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)

Point-by-point calculation of the mean transit time based on gamma fit was used to analyze brain perfusion studies in a vertex view. The algorithm and preliminary results in normal brain and in different stages of cerebral perfusion abnormality (ischemia, stroke, migraine, tumor, abscess) are demonstrated. In contrast to the traditional methods using fixed, a priori defined regions of interest this type of mapping of the relative regional cerebral perfusion shows more clearly the irregular outlines of the disturbance. Right to left activity ratios in the arterial part of the time-activity curves showed significant correlation with the mean transit time ratios (Qt = 1.185 - 0.192 Qa, n = 38, r = 0.716, P less than 0.001).
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PMID:Mean transit time image--a new method of analyzing brain perfusion studies. 630

Diltiazem, nifedipine, and verapamil inhibit calcium entry into cells via different mechanisms with different pharmacologies. They display different relative effects on different cardiovascular functions, a complex interplay of direct actions and adrenergic reflexes. Peripheral arterial vasorelaxation causes adrenergic reflex activity which opposes their direct negative chronotropic, dromotropic, inotropic, and hypotensive actions. Verapamil's most potent activity is electrophysiologic, and nifedipine's effects are hemodynamic; diltiazem acts like a less-potent combination of verapamil and nifedipine. All three drugs are efficacious in angina. These three drugs may not be interchangeable in all patients, but individualization of therapy is possible. Future indications for calcium channel blocker therapy may include hypertrophic cardiomyopathy, cerebral vasospasm, migraine headaches, pulmonary hypertension, asthma, esophageal spasm, intestinal ischemia, Raynaud's phenomenon, dysmenorrhea, and premature labor.
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PMID:Calcium channel blockers in emergency medicine. 638 Mar 52

Considerable experimental evidence has accumulated to indicate that brain ischemia or stroke-like events will lead to rapid losses of brain potassium, magnesium, ATP, creatine phosphate and glucose. These events are usually followed by an uptake of sodium and calcium ions. Increased uptake or excess Ca2+ uptake in neuronal cells is thought to be the prime cause of neuronal death in the brain. Mg2+ deficiency is known to produce a host of neurological disturbances in man; experimentally, Mg2+ deficiency leads to excess uptake of Ca2+ in the brain. Strokes and transient ischemic attacks also are known to be associated with neurological disturbances and ionic changes in the brain. Stroke patients have been reported to exhibit deficits in serum and CSF [Mg]. Acute Mg or K deficiency can produce cerebrovasospasm, at least experimentally. The lower the extracellular concentration of either Mg2+ or K+, the greater the magnitude of cerebral arterial contraction. These cerebrovascular contractions induced by lowering either the [Mg2+]0 or [K+]0 cannot be antagonized or attenuated by known pharmacologic antagonists. The cerebrovasospasms produced upon lowering [Mg2+]0 can be modulated by [K+]0 and vice versa; e.g. the lower the [K+]0, the greater the degree of vasospasm upon withdrawal of [Mg2+]0 and vice versa. Lowering [Mg2+]0 in situ and in vitro results in increased uptake of Ca2+ in the brain and the cerebral arteries. Cerebrovasospasms induced by substances that are known to be released in the brain on injury, such as prostanoids and serotonin, are relaxed dramatically by addition of [Mg2+]0. Infusions of MgSO4 into the brain via the internal carotid artery produces dose-dependent lowering of systolic and diastolic blood pressure as well as dose-dependent vasodilatation of arterioles (17-30 micron) and venules (18-40 micron) in the cerebral microcirculation, as observed by direct in situ high-resolution TV image-intensification microscopy. In clinical studies, infusion of MgSO4 has been reported to alleviate cerebrovasospasms. Epidemiological evidence is accumulating to suggest that consumption of fruit and vegetables (foodstuffs relatively high in K and Mg, and low in Na) is associated in certain geographic regions with a lower than normal incidence of strokes, particularly that of cerebral hemorrhage. On the basis of such data, and the findings reported herein, we believe one must consider that certain types of cerebrovascular accidents, transient ischemic attacks and 'classical' migraine attacks may be associated with a 'true' Mg deficiency and altered fluxes of K+ ions in the brain and CSF.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions of Mg and K on cerebral vessels--aspects in view of stroke. Review of present status and new findings. 639 42

The case is described of a 32-year-old female patient who has suffered since puberty from acute migraine attacks and Raynaud syndrome of both hands. In June 1981 acute posterior cerebral ischemia occurred. 11/2 years later the patient was hospitalized for acute myocardial infarction with normal and patent coronary arteries. Thereafter, the patient was treated with nifedipin and anticoagulation, and no other vascular complications have since occurred. The authors suggest that the patient is suffering from a diffuse vasospastic disorder leading to migraine attacks, Raynaud syndrome, cerebrovascular ischemia and myocardial infarction, in view of the fact that the patient has no other known risk factors for early vascular complications.
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PMID:[Vasospastic syndrome in a young women with migraine, Raynaud's disease, cerebral ischemia and myocardial infarction]. 650 63

