By Dr. Richard Lauer;

While cerebral palsy (CP) is characterized by impairments in the development of movement and posture that are attributed to disturbances that occurred in the developing fetal or infant brain, many interventions used to treat children with CP do not address the underlying neurological changes. Instead, interventions focus on the end-stage consequences of CP such as altered movement patterns, or the fatigue that occurs during the execution of a task. However, there is now considerable evidence that the sensory and motor areas of the brain are dynamically maintained in both normal and brain-injured animals, as well as humans, and these areas are continuously modulated in response to activity, behavior, and skill acquisition2,3. The evidence suggests a form of neural plasticity – the ability of the brain to remodel itself through experience.

Multiple mechanisms have been proposed to explain the varied nature of neural plasticity. Functional changes in the brain may be due to deafferentation, removal of inhibition, activity-dependent synaptic changes, changes in membrane excitability, axonal regeneration and sprouting, or unmasking of pre-existing conditions2,3. These events can occur within minutes following a brain insult, or more slowly over months or years4,5. Rapid changes in cortical representations are a likely result from the unmasking of latent synaptic connections with the removal of inhibition. Plasticity over longer time periods likely involves cellular changes associated with long-term potentiation and activity-dependent growth of new connections2,3. Such findings in basic neuroplasticity have coupled with a growing knowledge of motor learning, biomechanics, and exercise science to provide the stimulus for motor rehabilitation research and the development of neural rehabilitation therapies6.

Interestingly, multiple imaging studies in children with CP have demonstrated unusual patterns of bilateral cortical activity during the execution of motor tasks using both the upper and lower extremities7,8. These studies suggest that the clinical features of the movement disorders seen in these children are the consequence of the unusual activity patterns in the brain and spinal cord. It should also be noted that the findings demonstrate the plasticity of central motor pathways in response to supraspinal lesions in children with CP. Given the highly adaptive nature of the brain and spinal cord in response to behavior, activity, and skill acquisition, interventions that have an effect on the activity of the neural cells at any level could also induce plastic changes.

Functional electrical stimulation (FES), by direct excitation of motor and sensory pathways, can provide a unique and powerful resource that has the potential to induce long term changes within the brain, with immediate improvements in movement. A great deal of research has already been done in the area of FES applications to children with CP, but application to the wider population with CP is hampered by the fact that many of the reported outcomes are case or pilot studies. A recent review article on FES on walking ability in children with CP highlighted this discrepancy, bringing much needed attention to the great deal of variation that exists in the protocols across studies, and the need for more rigorous research designs9. Furthermore, the effects of FES on the central nervous system with regards to spinal and cortical control of movement and neural plasticity, while speculated, are not fully understood. These are avenues of future investigation that need to be addressed before the clinical acceptance and utilization of this intervention.

References
1. Rosenbaum P, Paneth N, Leviton A et al. A report: the definition and classification of cerebral palsy April 2006. Dev Med Child Neurol Suppl 2007; 109: 8-14.
2. Butefisch CM, Davis BD, Wise SP, Sawaki L, Kopylev L, Classen J, et al. Mechanisms of use dependent plasticity in the human motor cortex. Proceedings National Academy of Science 2005;97: 3661-3665.
3. Chen R, Cohen LG, Hallet M. Nervous system reorganization following injury. Neuroscience 2002; 111(40):761-773.
4. Jones EG, Pons TP. Thalamic brainstem contributions to large scale plasticity of the primate somatosensory cortex. Science 1998;282(5391):1121-1125.
5. Nicholelis MA. Dynamic and distributed somatosensory representations as the substance for cortical and subcortical plasticity. Pediatric Research 1997;45(1):559-567.
6. Shepherd RB. Exercise and training to optimize functional motor performance in stroke: Driving neural reorganization? Neural Plasticity 2001;8(1-2):121-129.
7. Briellmann RS, Abbott DF, Caflisch U, Archer JS, Jackson JD. Brain reorganization in cerebral palsy: A high-field functional MRI study. Neuropediatrics 2002;33(3):162-165.
8. Farmer SF, Harrison LM, Ingram DA, Stephens JA. Plasticity of central motor pathways in children with hemiplegic cerebral palsy. Neurology 1991;41(9):1505-1510.
9. Seifart A, Unger M, Burger M. The effect of lower limb functional electrical stimulation on gait of children with cerebral palsy. Pediatr Phys Ther. 2009; 21(1):23-30.