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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated 36 patients with cerebral ischemia and mitral valve prolapse and compared them with 36 age-matched controls with cerebral ischemia who had similar attributes but who did not have mitral valve prolapse. Stepwise logistic regression analysis revealed an inverse relation between cerebral ischemia in the presence of mitral valve prolapse and hypertension, diabetes mellitus, occlusive cerebrovascular disease, and completed stroke at p less than 0.01. We also found, by correlation analysis, a negative correlation between both hypertension and diabetes mellitus versus mitral valve prolapse at p less than 0.05. Overall, 10 study patients compared with two control patients had no risk factors for cerebrovascular disease detected (chi 2 = 4.9, p less than 0.05). These data indicate that the association of mitral valve prolapse and cerebral ischemia is of special importance in patients who do not have other detected risk factors for cerebrovascular disease.
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PMID:Cerebral ischemia and mitral valve prolapse: case-control study of associated factors. 336 72

We studied the ability of serum glucose concentration and neurologic deficits at admission in predicting the outcome of acute cerebral ischemia in 65 patients given naloxone. Among our patients, the volume of infarction on computed tomograms and outcome were strongly related to the severity of neurologic deficits found at admission. Neither a history of diabetes nor hyperglycemia when added to the results of the initial neurologic assessment improved prediction of outcome after acute cerebral infarction.
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PMID:Comparison of admission serum glucose concentration with neurologic outcome in acute cerebral infarction. A study in patients given naloxone. 336 74

The impact of diabetes was prospectively studied during a 5-year period in 428 unselected and consecutive patients with acute cerebrovascular disease of whom 18% were diabetic. Cerebral infarction was more frequent in diabetics (81 vs 70%, p less than 0.02) whereas transient cerebral ischaemia was less frequent (4 vs 14%, p less than 0.01). Case fatality rate during hospitalization was higher in the diabetic than in the non-diabetic patients (28 vs 15%, p less than 0.02). Patients who died during hospitalization, diabetic as well as non-diabetic, had significantly higher blood glucose concentrations on admission compared with patients who survived. Hematocrit values were higher in the diabetic than in the non-diabetic patients (p less than 0.02). Diabetics had higher systolic blood pressure levels than the non-diabetics in the acute phase (p less than 0.005). The diabetic stroke patients more often had a history of hypertension, atrial fibrillation, heart failure and angina pectoris than non-diabetics stroke patients and diabetic control patients without stroke. Stroke patients, not known to be diabetic, had larger mean oral glucose tolerance test curve areas when compared with healthy controls but not when compared with hospitalized controls. We propose that diabetes increases the risk for stroke through other concurrent risk factors, cardiac disorders in particular.
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PMID:Clinical characteristics in diabetic stroke patients. 339 27

This study examined the hypothesis that diabetes mellitus predisposes the brain to irreversible ischaemic damage rather than to reversible transient ischaemic attacks. Of 525 patients presenting with transient or minor strokes, 54 patients were found to have diabetes mellitus and 471 patients had no evidence of diabetes. The diabetic subgroup was significantly more hypertensive than the non-diabetic subgroup (P less than 0.001). In an overall comparison of the prevalence of strokes and transient ischaemic attacks in diabetic and non-diabetic subgroups, 26 (6.7%) of 388 patients with transient ischaemic attacks had diabetes mellitus, and 362 (93.3%) of 388 patients with transient ischaemic attacks were non-diabetic. Thus diabetes was not a significant risk factor for TIAs (P less than 0.001). However when the role of diabetes in causing strokes was assessed in all 525 patients evaluated in the study, 28 of 54 diabetics presented with strokes whereas 109 of 471 non-diabetics presented with strokes. Statistically diabetics were 3-4 times more likely to present with a stroke than non-diabetics (P less than 0.0001) in keeping with the findings in other centres. The findings of this study appear to support the hypothesis that diabetics are at a greater risk of permanent cerebral ischaemia without prior warning of a transient ischaemic event than their non-diabetic counterparts. It may be advisable to screen asymptomatic diabetic patients aggressively and to consider these patients as a high risk subgroup for potential stroke if extracranial carotid vascular disease is present.
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PMID:Diabetes as risk factor for transient ischaemic attacks as opposed to strokes. 345 57

