Parkinsonism & related disorders · 2024
TMS-evoked potentials provide novel neurophysiological features of Tourette syndrome.
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Lassman Simon, Zifman Noa, Fogel Hilla, Hassin-Baer Sharon, Anis Saar
Аннотация
INTRODUCTION: Gilles de la Tourette syndrome (TS) is a neuropsychiatric disorder associated with abnormal activation of the cortico-striatal-thalamo-cortical circuits and dopaminergic system. We sought to examine changes in neurotransmission relating to cortical excitation/inhibition of TS by measuring TMS-evoked potentials (TEPs) of selected networks.
METHODS: Thirty-three adult TS patients and 18 healthy controls underwent evaluation of symptom severity using the YGTSS (tics), PUTS (premonitory urge), Y-BOCS (OCD), CAARS (ADHD), BDI (depression), and BAI (anxiety). TMS-EEG was performed to measure TEPs obtained from the primary motor cortex (M1), dorsolateral prefrontal cortex (DLPFC), and primary visual cortex (V1).
RESULTS: TEP analysis revealed a delayed P180 latency in M1 for TS patients compared to controls (p = 0.006). Lower early amplitude of TEP in response to stimulation of DLPFC (50-70 ms), and delayed DLPFC P180 latency were associated with higher tic severity (p = 0.001 and p = 0.003, respectively). M1 early amplitude (50-70 ms) also effectively differentiated TS with mild-moderate from severe tics (p = 0.003). Significant correlation was found between TEP V1 early amplitude (15-45 ms) and severity of TS anxiety.
CONCLUSION: Distinct TEP patterns registered in response to DLPFC, M1, and V1 stimulation may shed light on the underlying pathophysiology of TS and are associated with tic severity and comorbidities.
METHODS: Thirty-three adult TS patients and 18 healthy controls underwent evaluation of symptom severity using the YGTSS (tics), PUTS (premonitory urge), Y-BOCS (OCD), CAARS (ADHD), BDI (depression), and BAI (anxiety). TMS-EEG was performed to measure TEPs obtained from the primary motor cortex (M1), dorsolateral prefrontal cortex (DLPFC), and primary visual cortex (V1).
RESULTS: TEP analysis revealed a delayed P180 latency in M1 for TS patients compared to controls (p = 0.006). Lower early amplitude of TEP in response to stimulation of DLPFC (50-70 ms), and delayed DLPFC P180 latency were associated with higher tic severity (p = 0.001 and p = 0.003, respectively). M1 early amplitude (50-70 ms) also effectively differentiated TS with mild-moderate from severe tics (p = 0.003). Significant correlation was found between TEP V1 early amplitude (15-45 ms) and severity of TS anxiety.
CONCLUSION: Distinct TEP patterns registered in response to DLPFC, M1, and V1 stimulation may shed light on the underlying pathophysiology of TS and are associated with tic severity and comorbidities.