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Lack of post‐exercise depression of corticospinal excitability in patients with Parkinson's disease
Author(s) -
Khedr E. M.,
Galal O.,
Said A.,
Abdelsameea M.,
Rothwell J. C.
Publication year - 2007
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2007.01858.x
Subject(s) - medicine , depression (economics) , parkinson's disease , physical medicine and rehabilitation , disease , neuroscience , physical therapy , psychiatry , psychology , economics , macroeconomics
There is lack of clarity in the literature over whether patients with Parkinson's disease (PD) show the same post‐exercise depression of corticospinal excitability as is usually observed in healthy control. This study set out to resolve the problem. Ten patients with idiopathic PD and 10 age‐matched controls were included in this study. Each subject performed a submaximal sustained voluntary contraction of the right first dorsal interosseous muscle (FDI) for 10 min or until force could no longer be sustained. Resting motor threshold, motor‐evoked potential (MEP), input–output curve, cortical silent period duration, interference pattern (IP) and M/F ratio were recorded at baseline, immediately after fatigue and after 20 min rest. Immediately after exercise, decreased MEP amplitude and increased cortical SP duration were observed in the control group whilst no such changes were observed in PD patients. The input–output curve was also significantly suppressed only in controls, but not in patients. The amplitude of IP was significantly reduced immediately after exercise in both PD patients and controls. Almost all these changes returned nearly to baseline values after 20 min rest. The amount of exercise was approximately equal in both groups because the effect on M‐waves and EMG amplitude was similar. However, the expected decline in corticospinal excitability was absent in PD patients. The absence of this effect in PD patients may reflect reorganization of motor commands in response to basal ganglia deficit.