18th Meeting of the European Neurological Society
07.06.2008 - 11.06.2008
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Home - 09.06.2008 - Multiple sclerosis


Multiple sclerosis

Monday, June 09, 2008, 11:30 - 13:00

Rapid onset central motor plasticity is not compromised in multiple sclerosis patients

D. Zeller, K. Aufm Kampe, K. Stefan, R. Gentner, K.V. Toyka, P. Rieckmann, J. Classen (Wurzburg, Rostock, DE)

Multiple sclerosis (MS) is an inflammatory demyelinating disease which also leads to substantial axonal injury. Neuronal plasticity is believed to represent an important substrate for recovery from and compensation of motor deficits resulting from demyelination and axonal lesions. The ability of the central nervous system to undergo plastic changes may have an important influence on the relationship between MS pathology and its clinical expression. Although chronic regional reorganization has been demonstrated in MS patients, it remains unknown if the mechanisms and the capacity to express central motor plasticity in MS patients are compromised in the short term. In the present study, we examined rapid onset central motor plasticity, and its relationship to motor impairment in 22 patients with MS (age 36.6 10.7 years; 16 women; EDSS 2.3 1.2). Motor plasticity was studied both neurophysiologically and behaviourally, at least 6 months after the last relapse. We used paired associative stimulation (PAS) which combines repetitive electric stimulation of the median nerve with subsequent transcranial magnetic stimulation (TMS) of the contralateral motor cortex. PAS models long-term potentiation of synaptic efficacy in the human primary motor cortex and thus may tap into an important physiological mechanism underlying neuronal plasticity. Additionally, dynamic motor learning was tested by an isometric force production task. Motor impairment was assessed neurophysiologically by the corticomuscular latency to the abductor pollicis brevis muscle as tested by TMS, and by a battery of five functional motor tests. MS patients had significantly longer corticomuscular latencies and performed significantly worse than healthy controls in a weighted measure of functional motor tests. Changes in corticospinal excitability induced by PAS were comparable between MS patients and controls. Baseline-adjusted training-induced motor performance increased similarly in patients and controls. Neither PAS-induced plasticity nor motor learning performance correlated with motor impairment. Comparing good and poor motor performers within the patient group, there were no significant differences with respect to either PAS-induced increases of cortical excitability or motor learning success. The present findings support the notion that, despite significant motor impairment, rapid motor system plasticity remains intact in MS patients, both neurophysiologically and behaviorally.