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Abstract
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.
Glossary
- 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.
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