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

We evaluated 14 patients with acute cardiogenic embolism who underwent open heart surgery soon after the onset to determine the cerebral and cardiac factors that influence neurologic outcome. The mean interval from onset of cerebral embolism to surgery was 5.3 (range 1-16) days. Five of the 14 patients had vegetations from infective endocarditis (including prosthetic valve endocarditis) as embolic sources, eight had intracardiac thrombi, and one had atrial myxoma. The diagnosed site of infarction before surgery was based on computed tomographic and/or angiographic findings. Of the 14 patients, four had infarcts due to major artery occlusion, seven due to cortical branch occlusion, and two due to perforating artery occlusion; one patient presented with a transient ischemic attack without computed tomographic abnormalities. Ten patients (71%) showed no clinical aggravation after open heart surgery; however, two patients died of massive cerebral hemorrhage, one died of deterioration of brain edema, and another became comatose from midbrain hemorrhage immediately after surgery. The four patients with clinical aggravation comprised three with septic embolism and one with aseptic occlusion of a major artery. From these results, infective endocarditis and a large infarct appear to be possible aggravating factors when patients with recent cerebral embolism undergo open heart surgery.
Stroke 1989 Oct
PMID:Brain damage after open heart surgery in patients with acute cardioembolic stroke. 279 61

A case of heat stroke is described in which the patient presented comatose with a rectal temperature exceeding 42.5 degrees C. Standard external evaporative cooling and iced gastric lavage failed to alter his temperature or mental status. Iced peritoneal lavage brought about a decrease in rectal temperature to 39.4 degrees C and significant improvement in mental status. The patient recovered uneventfully. Techniques of rapid cooling are discussed.
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PMID:The golden hour in heat stroke: use of iced peritoneal lavage. 280 56

Evidence has steadily accumulated to indicate that the rapid fluctuations in cyclic nucleotides during primary and secondary stroke are more than epiphenomena of the disease. During acute phases of ischemia, anoxia or hypoxia cyclic AMP rapidly accumulates in cerebral tissue, cerebrospinal fluid (CSF) and venous plasma, while cyclic GMP either remains unchanged or declines. The massive release of transmitters (catecholamines and adenosine) or ionic fluxes (Na+ and K+) may account for these observations. If reflow is established through a previously occluded vessel cyclic AMP content rises even higher in conjunction with a sharp rise in cyclic GMP. It is during this reflow period subsequent to longer term stroke (30-60 min) that the synaptic membrane enzyme, adenylate cyclase, is especially vulnerable. Presumably the cause of injury to cell membrane systems results from excess lactic acid accumulation and/or Ca++ entry through the damaged blood-brain barrier. The latter initiates breakdown of membrane phospholipids with resultant synthesis of vasoactive prostaglandins and formation of free radicals causing further insult to membrane phospholipids. Thus drugs acting to inhibit formation of prostaglandins, scavenge free radicals, reduce lactate formation, inhibit Ca++ entry or stabilize cell membranes have been shown to possess varying degrees of protective action toward adenylate cyclase. Moreover, cyclic AMP has been found to reverse stroke-induced vasospasm in central vessels. Reduced cyclic AMP content in CSF has been used to monitor the severity of coma, whereas clinical improvement was associated with predictable increases in the cyclic nucleotide. Therefore, cyclic nucleotides and related membrane enzyme systems might be used as target molecules in which to develop future therapeutic strategies for prevention or treatment of stroke.
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PMID:Cyclic nucleotides in stroke and related cerebrovascular disorders. 286 May 49

The clinical-angiologic data and the clinical outcome in 66 patients with acute vertebro-basilar thrombosis treated with antiplatelet agents, anticoagulants, or fibrinolytic agents are presented. Forty-three patients were treated with local intraarterial infusion of streptokinase or urokinase proximal to the thrombotic occlusion; 14 patients in this group (33%) survived, only one of whom was in deep coma when therapy was started. Twenty-three patients did not receive fibrinolytic therapy; 4 of these patients (17%) who exhibited mild brainstem-related symptoms survived. This study implies that early diagnosis and treatment in vertebrobasilar stroke in progression may achieve improved survival.
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PMID:Acute vertebral-basilar thrombosis. Angiologic-clinical comparison and therapeutic implications. 298 May 2

SEPs may be recorded over the spine and scalp to stimulation of any accessible mixed or sensory nerve in the extremities. SEP abnormalities are useful in detecting lesions in central somatosensory pathways. They do not establish a specific diagnosis, but they may suggest or support a diagnosis made on clinical grounds. They have been used particularly to detect subclinical lesions in multiple sclerosis, but their role in following the course of this disorder is unclear. SEPs have been used as a prognostic guide in patients with hemispheric stroke and in patients who are comatose following head injury or severe cerebral anoxia; in such instances, however, the SEP often adds little to what can be determined by clinical examination. Their role in the evaluation of patients with brain death is controversial. Preserved SEPs or their early return after a spinal injury suggests an incomplete lesion, and therefore a better prognosis than otherwise. SEPs have been used to minimize or prevent intraoperative neurologic complications by monitoring spinal cord function, but their role in this regard awaits adequate validation. In patients with cervical spondylosis, SEPs elicited by stimulation of a nerve in the lower extremities may be helpful in indicating which patients are liable to develop a significant cord deficit, so that surgical treatment can be considered at an early stage. SEP abnormalities have been described in a number of other neurologic contexts, but the findings may be of more academic than clinical relevance in that they help to define the extent of neuropathologic involvement without altering the management of individual patients.
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PMID:The use of somatosensory evoked potentials in the evaluation of the central nervous system. 307 Mar 40

