Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 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

Until the second half of the eighteenth century, the very definition of migraine as hemicrania (pain felt in one side of the head) eclipsed symptoms that were then considered as "marginal", although tingling sensations, speech impairment and visual impairment had already been described by Piso and Wepfer. The possibility of a migraine without a headache nevertheless started to be envisaged, inviting one to re-evaluate the status of these phenomena. But, as paradoxical as it may seem, it is in the field of astronomy that some of these phenomena such as visual aberrations were analyzed systematically and acknowledged to be migrainous. Scintillating scotoma is no exception: it was indeed mentioned as early as in the Hippocratic corpus, but until the end of the nineteenth century it was addressed as a separate condition to migraine. We limit our study to the visual aura. Our purpose is to show that the ophthalmic symptoms affecting migraine sufferers were not, by themselves, a medical object--which somehow calls into question the very functioning of science.
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PMID:[An encounter between medicine and astronomy: migraine visions]. 2204 98