. In present article the pictures of visual aura experienced by migraine patient are presented and discussed.
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PMID:[Migraine with visual aura: visual aura pictured by the patient]. 1753 May 82