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

Body fluid gas pressure and electrolytes of patients with ruptured aneurysm were continuously analyzed. Intracranial pressure (ICP) was regulated at the level of 120-100 mm H2O by cerebral ventricular drainage. There was no significant change in the pH, PCO2, HCO3-, Na+, K+, Ca++ in the cerebrospinal fluid (CSF) of patients with slight or moderate disturbance of consciousness (lethargic-drowsy state). The PcsfO2 of the patients with marked disturbances of consciousness (semicoma-coma) was significantly low. PcsfO2 of the patients with cerebral vasospasm was significantly lower than for those without vasospasms. PcsfO2/PaO2 was 0.27 +/- 0.01 in the patients with vasospasm and 0.50 +/- 0.01 in those with vasospasm. PcsfO2 tended to decrease in patients with markedly bloody CSF. When the bloody CSF was cleared by ventricular drainage, PcsfO2 increased. PcsfO2 did not return to a normal value in the patients with marked disturbances of consciousness despite sufficient arterial oxygen tension. This suggests that PcsfO2 and PcsfO2/PaO2 should provide a convenient index for the prognosis of patients with ruptured aneurysm.
Stroke
PMID:Body fluid oxygen tension and prognosis in patients with ruptured aneurysm. 4 45

In a previous study occlusion of a middle cerebral artery (MCA) followed by 48 h of hypothermia (29 degrees) was lethal in 5 of 5 monkeys as compared to only 3 of 9 normothermic animals. The present study extended these observations in monkeys and cats with or without MCA occlusion. In monkeys MCA occlusion plus 48 h of hypothermia was consistently lethal. Without MCA occlusion of 2 of 3 monkeys survived, but were comatose the first 12 h post-hypothermia. In normothermic cats, MCA occlusion was lethal in only one of 5 animals whereas hypothermia was lethal in 20 of 21 cats with or without MCA occlusion. The detrimental effects of hypothermia were not favorably influenced either by hemodilution or by deliberate alterations in PaCO2. The effect of 48 h of hypothermia and rewarming on cerebral blood flow (CBF) and cerebral metabolites was evaluated in 6 normal monkeys. CBF was reduced 60 to 70 percent at 29 degrees C and returned to only a maximum of 50 percent of control with re-warming. Prior to re-warming distribution of CBF was inhomogeneous. Cerebral metabolites were borderline normal prior to re-warming but energy stores decreased while lactate increased with re-warming.
Stroke
PMID:Deterimental effect of prolonged hypothermia in cats and monkeys with and without regional cerebral ischemia. 11 94

In 53 patients in different periods of brain strokes the authors studied the functional state of spinal centers by means of registration of H-reflex and F-wave of the skeleton muscles. In spite of the stroke character a marked increase of excitation of the spinal centers was observed, it being especially significant in the subacute period of the disease. The increase of H-reflex amplitude was maximal in extremities, contralateral to the focus of the lesion, but it was observed on the lesion side as well. The patients with cerebral coma in the acute stage of the stroke demonstrated a descrease of relation between central and motor responses up to 12--13%, it gradually increased as the coma ceased. The latent period of F-wave on the both extremities was reliably lower than the control indices along the whole period of the study. The authors show the significance of registration in the dynamics of the muscle evoked potentials for topical diagnosis of the cerebral vessel process and for effective control of the administered therapy.
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PMID:[Functional state of spinal centers in patients with cerebral circulatory disorders according to the results of stimulation electromyography]. 14 84

Two cases of fatal heat stroke, concerning a 20 year-old soldier and a 44 year-old psychiatric patient, treated with neuroleptics, are reported. The clinical picture, starting suddenly with coma and hyperthermia, was quite identical for both. Secondarily, while hyperthermia decreases and the conscience improved partially, an hemorrhagic syndrome similar to a consumption coagulopathy, acute renal insufficiency and acute hepatic failure appear. Death occurred after aggravated neurological disorders and respiratory distress. The anatomical lesions spread on all the viscera include tubular nephritis, and hepatic centro-lobular necrosis and an interstitial and alveolar oedema with hemorrhages and hyaline membranes in the lungs.
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PMID:[Heat stroke and disseminated intravascular coagulation. Apropos of 2 cases]. 21 8

