Articles: brain-injuries.
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The combination of central fluid percussion traumatic brain injury (TBI) followed 24 h later by a bilateral entorhinal cortical deafferentation (BEC) produces profound cognitive morbidity. We recently showed that MK-801 given prior to TBI in this insult improved spatial memory for up to 15 days. In the present study we examine whether MK-801 treatment of the BEC component in the combined insult model affects cognitive recovery. ⋯ Immunocytochemical localization of parvalbumin showed that chronic administration of MK-801 in the combined insult cases attenuated the injury-induced dendritic atrophy of inhibitory neurons in the dentate gyrus and area CA1. Synaptophysin immunobinding revealed that chronic MK-801 treatment of the BEC component of the combined insult normalized the distribution of presynaptic terminals within the dentate gyrus. These results suggest that cognitive deficits produced by head trauma involving both neuroexcitation and deafferentation can be attenuated with chronic application of glutamatergic antagonists during the period of deafferentation injury and that this attenuation is correlated with axo-dendritic integrity.
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Acta Neurochir. Suppl. · Jan 1998
Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia?
Hyperventilation (HV) is routinely used in the management of increased intracranial pressure (ICP) in severe head injury. However, this treatment continues to be controversial because it has been reported that long-lasting reduced cerebral blood flow (CBF) due to profound sustained hypocapnia may contribute to the development or deterioration of ischemic lesions. Our goal in this study was to analyze the effects of sustained hyperventilation on cerebral hemodynamics (CBF, ICP) and metabolism (arterio jugular differences of lactates = AVDL). ⋯ According to AVDO2 and AVDL, no adverse effects were found during four hours of HV in hyperemic patients. Nevertheless, AVDO2 and AVDL are global measurements and might not detect regional ischemia surrounding focal lesions such as contusions and haematomas. We suggest that monitoring of AVDO2 or other haemometabolic variables should be mandatory when sustained HV is used in the management of head injury patients.
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Acta Neurochir. Suppl. · Jan 1998
Monitoring of brain tissue PO2 in traumatic brain injury: effect of cerebral hypoxia on outcome.
This study investigates the effect of hypoxic brain tissue PO2 on outcome, and examines the incidence of possible causes for cerebral hypoxia. We studied 35 patients with severe head injury (GCS < or = 8). Age was 33.2 (+/- 11.3) years. ⋯ Hypocarbia (ETCO2 < 28 mm Hg) was present in 48.0% of the time of PtiO2 < 10 mm Hg. No obvious cause for cerebral hypoxia was found in 45% of the data. These result underscore the association of cerebral hypoxia with poor neurological outcome and stress the meaning of monitoring of PtiO2 as an independent parameter in patients following TBI.
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Acta Neurochir. Suppl. · Jan 1998
Continuous intracranial multimodality monitoring comparing local cerebral blood flow, cerebral perfusion pressure, and microvascular resistance.
Maintaining cerebral perfusion pressure (CPP) above 70 mmHg is currently a mainstay of neurosurgical critical care. Shalmon, et al. recently showed poor correlation between CPP and regional cerebral blood flow (CBF) [1]. To study the relationship between CPP and CBF, at a microvascular level, we retrospectively analyzed multimodality digital data from 12 neurosurgical critical care patients in whom a combined intracranial pressure (ICP)--laser Doppler flowmetry (LDF) probe (Camino, San Diego) had been placed. ⋯ Autoregulation was impaired or absent in all monitored patients. We conclude that with disrupted autoregulation, CPP above 70 mmHg does not necessarily insure adequate levels of cerebral perfusion. Restoration and maintenance of adequate cerebral perfusion should be performed under the guidance of direct CBF monitoring.
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Acta Neurochir. Suppl. · Jan 1998
Effects of cerebral perfusion pressure on brain tissue PO2 in patients with severe head injury.
Ischemia causes secondary brain damage after severe head injury (SHI). Cerebral perfusion is commonly estimated by monitoring CPP, but the adequacy of cerebral oxygenation requires further measurements, such as jugular oxygen saturation or, more recently, PtiO2 monitoring. In 7 patients with severe head injury, ICP, MAP, CPP, SjO2 and PtiO2 were monitored for a mean time of 9.0 +/- 2.2 days. ⋯ Focusing on values under the thresholds of 60 mm Hg for CPP and 20 mm Hg for PtiO2, we found a relationship between CPP and PtiO2. Looking at the PtiO2 time-course, we observed a quite constant increasing trend during the first 48 hours of monitoring, then the values remained relatively constant within a normal range. Our data show that decreases of PtiO2 are not uncommon after severe head injury and therefore it seems that monitoring of PtiO2 in SHI may be useful in order to minimize secondary insults.