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Brainstem Reflexes in Idiopathic Cervical Dystonia: Does Medullary Dysfunction Play a Role?
Author(s) -
Manzo Nicoletta,
Tocco Pierluigi,
Ginatempo Francesca,
Bertolasi Laura,
Rocchi Lorenzo
Publication year - 2021
Publication title -
movement disorders clinical practice
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.754
H-Index - 18
ISSN - 2330-1619
DOI - 10.1002/mdc3.13149
Subject(s) - cervical dystonia , dystonia , brainstem , medicine , audiology , silent period , reflex , latency (audio) , psychology , neuroscience , anesthesia , stimulation , transcranial magnetic stimulation , electrical engineering , engineering
Background Neurophysiological markers in dystonia have so far not been sistematically applied in clinical practice due to limited reproducibility of results and low correlations with clinical findings. Exceptions might be represented by the blink reflex (BR), including its recovery cycle (BRRC) and the trigemino‐cervical reflex (TCR) which, compared to other neurophysiological methods, have shown more consistent alterations in cervical dystonia (CD). However, a comparison between the two techniques, and their possible correlation with disease symptoms, have not been thoroughly investigated. Objectives To assess the role of BR, BRCC and TCR in the pathophysiology of idiopathic cervical dystonia. Methods Fourteen patients and 14 age‐matched healthy controls (HC) were recruited. Neurophysiological outcome measures included latency of R1 and R2 components of the BR, R2 amplitude, BRRC, latency and amplitude of P19/N31 complex of TCR. Clinical and demographic features of patients were also collected, including age at disease onset, disease duration, presence of tremor, sensory trick and pain. The Toronto Western Spasmodic Torticollis Rating Scale was used to characterize dystonia. Results Compared to HC, CD patients showed increased latency of the BR R2 and decreased suppression of the BRRC. They also showed increased latency of the P19 and decreased amplitude of P19/N31 complex of TCR. The latency of P19 component of TCR was positively correlated with disease duration. Conclusions We propose that the increased latency of R2 and P19 observed here might be reflective of brainstem dysfunction, mediated either by local interneuronal excitability changes or by subtle structural damage.