Movement disorders : official journal of the Movement Disorder Society · 2000
Abnormalities of motor cortical excitability are not correlated with clinical features in atypical parkinsonism.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Marchese R, Trompetto C, Buccolieri A, Abbruzzese G
Аннотация
OBJECTIVE: To evaluate the specificity of motor cortical excitability changes in parkinsonian syndromes and their relevance to the pathophysiology of cardinal parkinsonian features.
METHODS: Paired transcranial magnetic stimulation (TMS) was used to assess cortico-cortical inhibition (CCI) and facilitation (CCF) in the opponens pollicis muscle of patients with atypical, non-L-dopa- (LD) responsive parkinsonism.
RESULTS: Compared with age-matched normal control subjects, CCI (interstimulus interval [ISI], 3 ms) was significantly reduced in 10 patients with predominantly parkinsonian multiple system atrophy (MSA-P) and in seven with vascular parkinsonism (VP), but not in four with predominantly cerebellar MSA. No significant change of CCF (ISI, 12 ms) was observed. No correlation was found between the amount of CCI and clinical status as evaluated with the Unified Parkinson's Disease Rating Scale (UPDRS). In 10 patients (5 MSA-P, 5 VP), CCI was significantly increased by LD acute administration without concurrent clinical changes.
CONCLUSIONS: Abnormalities of CCI are not peculiar to idiopathic Parkinson's disease and seem unlikely to underlie any specific parkinsonian feature, but rather possibly reflect a nonspecific imbalance of inhibitory and facilitatory motor cortical circuits.
METHODS: Paired transcranial magnetic stimulation (TMS) was used to assess cortico-cortical inhibition (CCI) and facilitation (CCF) in the opponens pollicis muscle of patients with atypical, non-L-dopa- (LD) responsive parkinsonism.
RESULTS: Compared with age-matched normal control subjects, CCI (interstimulus interval [ISI], 3 ms) was significantly reduced in 10 patients with predominantly parkinsonian multiple system atrophy (MSA-P) and in seven with vascular parkinsonism (VP), but not in four with predominantly cerebellar MSA. No significant change of CCF (ISI, 12 ms) was observed. No correlation was found between the amount of CCI and clinical status as evaluated with the Unified Parkinson's Disease Rating Scale (UPDRS). In 10 patients (5 MSA-P, 5 VP), CCI was significantly increased by LD acute administration without concurrent clinical changes.
CONCLUSIONS: Abnormalities of CCI are not peculiar to idiopathic Parkinson's disease and seem unlikely to underlie any specific parkinsonian feature, but rather possibly reflect a nonspecific imbalance of inhibitory and facilitatory motor cortical circuits.