ABSTRACT
It is commonly acknowledged that rehabilitative interventions, particularly in neurorehabilitation, do not affect the underlying disease process. However, the concept of neural plasticity opens the possibility of helping recovery at the cellular level through rehabilitation. Plasticity is defined as ‘the tendency of synapses and neuronal circuits to change because of activity’4. ‘Fast’ short-term plasticity is related to down-regulation of γ-aminobutyric acid (GABA), while ‘slow’ long-term plasticity involves structural
changes and long-term potentiation. The assessment of plasticity can be performed at the microscopic level, but in the clinical setting, non-invasive procedures including functional imagery (such as positron emission tomography (PET), single photon emission computed tomography (SPECT) and functional magnetic resonance imaging (fMRI) and transcranial magnetic stimulation (TMS) are obviously preferred. Most of the literature on plasticity and rehabilitation deals with stroke and spinal cord or brain injury. In stroke survivors, for example, where most of the rehabilitation is aimed at compensating for impairments and functional limitations, a more active strategy for stimulating recovery has been advocated, with the use of oral medications (e.g. dextroamphetamine, methylphenidate), and increasing focus on the impaired limbs (e.g. constraintinduced movement therapy, bilateral movement rehabilitation, partial body weight-supported treadmill training, neurostimulation)5,6. It is conceivable to apply the same concepts to MS, even though limitations can be expected due to the presence of multiple lesions and to the ongoing disease process7.
