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)

Eighteen patients with idiopathic optic neuropathy lacked symptoms and signs of cardiovascular and cerebrovascular disease, especially when compared to three groups of patients with sudden visual loss caused by retinal infarction, transient ischemia, and cerebral infarction. Many patients in the latter groups had hypertension, carotid bruits, heart disease, transient ischemic attack, and stroke. But among the patients with ischemic optic neuropathy, hypertension was the only evidence of cardiovascular disease, affecting 44% of the patients. We argue that, in many cases, ischemic optic neuropathy represents a direct and early complication of hypertension arterial disease affecting small arterioles supplying the anterior part of the optic nerve. The pathologic process may thus be similar or identical to lacunar infarction of the brain.
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PMID:Ischemic optic neuropathy as a possible early complication of vascular hypertension. 51 8

The clinical features of 102 cases with transient attacks due to cerebral ischemia were evaluated, and 94 out of 102 cases were followed for an average of 6 years. 1) The clinical study makes comparisons between two groups of patients grouped under the somewhat new definition of Reversible Ischemic Attacks (RIA): classical Transient Ischemic Attacks (TIA) and Stroke with Full Recovery (SFR), in which a complete recovery took place over a longer period, on the average 3 weeks. 2) SFR constitutes the 34.31% of the total cases with transient ischemic episodes. In the carotid district the onset was more frequently gradual in SFR than in TIA and aphasia more frequent in TIA than in SFR. Multiple attacks prevailed in TIA over the SFR group. The definition of transient attack due to ischemia is discussed. 3) Completed strokes occurred in 11 cases (11.7%) with RIA. Hypertension and cardiac disease were significantly frequent in cases with subsequent stroke. The conclusion was reached that TIA is a symptom, not a pathological state, and TIA should be considered an important symptom but not a specific harbinger of completed stroke.
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PMID:Clinical features and long-term follow-up of patients with reversible ischemic attacks (RIA). 69 35

During the past few years CT has emerged as an unsurpassed diagnostic modality in cerebrovascular disease. CT is of limited value in TIA, but reveals a wide variety of findings in completed infarcts. Ischemic, petechial, and hemorrhagic infarcts can be distinguished. Contrast enhancement, varying with the age of the infarct, is frequent. Also the general density of the infarct varies with time. Differential diagnosis, primarily infarct vs tumor, is made by angiography or by followup CT scans. Saccular aneurysms are directly demonstrable by CT if larger than 0.5 cm in diameter. Sequelae of ruptured aneurysm--hematoma, hydrocephalus, ischemia--are consistently visible. This generally also applies to arteriovenous malformations. Angiography is necessary to clarify anatomical details of aneurysms and vascular malformations, and is often indispensable for differential diagnosis.
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PMID:CT diagnosis of cerebrovascular disorders--a review. 71 88

In the elderly, a transient ischemic attack (TIA) and a hypersensitive carotid sinus reflex (HCSR) often co-exist and can pose a diagnostic challenge. Seven cases are presented. HCSR is a relative condition; besides increased irritability of the receptor or target organs, susceptibility of the nerve center to ischemia probably is induced by a slow heart rate or low blood pressure in any patient with pre-existing occlusive cerebrovascular disease. Dizziness and syncope of this type represent hemodynamic TIA in contrast to thromboembolic TIA. The carotid sinus massage test is recommended for differentiating the two types of TIA; the treatments differ. At present there is no uniform management that can be applied to either TIA or HCSR routinely. Therefore, treatment should be approached on an individual basis, keeping in mind the different pathophysiologic factors operating in the specific patient.
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PMID:The problem of dizziness and syncope in old age: transient ischemic attacks versus hypersensitive carotid sinus reflex. 124 91

