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)

During the migraine-aura cerebral blood flow (CBF) is reduced in areas corresponding to the neurological deficits and symptoms. Whether this CBF reduction is the primary cause of the neurological deficits (the vascular theory) or a secondary result of primary neuronal dysfunction in particular "spreading depression" (SD) (the neurogenic theory) is still under discussion. The latter theory is supported by CBF investigations performed during attacks of migraine with aura (MA). The CBF reduction was found to be modest (20-35%) and not sufficient to cause ischemia which usually demands reduction of CBF by more than 50%. In addition the low-flow area appeared to "spreading" in the same manner as that seen in SD in the rat ("spreading oligemia"). Recent studies indicate, however, that the CBF reduction in most cases, after all, is sufficient to cause ischemia and that "spreading oligemia" might be an artifact caused by "scattered radiation". Persistent neurological deficits, EEG abnormalities and infarcts on CT-scans are seen after MA, thus further supporting the theory of vascular dysfunction (vasospasm) and ischemia as the cause of the migraine-aura.
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PMID:[Migraine aura--vascular or neuronal disease?]. 219 47

Three women with well-documented migraine associated with intracerebral hemorrhage are described. In each case, migraine headaches began during adulthood. Unusually severe and protracted headache heralded the onset of fixed neurological deficits associated with lobar intracerebral hemorrhage. Striking carotid artery tenderness was characteristic. Except for a history of migraine, no cause for intracerebral hemorrhage could be established. In each case arteriography showed extensive spasm of the appropriate extracranial or intracranial artery. Surgical pathology following evacuation of two hematomata demonstrated signs of vessel wall necrosis associated with subacute inflammatory changes. Vasospasm associated with severe migraine attacks may result in ischemia of intracranial vessel walls, leading to necrosis and subsequent vessel rupture when perfusion pressure is restored.
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PMID:Migraine with vasospasm and delayed intracerebral hemorrhage. 198 18

The authors investigated 100 patients (55 males and 45 females) aged 16 to 45 years who experienced cerebral ischemic attack, excluding venous thrombosis. Transient ischemic attacks accounted for 12% only. Attacks were related to usual causes of brain ischemia in 49 cases (premature atherosclerosis in 26, cardiopathy in 20 and lacunar stroke in 3). Thirty-eight events were attributed to most uncommon etiologies. Nonatherosclerotic arteriopathies (10 cases) such as spontaneous dissection, dysplasia or megadolichoarteries were easily diagnosed by angiography. Oral contraceptives (14 cases) and migraine (2 cases) were diagnosis of exclusion. Hematological disorders were a possible cause in 10 patients. Etiology remained undetermined in 13 cases. Four patients died acutely. Follow-up data were obtained in 93 survivors with a mean duration of 26 months (range, 6 to 60 months). Four subjects died during follow-up and 6 experienced recurrent stroke (annual recurrence rate: 3%). In activities of daily living, 64% of patients had complete autonomy while 13% had mild residual disability and 23% had severe handicap.
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PMID:[Cerebral arterial ischemic complications in young adults. Etiology and prognosis]. 232 55

Brainstem auditory evoked potentials (BAEPs) are affected by stroke or migraine in the vertebrobasilar arterial system. Some studies have reported BAEP changes in vertebrobasilar transient ischemic attacks (TIAs), but others have shown no alterations. We recorded BAEPs in 35 patients with TIAs in the vertebrobasilar system who did not have a stroke, other neurologic disease or significant hearing loss. Thirty patients were recorded after resolution of symptoms, while five individuals still had some resolving signs or symptoms. TIA patients as a group had longer interpeak latencies, but I-III, III-V, and I-V latencies were not significantly longer than in controls. Wave V was significantly longer in latency and lower in amplitude in TIA patients, however. The patients whose TIAs had resolved at absolute and interpeak latencies were within normal limits, but three of five had interpeak latencies at or above three standard deviations beyond the normal mean in the still symptomatic group. One of these was later tested and found to be within normal limits. BAEPs after subsidence of symptoms may add little to the evaluation of vertebrobasilar ischemia, but further AEP analysis may show more definitive differences of diagnostic use. The occasional BAEP abnormality during the resolving transient ischemia supports the recently suggested continuum between ischemia and infarction in the vertebrobasilar territory.
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PMID:Auditory evoked potentials in vertebrobasilar transient ischemic attacks. 233 45

A 38-year-old woman developed intermittent oscillopsia occurring every 45 to 90 minutes and lasting 20 to 40 seconds. She had a right-beating jerk nystagmus during these episodes. At other times, her neurologic examination was normal, and no nystagmus could be elicited. The nystagmus resolved when her classic migraine headaches were controlled with medical therapy. This intermittent unidirectional nystagmus may represent dormant periodic alternating nystagmus or another type of dormant nystagmus appearing intermittently due to episodic migrainous brainstem ischemia.
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PMID:Intermittent unidirectional nystagmus. 236 28

