Relief of primary cervical dystonia symptoms by low frequency transcranial magnetic stimulation of the premotor cortex: case report

Allam, Nasser; Brasil‐Neto, Joaquim P.; Brandão, Pedro Renato de Paula; Weiler, Fernanda; Filho, Jairo de Barros; Tomaz, Carlos

doi:10.1590/s0004-282x2007000400030

Cited by 26 publications

(13 citation statements)

References 22 publications

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“…Given that the plasticity induced by TMS has been shown to differ in patients with focal hand dystonia [121], determining what will work best for treatment will take some development. However, significant progress has already been made in this direction, and there is convergence with the fMRI findings discussed above, given it appears premotor stimulation is particularly effective in treating some focal dystonias [25, 26, 108, 109]. …”

Section: Using Imaging To Evaluate and Guide Treatment Of Dystoniamentioning

confidence: 95%

“…Premotor cortex has also been used as the target for successful treatment of cervical dystonia using either TMS or epidural stimulation (see Fig. ( 3C )) [24-26] (see Using imaging to evaluate and guide treatment of dystonia). Finally, premotor activation abnormalities (reduced activation) have also been shown in spasmodic dysphonia, during vocalization [27].…”

Section: Dystonia Appears To Be a Circuit Disorder: What Is The Functmentioning

confidence: 99%

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Imaging Studies in Focal Dystonias: A Systems Level Approach to Studying a Systems Level Disorder

Blood

2013

Current Neuropharmacology

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Focal dystonias are dystonias that affect one part of the body, and are sometimes task-specific. Brain imaging and transcranial magnetic stimulation techniques have been valuable in defining the pathophysiology of dystonias in general, and are particularly amenable to studying focal dystonias. Over the past few years, several common themes have emerged in the imaging literature, and this review summarizes these findings and suggests some ways in which these distinct themes might all point to one common systems-level mechanism for dystonia. These themes include (1) the role of premotor regions in focal dystonia, (2) the role of the sensory system and sensorimotor integration in focal dystonia, (3) the role of decreased inhibition/increased excitation in focal dystonia, and (4) the role of brain imaging in evaluating and guiding treatment of focal dystonias. The data across these themes, together with the features of dystonia itself, are consistent with a hypothesis that all dystonias reflect excessive output of postural control/stabilization systems in the brain, and that the mechanisms for dystonia reflect amplification of an existing functional system, rather than recruitment of the wrong motor programs. Imaging is currently being used to test treatment effectiveness, and to visually guide treatment of dystonia, such as placement of deep brain stimulation electrodes. In the future, it is hoped that imaging may be used to individualize treatments across behavioral, pharmacologic, and surgical domains, thus optimizing both the speed and effectiveness of treatment for any given individual with focal dystonia.

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Section: Using Imaging To Evaluate and Guide Treatment Of Dystoniamentioning

confidence: 95%

Section: Dystonia Appears To Be a Circuit Disorder: What Is The Functmentioning

confidence: 99%

Imaging Studies in Focal Dystonias: A Systems Level Approach to Studying a Systems Level Disorder

Blood

2013

Current Neuropharmacology

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“…The BFM score did not improve either immediately or after 1 and 4 months after the last rTMS session. However, the cervical subset of the BFM score improved by 50% and was sustained for 4 months (Allam et al, 2007). …”

Section: Therapeutic Procedures In Dystoniamentioning

confidence: 99%

Contribution of TMS and rTMS in the Understanding of the Pathophysiology and in the Treatment of Dystonia

Lozeron

Poujois

Richard

et al. 2016

Front. Neural Circuits

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Dystonias represent a heterogeneous group of movement disorders responsible for sustained muscle contraction, abnormal postures, and muscle twists. It can affect focal or segmental body parts or be generalized. Primary dystonia is the most common form of dystonia but it can also be secondary to metabolic or structural dysfunction, the consequence of a drug’s side-effect or of genetic origin. The pathophysiology is still not elucidated. Based on lesion studies, dystonia has been regarded as a pure motor dysfunction of the basal ganglia loop. However, basal ganglia lesions do not consistently produce dystonia and lesions outside basal ganglia can lead to dystonia; mild sensory abnormalities have been reported in the dystonic limb and imaging studies have shown involvement of multiple other brain regions including the cerebellum and the cerebral motor, premotor and sensorimotor cortices. Transcranial magnetic stimulation (TMS) is a non-invasive technique of brain stimulation with a magnetic field applied over the cortex allowing investigation of cortical excitability. Hyperexcitability of contralateral motor cortex has been suggested to be the trigger of focal dystonia. High or low frequency repetitive TMS (rTMS) can induce excitatory or inhibitory lasting effects beyond the time of stimulation and protocols have been developed having either a positive or a negative effect on cortical excitability and associated with prevention of cell death, γ-aminobutyric acid (GABA) interneurons mediated inhibition and brain-derived neurotrophic factor modulation. rTMS studies as a therapeutic strategy of dystonia have been conducted to modulate the cerebral areas involved in the disease. Especially, when applied on the contralateral (pre)-motor cortex or supplementary motor area of brains of small cohorts of dystonic patients, rTMS has shown a beneficial transient clinical effect in association with restrained motor cortex excitability. TMS is currently a valuable tool to improve our understanding of the pathophysiology of dystonia but large controlled studies using sham stimulation are still necessary to delineate the place of rTMS in the therapeutic strategy of dystonia. In this review, we will focus successively on the use of TMS as a tool to better understand pathophysiology, and the use of rTMS as a therapeutic strategy.

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“…Previously we have suggested that the enhanced dPMI is a reflection of compensatory mechanisms—supported by rTMS trials aimed at enhancing inhibition over the premotor cortex demonstrating symptom improvement (Allam et al, 2007; Lefaucheur et al, 2004; Murase et al, 2005). Although we were unable to directly measure dPMI over the SCM as described above, we have indirect evidence that dPMI is compensatory in nature.…”

Section: Discussionmentioning

confidence: 92%

“…This enhanced inhibition is hypothesized to be due to compensatory networks that play a role in reducing unwanted motor output. This is supported by studies using low-frequency repetitive transcranial magnetic stimulation (rTMS) over the premotor cortex that have modulated symptoms in FHD and in secondary dystonia with significant improvement in painful spasms (Allam et al, 2007; Lefaucheur et al, 2004; Murase et al, 2005). …”

Section: Introductionmentioning

confidence: 90%

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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Relief of primary cervical dystonia symptoms by low frequency transcranial magnetic stimulation of the premotor cortex: case report

Cited by 26 publications

References 22 publications

Imaging Studies in Focal Dystonias: A Systems Level Approach to Studying a Systems Level Disorder

Imaging Studies in Focal Dystonias: A Systems Level Approach to Studying a Systems Level Disorder

Contribution of TMS and rTMS in the Understanding of the Pathophysiology and in the Treatment of Dystonia

Enhanced dorsal premotor–motor inhibition in cervical dystonia

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