Neuroplasticity Research

KEY FINDING: Spinal cord injury (SCI) leads to severe sensorimotor dysfunction by damaging the corticospinal system, but the CNS possesses considerable plasticity that can be harnessed for recovery.

KEY FINDING: New myelin generation peaks at 3 months post-injury but continues for at least 6 months after SCI, indicating a prolonged remyelination response.

KEY FINDING: Spinal interneuron reorganizations are subtype specific and may be adaptive or maladaptive for a given functional output.

KEY FINDING: Exercise enhances neuroplasticity by increasing BDNF, IGF-1, and VEGF production, creating a neural environment primed for change in neurological disorders and injuries.

KEY FINDING: Following CSCI, patients may experience shallow and rapid breathing to maintain minute ventilation, but tidal volume tends to decrease under these circumstances.

KEY FINDING: A low dose of 4-MU (1.2 g/kg/day) reduced hyaluronan and chondroitin sulfate levels in uninjured spinal cords.

KEY FINDING: A single arm cycling session increased the excitability of the corticospinal pathway to the erector spinae (ES) muscle in both SCI and able-bodied individuals.

KEY FINDING: Overall, inhibiting the Nogo-A pathway led to an 18.9% improvement in neurobehavioral outcomes across all studies.

KEY FINDING: T12-L3 nerve transfer (NT) qualitatively improved locomotion in rats with mild thoracolumbar contusion (SCImi) and in animals with subacute moderate contusion (SCImo).

KEY FINDING: Significant differences were found in SSEP signal amplitudes when stimulating either forelimb in rats with normothermia compared to those treated with hypothermia on days 4 and 7 post-SCI.