Articles: brain-injuries.
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Brain injury : [BI] · Jul 1997
Case ReportsPsychomotor agitation following gabapentin use in brain injury.
Gabapentin, an anticonvulsant structurally related to gamma-aminobutyric acid (GABA) was recently reported to be effective in pain associated with reflex sympathetic dystrophy (RSD) and in pain associated with neuropathy. Yet, to our knowledge, the use of gabapentin for neuropathic pain in the presence of cognitive impairment has not been reported. In this report, we describe two patients (one with a traumatic brain injury, one with a putative acquired brain injury) who presented to a neurorehabilitation unit complaining of pain that was diagnosed as neurologically mediated. ⋯ Correspondingly, each reported a diminution of psychological symptoms within 48 hours of gabapentin cessation. These two cases suggest that gabapentin may cause agitation in cognitive impaired patients. Physicians treating brain-injured patients and prescribing gabapentin for neuropathic pain may wish to closely monitor patients for similar signs of restlessness or anxiety.
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Cerebrovascular vasomotor reactivity reflects changes in smooth muscle tone in the arterial wall in response to changes in transmural pressure or the concentration of carbon dioxide in blood. We investigated whether slow waves in arterial blood pressure (ABP) and intracranial pressure (ICP) may be used to derive an index that reflects the reactivity of vessels to changes in ABP. ⋯ Computer analysis of slow waves in ABP and ICP is able to provide a continuous index of cerebrovascular reactivity to changes in arterial pressure, which is of prognostic significance.
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Intraischemic reduction in temperature of 2-3 degrees C (modest hypothermia) has been demonstrated to provide partial neuroprotection in neonatal animals. This investigation determined if modest hypothermia initiated immediately after brain ischemia provides neuroprotection. Piglets were studied with rectal temperature maintained during the 1st h after 15 min of brain ischemia at either 38.3 +/- 0.3 degrees C (normothermia, n = 11) or at 35.8 +/- 0.5 degrees C (modest hypothermia, n = 11). ⋯ Postischemic hypothermia was associated with less severe stages of encephalopathy compared with normothermia (p = 0.05). Histologic neuronal injury was assessed categorically in 16 brain regions, and postischemic hypothermia resulted in less neuronal injury in temporal (p = 0.024) and occipital (p = 0.044) cortex at 10 mm beneath the cortical surface, and in the basal ganglia (p = 0.038) compared with that in normothermia. Modest hypothermia for 1 h immediately after brain ischemia provides partial neuroprotection and may represent an adjunct to resuscitative strategies.
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The management of malignant posttraumatic cerebral edema remains a frustrating endeavor for the neurosurgeon and the intensivist. Mortality and morbidity rates remain high despite refinements in medical and pharmacological means of controlling elevated intracranial pressure; therefore, a comparison of medical management versus decompressive craniectomy in the management of malignant posttraumatic cerebral edema was undertaken. ⋯ Decompressive bifrontal craniectomy provides a statistical advantage over medical treatment of intractable posttraumatic cerebral hypertension and should be considered in the management of malignant posttraumatic cerebral swelling. If the operation can be accomplished before the ICP value exceeds 40 torr for a sustained period and within 48 hours of the time of injury, the potential to influence outcome is greatest.
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Experimental neurology · Jul 1997
Time course of changes in lactate and free fatty acids after experimental brain injury and relationship to morphologic damage.
Regional levels of lactate and free fatty acids (FFA) were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min after injury, tissue concentrations of lactate were elevated in the cortices and hippocampi of both ipsilateral and contralateral hemispheres. Whereas lactate levels had returned to normal by about 20 min after injury in the penumbra and contralateral cortices, their elevation persisted in the ipsilateral injured cortex and hippocampus for 24 h after injury. ⋯ In general, these elevations persisted for as long as 6 to 24 h in the injured cortex and for 2.5 to 24 h after injury in the ipsilateral hippocampus. Histologic studies revealed a similar extent of damage in the cortex between 5 min and 24 h after injury, whereas damage in the CA3 region of the ipsilateral hippocampus increased during that period. These findings suggest a role for lactic acid and FFA, two secondary injury factors, in neuronal cell loss after brain injury.