The three Community Hospital-based Stroke Programs collected data on 4132 stroke patients admitted to acute care hospitals during 1979 and 1980. White female stroke patients were older than the white male, nonwhite female and nonwhite male stroke patients. Nearly one-fourth (23%) of stroke patients were employed at the time of the event. Most (77%) of the patients were hospitalized for first stroke episodes. Eighty-three percent of the patients had at least one of the four major risk factors for stroke, namely, hypertension, diabetes, transient ischemic attacks and cardiac disease. Half (49%) of the patients were alert at the time of admission. The three diagnostic categories included infarction (60%), stroke not otherwise specified (30%) and hemorrhage (10%). Fourteen days was the median length of hospitalization; 50% of the stroke patients were discharged to a home setting, 31% were institutionalized and 19% died while in the hospital. The mean Barthel Index score for 2400 patients at the time of discharge was 61.8 (normal is 100). Of those patients who were working at the time of the stroke, 22% returned to work. In comparison to the patients in the National Survey of Stroke, patients in this Study were less severe at the time of admission (49% of patients in the National Survey of Stroke were stuporous or comatose compared to 21% of the patients in the current Study). The inhospital fatality was 30.7% in the National Survey of Stroke, and 19.7% in the current Study.
Stroke
PMID:Community Hospital-based Stroke Programs: North Carolina, Oregon, and New York. II: Description of study population. 308 36

A review of recent research conducted at the Rusk Institute of Rehabilitation Medicine in New York City concerning speech and language deficits in closed head injured patients (CHI). One hundred and twenty-five consecutive admissions of 125 closed head injured post coma patients were administered standardized aphasia tests to determine the presence and nature of verbal deficits. Mean time since injury for the group was 45 weeks. All patients, without exception, evidenced linguistic impairment. The population fell into three relatively equally sized groups: classic aphasia, dysarthria accompanied by linguistic deficits, and "subclinical" aphasic deficits. The study results suggest that linguistic functions are particularly vulnerable in severe head injury. A second study compared aphasia secondary to CVA and CHI. When age and time since onset were controlled, aphasic CHI and CVA patients are more similar than different in linguistic task performance and overall functional communication effectiveness. The results suggest that the therapeutic approaches traditionally implemented with CVA aphasic patients are appropriate for the management of CHI aphasic patients as well.
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PMID:Language and speech defects. 316 12

Using logistic regression, we analyzed the predictive value of a number of entry variables with respect to the outcome variables delayed cerebral ischemia, rebleeding, and poor outcome (death or severe disability) in patients with aneurysmal subarachnoid hemorrhage. The entry variables were clinical condition on admission (grades on the Glasgow Coma Scale, Hunt and Hess system), the amount of subarachnoid and intraventricular blood and the presence of hydrocephalus on the admission computed tomogram, and antifibrinolytic treatment with tranexamic acid. We used data from a prospectively studied population of 176 patients admitted within 72 hours after subarachnoid hemorrhage. The risk of delayed cerebral ischemia was best predicted by the amount of subarachnoid blood, intraventricular blood, and antifibrinolytic treatment irrespective of clinical condition and hydrocephalus. The site of delayed cerebral ischemia was not related to the location of the subarachnoid hemorrhage. Antifibrinolytic treatment was the only entry variable (negatively) predicting the risk of rebleeding. Death or severe disability after 3 months was best predicted by the amount of subarachnoid blood and the initial clinical condition reflected by the grade on the Glasgow Coma Scale.
Stroke 1988 Oct
PMID:Prediction of delayed cerebral ischemia, rebleeding, and outcome after aneurysmal subarachnoid hemorrhage. 317 85

The Pilot Stroke Data Bank obtained information on 94 patients with intracerebral hemorrhage. These data were used to identify factors predictive of 30-day outcome from among 85 demographic, historical, clinical, and laboratory variables generally available to clinicians on the day of admission. The 9 univariate factors statistically associated with outcome were Glasgow Coma Scale score, systolic blood pressure, pulse pressure, horizontal and vertical gaze palsies, severity of weakness, presence of brainstem-cerebellar deficits, interval stroke course, and parenchymal hemorrhage size. Beginning with these factors, a step-down variable selection procedure was used to derive a logistic regression model, containing only Glasgow Coma Scale score, pulse pressure, and hemorrhage size, that could be used to categorize correctly 92% of the patients as alive or dead at 30 days after onset.
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PMID:Prediction of intracerebral hemorrhage survival. 277

Six alcoholic patients developed extensive cerebral hemispheric hemorrhages with both intraventricular and subarachnoid blood. All patients had evidence of liver damage, low platelet counts, and abnormal prothrombin and partial thromboplastin times. Four patients presented with seizures; in two of the four, these seizures were initially diagnosed as alcohol withdrawal seizures. Four patients were comatose with lateralizing neurologic deficit; two patients were comatose without lateralizing neurologic deficit, suggesting a metabolic encephalopathy. In one patient there was delayed neurologic deterioration. In all six patients, computed tomography showed large diffuse cerebral hemispheric hemorrhages, prominent intraventricular blood, and breakthrough into the subarachnoid spaces, which was confirmed by necropsy findings. There was marked mass effect but minimal surrounding edema. All six patients died. In three, autopsy showed no evidence of aneurysm, vascular malformation, neoplasm, or amyloid angiopathy and no arteriolar hypertensive changes.
Stroke 1988 Dec
PMID:Alcoholic intracerebral hemorrhage. 320 17


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