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

The possible role of displaced neurotransmitter acetylcholine (ACHh) in dysautoregulation was examined after experimental regional cerebral infarction was produced by occluding the middle cerebral artery (MCA) in babons. Regional cerebral blood flow (rCBF) was measured after intracarotid injection of 133Xenon using the gamma camera. Autoregulation was tested with metaraminol or angiotensin infusion and the autoregulation index (A.I.) was calculated. Acetylcholinesterase (ACHhE) was measured in brain tissue of noninfarcted and infarcted hemispheres. Cerebral arteriovenous (A-V) differences for cholinesterase (ChE) were also measured. Regional dysautoregulation was found in infarcted gray matter and correlated with increased AChE levels in the same zones of cortex and basal ganglia. The time course of onset of dysautoregulation correlated with increased ChE uptake by the brain. Intravenous infusion of the cholinergic neurotransmitter blocker, scopolamine, restored autoregulation to the ischemic zones. Autoregulation appears to be a myogenic reflex, influenced by neurogenic and metabolic mechanisms.
Stroke
PMID:Disordered cholinergic neurotransmission and dysautoregulation after acute cerebral infarction. 16 7

The fluorescence of reduced nicotinamide adenine dinucleotide (NADH) from cerebral cortex was measured before, during, and after middle cerebral artery (MCA) occlusion and then at death of the animal. In normal cortex, NADH remained constant throughout a wide range of variations in blood pressure and Paco2. In ischemic cortex, NADH levels were higher in hypovolemic hypotensive animals than in normotensive normovolemic animals. Neither hypercapnia nor hypocapnia was effective in decreasing NADH in regions of ischemia, but the latter was associated with a degree of hypotension that interfered with interpretation of data. NADH returned to normal with restoration of flow, supporting the reversibility of this degree of ischemia. The high levels of NADH at death, compared to those during ischemia, are consistent with incomplete ischemia in this model of cerebral infarction.
Stroke
PMID:Reduced nicotinamide adenine dinucleotide fluorescence and cortical blood flow in ischemic and nonischemic squirrel monkey cortex. 2. effects of alterations in arterial carbon dioxide tension, blood pressure, and blood volume. 16 73

Antecubital venous blood was sampled from stroke patients in the presence of disodium ethylenediamine tetraacetate. Plasma was analyzed for cyclic AMP applying a competitive protein binding method without any special pretreatment. In mild hemispheric infarction as manifested by moderate hemiparesis and/or dysarthria, plasma cyclic AMP remained in the normal range (8-18 picomoles/ml). In most of the cases with moderate infarction, the cyclic AMP level was distinctly below the normal range several days after the onset of symptoms. However, cyclic AMP remained in the normal range in severe infarction with signs of brain edema, and in two cases with moderately severe symptoms. One of the two cases suffered from later development of brain edema, and the other revealed a large lesion in brain scintigrams. The sizes of the lesion revealed in brain scintigrams were smaller in the moderate cases and larger in the severe cases, except in one of the cases mentioned above. It appeared that with plasma cyclic AMP levels we could predict the extent of the lesion, and perhaps the subsequent development of impending brain edema in a few days after the onset of cerebral infarction. In moderate cases of cerebral hemorrhage, judged from the consciousness, cyclic AMP decreased to a subnormal level 2-4 days after the onset. In severe cases it remained in the normal range. Subarachnoid hemorrhage showed significantly elevated cyclic AMP levels in the early stage.
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PMID:Venous plasma cyclic AMP in acute cerebrovascular disease. 18 49

The clinical and pathological features of 24 patients with cerebral emboli complicating 66% of our cases of nonbacterial thrombotic endocarditis (NBTE) associated with carcinoma are reviewed. Twelve patients were admitted for a cerebrovascular accident (CVA) while 4 patients developed a CVA during hospitalization. Transient ischemic attacks preceded the CVA in 3 patients. More often the CVA took the form of a single sudden accident. Cerebral infarcts however were generally multiple and hemorrhagic and varied in size and age. In 4 patients large softenings were directly responsible for death. 8.6% of cerebral embolisms were caused by NBTE and in 10 patients cerebral embolization was the first symptom of a carcinoma. The frequency of NBTE in ovarian carcinoma even in the absence of metastases may motivate a more aggressive approach towards unexplained cerebral embolism.
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PMID:Cerebral embolism in nonbacterial thrombotic endocarditis associated with carcinoma. A clinico-pathological study. 23 5