Transient cerebral ischemia demonstrates an increase in activated oxygen species in the brain that could lead to eventual neuronal cell death. Neuronal cells respond to oxygen free radicals through the restructuring of the cytoskeleton and membranes, mobilization of calcium and gene expression which play a role in cell injury. Ten min of bilateral carotid artery occlusion resulted in a decrease in calcium/calmodulin dependent protein kinase II (CaM kinase II) phosphorylation and activity detected in the brain immediately following ischemia and was partially restored within 24 h of reperfusion. Pretreatment of animals with an anesthetic dose of pentobarbital (40 mg/kg) resulted in partial protection of inactivation of CaM kinase II following ischemia. CaM kinase II activity was maintained following pretreatment of animals with alpha-phenyl N-tert-butyl nitrone (PBN), which traps oxygen free radicals. Infusion of superoxide dismutase or catalase prior to ischemia, blocked CaM kinase II inactivation. Blockage of calcium uptake with bepridil resulted in a marked protection of CaM kinase II inactivation. In addition, trifluoperazine, a calmodulin antagonist also diminished the inhibition of CaM kinase II phosphorylation in our model. These results suggest that ischemia and reperfusion injury results in the generation of activated oxygen and the mobilization of calcium which inactivate CaM kinase II. These results indicate that changes associated with protein kinase activity in the brain following an ischemic insult may have profound effects upon neurodegeneration and neuronal survival.
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PMID:Role of calcium in inactivation of calcium/calmodulin dependent protein kinase II after cerebral ischemia. 133 39

Forty patients who fulfilled the DSM-III-R criteria for multi-infarct dementia and had a score of 7 points or more on Hachinski ischemia score (HIS) were analyzed with the purpose to correlate the rating scales and CT scans. Among the examined patients there were 32 women with the average age of 68.5 +/- 9.8 years and 8 men with the average age of 68.8 +/- 10.4 years. No significant difference between sex in relation to Folstein Mini-mental state examination (MMSE), Gottfries-Brane-Steen scale (GBS) and Sandoz clinical assessment-geriatric scale (SCAG) was found. There is no correlation of GBS and SCAG on MMSE. With regression analysis a good correlation was found between GBS and SCAG, and we suggest that in such studies only one of these two scales is sufficient. CT abnormalities were found in about 77% of examined patients without difference according to sex. But, GBS score demonstrated greater disability among MID patients with abnormal CT scans than in MID patients with normal CT scans. In medical history of male MID patients completed stroke was significantly more common than among women, while the female MID patients had in their history significantly more frequent transient ischemic attack (TIA). This finding should be checked in a greater patient population. It is stressed that in everyday clinical practice it is necessary to use the diagnosis of multi-infarct dementia, e.g. to differentiate cerebral diseases according to etiology and pathogenesis.
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PMID:Rating scales and computed tomography in multi-infarct dementia. 146 3

Antiphospholipid antibodies are a marker for an increased risk of thrombosis, including stroke and transient ischemic attacks. Prior studies suggest that patients with these antibodies and thrombosis may be at increased risk for recurrent thrombotic events. We prospectively evaluated 75 patients with antiphospholipid antibodies and cerebral or ocular ischemia for recurrence of thrombosis. Twenty-six patients (35%) experienced a recurrent stroke or transient ischemic attack, with a mean time to recurrence of 1.18 years. Hypertension significantly increased the risk of a recurrent transient ischemic attack. Patients with coronary artery disease were three times as likely as those without to have a recurrent stroke or transient ischemic attack. There was a trend for treatment with a combination of aspirin and dipyridamole to reduce the risk of recurrent thrombotic events after adjusting for sex and ethnicity.
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PMID:Risk of recurrent thromboembolic events in patients with focal cerebral ischemia and antiphospholipid antibodies. The Antiphospholipid Antibodies in Stroke Study Group. 156 71

1. We investigated the alterations in binding sites of three major second messengers, phorbol 12,13-dibutyrate, inositol 1,4,5-trisphosphate and forskolin following transient cerebral ischemia in gerbils, and examined the effects of a novel vinca alkaloid derivative, vinconate against the alterations in the binding of the second messengers following ischemia. 2. Transient cerebral ischemia produced by bilateral occlusion of the common carotid arteries was induced for 10 min, and intraperitoneal administration of vinconate (100 mg/kg and 300 mg/kg) was given 10 min before ischemia. 3. Morphological study indicated that transient ischemia can produce severe neuronal damage in striatum, hippocampal CA1 sector and hippocampal CA3 sector. 4. Transient cerebral ischemia caused the postischemic alterations in the binding of three second messengers. 5. The postischemic alterations in the binding of second messengers were ameliorated by pretreatment with vinconate. This effect was especially observed in the striatum which was most vulnerable to ischemia. 6. These findings are discussed in relation to the mechanism of ischemic neuronal damage.
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PMID:Protective effect of a novel vinca alkaloid derivative, vinconate, against alterations in binding sites of second messengers after transient cerebral ischemia in gerbils. 159 19

