Abstract

Corticobasal syndrome (CBS) is characterized by asymmetric cortical sensorimotor dysfunction and parkinsonism diagnosed during life. Transcranial magnetic stimulation (TMS) in CBS has shown many cortical physiological abnormalities, on the whole indicating a reduced inhibition and increased excitability in some cortical circuits and a reduced excitability in other circuits ( Pal et al., 2008 ). Repetitive low-frequency TMS trains (<1 Hz) decrease cortical excitability in the motor cortex when delivered for 5 min or more ( Cincotta et al., 2003 ). To explore in CBS motor cortical excitability and the effects of a single session of LF-rTMS. We studied with TMS two CBS patients: a 70-year-old man, (disease duration 3 years; right alien hand syndrome) and a 56-year-old woman (disease duration 1 year; vertical gaze palsy; postural instability; left hand dystonic posture). We used a Magstim 200 stimulator with figure-of-eight coils at the hot-spot for the FDI muscle. We measured bilaterally: relaxed (rT) and active Threshold (aT); and Contralateral Silent Period (CSP) 1.3xrT, 20% maximum effort. In a random order-active/sham-we used a 10′ low frequency (0,3 Hz) rTMS over the more affected M1. We used two focal coils, which were one above the other, for “active” stimulation, the coil directly contacting the scalp was connected to the stimulator, whereas the other was not. We evaluated immediately after the active/sham treatment (T1) and after 30′ (T2) rT, CSP length and clinical effect. For the statistic we compared with t-test in each of the subject the separately values from individual trials for the less affected side (LA) and more affected side (MA) and before-after rTMS. In CBS CSP was shortened ( Fig. 1 ) and rT/aT were increased especially in the MA. The novel finding was the effects of active LF-rTMS on the contralateral silent period ( Fig. 2 ), although we did not observed any clinical effect, that disappeared after 30 min. In CBS TMS confirmed a decrease of cortical inhibitory phenomenon bilaterally as shown by CSP reduction and increased of cortical excitability. TMS changes differed among our two patients more prominent on the more affected side and in the patient with longer disease duration. A brief LF-rTMS applied on the MA hand prolonged transiently CSP length probably through a GABA-B modulation. This report represents the first experience with slow frequency rTMS in CBS and it might well be that with the same experimental setting with a longer train repeated over the course of several days would be able to induce more pronounced effects on cortical excitability.

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