Dexamethasone in acute stroke.
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Acute Disease↗
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Dexamethasone in acute stroke.
Explore the source record for details and available documents.
Acute Disease↗
Aphasia in acute stroke.
Previous surveys of stroke populations have offered only cursory information on language disturbance, and, conversely, few surveys of aphasic populations have dealth exclusively with stroke or with acute phenomena. This paper describes aphasia in 850 acute stroke patients consecutively registered by the Harlem Regional Stroke Program, of whom 177 (21%) were aphasic; of these, nine were of Broca's type, 24 were of Wernicke's type, 14 were of anomic, ten were conduction, seven were of "isolation" type, and 107 were "mixed." An unexpected finding was a significant over-representation of men among the nonfluent aphasics. During the following four to 12 weeks, 12% of fluent aphasics died, and 12% remained moderately or severely impaired; among survivors, aphasia improved in 74%, and in 44% it cleared completely. During the same period, 32% of nonfluent aphasics died, and 34% remained moderately or severely impaired; among survivors, aphasia improved in 52%, and in only 13% did it clear completely. In both fluent and nonfluent groups, hemiparesis and/or visual field cut were associated with poor prognosis.
Acute Disease↗
Haemorheological factors in the pathophysiology of acute stroke.
Blood viscosity studies were carried out in fourteen patients with acute stroke, eight with cerebral infarction, six with cerebral haemorrhage and in thirteen controls. We observed a statistically significant higher values of plasma, red cell and whole viscosity in patients with acute stroke than in normal controls. Plasma fibrinogen levels were statistically higher (p less than 0.01) in patients than in normal controls. The platelet aggregation was increased in two young adults with acute stroke. The results suggest that the haemorheological factors play an important role in the pathophysiology of stroke patients.
Acute Disease↗
Reactive hyperglycaemia in patients with acute stroke.
Initial and follow-up fasting serum glucose levels following acute stroke were evaluated retrospectively in 392 selected hospitalized patients. Transitory reactive hyperglycaemia was observed in a large number of patients (28% of the total series) without a history of diabetes prior to the acute cerebrovascular event. The data from this group suggest a possible relationship between the impairment of carbohydrate metabolism and the type and location of stroke since both the frequency and severity of the hyperglycaemic response were higher in patients with haemorrhagic stroke and brainstem infarction as compared with cerebral infarction. The incidence and degree of the reactive hyperglycaemia were also related to the severity of the acute stroke. There were more comatose patients in the group showing this phenomenon. Initial serum glucose levels in the latter group were higher in unconscious patients than in alert ones. In addition, hospital mortality was significantly higher in these patients. Transitory reactive increases of serum glucose levels were also observed in the majority of patients with a history of overt diabetes prior to the acute stroke. The hyperglycaemic reaction following acute stroke may be attributed to several underlying mechanisms. These include: a non-specific reaction to acute stress and tissue injury with the associated autonomic, hormonal and metabolic alterations; uncovering of underlying latent diabetes by the acute stroke; increased secretion of growth hormone due to stroke-induced hypothalamic dysfunction; and irritation of the glucose regulatory centres in the hypothalamus and brain stem by blood-laden cerebrospinal fluid or local ischaemia.
Acute Disease↗
Stroke: Acute nursing care in the stroke unit.
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Acute Disease↗
Surgical treatment of the acute stroke caused by proven vertebral-basilar artery insufficiency.
Five patients with acute strokes caused by proven vertebral-basilar artery insufficiency had restoration of acutely lost neurologic function with revascularization of ischemic tissue and cells of the hindbrain, including upper and lower motor neurons of the brainstem. This was done with an operation to correct partial extralumenal obstruction of the proximal vertebral artery. The operations were performed three to seven days after the onset of the acute strokes. Patient selection is dependent on angiography of the aortic arch with visualization of the vessels of the neck, the vertebral and carotid arteries. There was no mortality and no significantly morbidity among these patients.
Aged↗
Early time course of N-acetylaspartate, creatine and phosphocreatine, and compounds containing choline in the brain after acute stroke. A proton magnetic resonance spectroscopy study.
