Impaired motor cortical inhibition in Parkinson's disease: motor unit responses to transcranial magnetic stimulation

Citation
Bu. Kleine et al., Impaired motor cortical inhibition in Parkinson's disease: motor unit responses to transcranial magnetic stimulation, EXP BRAIN R, 138(4), 2001, pp. 477-483
Citations number
45
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EXPERIMENTAL BRAIN RESEARCH
ISSN journal
00144819 → ACNP
Volume
138
Issue
4
Year of publication
2001
Pages
477 - 483
Database
ISI
SICI code
0014-4819(200106)138:4<477:IMCIIP>2.0.ZU;2-R
Abstract
Transcranial magnetic stimulation (TMS)-induced corticospinal volleys can b e investigated in detail by analysing the firing pattern modulation of acti ve motor units (MUs) at close to threshold stimulation strengths. In amyotr opic lateral sclerosis (ALS) these volleys are dispersed and prolonged, att ributed to altered motor cortical excitability. Impaired intracortical inhi bition, as found in ALS, is not unique to this disease, but is also a well- established finding in Parkinson's disease (PD). The present study explored whether reduced inhibition in the motor cortex in PD is accompanied by sim ilar changes in motor unit firing modulation by TMS as are found in ALS. TM S was applied to the contralateral motor cortex during a low-force voluntar y elbow flexion while 126-channel surface electromyography (SEMG) was recor ded from the brachial biceps muscle. A recently developed method for SEMG d ecomposition was used to extract the firing pattern of up to five simultane ously active MUs. Sixteen MUs in 7 PD patients and 17 MUs in 5 healthy cont rol subjects were analysed and peristimulus time histograms (PSTHs) and int erspike interval change functions (IICFs) were calculated. The IICF provide s an estimate of the modulation of the postsynaptic membrane potential at t he spinal motoneuron, evoked by the stimulus. In PD the duration of the PST H peak was significantly increased and the synchrony was decreased. The exc itatory phase at 20-50 ms of the IICF was broader in PD, reflecting a longe r duration of the TMS-evoked excitatory postsynaptic potential. It is propo sed that these results are due to prolonged corticospinal volleys resulting from impaired intracortical inhibition.