Deficient activation of the motor cortical network in patients with writer’s cramp

Ibáñez, Vicente; Sadato, Norihiro; Karp, Barbara I.; Deiber, Marie-Pierre; Hallett, Mark

doi:10.1212/wnl.53.1.96

Cited by 189 publications

(143 citation statements)

References 42 publications

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“…13 Although BG activity during tapping (defined as percent-signal change from pre-tapping activity) was also greater in patients in this study, the sustained activity observed during rest can be more confidently attributed to dystonic pathophysiology, because secondary variables during movement itself (e.g., task difficulty, performance) may confound interpretation of patient/control differences. In addition, our finding may explain why previous imaging studies have not detected abnormal increases in BG activity during movement in FHD patients, 6,8,10 because standard "task versus rest" contrast analyses assume that the fMRI signal returns to pretask levels during posttask rest periods. This is the first demonstration of abnormally sustained BG activity after motor task performance in FHD patients.…”

Section: Fig 2 Hemodynamic Time Courses Illustrating That Rest Blockmentioning

confidence: 65%

“…8 In this study, we aimed to detect BG abnormalities in FHD patients by capitalizing on the spatiotemporal resolution of functional magnetic resonance imaging (fMRI). Specifically, we evaluated hemodynamic time courses in the BG and primary sensorimotor cortices at intervals before, during, and after FHD patients performed finger-tapping tasks.…”

Section: Ann Neurol 2004;55:744 -748mentioning

confidence: 99%

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Basal ganglia activity remains elevated after movement in focal hand dystonia

Blood

Flaherty

Choi

et al. 2004

Annals of Neurology

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Although previous studies of focal hand dystonia have detected cortical sensorimotor abnormalities, little is known about the role of the basal ganglia in this disorder. We report here that when focal hand dystonic patients performed finger-tapping tasks, functional magnetic resonance imaging showed persisting elevations of basal ganglia activity after the tasks ended. We posit that inhibitory control of the basal ganglia may be faulty in focal hand dystonia, and that the increases we observe in "resting" activity may mask basal ganglia abnormalities in standard imaging contrast analyses.

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Section: Fig 2 Hemodynamic Time Courses Illustrating That Rest Blockmentioning

confidence: 65%

Section: Ann Neurol 2004;55:744 -748mentioning

confidence: 99%

Basal ganglia activity remains elevated after movement in focal hand dystonia

Blood

Flaherty

Choi

et al. 2004

Annals of Neurology

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“…The exact pathophysiology of writer's cramp remains unknown. Structural changes in the sensorimotor cortex, basal ganglia and cerebellum (Garraux et al 2004;Egger et al 2007), abnormal activation in the basal ganglia-premotor cortex network during voluntary movements (Ibanez et al 1999), deficient inhibition at multiple levels of the motor system (Hallett 2006), impaired sensorimotor integration (Abbruzzese and Berardelli 2003), and excessive motor cortical plasticity (Quartarone et al 2006) have all been implicated.…”

Section: Introductionmentioning

confidence: 99%

Deficient Homeostatic Regulation of Practice-Dependent Plasticity in Writer’s Cramp

et al. 2010

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Homeostatic metaplasticity is important to maintain overall synaptic weight in neuronal networks. Previous work suggested that homeostatic metaplasticity in motor cortex is impaired in writer's cramp, the most common form of task-specific focal dystonia, when explored by the interactions between 2 successive plasticity inducing transcranial brain stimulation protocols (Quartarone Rizzo V, Bagnato S, Morgante F, Sant'angelo A, Romano M, Crupi D, Girlanda P, Rothwell JC, Siebner HR. 2005. Homeostatic-like plasticity of the primary motor hand area is impaired in focal hand dystonia. Brain. 128:1943Brain. 128: --1950. To which extent deficient homeostatic metaplasticity applies also to the behavioral level of practicedependent plasticity is unknown. Here, we examined the interactions of 3 paired associative transcranial magnetic stimulation protocols (motor cortical excitability-enhancing paired associative stimulation (PAS) 25ms , excitability-depressing PAS 10ms , and control PAS 100ms ) with subsequent practice-dependent plasticity. Ten patients with writer's cramp and 10 healthy controls practiced rapid thumb abductions for 30 min. Practice-dependent plasticity was quantified by the increase in peak acceleration of the trained movement. The healthy controls but not the writer's cramp patients showed homeostatic suppression of practice-dependent plasticity after PAS 25ms when compared with practice-dependent plasticity after PAS 10ms and PAS 100ms . The lack of the PAS 25ms -induced suppression of practice-dependent plasticity in writer's cramp correlated with clinical severity of the focal hand dystonia. Findings support the notion that deficient homeostatic metaplasticity of practicedependent plasticity plays a significant role in the pathophysiology of writer's cramp.

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“…Reduced inhibition of motor cortex occurs with writer's cramp. 39,80 Consistent with these physiological studies, individuals with writer's cramp exhibit reduced GABA levels in cortex. 81 As with many forms of dystonia, increased excitability or reduced inhibition is present at spinal and brainstem levels with writer's cramp.…”

Section: Focal Hand Dystoniamentioning

confidence: 55%

“…Most imaging studies in both generalized and focal dystonias report that the same brain regions exhibit increased glucose uptake or blood flow. 23,80,85,89,[123][124][125]127,173,174 In virtually all cases of primary dystonia, there is dysfunction of the thalamus, frontal cortex, cerebellum, and basal ganglia, particularly the striatum. These altered activity patterns at least partially reflect a reduction in cortical inhibition.…”

Section: Implications Of Animal Models Of Focal Dystoniamentioning

confidence: 99%

Animal models of focal dystonia

Evinger

2005

Neurotherapeutics

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Summary: Animal models indicate that the abnormal movements of focal dystonia result from disordered sensorimotor integration. Sensorimotor integration involves a comparison of sensory information resulting from a movement with the sensory information expected from the movement. Unanticipated sensory signals identified by sensorimotor processing serve as signals to modify the ongoing movement or the planning for subsequent movements. Normally, this process is an effective mechanism to modify neural commands for ongoing movement or for movement planning. Animal models of the focal dystonias spasmodic torticollis, writer's cramp, and benign essential blepharospasm reveal different dysfunctions of sensorimotor integration through which dystonia can arise. Animal models of spasmodic torticollis demonstrate that modifications in a variety of regions are capable of creating abnormal head postures. These data indicate that disruption of neural signals in one structure may mutate the activity pattern of other elements of the neural circuits for movement. The animal model of writer's cramp demonstrates the importance of abnormal sensory processing in generating dystonic movements. Animal models of blepharospasm illustrate how disrupting motor adaptation can produce dystonia. Together, these models show mechanisms by which disruptions in sensorimotor integration can create dystonic movements.

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Deficient activation of the motor cortical network in patients with writer’s cramp

Cited by 189 publications

References 42 publications

Basal ganglia activity remains elevated after movement in focal hand dystonia

Basal ganglia activity remains elevated after movement in focal hand dystonia

Deficient Homeostatic Regulation of Practice-Dependent Plasticity in Writer’s Cramp

Animal models of focal dystonia

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