Journal of neurotrauma
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Journal of neurotrauma · Feb 1995
The effect of acute cocaine or lidocaine on behavioral function following fluid percussion brain injury in rats.
One of the goals of our laboratory is to examine how the presence of drugs of abuse will influence traumatic brain injury. Previous studies in our laboratory have shown that cocaine or lidocaine treatment before experimental fluid percussion brain injury in rats reduces the cortical hypoperfusion normally found in the early posttraumatic period. The purpose of the current study was to determine if pretreatment with cocaine or lidocaine is also associated with changes in trauma-induced suppression of reflexes and motor and cognitive dysfunction that occurs following traumatic brain injury (TBI). ⋯ Lidocaine and cocaine did not affect cognitive function on days 11-15 postinjury. The mechanism by which lidocaine improves acute neurological and motor function following brain injury is unknown, but may involve improved posttraumatic cortical blood flow, as seen in our previous study. Our results, along with other studies showing lidocaine to be neuroprotective in animal models of ischemia, suggest that studies of the effect of posttraumatic administration of lidocaine are warranted.
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Journal of neurotrauma · Dec 1994
Combined fluid percussion brain injury and entorhinal cortical lesion: a model for assessing the interaction between neuroexcitation and deafferentation.
Laboratory studies suggest that excessive neuroexcitation and deafferentation contribute to long-term morbidity following human head injury. Because no current animal model of traumatic brain injury (TBI) has been shown to combine excessive neuroexcitation and significant levels of deafferentation, we developed a rat model combining the neuroexcitation of fluid percussion TBI with subsequent entorhinal cortical (EC) deafferentation. In this paradigm, moderate fluid percussion TBI was induced in each rat, followed 24 h later by bilateral EC lesion (BEC). ⋯ Specifically, the laminar pattern of presynaptic rearrangement induced by BEC lesion did not occur after TBEC injury. The present results show that axonal injury and its attendant deafferentation, when coupled with traumatically induced neuroexcitation, produce an enhancement of the morbidity associated with TBI. Moreover, they indicate that this model can effectively be used to study the interaction between neuroexcitation and synaptic plasticity.
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Journal of neurotrauma · Dec 1994
Widespread metabolic depression and reduced somatosensory circuit activation following traumatic brain injury in rats.
The effects of fluid percussion brain injury on the basal metabolic state and responsiveness of a somatosensory circuit to physiologic activation were investigated with [14C]2-deoxyglucose autoradiography. Under controlled physiologic conditions and normothermic brain temperature (37 degrees C), rats were injured with a moderate fluid percussion pulse ranging from 1.7 to 2.1 atm. At 4 or 24 h after traumatic brain injury (TBI), unilateral vibrissae stimulation was carried out, resulting in the metabolic activation of the whisker-barrel circuit. ⋯ Although the most severe and longer lasting metabolic consequences occurred in cortical and thalamic regions destined to exhibit histopathologic damage, milder abnormalities, most prominent in the early posttraumatic period, were also seen in noninjured areas. The inability to activate the somatosensory circuit metabolically indicates that circuit dysfunction is an acute consequence of TBI. Widespread circuit or synaptic dysfunction would be expected to participate in the functional and behavioral consequences of TBI.
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Journal of neurotrauma · Oct 1994
Different cerebral hemodynamic responses following fluid percussion brain injury in the newborn and juvenile pig.
The present study was designed to characterize the influence of early developmental changes on the relationship among systemic arterial pressure, cerebral hemodynamics, and cerebral oxygenation during the first 3 h following percussion brain injury. Anesthetized newborn (1-5 days old) and juvenile (3-4 weeks old) pigs equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. Brain injury of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. ⋯ These data show that the effects of comparable brain injury level were very different in newborn and juvenile pigs. Further, these data suggest that reductions in cerebral blood flow following brain injury are more dependent on changes in reactivity of arterioles. Finally, these data suggest that the decrease in cerebral oxygenation, an index of metabolism, coupled with reduced cerebral blood flow, could result in profound hypoperfusion after brain injury.