Articles: brain-injuries.
-
Intensive care medicine · Jan 1996
Event-related potentials--neurophysiological tools for predicting emergence and early outcome from traumatic coma.
To determine the prognostic value of multimodal evoked potentials (EPs) and event-related (ERPs) potentials in coma (Glasgow Coma Score <8), after severe traumatic brain injury (TBI). ⋯ Highly significant (P <0.001) correlations exist between long-latency ERP components and 3-month outcome. Short-latency EPs, brainstem (wave I-V) and somatosensory conduction times also correlate significantly with the GOS (P <0.01). Of the clinical measurements, pupillary response patterns, APACHE II and Glasgow Coma Scores (GCS) correlate significantly with outcome, as do the retrospective measures of duration of coma and post-traumatic amnesia (PTA) in survivors. Unfortunately, due to variance of long-latency responses, even in controls, absolute values cannot be relied upon as prognosticators. The presence of "mismatch negativity" predicted the return of consciousness (89.7% sensitivity and 100% specificity) and preceded changes in GCS. Its latency was the single best indicator of 90-day outcome from coma (r = -0.641).
-
Ischemia is one of the major factors causing secondary brain damage after severe head injury. We have investigated the value of continuous partial pressure of brain tissue oxygen (PbrO2) monitoring as a parameter for cerebral oxygenation in 22 patients with severe head injury (Glasgow Coma Scale score, < or = 8). Jugular bulb oxygenation, intracranial pressure, and cerebral perfusion pressure were simultaneously recorded. ⋯ The early occurrence of ischemia after head injury can be monitored on a continuous basis. Deficiency of oxygen autoregulatory mechanisms can be demonstrated, and their occurrence is inversely related to outcome. For practical clinical use, the method seemed to be superior to jugular oximetry.
-
J. Neuropathol. Exp. Neurol. · Jan 1996
Cytoskeletal derangements of cortical neuronal processes three hours after traumatic brain injury in rats: an immunofluorescence study.
Semiquantitative Western blot analyses have shown that traumatic brain injury (TBI) can produce significant loss of cytoskeletal proteins (neurofilament 68 [NF68], neurofilament 200 [NF200] and microtubule associated protein 2 [MAP2]) possibly by calpain-mediated proteolysis. Thus, we employed immunofluorescence (light and confocal microscopy) to study the histopathological correlates of acute neurofilament and MAP2 protein decreases observed 3 hours following unilateral cortical injury in rats. TBI induced dramatic alterations in NF68, NF200, and MAP2 immunolabeling in dendrites within and beyond contusion sites ipsilateral and contralateral to the injury site. ⋯ Acute axonal alterations detected with NF68 were minimal compared to immunofluorescence changes seen in dendritic regions. Therefore, preferential dendritic cytoskeletal derangements may be an early morphological feature of experimental traumatic brain injury in vivo. In addition, these cytoskeletal derangements may not be exclusively restricted to sites of contusion and cell death.
-
Critical care medicine · Jan 1996
Hypertonic saline does not improve cerebral oxygen delivery after head injury and mild hemorrhage in cats.
To investigate the effects of hypertonic saline for resuscitation after mild hemorrhagic hypotension combined with fluid-percussion traumatic brain injury. Specifically, the effects of hypertonic saline on intracranial pressure, cerebral blood flow (radioactive microsphere method), cerebral oxygen delivery (cerebral oxygen delivery = cerebral blood flow x arterial oxygen content), and electroencephalographic activity were studied. ⋯ After a combination of hemorrhage and traumatic brain injury, neither 10% hydroxyethyl starch nor 3.0% hypertonic saline restored cerebral oxygen delivery. Although neither trauma alone nor hemorrhage alone altered electroencephalographic activity, the combination produced significant decreases in electroencephalographic activity at 60 and 120 mins after resuscitation in groups 3 and 4, suggesting that cerebral oxygen delivery is inadequately restored by either resuscitation fluid. Therefore, traumatic brain injury abolished compensatory cerebral blood flow increases to hemodilution, and neither hydroxyethyl starch nor 3.0% hypertonic saline restored cerebral blood flow, cerebral oxygen delivery, or electroencephalographic activity after hemorrhagic hypotension after traumatic brain injury.
-
The purpose of this study was to evaluate the effects of mannitol (Man), dexamethasone (DM), dichloroacetic acid (DCA) and 1,3-butanediol (BD) in reduction of posttraumatic cortical edema following brain deformation injury to rats. Ten minutes prior to fluid percussion injury, each animal received one of four pretreatments or placebo: Man, 1 g/kg intravenously, DM 3.0 mg/kg intravenously, DCA 25 mg/kg intraperitoneally BD 0.5 mg/kg intraperitoneally (n = 12 per treatment group), or equivolume saline (n = 8 per corresponding trauma group). Six hours after trauma, cortical tissue was harvested. ⋯ The measured cortical SpG from traumatized animals receiving Man (mean 1.037 +/- SEM .001), DCA (1.038 +/- .001), and BD (1.039 +/- .001) were equal to SpG from untraumitized cortex (1.041 +/- .001), and were significantly greater than SpG from traumatized cortex for animals receiving DM (1.035 +/- .001) or placebo (1.033 +/- .002). Pretreatment with DCA, Man, and BD appears to protect against development of posttraumatic cortical edema when measured 6 hours after blunt head trauma in the rat. Each of these chemical treatments appears effective in preventing or reducing posttraumatic cortical edema.