Objective: To determine how intracortical circuits interact with one another in Parkinson’s disease.

Background: Using transcranial magnetic stimulation (TMS), previous work has established that motor cortical inhibitory and facilitatory circuits are abnormal in patients with Parkinson’s disease (PD). Three such circuits are short interval intracortical inhibition (SICI), short interval intracortical facilitation (SICF) and short-latency afferent inhibition (SAI). They assess GABAAergic, glutamatergic and cholinergic function, respectively. Importantly, these circuits interact with each other and their interactions can be tested using a triple-pulse TMS paradigm, which elicits one circuit in the presence of another. However, these interactions have not been studied in PD.

Methods: 15 right-handed PD patients (aged 64.8±7.9 years) were studied ON and OFF dopaminergic medications. Unified Parkinson’s Disease Rating Scale Part III was used to assess disease severity. 16 right-handed, healthy participants (aged 64.1±6.9 years) served as controls. Surface electromyography measured motor evoked potentials from the first dorsal interosseous generated by TMS of left M1 in controls and of M1 in the more affected hemisphere in PD patients. SICI was tested at an interstimulus interval (ISI) of 2 ms and SICF at an ISI of 1.5 ms. The interactions between SICI and SICF were evaluated by comparing SICF alone to SICF in the presence of SICI. The latency of the median nerve N20 somatosensory evoked potential plus 2 ms was used as the ISI for SAI. The interactions between SAI and SICI were evaluated by comparing SAI alone to SAI in the presence of SICI and by comparing SICI alone to SICI in the presence of SAI.

Results: SICF was increased in PD OFF compared to both controls and PD ON. SICF was facilitated by SICI in controls, but not PD ON or PD OFF. SICI and SAI inhibit each other in PD ON, PD OFF and controls with no significant difference among groups.

Conclusions: Facilitation of SICF by SICI is impaired in PD and is not corrected by dopaminergic medications. Impairment of cortical facilitation could be related to decreased M1 activation reported in imaging studies and could represent a non-dopaminergic feature of PD. Altered interactions between cortical circuits contribute to the pathophysiology of PD.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/motor-cortical-inhibitory-and-facilitatory-circuit-interactions-in-parkinsons-disease/