The occurrence of cerebrovascular diseases under the age of 50 years has been analyzed. It has been found that 230 cases of cerebrovascular diseases have been established between 1970 and 1976 in the 7th district of Budapest. With reference to clinical forms transitory cerebral ischemia and thrombosis of the cerebral arteries showed highest frequency. Risk factors were compared to those in patients over the age of 50 years. The matched pair analysis was used to determine relative risk and objective real circumstances. In this analysis the McNemar test was found positive in numerous cases. Based on the results the multifactorial origin was considered responsible of arteriosclerosis, hypertension, heart disease, diabetes mellitus, alcohol consumption, and smoking being the most important factors.
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PMID:[Cerebrovascular diseases in patients under 50 years of age]. 350 May 50

Focal cerebral ischemia was induced by occlusion of the right middle cerebral artery in hypoglycemic, normoglycemic, as well as in acute and chronic diabetic rats. The brain damage was studied after 4 days. The volume of infarction was decreased in hypoglycemia (29 +/- 19 mm3 (mean +/- SD) versus 58 +/- 35 mm3, P less than 0.0046), unaltered in acute diabetes (61 +/- 45 mm3), and increased in chronic diabetes (91 +/- 22 mm3, P less than 0.0463). The cortex adjacent to the infarct showed selective neuronal injury affecting the cortical layers 2 and 3. The damage was enhanced by hypoglycemia and prevented in most of the diabetic animals. The findings indicate that different mechanisms cause infarction and selective neuronal injury outside infarcts, but that both are influenced by the plasma glucose concentration.
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PMID:Focal ischemia of the rat brain, with special reference to the influence of plasma glucose concentration. 360 80

Characteristics, and the occurrence of other diseases, and complications related to diabetes mellitus of 91 consecutive diabetic patients who underwent vitreous surgery in 1979-1985 were examined. The mean age of the patients was 40 years (median 37, range 19-74), and the mean duration of diabetes 23 years (range 5-44). All, but one, had insulin therapy. Abnormalities in the cardiovascular and/or renal function were found in 89 of the 91 patients (98%). Signs of cardiovascular disease were observed in 58 patients (64%): 42% had elevated blood pressure (greater than or equal to 150/100 mmHg), 46% were on antihypertensive therapy, 14% had a history or signs of ischaemic heart disease, 12% had been digitalized, 7% had a history of cerebral ischaemia, and 8% had had surgery for gangrene of the lower limb. Signs of nephropathy were recorded in 64 patients (70%); 6 of them were on dialysis therapy, and two had received a kidney transplant. Symptoms possibly related to autonomic neuropathy e.g. postural hypotension, urinary tract symptoms, and gastric discomfort were found in 27%. Nine patients (10%) had some kind of thyroid disease, and two of them signs of multiple autoimmune endocrinopathy. The percentage surviving decreased from 96% at one year to 80% after 5 years of follow-up.
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PMID:Characteristics and survival of diabetic patients undergoing vitreous surgery. 360 10

Dichloroacetate (DCA) is known to prevent the phosphorylation of the pyruvate dehydrogenase complex (PDHC) by blocking the action of PDH kinase. This action allows the active PDHC to exert its effect on the metabolism of glucose, lactate and alanine to acetyl CoA. DCA has been shown to reduce serum lactate levels in humans and animals in such conditions as diabetes, phenformin-induced hepatic failure, exercise, and endotoxin-induced shock. Lactic acidosis in the brain has often been postulated as a cause of neuronal damage following ischemia and hypoxia. Therefore, we examined the effect of intravenously administered DCA (100 mg/kg) in rats that were rendered hyperglycemic by intravenous glucose (2 g/kg), and then made to undergo 15 minutes of incomplete cerebral ischemia by bilateral carotid ligation and systemic hypotension (mean arterial pressure of 50 mm Hg). DCA significantly reduced serum lactate levels pre-ischemia, but had no effect on serum lactate levels after ischemia induction. Brain levels of lactate, ATP and PCr after 15 minutes of incomplete ischemia were unaffected by DCA. We conclude that in this in-vivo model the control of PDHC activity in the brain may be different than that in the periphery, and that DCA was not effective in reducing brain tissue lactate levels.
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PMID:The effect of dichloroacetate on brain lactate levels following incomplete ischemia in the hyperglycemic rat. 371 55

