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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While the prevention of acute metabolic decompensation is no longer a serious problem in treating patients with non-insulin-dependent diabetes mellitus (NIDDM), target organ complications can have serious consequences, including blindness, renal failure, neuropathy, amputation, coronary artery disease, and stroke. The bulk of current evidence suggests that these complications can be minimized or perhaps even avoided by carefully monitoring and controlling the patient's blood glucose levels. Although criteria and standards of control differ widely in various centers, in general acceptable-to-good control in the NIDDM patient would consist of average fasting blood glucose (FBG) levels of less than 140 mg/dL and peak postprandial glucoses of less than 220 to 250 mg/dL. Treatment aimed at attaining these blood glucose levels should begin with dietary management and exercise prescription. General health measurements such as control of blood pressure and avoidance of smoking are especially important in the diabetic patient. When these approaches prove ineffectual, the addition of an oral hypoglycemic agent, preferably a second-generation sulfonylurea is indicated. Glipizide and glyburide are both excellent drug choices, although glyburide may cause hypoglycemia in older patients due to its longer half-life and especially in those with renal insufficiency because of accumulation of biologically active metabolites. In certain well-selected cases, the addition of insulin to oral sulfonylurea therapy may offer improved results over the use of either therapeutic modality alone. The advent of self blood glucose monitoring and periodic glycohemoglobin assessments, now well established in diabetic management, represents a major step forward in the endeavor to optimize standards of blood glucose control in the diabetic population.
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PMID:Monitoring and controlling the patient with non-insulin-dependent diabetes mellitus. 354 18

We report the clinical and autopsy findings in a young man of 18 with a chronic progressive disorder comprised of lactic acidosis, mental deterioration, and epileptic seizures which were sometimes accompanied by stroke-like episodes with transient hemiparesis and cortical blindness. He died of congestive heart failure. The autopsy showed lesions of the gray matter of the brain. Both the putamen and parieto-occipital cortex showed loss of neurons and proliferation of macrophages, astrocytes and vessels. There was marked loss of neurons in the inferior olives, and slight reduction of the number of Purkinje cells. Skeletal muscle studies revealed ragged-red fibers and structurally abnormal mitochondria. The heart was enlarged: accumulations of mitochondria occurred in the muscle fibers. The liver exhibited marked fatty degeneration. Biochemical analyses showed normal activities of pyruvate dehydrogenase in thrombocytes, pyruvate carboxylase in lymphocytes, biotinidase in serum as well as succinate dehydrogenase and cytochrome c oxidase. The features of this disorder differ in many respects from cases of mitochondrial encephalomyopathy previously reported and cannot be assigned to any specific disease entity.
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PMID:Mitochondrial encephalomyopathy. A variant with heart failure and liver steatosis. 367 21

Three (0.5%) of 612 patients with an acute ischemic stroke in the carotid territory also had ipsilateral optic nerve infarction. They had unilateral or bilateral internal carotid artery occlusion and reversed flow in the ophthalmic artery. Hemodynamic infarction was suggested by triggering by a drop in blood pressure, decreased ophthalmic artery flow and perfusion pressure, and cerebral infarction in a watershed area. The "optico-cerebral syndrome" suggests internal carotid artery occlusion with hemodynamic disturbances. In carotid disease, monocular blindness may be due to an optic nerve lesion sparing the retina.
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PMID:Optico-cerebral syndrome: simultaneous hemodynamic infarction of optic nerve and brain. 380 6

We examined 15 patients with cortical blindness, reviewed the records of 10 others, and compared these 25 patients to those in previous studies of cortical blindness. Although cerebrovascular disease was the most common cause in our series, surgery, particularly cardiac surgery, and cerebral angiography were also major causes. Only 3 patients denied their blindness, although 4 others were unaware of their visual loss. Electroencephalograms (EEGs) were performed during the period of blindness in 20 patients and all recordings were abnormal, with absent alpha rhythm. Visual evoked potentials recorded during blindness were abnormal in 15 of 19 patients, but did not correlate with the severity of visual loss or with outcome. Bioccipital lucencies were found in computed tomographic (CT) scans of 14 patients; none of the 14 regained good vision. Recovery of vision was poor in all 8 patients who had a spontaneous stroke, but fair or good in 11 of the other 17 patients. Prognosis was best in patients under the age of 40 years, in those without a history of hypertension or diabetes mellitus, and in those without associated cognitive, language, or memory impairments. We conclude that the prognosis in cortical blindness is poor when caused by stroke; EEGs are more useful than visual evoked potentials for diagnosis; and bioccipital abnormalities shown on CT scan are associated with a poor prognosis.
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PMID:Cortical blindness: etiology, diagnosis, and prognosis. 382 23

Studies suggesting that transplantation is better than dialysis for diabetic patients with renal failure may be biased by the more favorable pretreatment prognosis of transplanted patients. Therefore, to provide a fairer comparison we controlled for pretreatment clinical state, categorized treatment received, and assessed mortality, major morbid events, and hospitalization in 51 diabetic patients who began therapy between 1970 and 1980. Fourteen patients were treated by transplantation and 37 by dialysis. The mean waiting period for transplantation was 5 months. The average age of transplanted patients was 40.9 years and of dialyzed patients 59.6 years. When we controlled for this age disparity and other factors (duration of diabetes and heart failure) that affect prognosis in end-stage renal disease (ESRD), the mortality with both transplantation and dialysis was similar to that expected from the overall mortality rate of the 51 study patients. Treatment received had no effect on mortality; the observed deaths compared with deaths expected from pretreatment status were 8 and 7.3 for transplantation and 30 and 30.7 for dialysis. We also compared major morbid events (blindness, amputation, stroke, severe heart failure, and myocardial infarction) and hospitalization in transplanted patients with the 24 dialyzed patients who survived long enough (5 months) to be eligible for transplantation. The number of major morbid events was 2.7 per 10 patient-years in the transplanted group and 3.4 in the dialyzed group. Hospitalization was 151.3 d/yr in transplanted patients and 55.6 d/yr in dialyzed patients (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transplantation versus dialysis in diabetic patients with renal failure. 388 35

