Aggression after traumatic brain injury (TBI) is common but not well defined. Sixty-seven participants with first-time TBI were seen within three months of injury and evaluated for aggression. The prevalence of aggression was found to be 28.4% and to be predominantly verbal aggression. Post-TBI aggression was associated with new-onset major depression (p=0.02), poorer social functioning (p=0.04), and increased dependency on activities of daily living (p=0.03), but not with a history of substance abuse or adult/childhood behavioral problems. Implications of the study include early screening for aggression, evaluation for depression, and consideration of psychosocial support in aggressive patients.
In contrast to relapse, the mechanisms of multiple sclerosis (MS) disease progression are less understood and appear not to be exclusively inflammatory in nature. In this pilot study we investigated the relationship between disturbed CNS energy metabolism and MS disease progression. We tested the hypothesis that cerebrospinal fluid (CSF) concentrations of sorbitol, fructose, and lactate, all metabolites of extra-mitochondrial glucose metabolism, would be elevated in secondary progressive (SP) MS patients and would be associated with worsening neurologic disability. We measured metabolite concentrations by gas chromatographic/mass spectrometric and enzymatic methods in archived CSF samples from 85 MS patients [31 relapsing-remitting (RR) and 54 SP patients] and 18 healthy controls. We found that concentrations of all three metabolites, but not concentrations of glucose or myoinositol, were significantly increased in CSF from SP and, to a lesser degree, RR patients, compared to controls. Furthermore, CSF concentrations of sorbitol and fructose (polyol pathway metabolites), but not lactate (anaerobic glycolysis metabolite), correlated positively and significantly with Expanded Disability Status Scale (EDSS) score, an index of neurologic disability in MS patients. We conclude that extra-mitochondrial glucose metabolism is increased in MS patients and is associated with disease progression evidenced by increasing EDSS score. As extra-mitochondrial glucose metabolism increases with impaired mitochondrial metabolism of glucose, these findings implicate mitochondrial dysfunction in the pathogenesis of MS disease progression. CSF metabolic profiling may be useful in clarifying the role of mitochondrial pathology in progression and in targeting and monitoring therapies for disease progression that aim to preserve or boost mitochondrial glucose metabolism.
There is a high prevalence of SWCD in CHI patients admitted to a brain injury rehabilitation unit. Patients with SWCD have longer stays in both acute and rehabilitation settings and may be a marker for more severe injury.
Primary objective-To assess the prevalence of and risk factors for sleep disturbances in the acute post-traumatic brain injury (TBI) period.Research design-Longitudinal, observational study.Methods and procedures-Fifty-four first time closed-head injury patients were recruited and evaluated within 3 months after injury. Pre-injury and post-injury sleep disturbances were compared on the Medical Outcome Scale for Sleep. The subjects were also assessed on anxiety, depression, medical comorbidity and severity of TBI.Main outcomes and results-Subjects were worse on most sleep measures after TBI compared to before TBI. Anxiety disorder secondary to TBI was the most consistent significant risk factor to be associated with worsening sleep status.Conclusions-Anxiety is associated with sleep disturbances after TBI. Further studies need to be done to evaluate if this is a causal relationship.
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