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DOI 10.1016/j.clinph.2011.06.033

Медицинская библиотека · Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2011

Corticospinal excitability in patients with secondary dystonia due to focal lesions of the basal ganglia and thalamus.

Trompetto Carlo, Avanzino Laura, Marinelli Lucio, Mori Laura, Pelosin Elisa, Roccatagliata Luca, Abbruzzese Giovanni

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Аннотация

OBJECTIVE

To investigate the possible correlations between clinico-radiological features and pathophysiological mechanisms in patients with dystonia secondary to focal brain lesions.

METHODS

Single and paired-pulse transcranial magnetic stimulation was used to assess corticospinal excitability in 10 patients (4 females; mean age 61) and a group of normal controls. Active threshold, latency and amplitude of motor evoked potentials (MEPs), silent period (SP) duration and short-interval intracortical inhibition (SICI) were evaluated.

RESULTS

Patients with lesions involving the putamen and caudate presented with dystonic postures at rest. TMS assessment in these subjects showed increased MEP amplitude on the affected side and a bilateral decrease of SP duration and SICI. When the lesion spared the putamen and caudate, mainly involving the thalamus, the clinical picture was dominated by slow repetitive involuntary movements and tremor. In the affected side of these subjects the MEP amplitude was reduced and the MEP threshold was increased.

CONCLUSIONS

When putamen and caudate were lesioned, the patients presented with dystonic postures at rest; furthermore the patients showed changes of corticospinal excitability in comparison to both healthy subjects and other dystonic patients.

SIGNIFICANCE: There are correlations between type of dystonia, site of the lesion and neurophysiological findings.

Для цитирования: Trompetto Carlo, Avanzino Laura, Marinelli Lucio, Mori Laura, Pelosin Elisa, Roccatagliata Luca, Abbruzzese Giovanni. Corticospinal excitability in patients with secondary dystonia due to focal lesions of the basal ganglia and thalamus.. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2011. DOI: 10.1016/j.clinph.2011.06.033.

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