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Cerebellum‐dependent associative learning deficits in primary dystonia are normalized by r TMS and practice
Author(s) -
Hoffland B. S.,
Kassavetis P.,
Bologna M.,
Teo J. T. H.,
Bhatia K. P.,
Rothwell J. C.,
Edwards M. J.,
Warrenburg B. P.
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12186
Subject(s) - cerebellum , ctbs , eyeblink conditioning , neuroscience , dystonia , psychology , cerebellar hemisphere , motor learning , transcranial magnetic stimulation , stimulation , medicine , primary motor cortex , classical conditioning , conditioning , statistics , mathematics
Eyeblink classical conditioning ( EBCC ) is a cerebellum‐dependent paradigm of associative motor learning, and abnormal EBCC is a neurophysiological indicator of cerebellar dysfunction. We have previously demonstrated impaired EBCC in patients with primary dystonia, but it remains uncertain if this represents actual cerebellar pathology or reflects a functional cerebellar disruption. We examined this further by: (1) studying acquisition and retention of EBCC in a second session in eight patients with cervical dystonia ( CD ) who had a first session 7–10 days earlier; and (2) by investigating the potential of continuous theta burst stimulation (c TBS ) over the right cerebellar hemisphere to modify a first‐ever EBCC session in 11 patients with CD . EBCC data of eight healthy controls previously studied were used for additional between‐group comparisons. We observed an improvement of EBCC in a second session in patients with CD , which is in contrast to patients with proven cerebellar pathology who do not show further improvement of EBCC in additional sessions. We also found that cerebellar c TBS paradoxically normalized EBCC in patients with CD , while we previously showed that it disrupts EBCC in healthy volunteers. Combined, these two experiments are in keeping with a functional and reversible disruption of the cerebellum in dystonia, a phenomenon that is probably secondary to either cerebellar compensation or to cerebellar recruitment in the abnormal sensorimotor network.