Sensory integration in writer’s cramp: Comparison with controls and evaluation of botulinum toxin effect

Contarino, Maria Fiorella; Kruisdijk, José J. M.; Koster, Linda A M; Visser, B.W. Ongerboer de; Speelman, Johannes D.; Koelman, Johannes H. T. M.

doi:10.1016/j.clinph.2007.07.004

Cited by 29 publications

(16 citation statements)

References 37 publications

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“…In line with previous studies [7], [32], [38], the present study shows normal N20m and P35m responses in patients with WC. SEFs represent the responses of cortical neurons to changes in afferent activity [39].…”

Section: Discussionsupporting

confidence: 93%

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Reduced Motor Cortex Deactivation in Individuals Who Suffer from Writer's Cramp

et al. 2014

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This study investigated the neuromagnetic activities of self-paced finger lifting task and electrical median nerve stimulation in ten writer's cramp patients and fourteen control subjects. The event-related de/synchronizations (ERD/ERS) of beta-band activity levels were evaluated and the somatosensory cortical activity levels were analyzed using equivalent-current dipole modeling. No significant difference between the patients and control subjects was found in the electrical stimulation-induced beta ERS and electrical evoked somatosensory cortical responses. Movement-related beta ERD did not differ between controls and patients. Notably, the amplitude of the beta ERS after termination of finger movement was significantly lower in the patients than in the control subjects. The reduced movement-related beta ERS might reflect an impairment of motor cortex deactivation. In conclusion, a motor dependent dysregulation of the sensorimotor network seems to be involved in the functional impairment of patients with writer's cramp.

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Section: Discussionsupporting

confidence: 93%

“…Neruoimaging studies have shown normal electrophysiological processes in patients with dystonia [7], [32], [38]. In line with previous studies [7], [32], [38], the present study shows normal N20m and P35m responses in patients with WC.…”

Section: Discussionsupporting

confidence: 92%

Reduced Motor Cortex Deactivation in Individuals Who Suffer from Writer's Cramp

et al. 2014

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“…We also conclude that other cortical (pre-SMA, DLPFC) and subcortical areas (left lateral cerebellum) play a less prominent role in the STDT than S1. This new information giving further insight into the mechanisms involved in temporal discrimination of tactile stimuli – as tested with the STDT- in healthy subjects – helps interpret the sensory processing deficits in neurological diseases such as focal dystonia and Parkinson's disease and possibly prompts future studies applying TBS over S1 for therapeutic purposes in dystonic patients [15]–[18].…”

Section: Discussionmentioning

confidence: 91%

Theta-Burst Stimulation-Induced Plasticity over Primary Somatosensory Cortex Changes Somatosensory Temporal Discrimination in Healthy Humans

et al. 2012

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BackgroundThe somatosensory temporal discrimination threshold (STDT) measures the ability to perceive two stimuli as being sequential. Precisely how the single cerebral structures contribute in controlling the STDT is partially known and no information is available about whether STDT can be modulated by plasticity-inducing protocols.Methodology/Principal FindingsTo investigate how the cortical and cerebellar areas contribute to the STDT we used transcranial magnetic stimulation and a neuronavigation system. We enrolled 18 healthy volunteers and 10 of these completed all the experimental sessions, including the control experiments. STDT was measured on the left hand before and after applying continuous theta-burst stimulation (cTBS) on the right primary somatosensory area (S1), pre-supplementary motor area (pre-SMA), right dorsolateral prefrontal cortex (DLPFC) and left cerebellar hemisphere. We then investigated whether intermittent theta-burst stimulation (iTBS) on the right S1 improved the STDT. After right S1 cTBS, STDT values increased whereas after iTBS to the same cortical site they decreased. cTBS over the DLPFC and left lateral cerebellum left the STDT statistically unchanged. cTBS over the pre-SMA also left the STDT statistically unchanged, but it increased the number of errors subjects made in distinguishing trials testing a single stimulus and those testing paired stimuli.Conclusions/SignificanceOur findings obtained by applying TBS to the cortical areas involved in processing sensory discrimination show that the STDT is encoded in S1, possibly depends on intrinsic S1 neural circuit properties, and can be modulated by plasticity-inducing TBS protocols delivered over S1. Our findings, giving further insight into mechanisms involved in somatosensory temporal discrimination, help interpret STDT abnormalities in movement disorders including dystonia and Parkinson's disease.

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“…Several randomized, double-blind, controlled studies in limb dystonia have been performed investigating abobotulinumtoxinA (128, 129) and onabotulinumtoxinA (130–132). When comparing these studies, outcome measures and populations enrolled have marked variability.…”

Section: Therapymentioning

confidence: 99%

Research Priorities in Limb and Task-Specific Dystonias

et al. 2017

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Dystonia, which causes intermittent or sustained abnormal postures and movements, can present in a focal or a generalized manner. In the limbs, focal dystonia can occur in either the upper or lower limbs and may be task-specific causing abnormal motor performance for only a specific task, such as in writer’s cramp, runner’s dystonia, or musician’s dystonia. Focal limb dystonia can be non-task-specific and may, in some circumstances, be associated with parkinsonian disorders. The true prevalence of focal limb dystonia is not known and is likely currently underestimated, leaving a knowledge gap and an opportunity for future research. The pathophysiology of focal limb dystonia shares some commonalities with other dystonias with a loss of inhibition in the central nervous system and a loss of the normal regulation of plasticity, called homeostatic plasticity. Functional imaging studies revealed abnormalities in several anatomical networks that involve the cortex, basal ganglia, and cerebellum. Further studies should focus on distinguishing cause from effect in both physiology and imaging studies to permit focus on most relevant biological correlates of dystonia. There is no specific therapy for the treatment of limb dystonia given the variability in presentation, but off-label botulinum toxin therapy is often applied to focal limb and task-specific dystonia. Various rehabilitation techniques have been applied and rehabilitation interventions may improve outcomes, but small sample size and lack of direct comparisons between methods to evaluate comparative efficacy limit conclusions. Finally, non-invasive and invasive therapeutic modalities have been explored in small studies with design limitations that do not yet clearly provide direction for larger clinical trials that could support new clinical therapies. Given these gaps in our clinical, pathophysiologic, and therapeutic knowledge, we have identified priorities for future research including: the development of diagnostic criteria for limb dystonia, more precise phenotypic characterization and innovative clinical trial design that considers clinical heterogeneity, and limited available number of participants.

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Sensory integration in writer’s cramp: Comparison with controls and evaluation of botulinum toxin effect

Cited by 29 publications

References 37 publications

Reduced Motor Cortex Deactivation in Individuals Who Suffer from Writer's Cramp

Reduced Motor Cortex Deactivation in Individuals Who Suffer from Writer's Cramp

Theta-Burst Stimulation-Induced Plasticity over Primary Somatosensory Cortex Changes Somatosensory Temporal Discrimination in Healthy Humans

Research Priorities in Limb and Task-Specific Dystonias

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