Shortened cortical silent period in adductor spasmodic dysphonia: Evidence for widespread cortical excitability

Samargia, Sharyl; Schmidt, Rebekah; Kimberley, Teresa Jacobson

doi:10.1016/j.neulet.2013.12.007

Cited by 33 publications

(37 citation statements)

References 27 publications

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“…This however, is in contrast to much of the known physiology of focal dystonia that suggests a loss of inhibition (Quartarone and Hallett, 2013). Indeed, we showed shorter CSP latencies in our CD patients compared to healthy volunteers suggesting that our CD patients do have an overall reduction in inhibitory tone and are behaving in a physiologic manner consistent with the literature—yet they still show enhanced inhibition in a particular network (Samargia et al, 2014). …”

Section: Discussionsupporting

confidence: 82%

Enhanced dorsal premotor–motor inhibition in cervical dystonia

Richardson

2015

Clinical Neurophysiology

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Objective This study aims to understand whether the enhanced dPMI, seen in writer’s cramp patients previously, extends to other populations of focal dystonia patients (e.g. cervical dystonia) as an endophenotypic marker. Methods We studied 9 healthy subjects and 9 patients with CD. dPMI was tested by applying conditioning transcranial magnetic stimulation to the left dorsal premotor cortex and then a test pulse to the ipsilateral motor cortex at an interval of 6 ms. We also looked at the duration of the cortical silent period (CSP)—a measure of cortical excitability. Results CD patients had enhanced dPMI at rest (mean 57.0%, SD 16.2) in contrast to healthy volunteers (mean 124.1%, SD 35.7) (p<0.001). CSP latencies (in ms) in CD patients (mean 108.0, SD 33.1) were significantly shorter than in healthy volunteers (mean 159.1, SD 55.2) (p<0.05). Conclusions CD patients showed enhanced dPMI in a hand muscle—distant from their affected body part—similar to writer’s cramp patients. This enhanced inhibition was independent of disease severity and neck posture. This suggests that enhanced dPMI may be an endophenotypic marker of dystonia. Significance The abnormal dorsal premotor-motor connection in cervical dystonia is a potential novel and important avenue for therapeutic targeting.

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Section: Discussionsupporting

confidence: 82%

Enhanced dorsal premotor–motor inhibition in cervical dystonia

Richardson

2015

Clinical Neurophysiology

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“…This was also recently confirmed for SD 24 . With respect to processing of efferent motor commands, SD subjects were found to show increased activation of the primary sensorimotor cortices comprising both somatosensory (areas 3a, 3b, 1, and 2) and motor cortical regions (areas 4a, 4p, and 6) during symptomatic vocalization tasks 37 .…”

Section: Discussionsupporting

confidence: 75%

“…Given that muscle spindles in dystonic muscles are intact 21 and focal dystonia is not associated with known proprioceptive receptor or peripheral nervous system damage, the most plausible explanation is that the observed kinaesthetic deficits in focal dystonia are of central origin and not solely caused by the abnormal tone in the affected musculature or abnormal reflex circuitry in the brainstem. This assessment is corroborated by recordings of somatosensory evoked potentials (SEPs) and transcranial magnetic stimulation documenting that abnormal processing of somatosensory information in focal dystonia is associated with abnormally enhanced cortical excitability and decreased intracortical inhibition 22, 23 , which recently has also been confirmed for SD 24 .…”

Section: Introductionmentioning

confidence: 76%

Impaired Limb Proprioception in Adults With Spasmodic Dysphonia

et al. 2015

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Objectives Focal dystonia of the head, neck are associated with a loss of kinaesthetic acuity at muscles distant from the dystonic sites. That is, while the motor deficits in focal dystonia are confined, the associated somatosensory deficits are generalized. This is the first systematic study to examine, if patients diagnosed with spasmodic dystonia (SD) show somatosensory impairments similar in scope to other forms of focal dystonia. Methods Proprioceptive acuity (ability to discriminate between two stimuli) for forearm position and motion sense was assessed in 14 spasmodic dystonia subjects and 28 age-matched controls using a passive motion apparatus. Psychophysical thresholds, uncertainty area and a proprioceptive acuity index were computed based on the subjects’ verbal responses. Results The main findings are: First, the SD group showed significantly elevated thresholds and uncertainty areas for forearm position sense when compared to the control group. Second, 9 out of 14 dystonia subjects (64%) exhibited an acuity index for position sense above the control group maximum. Three SD subjects had a motion sense acuity index above the control group maximum. Conclusion The results indicate that impaired limb proprioception is a common feature of SD. Like other forms of focal dystonia, spasmodic dystonia does affect the somatosensation of non-dystonic muscle systems. That is, SD is associated with a generalized somatosensory deficit.

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“…Recently, by applying transcranial magnetic stimulation (TMS) over the dominant primary motor cortex (M1), Samargia et al . () found shortened cortical silent period (CSP) during contralateral hand muscle contraction in ASD, suggesting reduced cortical inhibition. However, Samargia et al .…”

Section: Introductionmentioning

confidence: 99%

“…However, Samargia et al . () did not examine M1 excitability during speech, leaving the ‘linguistic’ task‐specificity of ASD unexplained.…”

Section: Introductionmentioning

confidence: 99%

Abnormal motor cortex excitability during linguistic tasks in adductor‐type spasmodic dysphonia

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Marsili

Giovannelli³

et al. 2015

Eur J of Neuroscience

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In healthy subjects (HS), transcranial magnetic stimulation (TMS) applied during 'linguistic' tasks discloses excitability changes in the dominant hemisphere primary motor cortex (M1). We investigated 'linguistic' task-related cortical excitability modulation in patients with adductor-type spasmodic dysphonia (ASD), a speech-related focal dystonia. We studied 10 ASD patients and 10 HS. Speech examination included voice cepstral analysis. We investigated the dominant/non-dominant M1 excitability at baseline, during 'linguistic' (reading aloud/silent reading/producing simple phonation) and 'non-linguistic' tasks (looking at non-letter strings/producing oral movements). Motor evoked potentials (MEPs) were recorded from the contralateral hand muscles. We measured the cortical silent period (CSP) length and tested MEPs in HS and patients performing the 'linguistic' tasks with different voice intensities. We also examined MEPs in HS and ASD during hand-related 'action-verb' observation. Patients were studied under and not-under botulinum neurotoxin-type A (BoNT-A). In HS, TMS over the dominant M1 elicited larger MEPs during 'reading aloud' than during the other 'linguistic'/'non-linguistic' tasks. Conversely, in ASD, TMS over the dominant M1 elicited increased-amplitude MEPs during 'reading aloud' and 'syllabic phonation' tasks. CSP length was shorter in ASD than in HS and remained unchanged in both groups performing 'linguistic'/'non-linguistic' tasks. In HS and ASD, 'linguistic' task-related excitability changes were present regardless of the different voice intensities. During hand-related 'action-verb' observation, MEPs decreased in HS, whereas in ASD they increased. In ASD, BoNT-A improved speech, as demonstrated by cepstral analysis and restored the TMS abnormalities. ASD reflects dominant hemisphere excitability changes related to 'linguistic' tasks; BoNT-A returns these excitability changes to normal.

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Shortened cortical silent period in adductor spasmodic dysphonia: Evidence for widespread cortical excitability

Cited by 33 publications

References 27 publications

Enhanced dorsal premotor–motor inhibition in cervical dystonia

Enhanced dorsal premotor–motor inhibition in cervical dystonia

Impaired Limb Proprioception in Adults With Spasmodic Dysphonia

Abnormal motor cortex excitability during linguistic tasks in adductor‐type spasmodic dysphonia

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