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Distinct roles of brain activity and somatotopic representation in pathophysiology of focal dystonia.

ABSTRACT: Two main neural mechanisms including loss of cortical inhibition and maladaptive plasticity have been thought to be involved in the pathophysiology of focal task-specific dystonia. Such loss of inhibition and maladaptive plasticity likely correspond to cortical overactivity and disorganized somatotopy, respectively. However, the most plausible mechanism of focal task-specific dystonia remains unclear. To address this question, we assessed brain activity and somatotopic representations of motor-related brain areas using functional MRI and behavioral measurement in healthy instrumentalists and patients with embouchure dystonia as an example of focal task-specific dystonia. Dystonic symptoms were measured as variability of fundamental frequency during long tone playing. We found no significant differences in brain activity between the embouchure dystonia and healthy wind instrumentalists in the motor-related areas. Assessment of somatotopy, however, revealed significant differences in the somatotopic representations of the mouth area for the right somatosensory cortex between the two groups. Multiple-regression analysis revealed brain activity in the primary motor and somatosensory cortices, cerebellum, and putamen was significantly associated with variability of fundamental frequency signals representing dystonic symptoms. Conversely, somatotopic representations in motor-related brain areas were not associated with variability of fundamental frequency signals in embouchure dystonia. The present findings suggest that abnormal motor-related network activity and aberrant somatotopy correlate with different aspects of mechanisms underlying focal task-specific dystonia.

SUBMITTER: Uehara K

PROVIDER: S-EPMC6865568 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Distinct roles of brain activity and somatotopic representation in pathophysiology of focal dystonia.

Uehara Kazumasa K Furuya Shinichi S Numazawa Hidemi H Kita Kahori K Sakamoto Takashi T Hanakawa Takashi T

Human brain mapping 20181220 6

Two main neural mechanisms including loss of cortical inhibition and maladaptive plasticity have been thought to be involved in the pathophysiology of focal task-specific dystonia. Such loss of inhibition and maladaptive plasticity likely correspond to cortical overactivity and disorganized somatotopy, respectively. However, the most plausible mechanism of focal task-specific dystonia remains unclear. To address this question, we assessed brain activity and somatotopic representations of motor-r ...[more]

PMID: 30570801

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Project description:BackgroundFocal dystonias are severe and disabling movement disorders of a still unclear origin. The structural brain networks associated with focal dystonia have not been well characterized. Here, we investigated structural brain network fingerprints in patients with blepharospasm (BSP) compared with those with hemifacial spasm (HFS), and healthy controls (HC). The patients were also examined following treatment with botulinum neurotoxin (BoNT).MethodsThis study included matched groups of 13 BSP patients, 13 HFS patients, and 13 HC. We measured patients using structural-magnetic resonance imaging (MRI) at baseline and after one month BoNT treatment, at time points of maximal and minimal clinical symptom representation, and HC at baseline. Group regional cross-correlation matrices calculated based on grey matter volume were included in graph-based network analysis. We used these to quantify global network measures of segregation and integration, and also looked at local connectivity properties of different brain regions.ResultsThe networks in patients with BSP were more segregated than in patients with HFS and HC (p < 0.001). BSP patients had increased connectivity in frontal and temporal cortices, including sensorimotor cortex, and reduced connectivity in the cerebellum, relative to both HFS patients and HC (p < 0.05). Compared with HC, HFS patients showed increased connectivity in temporal and parietal cortices and a decreased connectivity in the frontal cortex (p < 0.05). In BSP patients, the connectivity of the frontal cortex diminished after BoNT treatment (p < 0.05). In contrast, HFS patients showed increased connectivity in the temporal cortex and reduced connectivity in cerebellum after BoNT treatment (p < 0.05).ConclusionsOur results show that BSP patients display alterations in both segregation and integration in the brain at the network level. The regional differences identified in the sensorimotor cortex and cerebellum of these patients may play a role in the pathophysiology of focal dystonia. Moreover, symptomatic reduction of hyperkinesia by BoNT treatment was associated with different brain network fingerprints in both BSP and HFS patients.

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Distinct roles of brain activity and somatotopic representation in pathophysiology of focal dystonia.

Publications

Distinct roles of brain activity and somatotopic representation in pathophysiology of focal dystonia.

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