Stroke; a journal of cerebral circulation
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Moderate elevations of brain temperature, when present during or after ischemia or trauma, may markedly worsen the resulting injury. We review these provocative findings, which form the rationale for our recommendation that physicians treating acute cerebral ischemia or traumatic brain injury diligently monitor their patients for incipient fever and take prompt measures to maintain core-body temperature at normothermic levels. ⋯ The acutely ischemic or traumatized brain is inordinately susceptible to the damaging influence of even modest brain temperature elevations. While controlled clinical investigations will be required to establish the therapeutic efficacy and safety of frank hypothermia in patients with acute stroke, the available evidence is sufficiently compelling to justify the recommendation, at this time, that fever be combatted assiduously in acute stroke and trauma patients, even if "minor" in degree and even when delayed in onset. We suggest that body temperature be maintained in a safe normothermic range (eg, 36.7 degrees C to 37.0 degrees C [98.0 degrees F to 98.6 degrees F]) for at least the first several days after acute stroke or head injury.
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Transcranial doppler ultrasound (TCD) is used after subarachnoid hemorrhage to detect cerebral vasospasm and is often treated with induced hypertension. Cerebral autoregulation, however, may be disturbed in this population, raising the possibility that TCD velocities may be elevated by induced hypertension. To study this possibility, we performed continuous TCD monitoring of the middle cerebral artery during the induction and withdrawal of induced hypertension in patients after subarachnoid hemorrhage. ⋯ In patients with disturbed autoregulation after subarachnoid hemorrhage, induced hypertension can alter cerebral blood flow velocities. The level of autoregulation needs to be considered when interpreting TCD velocities in patients after subarachnoid hemorrhage.
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Patients resuscitated from cardiac arrest have a high early mortality rate. Prognostic evaluation based on clinical observations is uncertain and would benefit from the use of biochemical markers of hypoxic brain damage. The astroglial protein S-100 is an established biochemical marker of central nervous system injury. The purpose of the present study was to validate the use of serum determinations of S-100 with regard to outcome after cardiac arrest. ⋯ The present study shows that hypoxic brain damage after cardiac arrest can be estimated by measurement of serum S-100 concentrations. The method can be used in early prognostic evaluation of short-term outcome after cardiac arrest.
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We sought to analyze the etiology and underlying vascular risk factors of transient ischemic attacks (TIAs) and minor ischemic strokes (MISs). ⋯ An etiologic classification of TIAs and MISs is feasible. The two most frequent pathogenetic mechanisms in our study were small-artery disease and cardioembolism. The prevalence of large-artery atherosclerosis was low.
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Case Reports Comparative Study
Pilot study of functional MRI to assess cerebral activation of motor function after poststroke hemiparesis.
Studies of cerebral activation of motor function after ischemic stroke may enhance our understanding of the underlying mechanisms of motor functional recovery, including the role of the noninfarcted hemisphere. ⋯ Synkinesia alone cannot explain the extent of ipsilateral activation in primary sensorimotor cortex. The explanation offered for our findings is that preexisting uncrossed motor neural pathways may be accessed or recruited to compensate for damage to the crossed motor pathways after ischemic stroke.