Cerebral infarction in diabetics: patterns and predictors of hospital mortality

Ischemic cerebrovascular disease accounts for substantial proportion of all strokes. Diabetes mellitus is a well established known risk factor for ischemic stroke and this due to the pathophysiological changes affecting blood vessels during the course of the disease. However it's unclear whether stroke features, severity and prognosis differ in diabetic and non-diabetic patients. This work is aiming to study and compare prospectively the characters and patterns of ischemic stroke in both diabetic and non-diabetic patients, with evaluation and predication of causes of hospital mortality. This study included 380 patients presenting with acute ischemic stroke, 120 were diabetic and 260 were non-diabetic. All were subjected to the following: Detailed history taking, complete general and neurological examination, assessment of stroke severity using Glasgow Coma Scale [GCS] and Canadian Stroke Scale [CANS] and Modified Rankin Scale [MRS] was done on the first and tenth day of admission to evaluate functional outcome, laboratory investigations including glycosylated haemoglobin [HbA1C], fasting and postprandial blood sugar, lipid profile, complete blood count and computed tomography of the brain. Our results showed that: The age of our diabetic patients was younger than non diabetic. We found that, hypertension, myocardial infarction, transient ischemic attack, obesity and hyperlipidemia were common in our diabetic patients, while atrial fibrillation and smoking were common in non diabetic patients. There was positive correlation between admission glucose level and HbA1c level and clinical presentation by CANS and MRS. Dysarthria, pure motor, pure sensory and sphincteric disturbance were higher in diabetic group. The size of infarctions were more medium and small size [lacunar] in our diabetic patients. Occipital lobe and thalamic infarctions were significantly higher in our diabetic group, while frontal infarction were higher in non-diabetic group. Outcome using CANS and MRS was more worse in diabetics indicating increasing disability and mortality. Causes of deterioration were hemorrhagic transformation, infarct expansion and stroke recurrence. In our diabetic group infarct expansion and stroke recurrence were higher than non-diabetic one. Mortality was higher in non diabetic group. Causes of mortality varies between infection and cardiac diseases. Diabetes mellitus has a negative effect on cerebral ischemia regarding occurrence and recovery. Furthermore uncontrolled diabetic patients were highly susceptible for stroke recurrence indicating the toxic role of hyperglycemia in cerebral tissues and also affection on blood brain barrier promoting hemorrhagic transformation of cerebral infarction

Nerve glucose, fructose, sorbitol and myo-inositol in experimental diabetes

In a trial to investigate the biochemical changes associated with diabetic polyneuropathy, nerve contents of glucose, fructose, sorbitol and myoinositol were studied in 20 normal healthy rats versus 20 rats with alloxan-induced diabetes. There was significant increase in the nerve contents of glucose, fructose and sorbitol of diabetic animals as compared to controls. On the contrary, nerve myoinositol showed significant decline in diabetic rats. It appears that the accumulation of alcohol sugars leads to tissue swelling, thickening of basement membranes and reduction in the nerve conduction velocity of the affected diabetic nerves. Moreover, the decreased nerve myoinositol found in diabetic animals, could be an integral factor in the pathogenesis of diabetic neuropathy, since decreased nerve myoinositol inhibits series of biochemical events responsible for maintaining nerve excitability and conductivity