Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with typical classic migraine, including clear-cut visual auras, who had been followed up clinically for more than 15 years developed permanent right homonymous hemianopia. The underlying cause of this clinical syndrome was established by computerized axial tomography as vascular infarction or ischemia, involving the contralateral visual cortex.
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PMID:Classic migraine with cerebral cortical infarction causing permanent hemianopia. 45 90

Basilar migraine has been studied by Bickerstaff who considers that there is a vasoconstriction in the basilar territory resulting in transient ischemia with the corresponding neurological symptoms including vertigo, and followed by the vasodilatation causing the headache. Three cases, treated in neurology, have had an audiovestibular investigation with an E.N.G. and an audiogram and are described herein. Nystagmus and hearing loss have been observed in one of these cases and it is suggested that the internal auditory artery participates in the basilar migrainous processes. The diagnosis of basilar migraine is impossible to prove and the investigation is very limited. Finally it is the evolution of the patient which helps in establishing the diagnosis of basilar migraine.
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PMID:[Basilar migraine]. 61 47

At the present time ergotism is due primarily to excessive use or abuse of ergot preparations for migraine headaches. The diagnosis may be made with the evidence of vascular ischemia in the presence of a history of migraines and its treatment with this drug. The therapy for the vasospasm is directed chiefly at the discontinuation of the ergot preparation, with further treatment aimed at the relief of symptoms or prevention of complications. A case is presented of lower extremity ischemia with impending gangrene of both feet in a patient with a history of chronic schizophrenia. Arteriograms revealed symmetrical vasospasm in the lower extremities as well as spasm of the superior mesenteric artery and its intestinal branches. This is believed to be the first documented case of mesenteric vasospasm due to ergotism. Treatment was instituted with low molecular weight dextran, tolazoline, and reserpine with rapid and complete resolution. Caution is advised in the use of ergot preparations in neuropsychiatric disorders.
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PMID:Mesenteric and peripheral vascular ischemia secondary to ergotism. 83 86

Older people often describe their headaches as starting with vague neck discomfort and eventually moving to the temples and forehead. These are muscle-tension headaches, by far the most common type in the elderly. Although cervical osteoarthritis often is at fault, depression can be a significant factor, patricularly when headaches are chronic. There is no sure cure for tension headache, and often, several of the many remedies-ethyl chloride spray, moist heat, massage, antidepressant drugs, analgesics, local anesthetics, etc.-must be tried before an effective one is found. But just as important to successful therapy are concern, compassion, and a willingness to listen on the part of the physician. True migraine headaches are rare in the elderly. More prevalent is the type of vascular headache associated with giant cell arteritis, which is severe and resistant to any form of analgesic except the strongest narcotics. Vascular headaches also may result from congestive heart failure (which produces venous congestion in the cranial cavity), transient ischemia, increased intracranial pressure, and a variety of metabolic disturbances.
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PMID:The types of headache that affect the elderly. 95 13

Acetazolamide, a carbonic anhydrase inhibitor, has proved to be useful in the assessment of "vasodilatory capacity" in cerebrovascular disease. To obtain further information on the nature of interictal low-flow regions in migraine, we reinvestigated 20 asymptomatic patients suffering from migraine with aura (n = 15) or without aura (n = 5) and who had either minor (n = 12) or marked (n = 8) regional hypoperfusion when examined in a previous 99mTc-HMPAO SPECT investigation. These patients received acetazolamide IV prior to tracer application. In 14/20 cases regional hypoperfusion resolved. Three patients with migraine with aura had less pronounced regional hypoperfusion compared to baseline. No change in baseline hypoperfusion was detectable in three older patients. No further decreases in flow were measured. In contrast to patients with cerebrovascular ischemia, in whom acetazolamide usually enhances low-flow regions, vasodilatory capacity appears intact in most migraine patients with interictal regional hypoperfusion. Thus, the "acetazolamide test" might be useful in the differential diagnosis of migraine with aura from transient cerebrovascular ischemia.
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PMID:The influence of acetazolamide on cerebral low-flow regions in migraine--an interictal 99mTc-HMPAO SPECT study. 142 58

Two hypotheses have dominated attempts to understand the etiology of migraine with aura or classic migraine; the vascular spasm model proposed by Wolff and colleagues, and the spreading cortical depression hypothesis. Neither can provide a fully satisfactory explanation for the syndrome, however. We propose that classic migraine is both spreading cortical depression and localized ischemia linked in a vicious cycle by potassium induced vasoconstriction. The cycle can be initiated by any event which raises the local cortical ECF potassium concentration to approximately 20 mM. Such an event could be a localized burst of activity of a group of cells, localized metabolic impairment, or a transient reduction in blood flow to a region of the cortex. Once this level of potassium concentration is reached, it may result in localized depolarization of neurons, releasing more potassium into the ECF. Glial siphoning can distribute the potassium preferentially toward the blood vessels in the area, leading to an elevation in potassium concentration in the ECF surrounding the vascular smooth muscle of the arterioles. Above approximately 15 mM, vascular smooth muscle increases its tension in response to elevations in potassium. Therefore, as cortical ECF potassium concentration rises above 15 to 20 mM, localized vasoconstriction occurs, thereby reducing both the supply of oxygen for aerobic metabolism and the removal of potassium in the blood. Under these conditions, the effectiveness of the mechanisms which control potassium concentration is impaired and unable to prevent additional elevations in potassium. As the concentration continues to rise, vasoconstriction becomes more intense, perpetuating the cycle that results in localized depression of cortical neuronal activity and ischemia. The condition is propagated to adjacent regions of the cortex by diffusion and glial-mediated spread of potassium. In many respects, the hypothesis unites the vascular spasm and spreading depression models. If verified, it may provide insight into the causes of classic migraine as well as give direction toward development of effective therapies.
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PMID:Migraine with aura: a vicious cycle perpetuated by potassium-induced vasoconstriction. 155 28

