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

There is continuing controversy about the benefits of decompressive craniectomy in the treatment of lesions causing increased intracranial pressure (ICP) and brain edema. Laboratory work has shown a decrease in ICP after craniectomy, but also a paradoxical enhancement in the formation of underlying cerebral edema, which may act to the detriment of the patient. Since Rengachary et al. advocated craniectomy for massive cerebral infarction and reported their group of three patients, we have managed five patients with acute supratentorial cerebral infarction who progressed to uncal herniation and impending death from raised ICP and brain stem compression. All were treated with frontotemporal craniectomy after conventional medical therapy failed to achieve a response. All patients survived and are walking, despite a paresis appropriate to their original stroke. Two have returned to work. Good results with supratentorial craniectomy after infarction show that this procedure is life-saving and can also give acceptable functional recovery.
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PMID:Functional recovery after decompressive craniectomy for cerebral infarction. 318 72

To study the relation of blood glucose soon after the onset of stroke and outcome in terms of fatality and functional recovery 6 months later, two prospective studies were performed. Fasting blood glucose measured within 48 hours of onset was significantly higher in those who died than in those who survived. However, random blood glucose, mean daily blood glucose and HbA1 were not related to fatality or functional recovery. Fasting blood glucose levels soon after the stroke were significantly higher than those in the same patients measured 1 month later. These results suggest that the hyperglycaemia related to decreased survival is a stress response rather than an indication of preexisting diabetes mellitus but do not support the view that a high blood glucose level is itself harmful to the brain.
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PMID:Blood glucose and prognosis of acute stroke. 338 45

Quantification of myocardial performance after regional ischemic injury is difficult because available performance indexes are markedly dependent on concurrent load changes. To develop a more load-insensitive index of myocardial function during ischemia, eight conscious dogs were instrumented to measure left ventricular pressure with micromanometers and myocardial segment length with ultrasonic dimension transducers. Preload was varied by transient vena caval occlusion during control conditions, after 15 min of coronary occlusion, and at intervals during 24 h of reperfusion. Acute ischemia shifted the linear relationship between segmental stroke work (SW) and end-diastolic segment length (EDL) rightward, diminishing the slope and increasing the chi-intercept. Preload recruitable work area (PRWA), defined as the area under the SW-EDL curve, reflected changes in both slope and intercept. During acute ischemia, conventional performance indexes and PRWA decreased significantly and required up to 24 h of reperfusion to return to control values. Of all parameters examined, PRWA was most responsive to prolonged ischemic dysfunction after reperfusion and was insensitive to concurrent load changes. Thus PRWA provides improved precision in quantifying of myocardial dysfunction after regional ischemic injury. This parameter should be especially useful in assessing the subtle effects of acute interventions designed to modify functional recovery.
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PMID:Quantification of regional myocardial dysfunction after acute ischemic injury. 339 29

Electromyographically triggered electric muscle stimulation (EMS) was evaluated in combination with conventional treatment in 69 consecutive postcerebrovascular accident outpatients whose onset of hemiplegia was four months to 14 years earlier. Six subjects initially exhibited no residual volitional activity in targeted muscles, and all patients had undergone conventional therapy with little or no functional recovery. Electromyographic (EMG) recordings and EMS directed to prime movers of impaired movements were accomplished by way of skin-surface electrodes. Prescribed treatment (patient compliance was frequently substandard) involved several months of four to five sessions per week, focusing on wrist extension and/or ankle dorsiflexion initially, and often other movements later. During 30 to 300 movement attempts per session, EMGs that exceeded a preset threshold triggered immediate stimulation to force movement completion. Over sessions, patients commonly realized substantially improved increases in voluntary EMG capabilities generally proportionate to the frequency of treatment sessions. Parallel improvements were also found for subjectively scaled functional measures of range-of-motion and ambulation. Motivation was important to success, but side and nature of stroke, age, and poststroke interval were not. Progress often far exceeded that of previous conventional therapy (each patient served as his/her own control). Regarding mechanisms, impaired proprioceptive feedback is considered central to stroke-disrupted sensorimotor control. EMG-triggered EMS is intended to improve brain relearning by reinstating proprioceptive feedback time-locked to each attempted movement. Clinical results were consistent with this theory; further assessment of the new EMG-triggered EMS modality intergrated into conventional treatment regimens seems warranted.
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PMID:Electromyographically triggered electric muscle stimulation for chronic hemiplegia. 349 65

It has been questionable whether the lack of proven pharmacological treatments in acute cerebral infarction (ACI) reflects ineffective drugs or only inadequacies in their assessment. The difficulties in developing a rationale for drug therapy in this condition favoured the former, although the latter possibility was supported by re-evaluation of most published trials. In this paper, a plausible rationale, in terms of our current understanding of both the drug and the condition, is expounded for treatment of ACI with naftidrofuryl. Guidelines for the design and conduct of clinical trials in acute stroke are discussed in relation to the particular problems posed: need for early initiation of treatment; need for, and difficulties of, diagnostic confirmation; matching of treatment groups by prognostic indicators of uncertain significance, and requirements for large numbers of patients and long-term follow-up. The practical application of these guidelines is tested in a clinical trial of naftidrofuryl conducted in a single centre on 100 patients with proven diagnoses. Rigorous attention to all aspects of selection, treatment and follow-up, with an explanatory approach to the trial design, was predicted to produce a positive result if the drug was effective. The findings were that naftidrofuryl treatment was associated with no change in death rate but with clinically and statistically significant improvements in neurological recovery and bed-occupancy. Better functional recovery was also noted, so that the trial result was coherent. It was concluded that a beneficial effect had been recorded, and consistency of this outcome with those of previous studies is demonstrated. A case is made for further studies to define exactly the role of this drug in the management of ACI.
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PMID:Towards a model stroke trial. The single-centre naftidrofuryl study. 353 23

