AA

Neuroplasticity

Spontaneous neuronal plasticity occurs through various mechanisms and has been demonstrated primarily in animal models.  Recovery mechanisms following complete injuries may include recovery of nerve roots beside the lesion level, changes in the gray matter of the spinal cord at the lesion level, reorganization of existing spinal circuits and peripheral changes (Bradbury & McMahon 2006; Kern et al. 2005; Ding et al. 2005; Hagg & Oudega 2006; Ramer et al. 2005).  The evidence for spontaneous axonal regeneration is limited as a small proportion of fibres regenerate and over a modest distance (Bradbury & McMahon 2006). However, cortical re-organization can occur, for example, Lotze et al. (2006) showed that cortical representation of elbow movements following a complete thoracic injury in humans was moved toward cortical areas which represented the injured thoracic regions.  There is evidence that a pattern-generating spinal circuitry (also known as a central pattern generator) is retained following a complete injury which can produce stepping-like movements and activation patterns with epidural lumbar cord stimulation (Kern et al. 2005) or treadmill stimulation (Dietz et al. 2002). However, the functional consequences of these observations are yet to be determined.

Incomplete injuries may have a greater extent of axonal sprouting and axonal growth (Ding et al. 2005; Hagg & Oudega 2006).  In incomplete spinal cord injury in rats, transected hindlimb corticospinal tract axons sprouted into the cervical gray matter to contact short and long propriospinal neurons (Bareyre et al. 2004).  Following cervical lesions of the rat dorsal corticospinal motor pathway which contains more than 95% of all corticospinal axons, there was spontaneous sprouting from the ventral corticospinal tract onto medial motoneuron pools (Weidner et al. 2001).  This sprouting was paralleled by functional recovery.  Ramer et al. (2005) suggested that if axonal regeneration occurs or if synaptic spaces become occupied with different axons, functional recovery will require retraining to optimize these new circuits.  The neuroplastic changes which underlie spontaneous recovery may be enhanced by physical interventions (e.g., exercise, electrical stimulation) and pharmacological agents (Ramer et al. 2005).