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.
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.
Authors: Masoud Tahmasian; Simon B Eickhoff; Kathrin Giehl; Frank Schwartz; Damian M Herz; Alexander Drzezga; Thilo van Eimeren; Angela R Laird; Peter T Fox; Habibolah Khazaie; Mojtaba Zarei; Carsten Eggers; Claudia R Eickhoff Journal: Cortex Date: 2017-04-08 Impact factor: 4.027
Authors: Rick C Helmich; Avner Thaler; Bart F L van Nuenen; Tanya Gurevich; Anat Mirelman; Karen S Marder; Susan Bressman; Avi Orr-Urtreger; Nir Giladi; Bastiaan R Bloem; Ivan Toni Journal: Neurology Date: 2014-12-24 Impact factor: 9.910
Authors: Douglas N Martini; Rosie Morris; Valerie E Kelly; Amie Hiller; Kathryn A Chung; Shu-Ching Hu; Cyrus P Zabetian; John Oakley; Kathleen Poston; Ignacio F Mata; Karen L Edwards; Jodi A Lapidus; Thomas J Grabowski; Thomas J Montine; Joseph F Quinn; Fay Horak Journal: Front Neurol Date: 2020-09-04 Impact factor: 4.003