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

Twenty-one consecutive patients with testicular cancer treated with bleomycin, vinblastine, and cisplatin (PVB) were evaluated for acute vascular ischaemic events during chemotherapy. Angina pectoris occurred in 8/21 (38%) patients, a median 5.6 weeks after initiation of chemotherapy and persisted for 2-7 days. Raynaud's phenomenon was detected in seven (33%) subjects, transient ischaemia of the toes was found in six (29%) patients, one patient complained of migraine, but none had major cerebrovascular accidents. Patients with and without angina pectoris and/or Raynaud's phenomenon did not differ in respect of age, histology of tumor or medication. Ischaemia occurred at any time during the course of chemotherapy. No correlation was found between dosage of drugs and time of onset of ischaemic reactions. However, arterial occlusive event is a frequent and common toxicity and a result of treatment with PVB.
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PMID:Acute vascular toxicity after combination chemotherapy with cisplatin, vinblastine, and bleomycin for testicular cancer. 245 30

Transient global amnesia (TGA) is an unusual form of the amnestic syndrome, clinically characterized by profound disturbance of short-term memory with preservation of immediate recall and long-term memory. Spontaneous recovery is the rule and is usually complete within several hours. The etiology of TGA is not clear. It is considered to be caused by transient ischemia confined to the medial temporal lobe, an area supplied by branches of the vertebrobasilar system. Basilar artery migraine is a well-known syndrome, first described by Bickerstaff. Besides pulsating headache, the dominant symptoms are vertigo, ataxic gait, tinnitus, dysarthria, paraeshesia in the hands, homonymous hemianopsia and sometimes drop-attacks. These symptoms are associated with vertebrobasilar system dysfunction. In this paper, three migraine patients, suffering from one episode of TGA, were reported. All patients were women. Case 1 was a 48-year-old woman with a history of common migraine. Case 2 was a 48-year-old woman with a history of classic migraine. Case 3 was a 59-year-old woman with a common migraine. Family history of migraine exists in case 1 and case 3. Their migrainous attacks began in their twenties and thirties. They suddenly suffered migraine with the symptoms of vertebrobasilar dysfunction. These symptoms are ataxic gait (Case 1, 2, 3), dysarthria (Case 1, 2), vertigo (Case 1, 3) and homonymous hemianopsia (Case 1, 3). Simultaneously three patients had TGA. Duration of retrograde amnesia were about twenty-four hours (Case 1), about thirty minutes (Case 2) and about three hours (Case 3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Basilar artery migraine associated with transient global amnesia]. 262 11

Migraine, a clinical syndrome of unknown etiology, is a common cause of a variety of visual disturbances. This review describes the visual alterations associated with migraine syndromes of particular interest to the ophthalmologist; acephalgic, ocular, and ophthalmoplegic. Several current theories of migraine pathophysiology are discussed. Migrainous episodes are common and must be differentiated from neurologic dysfunction due to ischemia, inflammation, seizure, and compression. The differentiating characteristics of these conditions as well as a diagnostic algorithm are presented.
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PMID:Visual disturbances of migraine. 265 58

This paper summarizes what has been learned over the years about the role of eicosanoids in the pathogenesis of primary dysmenorrhea, endometriosis and menstrual migraine. The role of prostaglandins (PGs) in the pathogenesis of primary dysmenorrhea is inferred from four main observations: firstly, the clinical symptoms of primary dysmenorrhea are similar to those induced by the administration of PGF2 alpha and PGE2 for the induction of labour; secondly, the increased production of PGs by the endometrium during the luteal and menstrual phases of ovulatory cycles is consistent with the occurrence of primary dysmenorrhea mainly in ovulatory cycles; thirdly, the concentrations of PGF2 alpha and PGE2 in the endometrium and menstrual fluid of dysmenorrheic women are significantly higher than in controls; fourthly, certain PG inhibitors have been proved to be effective in the treatment of dysmenorrhea. The change in PG production can explain the major symptoms of primary dysmenorrhea, including the increased uterine contractility, uterine ischemia and the lowering of the pain threshold to chemical and physical stimuli in the pelvic nerve terminals. Moreover, recent experimental data suggest that leukotrienes (LTs) might be among the alternative pathogenetic causes of primary dysmenorrhea. The data which support a relationship between eicosanoids and endometriosis are as follows: endometriotic tissue produces PGs; the peritoneal fluid concentration of PGF2 alpha increases significantly after the induction of endometriosis in laboratory animals; the concentration of PGs in peritoneal fluid of some patients with endometriosis is greater than in controls and, finally, the number and activation of pelvic macrophages which are able to synthesize eicosanoids increase in patients with endometriosis. Possible roles for eicosanoids in the pathogenesis of infertility and secondary dysmenorrhea induced by endometriosis have been suggested. Eicosanoids are probably also involved in the pathogenesis of menstrual migraine. Different types of PGs might play a role both in the initial vasoconstriction during the prodromal phase of migraine and in the vasodilation and sensitization to pain typical of the pain phase.
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PMID:Eicosanoids in primary dysmenorrhea, endometriosis and menstrual migraine. 265 74


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