期刊
MOVEMENT DISORDERS
卷 32, 期 5, 页码 750-756出版社
WILEY
DOI: 10.1002/mds.26931
关键词
Parkinson disease; LRRK2; TMS; cortical plasticity; levodopa
Objectives: A mutation in leucine-rich repeat kinase 2 is the most common cause of hereditary Parkinson's disease (PD), yet the neural mechanisms and the circuitry potentially involved are poorly understood. Methods: We used different transcranial magnetic stimulation protocols to explore in the primary motor cortex the activity of intracortical circuits and cortical plasticity (long-term potentiation) in patients with the G2019S leucine-rich repeat kinase 2 gene mutation when compared with idiopathic PD patients and age-matched healthy subjects. Paired pulse transcranial magnetic stimulation was used to investigate short intracortical inhibition and facilitation and short afferent inhibition. Intermittent theta burst stimulation, a form of repetitive transcranial magnetic stimulation, was used to test long-term potentiation-like cortical plasticity. Leucinerich repeat kinase 2 and idiopathic PD were tested both in ON and in OFF L-dopa therapy. Results: When compared with idiopathic PD and healthy subjects, leucine-rich repeat kinase 2 PD patients showed a remarkable reduction of short intracortical inhibition in both ON and in OFF L-dopa therapy. This reduction was paralleled by an increase of intracortical facilitation in OFF L-dopa therapy. Leucinerich repeat kinase 2 PD showed abnormal long-term potentiation-like cortical plasticity in ON L-dopa therapy. Discussion: The motor cortex in leucine-rich repeat kinase 2 mutated PD patients is strongly disinhibited and hyperexcitable. These abnormalities could be a result of an impairment of inhibitory (gamma-Aminobutyric acid) transmission eventually related to altered neurotransmitter release. (C) 2017 International Parkinson and Movement Disorder Society
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