Sixty-seven patients who underwent carotid-subclavian bypass (CSBP) (28 CSBPs only and eight with carotid endarterectomy) or axilloaxillary artery bypass (n = 31) with polytetrafluoroethylene grafts were followed up for a mean of 69.2 and 71.9 months, respectively. Indications for surgery in the CSBP group included hemispheric transient ischemic attack (TIA)/cerebrovascular accident in five, nonhemispheric TIA in seven, upper extremity ischemia in 15, and combined TIA and arm ischemia in nine patients. In the axilloaxillary artery group, two patients had hemispheric TIA, five had nonhemispheric TIA, 12 had upper extremity ischemia, and 12 had combined TIA and arm ischemia. Graft patency was determined clinically and confirmed by segmental Doppler pressures, duplex ultrasonography, or angiography. The 30-day mortality rate was approximately 3% in both groups. The 30-day complication rate was 3% for the axilloaxillary artery group and 8% for the CSBP group (not statistically significant). Relief of symptoms was achieved in 100% of patients in both groups; however, 20% of the patients in the axilloaxillary artery group had a recurrence of symptoms, in contrast to 5.6% in the CSBP group. The cumulative 10-year primary and secondary patency rates, calculated by life-table analysis, were 66% and 84.6% for the axilloaxillary artery procedures and 93.8% and 93.8% for the CSBP procedures, respectively (statistically significant). Concomitant carotid endarterectomy with CSBP did not influence graft patency. In conclusion, both bypasses have comparable morbidity and mortality rates; however, the CSBP has a statistically significantly better primary patency rate than the axilloaxillary artery bypass. Therefore CSBP should be the procedure of choice and the axilloaxillary artery bypass should be restricted to high-risk patients.
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PMID:Brachiocephalic revascularization: a comparison between carotid-subclavian artery bypass and axilloaxillary artery bypass. 823 26

To evaluate possible involvement of phospholipid metabolism and related second messenger systems in the selective neuronal damage after ischemia, we measured changes of polyphosphoinositides (PPIs) and free fatty acids (FFAs) in a model of 5-min or 10-min ischemia and reperfusion in gerbils. The binding activity of 3H-phorbol 12,13-dibutyrate (PDBu) for protein kinase C (PKC) and 3H-inositol 1,4,5-triphosphate (IP3) for IP3 receptors was demonstrated autoradiographically. Induction of 70 KDa heat shock protein (HSP70) mRNA and amyloid precursor protein (APP) mRNA was also examined using Northern blot analysis. In the parietal cortex (an area resistant to transient ischemia), PPIs decreased during ischemia and recovered rapidly after reperfusion. However, recovery did not occur in the hippocampal CA1 area (an area more vulnerable to transient ischemia). In the cortex, arachidonic acid (AA) increased during ischemia and returned to baseline by 7 days after reperfusion; in the CA1 area, the AA level remained elevated even after 7 days of reperfusion. PDBu binding decreased in CA1 cells after 2 days of reperfusion. IP3 binding began to decrease at 5 hr of reperfusion, which is far earlier than either the onset of decreased PDBu binding or the observation of neuronal damage by light microscopy. The induction of HSP70 mRNA occurred, but the induction of APP mRNA did not. Regional differences in the induction of HSP70 mRNA were found; CA1 cells produced less HSP70 mRNA than cortical cells 8 hr after transient ischemia. These results suggest that CA1 cell membranes may not recover after transient ischemic attack, and that the membranes of the endoplasmic reticulum, which have IP3 receptors, may undergo alterations earlier than cytoplasmic membranes. The variable induction of HSP70 mRNA may be related to regional differences in vulnerability in cortical and hippocampal CA1 cells after transient ischemia. Involvement of excitatory neurotransmission in the induction of HSP70 has been suggested. The combined data may support a role for inositol phospholipid metabolism, changes in related second messenger systems, and induction of HSP70 in the excitotoxic mechanism of hippocampal CA1 neuronal damage, death, and repair.
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PMID:Phospholipid metabolism and second messenger system after brain ischemia. 163 89


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