BACKGROUND AND PURPOSE: The early time course after acute stroke of cerebral N-acetylaspartate, creatine and phosphocreatine, and compounds containing choline was studied in vivo by means of localized water-suppressed proton magnetic resonance spectroscopy. METHODS: Eight patients with acute stroke were studied serially in the acute phase, 1 week after, and 2-4 weeks after the onset of clinical symptoms. Ten healthy volunteers served as controls. A stimulated echo (STEAM) sequence was used for measurement of the brain metabolites in a volume of interest located within the infarcted area as visualized by magnetic resonance imaging. For quantification, the unsaturated water signal was used as the internal standard. Regional cerebral blood flow in the infarcted area was measured relative to a symmetrically located unaffected area by means of single-photon emission computed tomographic scanning, using 99mTc-labeled d,l-hexamethylenepropyleneamine oxime as the flow tracer. RESULTS: Relative regional cerebral blood flow was considerably reduced in the infarcted area in the acute phase. After 1 week, hyperemia was seen in all but one patient. The N-acetylaspartate content was significantly reduced, with the loss appearing to occur between 6 and 24 hours after the stroke incident. The reduction in N-acetylaspartate content was greater in the central part than in the peripheral part of the infarcted area. Creatine and phosphocreatine were also reduced in the infarcted area, whereas no significant change was seen in the choline content. CONCLUSIONS: Assuming that N-acetylaspartate content reflects neuronal survival or loss, our results may suggest that treatment procedures with restoration of blood flow to severely ischemic areas should be initiated within the first 6 hours after stroke onset.
Acute Disease↗
Naftidrofuryl after acute stroke: a review and a hypothesis.
With demographic change, Western populations are becoming older. The prolonged decline in incidence of stroke, already a very costly illness, may soon reverse. This paper briefly reviews medical treatments of acute stroke that have been popular in the past and finds that they have been generally of little value. The place of naftidrofuryl, a drug with a complex pharmacological profile that includes selective S2-receptor blockade, is discussed in greater detail. Two clinical studies have indicated that, although it may not alter death rate in acute stroke, naftidrofuryl therapy enhances recovery from the disabling effects of cerebral infarction. One important consequence of this is a potentially major reduction in time spent in hospital by stroke patients. Hospital bed occupancy has been identified as a principal component in the cost of stroke to health services. Drug treatments that reduce death rate without improving recovery in survivors have an opposite effect, as has been seen in an important trial of glycerol.
Acute Disease↗
Dexamethasone in acute stroke.
Over 13 months 118 patients admitted to hospital with acute stroke were allocated at random to treatment with either dexamethasone or placebo. At one year there was no significant difference in the numbers of survivors or in the quality of life between the two groups. The results suggest that there is no indication for the routine administration of dexamethasone to a heterogeneous group of patients with stroke.
Acute Disease↗
Acute gastric changes in patients with acute stroke. Part 1: with reference to gastroendoscopic findings.
A gastroendoscopic study was performed on 177 patients with acute stroke. Gastric changes were found in 92 among them (52%), including ten with acute ulcer. A high frequency of gastric changes was found in patients with serious stroke and/or in patients whose cerebral lesions were located close to the hypothalamus or its centrifugal tract. The mortality in patients with gastric changes was high, especially in patients with acute ulcers, multiple erosions and petechiae. The frequency of brown gastric juice and coffee grounds at gastroendoscopic examination (gastric hemorrhage) was three times as high as that of melena and/or hematoemesis. On the other hand, the mortality of patients with gastric hemorrhage differed little from that of patients with melena and/or hematoemesis.
Adult↗
Cardiac and respiratory monitoring of acute stroke patients.
This study evaluates physiologic monitoring as a tool for improved nursing observation of acute stroke patients. Forty-four patients admitted within 48 hours of onset of stroke were monitored using an automated arrhythmia detection system and impedance pneumography. Cardiac arrhythmias were observed in 25 of 44 patients. Three patients with episodes of atrial fibrillation were digitalized and converted to normal sinus rhythm. Respiratory patterns were intermittently abnormal in 39 of 44 patients. The presence of intermittent Cheyne-Strokes respirations or tachypnea was associated with an increased mortality rate. Cardiac monitoring appears to be a useful tool for prompt detection of potentially serious arrhythmias in stroke patients. Respiratory monitoring is useful for detection of abnormalities of respiratory rate and pattern; these abnormalities may serve as an early indicator of change in neurologic status.
