Abnormal perception of the tonic vibration reflex in idiopathic focal dystonia

Yoneda, Y.; Rome, Scott; Sagar, H. J.; Grünewald, Richard A.

doi:10.1046/j.1468-1331.2000.t01-1-00102.x

Cited by 39 publications

(24 citation statements)

References 19 publications

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“…Although visual processing is normal in cervical dystonia, previous studies have described deficits in proprioceptive tasks dystonic subjects are less sensitive at detecting passive movements of the fingers [40] and arms are abnormal in their perception of the vibration induced illusion of movement (which is induced by stimulating muscle spindles with a vibration stimulus) [36, 41, 42]. How can performance in our tasks be normal in the face of such obvious deficits?…”

Section: Discussionmentioning

confidence: 97%

Normal Motor Adaptation in Cervical Dystonia: A Fundamental Cerebellar Computation is Intact

et al. 2014

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The potential role of the cerebellum in the pathophysiology of dystonia has become a focus of recent research. However, direct evidence for a cerebellar contribution in humans with dystonia is difficult to obtain. We examined motor adaptation, a test of cerebellar function, in 20 subjects with primary cervical dystonia and an equal number of aged matched controls. Adaptation to both visuomotor (distorting visual feedback by 30°) and forcefield (applying a velocity-dependent force) conditions were tested. Our hypothesis was that cerebellar abnormalities observed in dystonia research would translate into deficits of cerebellar adaptation. We also examined the relationship between adaptation and dystonic head tremor as many primary tremor models implicate the cerebellothalamocortical network which is specifically tested by this motor paradigm. Rates of adaptation (learning) in cervical dystonia were identical to healthy controls in both visuomotor and forcefield tasks. Furthermore, the ability to adapt was not clearly related to clinical features of dystonic head tremor. We have shown that a key motor control function of the cerebellum is intact in the most common form of primary dystonia. These results have important implications for current anatomical models of the pathophysiology of dystonia. It is important to attempt to progress from general statements that implicate the cerebellum to a more specific evidence-based model. The role of the cerebellum in this enigmatic disease perhaps remains to be proven.

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Section: Discussionmentioning

confidence: 97%

Normal Motor Adaptation in Cervical Dystonia: A Fundamental Cerebellar Computation is Intact

et al. 2014

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“…Patients can match the movement of one elbow with the other one for passive movements, but not if the movement is produced by the tonic vibration reflex (Grunewald et al, 1997). Perception of the vibration-induced illusion of movement is abnormal for patients with different types of focal dystonia in multiple body joints (Yoneda et al, 2000). Similar to temporal discrimination abnormalities, a deficit of vibration-induced illusion was also identified in asymptomatic first degree relatives of patients (Frima et al, 2008).…”

Section: Sensory Abnormalitiesmentioning

confidence: 99%

Neurophysiology of dystonia: The role of inhibition

Hallett

2011

Neurobiology of Disease

317

263

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The pathophysiology of dystonia has been best studied in patients with focal hand dystonia. A loss of inhibitory function has been demonstrated at spinal, brainstem and cortical levels. Many cortical circuits seem to be involved. One consequence of the loss of inhibition is a failure of surround inhibition, and this appears to directly lead to overflow and unwanted muscle spasms. There are mild sensory abnormalities and deficits in sensorimotor integration; these also might be explained by a loss of inhibition. Increasing inhibition may be therapeutic. A possible hypothesis is that there is a genetic loss of inhibitory interneurons in dystonia and that this deficit is a substrate on which other factors can act to produce dystonia.Dystonia is a syndrome characterized primarily by unwanted muscle spasms giving rise to involuntary movements and abnormal postures. There are many types of dystonia, and while some aspects of the physiology may well be shared among them, this is not at all certain (Breakefield et al., 2008). Much of the physiology has been obtained in patients with focal hand dystonia, and this review will emphasize that entity. It is likely that the adult onset focal dystonias, the group that focal hand dystonia belongs to, are all related to each other (Defazio et al., 2007). Some patients have more than one of them, and the different entities can be seen in different members of the same family. Hence, the physiology of these disorders is likely to be shared. Dystonia, like almost any other disorder, is a product of genetic factors and modifiers, including environmental modifiers. Some of the physiology should represent the endophenotype stemming from the genetic makeup of the person, while other physiology should correlate with the overt manifestations of the specific entity from which the person suffers. Which is endophenotypic and which is correlative is not always clear by our current understanding.Focal hand dystonia commonly starts as an "occupational cramp". This is a task specific disorder very much related to a repetitive action often done in the context of an occupation

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“…However, and unlike healthy subjects, tracking during induced movements was impaired, even if the vibration-induced flexion was normal (Grünewald et al, 1997). With respect to other movement disorders, this impairment is specific for focal dystonias (Rome and Grunewald, 1999), regardless of the stimulated body segment (Yoneda et al, 2000). The detection of postural changes is preserved in the passive condition but not in the induced condition.…”

Section: Sensory-motor Deficits In Focal Dystoniamentioning

confidence: 99%

Focal dystonia and the Sensory-Motor Integrative Loop for Enacting (SMILE)

Perruchoud

Murray

Lefebvre

et al. 2014

Front. Hum. Neurosci.

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Performing accurate movements requires preparation, execution, and monitoring mechanisms. The first two are coded by the motor system, the latter by the sensory system. To provide an adaptive neural basis to overt behaviors, motor and sensory information has to be properly integrated in a reciprocal feedback loop. Abnormalities in this sensory-motor loop are involved in movement disorders such as focal dystonia, a hyperkinetic alteration affecting only a specific body part and characterized by sensory and motor deficits in the absence of basic motor impairments. Despite the fundamental impact of sensory-motor integration mechanisms on daily life, the general principles of healthy and pathological anatomic–functional organization of sensory-motor integration remain to be clarified. Based on the available data from experimental psychology, neurophysiology, and neuroimaging, we propose a bio-computational model of sensory-motor integration: the Sensory-Motor Integrative Loop for Enacting (SMILE). Aiming at direct therapeutic implementations and with the final target of implementing novel intervention protocols for motor rehabilitation, our main goal is to provide the information necessary for further validating the SMILE model. By translating neuroscientific hypotheses into empirical investigations and clinically relevant questions, the prediction based on the SMILE model can be further extended to other pathological conditions characterized by impaired sensory-motor integration.

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Abnormal perception of the tonic vibration reflex in idiopathic focal dystonia

Cited by 39 publications

References 19 publications

Normal Motor Adaptation in Cervical Dystonia: A Fundamental Cerebellar Computation is Intact

Normal Motor Adaptation in Cervical Dystonia: A Fundamental Cerebellar Computation is Intact

Neurophysiology of dystonia: The role of inhibition

Focal dystonia and the Sensory-Motor Integrative Loop for Enacting (SMILE)

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