Journal of neurotrauma
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Journal of neurotrauma · Oct 2010
Development of autonomic dysreflexia after spinal cord injury is associated with a lack of serotonergic axons in the intermediolateral cell column.
Autonomic dysreflexia consistently develops in patients and in rats after severe upper thoracic spinal cord injury (SCI) as a result of exaggerated spinal sympathetic excitation. In this study we induced episodic hypertension in rats after varying degrees of SCI severity to investigate the contribution of serotonergic bulbospinal axons to the development of autonomic dysreflexia after SCI. Female Wistar rats (250-300 g) were used in all experiments in the following groups: (1) uninjured, (2) clip compression at T4 of 20, 35, or 50 g, (3) spinal cord transection at T4, and (4) intrathecal 5,7-dihydroxytryptamine creatinine sulfate (5,7-DHT). ⋯ Intrathecal administration of the 5-HT(2A) agonist dimethoxy-4-iodamphetamine increased resting MAP and blocked colon distension-induced hypertension, whereas the 5-HT(2A) antagonist ketanserin decreased resting MAP and was permissive to the colon distension-induced pressor response in SCI rats. These results suggest that the SCI-induced loss of serotonergic inputs into the spinal cord IMLC is proportional to the pathogenesis of autonomic dysreflexia and hypotension seen after SCI. We thus conclude that sparing of serotonergic axons beyond a critical threshold preserves cardiovascular regulation and prevents the development of autonomic dysreflexia.
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Journal of neurotrauma · Oct 2010
Docosahexaenoic acid prevents white matter damage after spinal cord injury.
We have previously shown that the omega-3 fatty acid docosahexaenoic acid (DHA) significantly improves several histological and behavioral measures after spinal cord injury (SCI). White matter damage plays a key role in neurological outcome following SCI. Therefore, we examined the effects of the acute intravenous (IV) administration of DHA (250 nmol/kg) 30 min after thoracic compression SCI in rats, alone or in combination with a DHA-enriched diet (400 mg/kg/d, administered for 6 weeks post-injury), on white matter pathology. ⋯ By 6 weeks, damage to myelin and serotonergic fibers was also reduced. For some of the parameters measured, the combination of DHA injection and DHA-enriched diet led to greater neuroprotection than DHA injection alone. These findings demonstrate the therapeutic potential of DHA in SCI, and clearly indicate that this fatty acid confers significant protection to the white matter.
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Journal of neurotrauma · Sep 2010
Multicenter Study Comparative StudyClinical evaluation of a portable near-infrared device for detection of traumatic intracranial hematomas.
The purpose of this multicenter observational clinical study was to evaluate the performance of a near-infrared (NIR)-based, non-invasive, portable device to screen for traumatic intracranial hematomas. Five trauma centers collected data using the portable NIR device at the time a computed tomography (CT) scan was performed to evaluate a suspected traumatic brain injury (TBI). The CT scans were read by an independent neuroradiologist who was blinded to the NIR measurements. ⋯ For all 96 cases with intracranial hemorrhage, regardless of size and type of hemorrhage, the sensitivity was 68.7% (CI 58.3,77.6%), and specificity was 90.7% (CI 86.4,93.7%). These results confirm the results of previous studies that indicate that a NIR-based portable device can reliably screen for intracranial hematomas that are superficial and of a size likely to be of clinical importance. The NIR device cannot replace CT scanning in the diagnosis of TBI, but the device might be useful to supplement clinical information used to triage TBI patients, and in situations in which CT scanning is not readily available.
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Journal of neurotrauma · Sep 2010
Multicenter Study Comparative StudyOutcomes of patients with severe traumatic brain injury who have Glasgow Coma Scale scores of 3 or 4 and are over 65 years old.
The goal of this study was to investigate the outcomes of patients with traumatic brain injury (TBI) who had Glasgow Coma Scale (GCS) scores of 3 or 4, and were aged 66 years or older. Between January 2001 and December 2005, 13 European centers enrolled patients with severe brain trauma. Data sets of all patients who had a GCS score of 3 or 4 and were 66 years of age or older were analyzed. ⋯ Patients with GCS scores of 3 or 4 who are older than 65 years have a poor, but not hopeless, prognosis. Confirmed factors predicting poor prognosis for this group of patients were closed basal cisterns and midline shift >15 mm on the first CT scan. Factors possibly related to favorable outcomes were female gender, lower trauma severity, open or partially open basal cisterns, and no midline shift on the first CT scan.
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Journal of neurotrauma · Sep 2010
Randomized Controlled Trial Comparative StudyHow mild traumatic brain injury may affect declarative memory performance in the post-acute stage.
Memory deficits are among the most frequently reported sequelae of mild traumatic brain injury (MTBI), especially early after injury. To date, these cognitive deficits remain poorly understood, as in most patients the brain is macroscopically intact. To identify the mechanism by which MTBI causes declarative memory impairments, we probed the functionality of the medial temporal lobe (MTL) and the prefrontal cortex (PFC), within 6 weeks after injury in 43 patients from a consecutive cohort, and matched healthy controls. ⋯ In contrast, no difference in prefrontal activation was found between patients and controls, nor was there a relation with injury severity. On a behavioral level, injury severity was inversely related to declarative memory performance. In all, these findings suggest that reduced medial temporal functionality may contribute to poorer declarative memory performance in the post-acute stage of MTBI, especially in patients with longer post-traumatic amnesia.