Arrhythmias, Cardiac↗
Failure of prolonged hypocapnia, hypothermia, or hypertension to favorably alter acute stroke in primates.
The effects of induced hypocapnia, hypothermia, and hypertension were surveyed in a primate model of acute stroke during and following a 48-hour period of intensive care. The results were compared to a group of nine control animals previously studied. Hypocapnia (PaCO2=25 torr) was examined in five animals and did not appear to alter the expected mortality, degree of neurological deficit, or frequency of infarction. There was, however, a suggestion that the size of infarction may be reduced. Hypothermia (29 degrees C) in five animals had a detrimental effect in that no animals survived following the intensive care period and all had infarction with massive edema. We speculate that hypothermia caused a sufficient increase in blood viscosity as to compromise collateral flow, thereby accounting for this detrimental effect. Induced hypertension (to 20% above control levels) was abandoned after three animals because of severe systemic effects (cardiac failure and pulmonary edema) resulting in death during the period of intensive care.
Acute Disease↗
Acute gastric changes in patients with acute stroke. Part 2: gastroendoscopic findings and biochemical observation of urinary noradrenalin, adrenalin, 17-OHCS and serum gastrin.
To investigate the relationships between gastric change accompanying patients with acute stroke and the function of the autonomic nervous system and pituitary-adrenal system, studies on the gastroendoscopic technique and biochemical observations were done in 122 patients. The mean urinary noradrenalin and adrenalin excretions were elevated in patients with acute gastric changes, especially in patients with multiple erosions and acute ulcers. An elevation of the mean fasting serum gastrin concentration was found in patients with acute ulcers and no acute gastric changes. The mean urinary 17-OHCS excretion was increased in patients with multiple erosions, petechiae and acute ulcers. In conclusion, the sympathetic and parasympathetic nervous system and the pituitary-adrenal system have respectively different roles in the production of various types of acute gastric changes in patients.
17-Hydroxycorticosteroids↗
Low-dose heparin as a prophylaxis against deep-vein thrombosis after acute stroke.
A trial of subcutaneous low-dose heparin in the prevention of deep-vein thrombosis was carried out in elderly patients admitted to hospital after an acute stroke. A statistically significant reduction was observed in deep-vein thrombosis as assessed by isotope leg scanning.
Acute Disease↗
Therapeutic interventions in acute stroke.
1. Potential therapies for ischaemic stroke include agents to reduce oedema, to improve cerebral perfusion, to reduce excitotoxic damage, to minimise free-radical induced injury and to reduce complications such as deep venous thrombosis. 2. Of the anti-oedema drugs, steroids are ineffective and possibly dangerous; intravenous glycerol is unproven. 3. Haemodilution to reduce whole blood viscosity and improve perfusion is ineffective. Thrombolytic drugs have not been adequately tested but several randomised multicentre trials are now commencing. Early treatment and CT scanning are essential. 4. Anticoagulants and antiplatelet drugs may have wide applicability but have not been tested in the acute phase of stroke. A multi-centre trial will address this issue. 5. Neuronal cytoprotection offers exciting prospects for acute stroke treatment. Antagonists of glutamate at the NMDA receptor, calcium and sodium channel blocking agents and free radical scavenging drugs have potent effects experimentally. Several agents are now reaching clinical trials. The calcium antagonist nimodipine has been disappointing in large scale trials but some studies were flawed by late treatment. 6. Successful treatment of acute stroke is likely to combine several approaches. 7. Therapeutic trials in stroke must include CT scanning, early treatment and a multicentre approach to achieve large numbers of patients.
Acute Disease↗
Predicting the outcome of stroke: acute stage after cerebral infarction.
On admission to hospital during the acute phase of a stroke presumed due to ischaemic infarction in one cerebral hemisphere 93 patients were examined to determine the factors associated with a poor prognosis for immediate survival. The patients particularly at risk were those who were overtly unconscious and those with any combination of impaired consciousness, dense hemiplegia, and failure of conjugate ocular gaze towards the side of the limb weakness. Necropsy evidence suggested that these signs usually indicate infarction of the whole of one middle cerebral artery territory which is often secondary to internal carotid artery occlusion and commonly produces fatal cerebral oedema.
Aged↗