Cerebellar Perfusion Changes After Repetitive Deep Transcranial Magnetic Stimulation in Parkinson’s Disease: A Five-Patient Case Series and Literature Review
TL;DR
A five-patient exploratory case series evaluating clinical measures and cerebral perfusion before and three months after high-frequency dTMS targeting the supplementary motor area (SMA) suggests network-level modulation of SMA–cerebellar circuitry may reflect network-level modulation of SMA–cerebellar circuitry.
Abstract
Background and Clinical Significance: Parkinson’s disease (PD) is a progressive neurodegenerative disorder for which nonpharmacological neuromodulatory approaches are being explored as adjunctive strategies. Deep transcranial magnetic stimulation (dTMS) using an H-coil can engage broader and deeper cortical networks than conventional focal coils, although anatomically distant structures are expected to be influenced through network modulation rather than direct electromagnetic stimulation. Case Presentation: We describe a five-patient exploratory case series evaluating clinical measures and cerebral perfusion before and three months after high-frequency dTMS targeting the supplementary motor area (SMA). Clinical outcomes included the Unified Parkinson’s Disease Rating Scale (UPDRS) Parts I-IV, Non-Motor Symptoms Scale (NMSS), Hoehn–Yahr stage, and Timed Up and Go test. Antiparkinsonian medication regimens and doses remained unchanged during the three-month follow-up. Cerebral perfusion was assessed using single-photon emission computed tomography (SPECT) and statistical parametric mapping. No clinical outcome reached nominal statistical significance at follow-up; given the sample size, this should be interpreted as limited statistical power rather than evidence of no effect. At an exploratory voxel-wise threshold of p < 0.001, uncorrected, SPECT identified a 28-voxel cluster of increased regional cerebral blood flow in the right cerebellar cortex (peak MNI coordinates: 22, −38, −44; t = 5.96; z = 3.11). Conclusions: These observations are hypothesis-generating and may reflect network-level modulation of SMA–cerebellar circuitry. Because only five patients were included, no sham-controlled arm was available, and the imaging analysis used an uncorrected exploratory threshold, causal or efficacy claims cannot be made. Larger sham-controlled studies with standardized dose-to-imaging timing, formal neuropsychological assessment, individualized targeting, and prespecified corrected imaging analyses are warranted.