Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-seven diabetics with symptoms and clinical features suggestive of autonomic neuropathy were followed up for 33 months. Of the twenty with abnormal Valsalva or handgrip tests initially, ten (50%) died. There were no other features at presentation that differentiated those who subsequently died from those who survived. The causes of death were renal failure (six patients), cerebrovascular accident (two patients), hypoglycaemic coma (one patient), and "sudden death" (one patient). Of the survivors whose autonomic-function tests were repeated 18 months to 2 years later, five had new or worsening symptoms of autonomic neuropathy with corresponding deterioration of their autonomic-function tests; while two, with initially normal tests, had improved symptomatically. It is concluded that in diabetics with the clinical features of autonomic neuropathy simple autonomic-function tests give a good guide to prognosis, and that abnormal tests are associated with a high mortality.
 ...
PMID:Mortality in diabetic autonomic neuropathy. 5 89

Recent data suggest that brain damage in ischemia, hypoglycemia, and several other brain diseases is caused by excitotoxic mechanisms which are triggered by presynaptic release of glutamate and related excitatory amino acids, and which involve an abnormal postsynaptic influx of calcium into cells containing a high density of glutamate receptors. This contention is supported by results demonstrating reduction of infarct size in focal ischemia due to middle cerebral artery (MCA) occlusion, and amelioration of neuronal necrosis in hypoglycemic coma, by antagonist which block the NMDA type of glutamate receptor. These results underscore the pathogenetic role of calcium influx into energy-compromised cells since the NMDA receptor-linked ion channel has a high conductance to calcium. The issue has been clouded by the inability of NMDA antagonists to ameliorate brain damage due to cardiac arrest, or to forebrain ischemia in rats and gerbils. In these conditions, however, an AMPA receptor blocker (NBQX) has been found efficacious. These results demonstrate that the pathophysiology of ischemic lesions is different in the cardiac arrest type of ischemia and in lesions due to MCA occlusion, and demand an explanation of the differences in therapeutic response. Tentatively, the cardiac arrest type of ischemia is so dense that multiple calcium conductances are activated in the energy-deprived tissue, explaining why any drug which acts on only one of them (such as an NMDA antagonist) cannot prevent cellular calcium overload. Furthermore the ultimate brain damage, which is often conspicuously delayed, may be secondary to upregulation of synaptic efficacy, causing increased calcium cycling and calcium-related damage. In this situation, an AMPA receptor blocker may be efficacious because it blocks "fast" excitation and Na+ influx, an "upstream" event which causes "downstream" calcium influx via multiple pathways. In the perifocal ("penumbra") zone of a stroke lesion, the situation is different since depolarisation is initially moderate and/or intermittent. Furthermore, since ATP is still produced (albeit at a reduced rate) the problem is one of a disturbed pump/leak relationship. Then, blockade of a major calcium-carrying channel by NMDA receptor blockers, or of the trigger to depolarisation by an AMPA receptor antagonist, may improve the pump/leak relationship and carry cells in the penumbra over a critical period.
 ...
PMID:Neurocytotoxicity: pharmacological implications. 168 4

The experiments were designed to test the possibility that calcium influx into neurons via voltage sensitive calcium channels (VSCCs) contribute to brain damage in two conditions in which any amelioration of neuronal necrosis may be assumed not to occur through an improvement of blood flow, viz., hypoglycemic coma and brief transient ischemia. Hypoglycemic coma is thought to lead to neuronal necrosis by release of glutamate and cellular influx of calcium during the insult, while damage due to brief transient ischemia may, at least in part, result from increased calcium cycling across cell membranes in the postinsult period. The insults were delivered to anesthetized rats, and the localization and density of neuronal necrosis were evaluated by histopathology following 1 week of recovery. One dihydropyridine calcium antagonist (isradipine), given in doses which have been reported to ameliorate ischemic damage due to stroke, failed to reduce damage incurred by 30 min of hypoglycemic coma, or 15 min of transient forebrain ischemia. Provided that it can be assumed that isradipine in the doses employed reduced calcium influx via VSCCs, the results support the notion that calcium influx through VSCCs plays only a minor pathogenetic role in global/forebrain ischemia or in hypoglycemia, and they suggest that the effect of blockers of VSCCs in stroke, if any, is due to both blockade of VSCCs and increase in blood flow.
 ...
PMID:The effect of a dihydropyridine calcium antagonist (isradipine) on selective neuronal necrosis. 183 Aug 97

Fructose-1,6-diphosphate has been shown to improve neurologic recovery following resuscitation from cardiac arrest and to restore brain electrical activity during hypoglycemic coma in rabbits. In view of these findings, we determined whether fructose-1,6-diphosphate protects the brain during ischemia-hypoxia. We subjected 16 rabbits to hypotension, hypoxemia, and bilateral common carotid artery occlusion. Five minutes after the onset of isoelectric electroencephalograms, seven randomly selected rabbits received 10% fructose-1,6-diphosphate (350 mg/kg bolus followed by 10 mg/kg/min infusion for 90 minutes) and the remaining nine rabbits (controls) received an equal volume of 1.5% NaCl (3.5 ml/kg bolus followed by 0.1 ml/kg/min infusion for 90 minutes). After isoelectricity lasting 7.86 +/- 0.8 minutes (mean +/- SEM) in the treated group and 6.44 +/- 0.38 minutes in the control group, the rabbits were reinfused with autologous shed blood and reoxygenated and the carotid artery occluders were removed. Treated rabbits recovered electrical activity more rapidly than the controls (p less than 0.005), and all seven treated rabbits survived. Only two controls (22%) survived (p less than 0.001), and they were severely disabled. Histology showed extensive cortical necrosis and focal necrosis in the hippocampi and cerebellum of brains from the two surviving controls. Brains from two treated rabbits exhibited minimal neuronal loss limited to the neocortex, and the brains from the remaining five treated rabbits were normal. This study suggests that fructose-1,6-diphosphate protects the brain from ischemic-hypoxic insults.
Stroke 1990 Apr
PMID:Prevention of ischemic-hypoxic brain injury and death in rabbits with fructose-1,6-diphosphate. 232 42

Hypoglycemic hemiplegia may lead to a mistaken diagnosis of stroke, although the symptoms resolve with correction of the hypoglycemia. We report a 27-year-old white man with insulin-dependent diabetes who developed right hemispheric infarcts and left hemiplegia associated with hypoglycemic coma. This report discusses the possible role of hypoglycemia in causing the stroke.
J Stroke Cerebrovasc Dis
PMID:Hypoglycemic coma associated with brain infarcts. 1789 73

We present the case of a 69-year old man who was brought to the hospital after being found unconscious; last seen at baseline 9 hours prior. On admission he was found to be severely hypoglycemic and received prompt glucose administration, with no immediate neurological improvement. Stroke was suspected. A brain MRI revealed abnormal hyperintense signal involving the head and tail of the left hippocampus. After close neurological monitoring and supportive care in the ICU, his condition improved over time, leaving no residual focal deficits. This case highlights the presence of MRI changes in patients with severe hypoglycemia as it happens in hypoglycemic coma.
 ...
PMID:Magnetic resonance imaging changes in a 69-year old man with hypoglycemia induced brain injury: case report and literature review. 3122 19