Twelve patients with transient global amnesia (TGA) were studied. Seven (58%) of the 12 had a headache during their attack; five (42%) of the 12 were migraineurs. Measurement of regional cerebral blood flow (rCBF) by the xenon Xe 133 inhalation method showed similar patterns of flow in five of the seven patients tested. The rCBF abnormalities were impaired vasomotor response in the watershed area between the middle cerebral artery and posterior cerebral artery territories, and/or focal ischemia in the inferior part of the temporal lobe. These rCBF abnormalities differed from those seen in patients with carotid transient ischemic attacks (TIAs) and vertebrobasilar TIAs. We speculate that the vasomotor phenomena in migraine may play a major role in the cause of TGA.
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PMID:The transient global amnesia-migraine connection. 668 94

In patients with transient ischemic attack (TIA), the risk of stroke increases greatly, especially in the months immediately following the initial attack. Diagnosis of TIA is based primarily on the patient's cerebrovascular history, since results of neurovascular examination are usually normal. TIA is often related to atherosclerotic arterial disease but can have numerous causes. Migraine, focal seizures, and other neurologic conditions can closely mimic TIA. Surgical and medical therapies help minimize the risk of stroke. The choice of therapy depends on the vascular territory of ischemia, the cause of the attack, the patient's medical and neurologic condition, the availability of a skilled surgeon, and other factors.
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PMID:Transient ischemic attacks. Strategies for minimizing stroke risk. 671 81

Three days after initiation of migraine headache therapy with ergotamine tartrate and propranolol, severe acute arterial insufficiency of the lower extremities developed in a 48-year-old woman who had been in general good health. Angiography revealed hypoplastic aortoiliac arteries, with tubular narrowing of the leg arteries. Lower extremity blood pressures rapidly returned to normal with a single intraarterial injection of 25 mg of tolazoline. Cases of peripheral ischemia due to either ergotamine or propranolol have been reported. Combined use of these two drugs may enhance the risk of acute arterial compromise.
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PMID:Lower extremity ischemia due to combined drug therapy for migraine. 681 34

The responses to work-test in ischemia (tourniquet technique), before and after I.V. injection of naloxone (2 mg) or saline, were investigated in healthy volunteers and patients suffering from various types of headache. The patients were examined during both painful and painless periods. We found that only the subjects suffering from migraine showed a significantly shortened pain tolerance at work-test in ischemia, after injection of naloxone, and only during painful periods. Psychogenic headache patients and migraine patients in painless periods showed responses during work-test similar to those in healthy volunteers, even after injection of naloxone. We believe that hyperalgesic effect of naloxone is due to involvement of beta-endorphin systems only during organic pain.
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PMID:Headache patients: different responses induced by naloxone during work-test. 715 Nov 48

Twelve patients with transient global amnesia (TGA) had prior migraines (six classical and six common). In three patients, classic migrainous phenomena accompanied TGA, and in nine patients severe headache accompanied the amnestic attack. Migrainous vascular dysfunction in the dominant posterior cerebral artery territory could explain TGA: (1) The pathophysiology and transient nature of TGA have led many to postulate posterior circulation vascular disease; migraine is a vascular disorder with a posterior circulation bias. (2) TGA and migraine share common precipitants. (3) Migraine differs from arteriosclerotic ischemia; the repetitive queries of TGA are absent in amnestic stroke. (4) TGA and migraine are usually benign.
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PMID:Transient global amnesia and migraine. 719 42

28 patients with transient global amnesia (TGA) were followed for a mean period of 73 months. The patients fell into 3 diagnostic groups: a group where patients had associated symptoms and signs of transient focal cerebral ischemia (TIA), a migraine group and a miscellaneous group. 22 patients had evidence of cerebrovascular disease or risk factors for cerebrovascular disease, and a vascular basis for the amnesic attack was highly suggestive in 25 patients. During the follow-up period 2 patients died, 3 had recurrent TGA and 13 developed a completed stroke or suffered from further TIA's. Permanent memory impairment was encountered in 9 cases. An unfavourable course was related to the presence of other TIA manifestations and/or risk factors for cerebrovascular disease. The study indicates that TGA is probably due to transient ischemia in the vertebrobasilar arterial distribution area. TGA per se has a good prognosis, but the coexistence of risk factor or manifest cerebrovascular disease implies a high rate of a subsequent completed stroke or permanent memory impairment.
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PMID:Transient global amnesia -- its clinical and pathophysiological basis and prognosis. 721 Nov 87


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