Etiology and longterm prognosis were prospectively investigated in 155 consecutive patients (96 men, 50 women) ages 16-45 years who were referred to the Neurosurgical Unit with cerebral transient ischemic attacks or infarction during the period 1978-88. All patients underwent neurological and medical-cardiological evaluation, cerebral computerized tomography scanning, electrocardiogram, and laboratory tests. 2-dimensional echocardiography was performed in 123 cases (79%), cerebral angiography in 147 (95%). Atherosclerosis was the leading etiology, occurring in 48 patients (31%). A cardioembolic disorder was considered the probable cause of ischemia in 8 cases (5.1%). Further possible etiologies were though to be: oral contraceptives (5.8% of the total, but 15.3% within the females), spontaneous arterial dissection (4.5%), migraine (4%), puerperium (2.6%), cervical trauma (2.6%), and other, more uncommon conditions. Despite extensive evaluation, the cause of cerebral ischemia remained unknown in 40% of the cases. All patients received antiplatelet medication and 16 underwent surgery. The longterm outcome at a mean followup of 5.8 years was favorable in that 91% of the subjects resumed their workload on a full or parttime basis.
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PMID:Etiopathogenesis and prognosis of cerebral ischemia in young adults. A survey of 155 treated patients. 177 5

I studied 9 patients with migraine and posterior circulation ischemia. Inclusion criteria were (1) brainstem or cerebellar infarcts or transient ischemic attacks, (2) satisfactory vertebrobasilar angiograms, and (3) migraine. Excluded were patients with only occipital lobe ischemia, known arteriosclerosis, or other nonmigrainous vascular disease. Two women and 7 men, ages 6 to 58 years (mean, 34.7), had transient attacks only (2), single strokes (4), single stroke followed by attacks (1), or multiple strokes (2). Five had antecedent classic, 2 common migraine, and classic migraine began only after the initial ischemic event in the other two. The 7 stroke patients all had CT- or MRI-documented brainstem (4) or cerebellar (6) infarcts. Angiography was normal (3) or demonstrated basilar artery (BA) narrowing (2) or occlusion (4), or branch occlusion (1). In 3 patients the initially occluded BA later reopened. At follow-up (average 4.3 years, range 1 to 9 years), 5 were normal and 4 had important clinical deficits. I conclude that (1) "basilar migraine" is not always benign; it affects both sexes and a wide age range; (2) the pattern of headaches, attacks, and strokes varies; (3) migraine may appear only after ischemia; (4) some patients have BA occlusion or diffuse narrowing; and (5) BA occlusion can be temporary.
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PMID:Migraine and vertebrobasilar ischemia. 192 34

Ca antagonists of the dihydropyridine class (DHPs) are a heterogeneous group of drugs that interfere with Ca entry into vascular smooth muscle cells of resistance arterioles through type-L calcium channels producing arteriolar vasodilation. This leads to a reduction of vascular tone and, therefore, they have been successfully used in the treatment of systemic hypertension, myocardial ischemia (stable, variant, and unstable angina and silent ischemia), and Raynaud's phenomenon. Furthermore, recent clinical trials have indicated that DHPs may induce regression or slowing the progression of atheroma in coronary arteries. The results obtained with DHPs in the prophylaxis of migraine headache and in treating ischemic stroke and cerebral artery vasospasm are encouraging. However, more carefully designed, double-blind, large-scale, long-term studies are needed to better define the therapeutic value of DHPs in these disorders, the severity of adverse effects, and the mechanism responsible for their therapeutic effects.
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PMID:Dihydropyridines and vascular diseases. 179 15

Flunarizine, a class IV Ca++ antagonist non-selective for slow Ca++ channels, has been shown to be beneficial in the prophylactic treatment of migraine, the treatment of vertigo, and as add-on treatment in therapy-resistant forms of epilepsy. Flunarizine protects the brain against functional and/or structural neuronal damage in various animal models of cerebral ischemia. In addition to its cerebrovascular effect, flunarizine has also direct neuroprotective actions. New data have emerged on flunarizine with regard to Ca++ and Na+ channels in neuronal cells. There are several possible mechanisms involved in the mode of action of flunarizine. Flunarizine may block Ca++ and Na+ channels, both of which may flux Ca++ as well as Na+. A decrease in Ca++ influx may prevent further release of glutamate, and activation of NMDA receptor gated Ca++ channels at physiological pH. A decrease in Na+ influx may prevent cytotoxicity secondary to a large gain in intracellular Ca++, by reverse operation of the Na+/Ca++ exchanger. This mechanism may be important when the glycolytic rate is increased with concomitant acidosis, and phospholipids are broken down as occurs typically during ischemia. Given the complexity of biochemical events leading to cell death, blocking exclusively one channel subtype is not likely to yield sufficient protection. Hence, it may be useful to develop anti-ischemic compounds which act on a series of pathways involved in Ca++ overload, rather than selectively block one such channel.
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PMID:Ca++ and Na+ channels involved in neuronal cell death. Protection by flunarizine. 185 Aug 15


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