Browse our collection of 12,052 research summaries, all carefully curated and simplified for the spinal cord injury community.
Showing 11,931-11,940 of 12,052 results
Arch Phys Med Rehabil, 2006 • October 1, 2006
The purposes of this study are (1) to determine the error attributable to external measurements of tibia length and (2) to establish the difference in BMD along the distal tibia that may occur as a re...
KEY FINDING: Absolute BMD error was greater for able-bodied than for SCI subjects (5.87mg/cm3 vs 4.5mg/cm3).
J Comp Neurol, 2006 • October 1, 2006
The study investigates the fate of endogenous stem/progenitor cells following spinal cord injury (SCI) in adult rats and mice. It demonstrates that constitutively dividing progenitor cells are vulnera...
KEY FINDING: Constitutively proliferating adult progenitor cells are vulnerable to spinal cord injury, leading to their death or reduced proliferation.
Health and Quality of Life Outcomes, 2006 • August 23, 2006
The study investigates the cross-diagnostic validity of the FIM™ motor items in patients with spinal cord injury, stroke, and traumatic brain injury using Rasch analysis. Results indicate that the ori...
KEY FINDING: The original seven-category scoring system for the FIM™ motor items was found to be invalid, necessitating extensive rescoring.
The Journal of Neuroscience, 2006 • August 23, 2006
The study developed a rat model of cauda equina injury and repair to examine if implantation of avulsed lumbosacral ventral roots into the spinal cord could restore lower urinary tract function. The f...
KEY FINDING: Avulsion injuries led to urinary retention, absence of bladder contractions and EUS EMG activation, increased bladder size, and retrograde death of autonomic and motoneurons.
Molecular Pain, 2006 • August 17, 2006
This study demonstrates that peripheral nerve injury induces changes in the excitability and sodium channel expression in the VPL nucleus of the thalamus. Specifically, the expression of Nav1.3 sodium...
KEY FINDING: Peripheral nerve injury (CCI) leads to increased firing rates of VPL neurons in response to peripheral stimuli.
J Neurosci Res, 2006 • August 15, 2006
This study evaluates lentiviral, adenoviral, and retroviral vectors for gene delivery to the spinal cord, focusing on transgene expression and inflammatory responses. Lentiviral vectors provided the m...
KEY FINDING: Lentiviral vectors had the most stable pattern of gene expression, with D15A levels remaining high at 4 weeks after both in vivo and ex vivo delivery.
Phil. Trans. R. Soc. B, 2006 • August 4, 2006
This review discusses some aspects of plasticity of connections after spinal injury in adult animal models as a basis for functional recovery of locomotion. It is concluded that recovery is partly due...
KEY FINDING: Locomotor training can modify the excitability of reflex pathways and complex neural circuits within the spinal cord.
J Appl Physiol, 2006 • August 1, 2006
The study quantified postfatigue potentiation in acutely and chronically paralyzed soleus muscles and determined the effect of long-term electrical stimulation training on potentiation characteristics...
KEY FINDING: Chronically paralyzed muscles show significant postfatigue potentiation, while acutely paralyzed muscles do not.
Nat Rev Neurosci, 2006 • August 1, 2006
The review discusses the inhibitory molecules in the adult CNS environment responsible for regenerative failure after injury. These inhibitors are associated with later stages of nervous system develo...
KEY FINDING: CNS myelin and glial scars inhibit axon outgrowth, but their relative importance in vivo is uncertain. Myelin inhibitors are constitutively expressed, while CSPGs are strongly upregulated following injury, with different time courses of expression ranging from 24 hours to 6 months post-lesion.
Phil. Trans. R. Soc. B, 2006 • July 31, 2006
CNS injuries have limited repair capabilities, but functional recovery is observed, which is variable. Neurite growth and new circuit formation require reactivation of developmental mechanisms, suppre...
KEY FINDING: Inactivation of Nogo-A promotes axonal regeneration and improved behavioral recovery after spinal cord injury.