Abnormal dorsal premotor–motor inhibition in writer's cramp

Richardson, Sarah Pirio; Beck, Sandra; Bliem, Barbara; Hallett, Mark

doi:10.1002/mds.25878

Cited by 19 publications

(31 citation statements)

References 14 publications

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“…It resulted in enhanced dorsal premotor–motor cortical inhibition, independent of the severity of the disease (Pirio Richardson, 2015). This enhanced inhibition is more consistent with an endophenotypic marker widespread in the brain, as it has been evidenced in the setting of task-specific dystonia, such as writer’s cramp (Pirio Richardson et al, 2014), and is hypothesized by the authors as compensatory to reduce abnormal motor output and sustained muscle contraction.…”

Section: Dystonia and Tms: A Window Into Pathophysiological Insightssupporting

confidence: 65%

Contribution of TMS and rTMS in the Understanding of the Pathophysiology and in the Treatment of Dystonia

Lozeron

Poujois

Richard

et al. 2016

Front. Neural Circuits

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Dystonias represent a heterogeneous group of movement disorders responsible for sustained muscle contraction, abnormal postures, and muscle twists. It can affect focal or segmental body parts or be generalized. Primary dystonia is the most common form of dystonia but it can also be secondary to metabolic or structural dysfunction, the consequence of a drug’s side-effect or of genetic origin. The pathophysiology is still not elucidated. Based on lesion studies, dystonia has been regarded as a pure motor dysfunction of the basal ganglia loop. However, basal ganglia lesions do not consistently produce dystonia and lesions outside basal ganglia can lead to dystonia; mild sensory abnormalities have been reported in the dystonic limb and imaging studies have shown involvement of multiple other brain regions including the cerebellum and the cerebral motor, premotor and sensorimotor cortices. Transcranial magnetic stimulation (TMS) is a non-invasive technique of brain stimulation with a magnetic field applied over the cortex allowing investigation of cortical excitability. Hyperexcitability of contralateral motor cortex has been suggested to be the trigger of focal dystonia. High or low frequency repetitive TMS (rTMS) can induce excitatory or inhibitory lasting effects beyond the time of stimulation and protocols have been developed having either a positive or a negative effect on cortical excitability and associated with prevention of cell death, γ-aminobutyric acid (GABA) interneurons mediated inhibition and brain-derived neurotrophic factor modulation. rTMS studies as a therapeutic strategy of dystonia have been conducted to modulate the cerebral areas involved in the disease. Especially, when applied on the contralateral (pre)-motor cortex or supplementary motor area of brains of small cohorts of dystonic patients, rTMS has shown a beneficial transient clinical effect in association with restrained motor cortex excitability. TMS is currently a valuable tool to improve our understanding of the pathophysiology of dystonia but large controlled studies using sham stimulation are still necessary to delineate the place of rTMS in the therapeutic strategy of dystonia. In this review, we will focus successively on the use of TMS as a tool to better understand pathophysiology, and the use of rTMS as a therapeutic strategy.

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Section: Dystonia and Tms: A Window Into Pathophysiological Insightssupporting

confidence: 65%

Contribution of TMS and rTMS in the Understanding of the Pathophysiology and in the Treatment of Dystonia

Lozeron

Poujois

Richard

et al. 2016

Front. Neural Circuits

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show abstract

“…This decreased inhibition is reflected in multiple levels from abnormal patterns of muscle activity, loss of spinal and brainstem reflexes and impaired inhibition at the motor cortical level (Cohen and Hallett, 1988; Chen et al, 1995; Kanovsky et al, 2003). In contrast to this literature, we have shown in previous studies that patients with writer’s cramp or focal hand dystonia consistently show enhanced dorsal premotor-motor cortical inhibition (dPMI) (Beck et al, 2009; Pirio Richardson et al, 2014). This enhanced inhibition is hypothesized to be due to compensatory networks that play a role in reducing unwanted motor output.…”

Section: Introductioncontrasting

confidence: 83%

“…At least 24 motor evoked potentials (MEPs) (12 test pulses and 12 conditioning + test pulses delivered randomly) were collected from the right FDI at rest. The interstimulus interval (ISI) between the conditioning dPM TMS pulse and the test motor TMS pulse was 6 ms (Pirio Richardson et al, 2014). The intensity of the conditioning pulse was at 90% of active motor threshold and the test intensity was 120% of resting motor threshold (Pirio Richardson et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

Enhanced dorsal premotor–motor inhibition in cervical dystonia

Richardson

2015

Clinical Neurophysiology

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Objective This study aims to understand whether the enhanced dPMI, seen in writer’s cramp patients previously, extends to other populations of focal dystonia patients (e.g. cervical dystonia) as an endophenotypic marker. Methods We studied 9 healthy subjects and 9 patients with CD. dPMI was tested by applying conditioning transcranial magnetic stimulation to the left dorsal premotor cortex and then a test pulse to the ipsilateral motor cortex at an interval of 6 ms. We also looked at the duration of the cortical silent period (CSP)—a measure of cortical excitability. Results CD patients had enhanced dPMI at rest (mean 57.0%, SD 16.2) in contrast to healthy volunteers (mean 124.1%, SD 35.7) (p<0.001). CSP latencies (in ms) in CD patients (mean 108.0, SD 33.1) were significantly shorter than in healthy volunteers (mean 159.1, SD 55.2) (p<0.05). Conclusions CD patients showed enhanced dPMI in a hand muscle—distant from their affected body part—similar to writer’s cramp patients. This enhanced inhibition was independent of disease severity and neck posture. This suggests that enhanced dPMI may be an endophenotypic marker of dystonia. Significance The abnormal dorsal premotor-motor connection in cervical dystonia is a potential novel and important avenue for therapeutic targeting.

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“…Long intracortical inhibition and silent period, which appear to be mediated by γ-aminobutyric acid (GABA) B inhibitory networks, may also be abnormal in patients with writing dystonia 37 38. Reduced dorsal and ventral premotor-motor inhibition has additionally been found 39 40. Paradigms which test inhibition of the motor cortex after peripheral nerve stimulation results have generated uncertain results so far 33 41–45.…”

Section: Pathophysiologymentioning

confidence: 99%

Task-specific dystonia: pathophysiology and management

Sadnicka

Kassavetis

Pareés

et al. 2016

J Neurol Neurosurg Psychiatry

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Task-specific dystonia is a form of isolated focal dystonia with the peculiarity of being displayed only during performance of a specific skilled motor task. This distinctive feature makes task-specific dystonia a particularly mysterious and fascinating neurological condition. In this review, we cover phenomenology and its increasingly broad-spectrum risk factors for the disease, critically review pathophysiological theories and evaluate current therapeutic options. We conclude by highlighting the unique features of task-specific dystonia within the wider concept of dystonia. We emphasise the central contribution of environmental risk factors, and propose a model by which these triggers may impact on the motor control of skilled movement. By viewing task-specific dystonia through this new lens which considers the disorder a modifiable disorder of motor control, we are optimistic that research will yield novel therapeutic avenues for this highly motivated group of patients.

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Abnormal dorsal premotor–motor inhibition in writer's cramp

Cited by 19 publications

References 14 publications

Contribution of TMS and rTMS in the Understanding of the Pathophysiology and in the Treatment of Dystonia

Contribution of TMS and rTMS in the Understanding of the Pathophysiology and in the Treatment of Dystonia

Enhanced dorsal premotor–motor inhibition in cervical dystonia

Task-specific dystonia: pathophysiology and management

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