Adouble-blind trial of aspirin for the treatment of cerebral ischemia was begun in 1972 and continued for 37 months. This was accomplished despite difficulties in controlling a long-term study of a drug which has widespread availability and consumption. The study design, criteria for selection of patients, follow-up surveillance, and methods of data analysis are presented. We report only subjects without carotid surgery before randomization. Patients (178) who had carotid transient ischemic attacks (TIAs) were randomly allocated to aspirin or placebo and followed to determine the incidence of subsequent TIAs,death, cerebral infarction or retinal infarction. Analysis of the first six months of follow-up revealed a statistically significant differential in favar of aspirin when death or cerebral or retinal infarction and the occurrence of TIAs were grouped and considered together as end points. Significance in favor of aspirin treatment was mainly revealed in patients with a history of multiple TIAs and was most evident in those individuals having carotid lesions appropriate to the TIA symptoms. It cannot be inferred from this study that aspirin prevents stroke because when end points were restriced to death or cerebral or retinal infarction, there was no statistically significant differential between the aspirin and placebo treatments.
Stroke
PMID:Controlled trial of aspirin in cerebral ischemia. 32 36

Patients (125) who had carotid transient ischemic attacks (TIAs) and one or more accessible carotid lesions visualized angiographically had reconstructive operations of the carotid artery and were then randomly assigned to aspirin or placebo treatment. The were followed to determine the incidence of subsecquent TIAs, death, cerebral infarction, or retinal infarction. Life table analysis (for 24 months follow up) that eliminated deaths which were not stroke-related revealed a significant difference in favor of aspirin. Because of the small number of patients and the short period of follow up, these results should be interpreted only as consistent with those reported in the initial publication but not conclusive of an aspirin effect in preventing cerebral infarction.
Stroke
PMID:Controlled trial of aspirin in cerebral ischemia. Part II: surgical group. 35 98

The indications for anticoagulant treatment to prevent cerebral infarction or progression of cerebral infarction are now clear. The indications are: (1) Prevention of recurrent embolization from a cardiac source (long-term anticoaguland treatment). (2) Transient ischemic attacks (particularly vertebrobasilar system) if a surgically accessible causative lesion, polycythemia, and thrombocytosis are not present (anticoagulants for a few months.) (3) Progressing stroke in either systme assuming that the neurological defect is partial and CT scan shows no evidence of bleeding (anticoagulants for a few months.) (4) Rarely, completed stroke (long-term).
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PMID:Anticoagulant treatment to prevent cerebral infarction. 38 11

The intact omentum of 13 monkeys was lengthened, placed subcutaneously, and laid on the left cerebral hemisphere prior to occluding the left middle cerebral artery. Two of these 13 monkeys developed left cerebral infarct and a right hemiparesis. Nine other monkeys had their left middle cerebral artery occluded without omental protection. All of these 9 developed a left cerebral infarct and 8 of them a right hemiparesis. Intact omentum may prevent a cerebral infarction when placed on the brain prior to MCA occlusion.
Stroke
PMID:Prevention of cerebral infarction in the monkey by omental transposition to the brain. 41 30

The clinical course of 16 consecutive patients with stenosis of the middle cerebral artery angiographically diagnosed between 1970 and 1977 was reviewed. All were managed nonsurgically with medical treatment including anticoagulation. Prior to therapy, transient ischemic attacks had occurred in 15 and cerebral infarction in 11. Initially, none exhibited more than a minor neurological deficit. Follow-up from one month to six years showed a benign course in 14 patients: 13 experienced no subsequent transient attacks or new stroke; 1 had repeated transient attacks for two years but not in the following four years. Two of the 16 developed a severe stroke early in the course, before medical therapy was started. No distinctive clinical or radiographic features were identified that permitted prediction of the outcome. This small series supports the need for a randomized study of bypass efficacy in these patients.
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PMID:Symptomatic middle cerebral artery stenosis. 42 78

Cerebral infarction was produced in paralyzed, ventilated rats by a 30 min period of right common carotid artery occlusion combined with systemic hypoxia (Pao2 21-25 mm Hg). After 30 min the arterial clamp was removed and the animals were reoxygenated and allowed to survive for 1 min (6 animals), 30 min (12 animals), or 1 1/2 to 2 h (6 animals). The animals were reanesthetized and sacrificed by perfusion-fixation with paraformaldehyde-glutaraldehyde. Light and electron microscopy revealed ischemic cell change in neurons in the ipsilateral cerebral cortex, striatum and hippocampus. These changes were mild to moderate in the early post-ischemic period and severe in the post-ischemic period. Cerebral infarction was present in one of the 30 min survivors and in all of the 1 1/2 to 2 h survivors. Electron microscopy showed platelet thrombi in the infarcted brain in 3 of the 7 animals with infarcts, and in an area of very severe ischemic cell change in a fourth animal. They were not present in areas of brain showing only mild to moderate ischemic cell change. These findings showed that platelet thrombi form in association with cerebral infarcts and suggested that they are induced by tissue necrosis rather than by neuronal ischemic cell change alone.
Stroke
PMID:Platelet thrombi in experimental cerebral infarction. 44 42


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