Articles: brain-injuries.
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J Int Neuropsychol Soc · Nov 1999
Comparative StudyPolysubstance abuse and traumatic brain injury: quantitative magnetic resonance imaging and neuropsychological outcome in older adolescents and young adults.
Few studies have examined the consequences of alcohol and drug abuse on TBI though they commonly co-occur. Both TBI and substance abuse independently result in neuropathological changes in the brain such as ventricular enlargement and cortical atrophy, thus it is reasonable to hypothesize that the combination of the two would result in more significant cerebral damage. In this study, 3 groups of patients--traumatically brain injured (TBI) with substance abuse (N = 19), TBI without substance abuse (N = 19), and substance abuse with no TBI (N = 16)--were compared with normal controls (N = 20) on several quantitative MRI (QMRI) measures. ⋯ When controlling for head injury severity, the effects of substance abuse in combination with TBI resulted in greater atrophic changes than seen in any other group. TBI and substance abuse patients' neuropsychological test performances also were examined, and no differences were found among patient groups on any measures. These findings have implications for the deleterious interaction of substance abuse combining with TBI to result in greater neuropathological changes that can be detected by QMRI techniques.
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Experimental neurology · Nov 1999
Cyclosporin A attenuates acute mitochondrial dysfunction following traumatic brain injury.
Experimental traumatic brain injury (TBI) results in a rapid and significant necrosis of cortical tissue at the site of injury. In the ensuring hours and days, secondary injury exacerbates the primary damage, resulting in significant neurological dysfunction. Recent reports from our lab and others have demonstrated that the immunosuppressant cyclosporin A (CsA) is neuroprotective following TBI. ⋯ Similarly, synaptosomes isolated from CsA-treated animals demonstrate a significant increase in mitochondria membrane potential, accompanied by lower levels of intramitochondrial Ca2+ and reactive oxygen species production than seen in vehicle-treated animals. These results suggest that the neuroprotective properties of CsA are mediated through modulation of the MPTP and maintenance of mitochondria homeostasis. Amelioration of cortical damage with CsA indicates that pharmacological therapies can be devised which will significantly alter neurological outcome after injury.
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Brain injury : [BI] · Nov 1999
Randomized Controlled Trial Clinical TrialCognitive and behavioural efficacy of amantadine in acute traumatic brain injury: an initial double-blind placebo-controlled study.
The objective of the current study was to determine the efficacy of amantadine in improving cognitive and behavioural performance in a traumatic brain injury (TBI) rehabilitation sample. The design was a prospective, randomized, double-blind, placebo-controlled, crossover design. Subjects were 10 adult traumatic brain injury patients in an acute brain injury rehabilitation unit. ⋯ In conclusion, although patients generally improved, this initial exploratory study found no differences in rate of cognitive improvement between subjects given amantadine versus those given placebo. However, the small sample size, heterogeneous population, acute time course, and large number of dependent variables limit power and generalizability. Implications are discussed for further research to better answer questions regarding efficacy of amantadine post-TBI.
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Comparative Study
The effects of acute and chronic alcohol ingestion on outcome following multiple episodes of mild traumatic brain injury in rats.
Recent studies suggest that in some circumstances, alcohol intoxication at the time of severe head injury may be neuroprotective. The objective of this study was to determine the effect of acute and chronic alcohol ingestion on outcome in rodents sustaining multiple episodes of mild traumatic brain injury while intoxicated. ⋯ The injured intoxicated CA animals had a more rapid recovery of reflexes compared with the injured intoxicated NA animals. Despite initial MWM deficits, the injured NA rodents eventually began to learn the MWM. The injured CA rats never learned the maze. Under the conditions of this study, acute alcohol intoxication at the time of multiple episodes of minor head trauma did not provide neuroprotection for NA or CA rodents.
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Critical care medicine · Nov 1999
Comparative StudyComparison of jugular venous oxygen saturation and brain tissue Po2 as monitors of cerebral ischemia after head injury.
To compare the characteristics of jugular venous oxygen saturation (Sjvo2) and brain tissue Po2 (Pbto2) as monitors for cerebral ischemia after severe head injury. Sjvo2 has been useful as a monitor for cerebral ischemia, but it is limited by its inability to identify regional cerebral ischemia. Pbto2 may be superior to Sjvo2 for this purpose, because oxygenation in localized areas of the brain can be monitored. ⋯ The two monitors provide complimentary information, and neither monitor alone identifies all episodes of ischemia. The best strategy for using these monitors is to take advantage of the unique features of each monitor. Sjvo2 should be used as a monitor of global oxygenation; but Pbto2 should be used as a monitor of local oxygenation, ideally with the catheter placed in an area of the brain that is vulnerable to ischemia but that may be salvageable with appropriate treatment.