Cogan syndrome is a multisystem inflammatory vascular disease, characterized by nonsyphilitic interstitial keratitis and vestibuloauditory symptoms. Recent reports have directed attention to involvement of other organ systems. Respiratory, cardiovascular, gastrointestinal, and musculoskeletal problems are common, as are laboratory abnormalities and general symptoms such as fever, chills, and weight loss. Prominent neurologic problems in two patients prompted a review of 79 cases of Cogan syndrome. More than half had nervous system involvement, including electroencephalographic or spinal fluid abnormality, headache, psychosis, coma, convulsion, neuropathy, and stroke. Cogan syndrome should be considered when neurologic deficits are accompanied by eye, ear, and systemic symptoms.
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PMID:Neurologic manifestations of Cogan syndrome. 30 11

The concentrations of homovanillic acid (HVA), 3-methoxy, 4-hydroxyphenylglycol (MHPG), and 5-hydroxyindolylacetic acid (5-HIAA) were measured in samples of ventricular cerebrospinal fluid (CSF) taken from 15 patients who were comatose as a result of an acute head injury, a tumour, or a cerebrovascular accident. The metabolite levels were not related to the ventricular fluid pressure. In the eight patients who recovered and from whom serial samples of CSF were obtained, the metabolite levels did not change, except for two patients in whom HVA increased as coma progressed. The concentration of MHPG, but not of HVA or 5-HIAA, was greater (P less than 0.02) in the five patients who died without regaining consciousness than in the 10 patients who recovered.
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PMID:Amine metabolites in ventricular cerebrospinal fluid in coma. 51 64

Using the life table method, 962 cases of infarction, 279 cases of hemorrhage, and 243 cases of undetermined type of stroke, occurring in Manitoba between Jan 1, 1970, and June 30, 1971, were analyzed for factors affecting survival. Survival until Dec 31, 1973, was found to be adversely affected by the presence of coma or unconsciousness and the absence of localizing signs and symptoms. Also, the prognosis was poor if the heart was enlarged on the x-ray film or the ECG was abnormal. On the other hand, the presence of individual clinical entities such as hypertension, hypertensive heart disease, myocardial infarction, atrial fibrillation, or diabetes did not affect the survival significantly. These findings will help in predicting the prognosis and in planning for management of stroke cases.
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PMID:Prognostic factors in the survival of 1,484 stroke cases observed for 30 to 48 months. II. Clinical variables and laboratory measurements. 63 54

Heat stroke following effort is not confined to hot regions. The authors have seen five cases in the Paris region between 1967 and 1974. It particularly affects young subjects, in pour training or living away from home. Clinically very similar to anaesthetic malignant hyperthermia, it has the same gravity, with a high mortality rate. It may be characterised by the triad: coma, muscular hypertonicity and hyperthermia of over 40 degrees C. Refrigeration, sedation and rehydration are all the more effective when started early. Improved knowledge of malignant hyperthermia of effort, within the more confused context of heat stroke, will ensure that it is recognised more frequently, limit its consequences and lead to better understanding of its underlying cause, the origin of which is undoubtedly muscular.
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PMID:[Malignant hyperthermia of effort or "heat stroke" (author's transl)]. 67 9

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

We measured cerebral oxygen extraction, cerebral blood flow(CBF), and cerebral metabolic rate (CMRO2) in comatose patients during the first 60 hours after resuscitation from cardiac arrest. Each patient was studied 2 or 3 times. CBF was determined by a modification of the Kety-Schmidt method using inhaled Xenon133. Over the study period jugular venous oxygen tension and saturation rose, while the oxygen content difference between arterial and jugular venous blood fell, indicating a progressive increase in the ratio of CBF to metabolism CBF and CMRO2 measurements confirmed this. Between 2 and 6 hours after resuscitation both measurements were severely but proportionately depressed to less than 50% of normal. After 6 hours CBF was increased disproportionately to CMRO2 so that a relative hyperemia developed and persisted for the duration of the study. Although regional inhomogeneity of flow and regional ischemia cannot be ruled out, we have found no evidence for global cerebral ischemia between 2 and 60 hours post-resuscitation as an explanation for failure of recovery. In man following cardiac arrest restoration of levels of global cerebral blood flow, which can be considered adequate relative to the depressed metabolic state of the tissue, is achieved within 2 hours of resuscitation.
Stroke
PMID:Cerebral blood flow and metabolism in man following cardiac arrest. 74 88


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