The literature points out the meaning of risk factors causing stroke as well as their therapy or elimination as an effective prevention of cerebrovascular disease. Hypertension increases the risk of apoplexy by 4-fold, with regard to the diastolic values of blood pressure by the 5-fold up to the 10-fold. Consistent hypertension therapy decreases significantly the incidence of cerebral apoplectic attacks. Manifested diabetes mellitus and even reduced glucose tolerance raise the risk of stroke by the 3-fold, even though factors frequently associated with diabetes are taken into consideration. Hyperlipidemia, hypercholesteremia, and hypertriglyceridemia stipulate an increase of stroke incidence by the 2-fold to the 3-fold. Morbidity rate rises if these abnormalities coincide with further risk factors, up to the 6-fold. Nicotine consumption alone increases the risk of cerebral apoplectic attacks in relation to age, by the 3-fold up to the 5-fold. In combination with the use of hormonal contraceptive drugs, the risk of morbidity rate in women rises to the 7-fold. Overweight of more than 30% aggravates twice the risk of stroke. Heart diseases of different kind increase the risk of apoplectic attacks by the 2-fold, in combination with hypertension by the 5-fold. The intake of oral contraceptives (OCs) causes an increase of cerebral thromboembolic attacks by the 3-fold up to the 5-fold, whereby a relation to estrogen content and to hemorheology disturbances is proven. Blood coagulation disturbances, especially hypercoagulability with increase of blood level of fibrinogen, fibrin, and enhanced adhesiveness of thrombocytes in cerebrovascular disease are proven to be valid. By combination of various risk factors apoplexy risk is additionally increased. The possibility of surgical and neurosurgical prophylactic treatment in all stages of cerebral ischemia, caused by occlusive disease of the cartoid, vertebral, and intracranial arteries, exists in 75% of patients. With regard to the longterm results of patients with extraintracranial bypass surgery, due to stenosis or occlusion of the carotid artery in its high cervical or intracranial course, or of the middle cerebral artery, the operated group clearly was better than the nonoperated group in frequency of cerebral ischemia recurrence. The therapeutic effect of inhibitors of thrombocytic aggregates and of anticoagulants for the chemotherapeutic prevention of cerebral ischemia, is proven for acetylsalicylic acid and derivatives of coumarin. Both diminish significantly the rate of cerebral ischemia when compared with placebo-treated control groups.
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PMID:[Prevention of cerebrovascular circulatory disorders]. 404 14

Prospective longitudinal cerebral blood flow values were serially plotted over a four-year interval against the course of cerebral ischemia before, during, and after onset of clinical symptoms. Of 161 normal subjects (mean age, 62 years), 86 were risk free and 75 had hypertension, heart disease, diabetes mellitus, and/or hyperlipidemia. Twenty-one subjects developed cerebrovascular symptoms during the prospective trial. Mean hemispheric cerebral blood flow values were significantly lower for at risk than for risk-free subjects. Symptomatic subjects showed lower values than those in either of the two asymptomatic groups at every session. Statistical analysis of cerebral blood flow values for symptomatic patients compared one and two years prior to onset of symptoms, at the onset of symptoms, and 1 year later showed reductions compared to asymptomatic risk-factored subjects tested in a similar prospective manner. Measurable declines in cerebral perfusion accompany development and progression of aortocerebral atherosclerosis prior to clinical appearance of signs and symptoms of cerebrovascular disease. If confirmed, these observations should permit the institution of preventive medical and/or surgical interventive measures and an evaluation of their outcome.
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PMID:Progressive cerebral ischemia antedates cerebrovascular symptoms by two years. 648 37


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