Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

TGA is a clearly recognisable clinical syndrome with many and varied aetiologies, the most ubiquitous being transient cerebral ischaemia. This entity is probably much more common than the literature suggests, many patients not coming to the attention of a physician due to the transient nature of the isolated memory defect and the risk of recurrence being low, it is of interest that many of the original patients described tended to be the more prominent members of the community, e.g. physicians and relatives of physicians, perhaps suggesting that the occurrence of TGA in such a person is less likely to pass unnoticed. In the differential diagnosis one should include the following: transient cerebral ischaemia, epilepsy, migraine, temporal lobe encephalitis, psychogenic fugues, post-traumatic, and rarely cerebral neoplasms.
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PMID:Transient global amnesia--a review of 213 cases from the literature. 36 12

Children with migraine, or, less commonly, with no previous history of migraine, may have agitated confusion lasting from several minutes to hours. There is a tendency for the confusional attacks to recur, but they are eventually replaced by typical migraine. The natural history of this syndrome with 1 1/2 to 5 years' follow-up in five children is reported. The mechanism is believed to be cerebral ischemia of one or both hemispheres.
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PMID:The natural history of acute confusional migraine. 65 10

The role of calcium as a second messenger which mediates the transmission of the signal and has an impact on cellular regulation of the majority of organs at all stages of development was confirmed during the past decade. In the submitted review the authors summarize mechanisms by which calcium exerts its regulatory function. At the same time the authors discuss the possible ratio of disorders in the above systems in various diseases in particular those of the central nervous system and possible pharmacotherapeutic interferences at different levels of transmission of the signal mediated by calcium. As in the mentioned area at the clinical level so far mainly calcium channel blockers were used, the authors summarize the use of these substances in the treatment of cerebral ischaemia, migraine, epilepsy and manic-depressive disease.
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PMID:[Possibilities of therapeutic applications of neuronal calcium homeostasis]. 166 83

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

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

The aetiology of strokes was studied in a hospital based series of patients aged up to 40 years with precise clinical and radiological criteria. One hundred and forty five patients (75 males and 73 females) aged five to 40 years with cerebral ischaemia were evaluated. Aetiology was heterogeneous and could be classified into seven groups. Cerebral arteriograms were performed in all cases and indicated the aetiological diagnosis in most patients. Embolism was the most frequent recognised abnormality (38.4%). There were no complications of arteriography. Arterial dissections discovered by arteriography were the cause of the stroke in 10.1% of the patients. Atherosclerosis was diagnosed in 32 cases and was the commonest cause (21.6%). In one fifth of cases no cause was found. Contraceptive drugs were considered as potential cause of ischaemic stroke in 11.5%, cardiac diseases in 12.8% and haematological disorders in 8.1%. Other potential causes included migraine, inflammatory diseases, pregnancy and lacunas. Follow up in 126 cases showed that many patients had good functional recovery.
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PMID:Cerebral infarction in young people. A study of 148 patients with early cerebral angiography. 189 19

Cortical spreading depression (SD) has been implicated in the pathophysiology of classical migraine headache and cerebral ischemia. A reduction in cerebral blood flow (CBF), mimicking that seen during the aura and headache phase of migraine, is typically observed following SD in the rat. This phenomenon may also play a role in potentiating ischemic brain damage. In the present study, brief cortical exposure to 1 M KCl produced a marked suppression of EEG amplitude which persisted 20 min in the rat. Upon normalization of the EEG, cortical blood flow declined 20-30% and remained low for at least 2 h. Treatment with a 1 mg/kg i.v. dose of the 21-aminosteroid antioxidant tirilazad mesylate (U-74006F), 2 min following KCl application, completely blocked the hypoperfusion while leaving the magnitude and duration of the EEG suppression and mean arterial pressure unchanged. Tirilazad mesylate is a potent inhibitor of oxygen radical-mediated lipid peroxidation both in vitro and in vivo. Thus, based on present results, an oxygen radical hypothesis is proposed to account for the SD-induced cerebral hypoperfusion.
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PMID:The 21-aminosteroid antioxidant tirilazad mesylate, U-74006F, blocks cortical hypoperfusion following spreading depression. 193 84

A 28 year old woman with a previous history of labile hypertension, migraine and transitory cerebral ischemia was admitted with cerebral infarction. One month later she developed livedo reticularis and amaurosis fugax, which led to the diagnosis of Sneddon's disease (livedo reticularis, labile hypertension and neurological symptoms) and the anticardiolipin antibody (ACA) syndrome. Treatment with prednisone and phenprocoumon resulted in lowering of ACA-titers, but the symptoms did not subside until acetylsalicylic acid was added.
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PMID:[Anti-cardiolipin antibody in cerebral infarction]. 198 66

We report a 26-year-old male who developed aphasia due to an ischemic cerebral infarction caused by MELAS (myoencephalophatic syndrome with lactic acidosis and cerebral ischemia). The most common causes of cerebral infarction in young patients were ruled out by laboratory investigations. The diagnosis of MELAS was suspected on the basis of past history of epilepsy, migraine and progressive sensory deafness, and increased resting blood lactic acid. Cerebral computed tomography showed bilateral caudate-putamen-pallidal calcification and nuclear magnetic resonance scan disclosed a left ischemic parietal-temporal-occipital infarction. The diagnosis was confirmed by muscular biopsy, which was characteristic of mitochondrial myopathy showing "red disarrayed" fibers in the histologic modified trichromic Gomori stain. Our patient showed that MELAS should be considered in young adults with cerebral infarction. The diagnosis should initially be suspected on a clinical basis, and confirmed by the presence of "red disarrayed" fibers with modified trichromic Gomori stain histologic muscle study.
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PMID:[Cerebral infarct in a young adult, as the presenting form of myeloencephalopathic syndrome with lactic acidosis and cerebral ischemia]. 236 6

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.
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PMID:Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases. 238 25


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