Journal of neurotrauma
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In order to quantify degenerative and regenerative changes and analyze the contribution of multiple factors to the outcome after neurite transection, we cultured adult mouse dorsal root ganglion neurons, and with a precise laser beam, we transected the nerve fibers they extended. Cell preparations were continuously visualized for 24 h with time-lapse microscopy. More distal cuts caused a more elongated field of degeneration, while thicker neurites degenerated faster than thinner ones. ⋯ Branching slowed the regenerative process, while simultaneous degeneration of uncut neurites increased it. Proximal lesions, small neuronal size, and extensive and rapid neurite degeneration were predictive of death of an injured neuron, which typically displayed necrotic rather than apoptotic form. In conclusion, this in vitro model proved useful in unmasking many new aspects and correlates of mechanically-induced neurite injury.
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Polyuria contributes to bladder overdistention, which confounds both lower and upper urinary tract management in individuals having a spinal cord injury (SCI). Bladder overdistention post-SCI is one of the most common triggers for autonomic dysreflexia, a potentially life-threatening condition. Post-SCI polyuria is thought to result from loss of vascular tone in the lower extremities, leading to edema and subsequent excess fluid, resulting in polyuria. ⋯ Step training (30 min/day, 6 days/week) did not alleviate polyuria in the moderate SCI contusion group. These results indicate that (1) mild injuries retaining weight-bearing locomotion that should have mild, if any, edema/loss of vascular tone still exhibit severe polyuria, and (2) step training was unable to reduce post-SCI polyuria. Taken together, these results indicate that the current mechanistic hypothesis of post-SCI polyuria may be incomplete.
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Journal of neurotrauma · Oct 2012
Persistence of disability 24 to 36 months after pediatric traumatic brain injury: a cohort study.
This study examined the outcome of 0- to 17-year-old children 36 months after traumatic brain injury (TBI), and ascertained if there was any improvement in function between 24 and 36 months. Controls were children treated in the emergency department for an arm injury. Functional outcome 36 months after injury was measured by the Pediatric Quality of Life Inventory (PedsQL), the self-care and communication subscales of the Adaptive Behavior Assessment Scale-2nd edition (ABAS-II), and the Child and Adolescent Scale of Participation (CASP). ⋯ Compared to the baseline assessment, children with moderate or severe TBI had significantly poorer functioning on the ABAS-II and poorer participation in activities (CASP). There was no significant improvement in any group on any outcomes between 24 and 36 months. Post-injury interventions that decrease the impact of these deficits on function and quality of life, as well as preventive interventions that reduce the likelihood of TBI, should be developed and tested.