HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bäumer, T. Articles by Münchau, A. Search for Related Content PubMed PubMed Citation Articles by Bäumer, T. Articles by Münchau, A. Related Collections Chromosomes All Movement Disorders Parkinson's disease/Parkinsonism Prognosis TMS All Genetics

Sensorimotor integration is abnormal in asymptomatic Parkin mutation carriers

A TMS study

From the Department of Neurology (T.B., S.S., C.G., A.M.), University of Hamburg, Germany; Department of Neurology, Central Hospital, and Institute of Genetic Medicine, European Academy-Research (P.P.P.), Bolzano-Bozen, Italy; NeuroImage Nord (H.R.S., M.P.), Hamburg-Kiel-Lübeck; Department of Neurology (H.R.S., M.P.), Christian-Albrechts-University, Kiel; and Neurology and Human Genetics (J.H., C.K.), University of Lübeck, Germany.

Address correspondence and reprint requests to Dr. Tobias Bäumer, Department of Neurology, University of Hamburg, Martinistraße 52, 20246 Hamburg, Germany baeumer{at}uke.de

Background: In patients with Parkinson disease (PD), transcranial magnetic stimulation (TMS) studies have consistently demonstrated a reduced inhibitory tone in the sensorimotor cortex. It remains unclear whether this is related to motor symptoms or represents adaptive compensatory changes to degeneration of dopaminergic neurons. Here we used short-interval afferent inhibition after digital stimulation (dSAI) and intracortical paired-pulse inhibition and facilitation to probe intracortical sensorimotor excitability in clinically asymptomatic carriers of a single mutant Parkin allele who have a latent nigrostriatal dopaminergic dysfunction.

Methods: Nine heterozygous mutation carriers and nine healthy controls were investigated. For dSAI testing, electrical pulses were applied to the right index finger followed by TMS pulses over the left motor cortex at interstimulus intervals (ISI) of 25, 30, and 40 msec. Intracortical paired-pulse excitability was tested at ISIs of 2 to 15 msec.

Results: dSAI was reduced at an ISI of 25 msec in carriers of a single mutant Parkin allele, whereas paired-pulse TMS was normal.

Conclusion: The relative decrease in sensorimotor inhibition may be a direct consequence of the Parkin mutation or represent adaptive changes at the cortical level in response to a subcortical dysfunction, but is not caused by motor symptoms.

Abbreviations: AMT = active motor threshold; ANOVA = analysis of variance; CS = conditioning stimulus; dSAI = short-interval afferent inhibition after digital stimulation; FDI = first dorsal interosseous; ICF = intracortical facilitation; ISI = interstimulus interval; M1 = primary motor cortex; MEP = motor evoked potential; MSO = maximum stimulator output; PD = Parkinson disease; RMT = resting motor threshold; SICI = short interval intracortical inhibition; TMS = transcranial magnetic stimulation; TS = test stimulus.

This research was funded by the EU (STREP FP-6 GENEPARK; Genepark). A. Münchau (grant I/78 553), H.R. Siebner (grant I/79 932), and C. Klein (Lichtenberg Grant) were supported by the Volkswagenstiftung. H.R. Siebner was also supported by the Bundesministerium für Bildung und Forschung (01GO 0511) and S. Schippling by the Forschungsförderungs-Fond of the University Medical Centre Hamburg-Eppendorf.

Disclosure: The authors report no conflicts of interest.

Received January 29, 2007. Accepted in final form May 17, 2007.