Cardiopulmonary arrest is a test of the brain's tolerance to global ischemia. New insights into the pathophysiology of global ischemia have led to the potential use of early prophylactic anticonvulsants, hypothermia, barbiturate coma, glucose manipulations, calcium-blocking agents, and hemodilution. A wide spectrum of neurologic sequelae may follow global ischemia, ranging from brain death, vegetative states, and impairment of higher intellectual function to syndromes of amnesia and cortical blindness, post-anoxic myoclonus, delayed leukoencephalopathy, and spinal stroke. The distinctive features of these sequelae and their pathophysiologic aspects are discussed. Special attention is given to brain death and prognostication.
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PMID:Cardiopulmonary arrest. Pathophysiology and neurologic complications. 390 62

Venous stasis retinopathy and ischemic oculopathy are ocular manifestations of ischemia in the distribution of the carotid artery. While not as common as transient monocular blindness or retinal arterial emboli, they are readily recognizable and indicate the presence of severe, often bilateral, carotid occlusive disease. Patterns of occlusion vary but usually include complete occlusion of at least one common or internal carotid artery, often accompanied by occlusion or narrowing in the opposite carotid system. The ocular findings in venous stasis retinopathy and ischemic oculopathy indicate ongoing ocular ischemia and may progress to intractable neovascular glaucoma. Therapy, individualized for the specific pattern of occlusive changes, may be directed toward prevention of stroke or may be indicated primarily for the reversal of ocular ischemia and prevention of blindness secondary to neovascular glaucoma.
Stroke
PMID:Chronic ocular ischemia and carotid vascular disease. 402 85

Although carotid endarterectomy (CE) is recommended in appropriate patients with bifurcation atheroma for the prevention of stroke, these patients are also at risk for visual loss, either temporary or permanent. The presentations of patients undergoing 512 consecutive CEs were reviewed to determine the preoperative frequency and risks of ocular disturbances. Visual symptoms occurred in 131 patients (25%). Temporary, monocular blindness (amaurosis fugax, AF) was reported by 99 patients (19%). Concomitant neurologic symptoms were present in 33 (33%) of the patients with AF, and carotid artery stenoses of greater than 75% diameter were documented in 82 (83%) of these patients. No visual deficits were observed following operation. Permanent visual loss ranging from scotoma to complete blindness was documented in 32 patients (6.2%). The permanent deficits were due to retinal artery occlusions (RAO) in 20 patients (4%), ischemic optic neuropathy (ION) in eight patients (1.5%), and homonymous hemianopsia (HH) in four patients (0.7%). Visual loss occurred without any warning in 27 of these 32 cases (84%). The five cases with warning had multiple episodes of AF and then sustained RAO and blindness. Neurologic symptoms occurred concomitantly but not prior to visual symptoms in 7 of the 12 patients (58%) with ION and HH. Stenoses greater than 75% were present in 22 of 32 cases (69%) and in every case of ION. Operation had no effect on the visual deficit. Permanent visual loss occurred in a significant number of patients with carotid atheroma (6.2%). Warning in the form of visual prodroma is uncommon in these patients (16%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ocular manifestations of carotid artery atheroma. 405 43

Eight weeks following streptozotocin-induced diabetes mellitus in rats, the sensitivity of adenylate cyclase to dopamine (DA) and norepinephrine (NE) was reduced in homogenates of retina. Furthermore, the activation of adenylate cyclase in cerebral microvessels (capillaries) by NE, 5'-guanylyl imidodiphosphate (alone or with NE) and forskolin was reduced in diabetic rats versus appropriate controls. In diabetic rats enzyme sensitivity to only NE was attenuated in homogenates of cerebral cortex and cortical piaarachnoid. No differences between controls and diabetics were noted with respect to guanylate cyclase or cyclic AMP phosphodiesterases. The damage observed in retina and microvessels may play an important pathogenic role in diabetes-induced blindness and stroke.
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PMID:Streptozotocin-induced diabetes produces alterations in adenylate cyclase in rat cerebrum, cerebral microvessels and retina. 613 68

A previously healthy young woman presented with sudden onset of quadriplegia, anesthesia below the C3 dermatome, respiratory paralysis, vertical nystagmus, ocular bobbing and cortical blindness. After partial resolution of the latter deficits, she remained quadriplegic, with a C3 level of anesthesia, and in respiratory paralysis until death from complications of a fulminant pulmonary infection. Autopsy disclosed bilateral infarctions of the medial aspect of the medulla and the upper cervical cord, in the distribution of the anterior spinal artery. Multiple sites of arterial occlusion by fibrocartilaginous material were found in branches of the anterior spinal artery, in correspondence with the sites of infarction. A review of the literature disclosed only 2 examples of medial medullary syndrome from embolism to the anterior spinal artery.
Stroke
PMID:Medial medullary infarction from fibrocartilaginous embolism to the anterior spinal artery. 665 10


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