To elucidate the incidence of severe disability due to cerebral stroke and its related factors, prospective data of 1,621 Hisayama residents aged 40 and over were examined. Severe disability resulting from stroke was defined as patients who were unable to dress, take care of their toilet needs, and feed themselves without assistance, or who required a wheel chair for ambulation three months after the most recent episode. During 20 years of follow-up 255 stroke patients were observed among the sample population. The annual incidence of stroke per thousand was 9.8, and rate of severe disability was 2.8 for men and 6.4 and 2.0 for women, respectively. Of the 74 cases with severe disability, approximately 92% were attributed to cerebral infarction. Related factors to severe disability due to cerebral infarction were recurrent attacks, hypertension, changes in ocular fundi and diabetes mellitus among predispositions and quadriplegia or muscular contraction, and intelligent or mental disorders among inhibiting factors for functional recovery. Furthermore, in 59 autopsy cases with multiple cerebral infarctions, the frequency of disability increased as the number of infarcts increased. Hypertension and diabetes mellitus, as risk factors for cerebral infarction and factors inhibiting post-ictal functional recovery were discussed.
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PMID:Severe disability related to cerebral stroke: incidence and risk factors observed in a Japanese community, Hisayama. 358 64

About 20% of the survivors from acute stroke are relocated from a general hospital to a rehabilitation centre or to a nursing and reactivation home. This occurs about one or two months after the stroke. At that point in time the most important period for spontaneous recovery has already passed. In 1981 a recent stroke was the somatic reason for admission in 21.4% of all patients in nursing-homes. In comparison to rehabilitation centres more elderly stroke patients with many other disorders are admitted to nursing-homes. It is also shown that the more disabled stroke patients are admitted to nursing-homes, but this appears to be influenced by the presence of a rehabilitation centre in the area. Urinary incontinence, a 'psychosyndrome', a relapse of stroke, a healthy partner and, to a lesser degree, aphasia determine the perspectives for discharge, besides functional recovery. But also the care setting and the facilities of a day hospital in a nursing-home are important factors that will influence the prognosis for discharge.
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PMID:[Role of the nursing home in the after care of CVA patients]. 359 Feb 80

We reviewed 6 computed tomography-documented cases of primary lateral pontine hemorrhage that occurred in our two institutions over a 2-year period. All patients survived the acute stroke, with excellent functional recovery in 4. The level of consciousness of the patient and the size of the hemorrhage had no consistent bearing on outcome. Both of these features have been considered important prognostic indicators in patients with pontine hemorrhage, but in our series benign outcomes were not restricted only to patients who were alert or had small hemorrhages; on the other hand, severe disability was noticed in 1 patient with a small hematoma strategically located in the pontine tegmentum. Our observations suggest that, although some patients with lateral pontine hemorrhage have a good prognosis, there is no single determinant that predicts outcome in a given patient.
Stroke
PMID:Lateral pontine hemorrhage: reappraisal of benign cases. 362 56

Corticomotor evoked potentials have recently been used in experimental animals and patients as a measure of neurologic function after stroke. However, little is known about the fundamental electrophysiologic properties contributing to the formation of these potentials. To define some of these properties, corticomotor evoked potentials were recorded from the contralateral hindlimb in response to transcortical stimulation in cats anesthetized with halothane. These potentials were obtained hourly for 6 hours after middle cerebral artery occlusion. Four major identifiable components were recorded in control responses. Immediately after infarction, all component amplitudes were significantly attenuated. However, after approximately 5 hours, the early latency components exceeded control values; late latency components were also increased. Corresponding somatosensory evoked potentials were abolished and did not return throughout the recording session. Based on classic neurophysiologic studies, the amplitude increment can be explained as combined activation of low-threshold brainstem facilitatory centers and/or direct activation of subcortical axonal pathways. With further study, corticomotor evoked potentials may be a valuable adjunct to current electrophysiologic monitoring techniques, particularly with regard to defining the extent and location of an infarct, as well as to assessing functional recovery.
Stroke
PMID:Early component changes in corticomotor evoked potentials following experimental stroke. 368 90

The flow threshold and time threshold for reversibility of cerebral ischemia were studied using a canine model of cerebral ischemia regulated by controlled perfusion of cerebral blood flow (CBF). CBF was continuously monitored with a laser Doppler flow meter, the brain was brought to a constant level of ischemia for a defined period of time, after which recirculation was instituted. The electroencephalogram (EEG) and somatosensory evoked potentials (SEP) were monitored and used as an index of brain function. No recovery of brain function was found following recirculation if the CBF was reduced to a level below 20% of the normal state for more than one hour. When residual blood flow was 30% of the normal level, however, recirculation after one hour of ischemia resulted in nearly complete recovery of brain function. Significant functional recovery was not seen after two or more hours of such ischemia. Nearly complete recovery was also seen following reperfusion within three hours with 40% of normal CBF. It was demonstrated that the reversibility in the ischemic brain was critically correlated to the level of blood flow and its duration. If these results can be applied to the human brain, emergency cerebral revascularization for ischemic stroke should be attempted when critical flow and time thresholds have not been crossed, namely, in less than 1 hour and 3 hours of insult when the residual blood flow is reduced to 30 and 40% of the normal state, respectively. In clinical situations, this "critical time" may be too short for acute revascularization unless cerebral protective measures are applied pre-operatively to prolong the viability period of ischemic cerebral tissue.
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PMID:Experimental study on the reversibility of cerebral ischemia. Residual blood flow and duration of ischemia. 368 99


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