2002
DOI: 10.1016/s0022-510x(02)00086-2
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Changes of cortical excitability of human motor cortex in spinocerebellar ataxia type 2

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Cited by 24 publications
(16 citation statements)
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References 30 publications
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“…Likewise, as in case of the BARS score, it was mainly the M-VEPs and the pattern reversal VEPs evoked by the smallest check size that showed a significant positive correlation. A similar positive correlation between cortical function and the worsening of the clinical state as assessed by the Inherited Ataxia Progression State or the duration of SCA2 disease was observed by Restivo et al [24] using the cortical silent period and transcranial magnetic stimulation. The authors speculated that the reason for this relationship was the gradual loss of the cerebellar neurons and a decrease of the facilitatory influence to the motor cortex.…”
Section: Cerebellar Deficit and Visual Pathologysupporting
confidence: 78%
See 1 more Smart Citation
“…Likewise, as in case of the BARS score, it was mainly the M-VEPs and the pattern reversal VEPs evoked by the smallest check size that showed a significant positive correlation. A similar positive correlation between cortical function and the worsening of the clinical state as assessed by the Inherited Ataxia Progression State or the duration of SCA2 disease was observed by Restivo et al [24] using the cortical silent period and transcranial magnetic stimulation. The authors speculated that the reason for this relationship was the gradual loss of the cerebellar neurons and a decrease of the facilitatory influence to the motor cortex.…”
Section: Cerebellar Deficit and Visual Pathologysupporting
confidence: 78%
“…It is generally accepted that clinical signs vary within a genetic subtype and between SCAs [26] and that the symptoms of progression can be different even for the same family members [27]. Also, Restivo et al [24] found no correlation between CAG repeats and the cortical silent period. Our group included a mother (S9) and daughter (S1), and they did not agree in the extent of visual pathologies.…”
Section: Cag Repeatsmentioning
confidence: 99%
“…In our sample of cerebellar patients there was, at baseline, a defective efficacy of the ICF that is consistent with previous studies. Several studies found a similar loss of ICF in cerebellar stroke patients (Liepert et al, 1998(Liepert et al, , 2004Restivo et al, 2002). Moreover, we previously demonstrated that in healthy subjects cerebellar iTBS was also effective in modulating ICF circuits in the contralateral M1 (Koch et al, 2008).…”
Section: Discussionsupporting
confidence: 61%
“…A prolonged SP has been observed previously in patients with degenerative cerebellar ataxia disease (Liepert et al, 1998;Nakashima et al, 1995;Oechsner and Zangemeister, 1999;Restivo et al, 2002;Schwenkreis et al, 2002;Wessel et al, 1996). The lengthening of the SP might not be a common phenomenon in all sub-types of SCA due to the genetic heterogeneity (Liepert et al, 1998;Nakashima et al, 1995;Oechsner and Zangemeister, 1999;Restivo et al, 2002;Schwenkreis et al, 2002;Wessel et al, 1996). The assessment method, such as the TMS intensity and definition of SP, could also affect the values of this parameter.…”
Section: Discussionmentioning
confidence: 84%
“…This made the absolute duration of the SP incomparable to its value in the studies using a higher TMS intensity (Liepert et al, 1998;Nakashima et al, 1995;Wessel et al, 1996). Furthermore, the onset of the SP was defined inconsistently in these studies, sometimes as beginning at the stimulation artifact (Cantello et al, 2007), sometimes at the onset of the MEP (Restivo et al, 2002), and others at the onset of EMG suppression. Likely, the average duration of the SP in our healthy controls was comparable to the studies that used a relatively low TMS-induced intensity with the SP measured from the onset of EMG suppression (Garvey et al, 2001;Ridding et al, 1995;Vry et al, 2008).…”
Section: Discussionmentioning
confidence: 98%