Abnormalities of sensory processing and sensorimotor interactions in secondary dystonia: A neurophysiological study in two patients

Tamburin, Stefano; Zanette, Giampietro

doi:10.1002/mds.20301

Cited by 7 publications

(4 citation statements)

References 27 publications

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“…However, these alterations may also in some circumstances, such as after an injury or the sustained performance of repetitive muscular activity, become maladaptive plastic changes that are thought to be responsible for initiating and perpetuating certain movement disorders and chronic pain syndromes. 24,[39][40][41][42][43][44][45][46][47][48][49][50][51] Furthermore, joint dysfunction originating from an injury may be a cause of ongoing pain and loss of function due to maladaptive sensorimotor integration from a hyperafferentiation of the CNS from the dysfunctional joints and associated structures. [52][53][54][55][56][57][58] Does Repetitive Muscular Activity and Joint Dysfunction Lead to Maladaptive Plasticity?…”

Section: Clinical and Research Implicationsmentioning

confidence: 98%

The Effects of Spinal Manipulation on Central Integration of Dual Somatosensory Input Observed After Motor Training: A Crossover Study

Taylor

Murphy

2010

Journal of Manipulative and Physiological Therapeutics

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Section: Clinical and Research Implicationsmentioning

confidence: 98%

The Effects of Spinal Manipulation on Central Integration of Dual Somatosensory Input Observed After Motor Training: A Crossover Study

Taylor

Murphy

2010

Journal of Manipulative and Physiological Therapeutics

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“…The measures of somatosensory inhibition applied in this study have never been investigated in SD, other than in SD caused by lesions in the somatosensory pathways. 34,35 None of our patients presented with lesions involving the somatosensory system, which was functionally intact. However, the results differed from those in idiopathic dystonia, in which there is reduced PP-SEP suppression, 20,23 impaired SIR, [18][19][20] and reduced HFO.…”

Section: Discussionmentioning

confidence: 93%

“…The measures of somatosensory inhibition applied in this study have never been investigated in SD, other than in SD caused by lesions in the somatosensory pathways 34,35 . None of our patients presented with lesions involving the somatosensory system, which was functionally intact.…”

Section: Discussionmentioning

confidence: 99%

Defective Somatosensory Inhibition and Plasticity Are Not Required to Develop Dystonia

et al. 2020

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Background Dystonia may have different neuroanatomical substrates and pathophysiology. This is supported by studies on the motor system showing, for instance, that plasticity is abnormal in idiopathic dystonia, but not in dystonia secondary to basal ganglia lesions. Objective The aim of this study was to test whether somatosensory inhibition and plasticity abnormalities reported in patients with idiopathic dystonia also occur in patients with dystonia caused by basal ganglia damage. Methods Ten patients with acquired dystonia as a result of basal ganglia lesions and 12 healthy control subjects were recruited. They underwent electrophysiological testing at baseline and after a single 45‐minute session of high‐frequency repetitive somatosensory stimulation. Electrophysiological testing consisted of somatosensory temporal discrimination, somatosensory‐evoked potentials (including measurement of early and late high‐frequency oscillations and the spatial inhibition ratio of N20/25 and P14 components), the recovery cycle of paired‐pulse somatosensory‐evoked potentials, and primary motor cortex short‐interval intracortical inhibition. Results Unlike previous reports of patients with idiopathic dystonia, patients with acquired dystonia did not differ from healthy control subjects in any of the electrophysiological measures either before or after high‐frequency repetitive somatosensory stimulation, except for short‐interval intracortical inhibition, which was reduced at baseline in patients compared to control subjects. Conclusions The data show that reduced somatosensory inhibition and enhanced cortical plasticity are not required for the clinical expression of dystonia, and that the abnormalities reported in idiopathic dystonia are not necessarily linked to basal ganglia damage. © 2020 International Parkinson and Movement Disorder Society

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“…Von Monakow,34 Bonhoeffer,24, 35 Pineles,37 and Halban and Infeld23 had previously hypothesized that, when the mesodiencephalic targets of afferent stimuli are diminished by a lesion or irritative impulses from areas surrounding a lesion, thus inadequate corticopetal impulses reach the cortex, compensatory impulses can be produced in the corticospinal tract resulting in involuntary movements. Recent studies confirm that impaired sensory functions, sensory gating, or sensorimotor integration contribute to chorea, dystonia, and tics 38–41. On the basis of his previous animal experiments, however, CvE contested that hyperkinesias are related to impaired centripetal (sensory) functions or that lesions or compensatory mechanisms of the corticospinal tract cause hemichorea.…”

Section: Posthemiplegic Choreamentioning

confidence: 99%

Constantin von Economo's contribution to the understanding of movement disorders

Ransmayr

2007

Movement Disorders

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Constantin von Economo's (CvE) main scientific achievements were his studies on the cytoarchitectonics of the cerebral cortex, sleep, and encephalitis lethargica (EL). He found a close relationship between motor symptoms and psychiatric and behavioral disorders in EL and postencephalitic Parkinsonism and identified the underlying neuropathology in the diencephalon and the brainstem. In agreement with Tretiakoff's findings in Parkinson's disease, CvE related postencephalitic Parkinsonism to neuronal loss in the substantia nigra. Several of CvE's early, less well-known publications also deal with the basal ganglia and movement disorders. He demonstrated in rabbits that the substantia nigra modulates automatization, coordination, and succession of masticatory movements and swallowing. In a study on the effects of experimental lesions of the cerebral peduncle in cats and monkeys, CvE hypothesized a corticotegmental pathway that maintains motor functions after pyramidal tract lesions. Recent studies have identified this pathway, which ends in the pedunculopontine nucleus. In a study on posthemiplegic chorea, CvE discussed various pathophysiological hypotheses that partly resemble modern concepts of chorea. In a clinicopathological study on Wilson's disease, CvE traced the striofugal fibers and visualized the basal ganglia outflow pathways. CvE was an outstanding multidisciplinary movement disorder specialist who contributed substantially to modern basal ganglia research.

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Abnormalities of sensory processing and sensorimotor interactions in secondary dystonia: A neurophysiological study in two patients

Cited by 7 publications

References 27 publications

The Effects of Spinal Manipulation on Central Integration of Dual Somatosensory Input Observed After Motor Training: A Crossover Study

The Effects of Spinal Manipulation on Central Integration of Dual Somatosensory Input Observed After Motor Training: A Crossover Study

Defective Somatosensory Inhibition and Plasticity Are Not Required to Develop Dystonia

Constantin von Economo's contribution to the understanding of movement disorders

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