Pallidal activity during dystonia: somatosensory reorganisation and changes with severity

Lenz, Frederick A.; Suárez, Jacqueline; Metman, Leo Verhagen; Reich, Stephen G.; Karp, Barbara I.; Hallett, Mark; Rowland, L. H.; Dougherty, Patrick M.

doi:10.1136/jnnp.65.5.767

Cited by 167 publications

(107 citation statements)

References 11 publications

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“…GPi firing rates(as well as GPe) are reduced in dystonic patients as compared to Parkinson's disease patients or parkinsonian primates, but slightly faster than reported in patients with hemiballismus 13,20,40,41 . Pallidal activity also seems to correlate inversely with dystonia severity 42 . No human data on normal firing rates are available for comparison.…”

Section: Discussionmentioning

confidence: 95%

Bilateral pallidotomy for generalized dystonia

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Grande

et al. 2001

Arq. Neuro-Psiquiatr.

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-Objective: To evaluate the efficacy and safety of bilateral pallidotomies in five patients with generalized dystonia. Background: Generalized dystonias are frequently a therapeutic challenge, with poor responses to pharmacological treatment. GPi (globus pallidus internus) pallidotomies for Parkinson's disease ameliorate all kinds of dyskinesias/dystonia, and recent studies reported a marked improvement of refractory dystonias with this procedure. Methods: Five patients with generalized dystonias refractory to medical treatment were selected; one posttraumatic and four idiopathic. The decision to perform bilateral procedures was based on the predominant axial involvement in these patients. Dystonia severity was assessed with the Burke-FahnMarsden Dystonia Scale (BFM). Simultaneous procedures were performed in all but one patient, who had a staged procedure. They were reevaluated with the same scale (BFM) by an unblinded rater at 1, 2, 3, 30, 60, 90, 120 and 180 days post-operatively. Results: The four patients with idiopathic dystonia showed a progressive improvement up to three months; the patient with posttraumatic dystonia relapsed at three months. One patient had a marked improvement, being able to discontinue all the medications. A mean decrease in the BFM scores of 52,58% was noted. One patient had a trans-operative motor seizure followed by a transient hemiparesis secondary to rack hemorrhage; other was lethargic up to three days after the procedure. Conclusions: Our results show that bilateral GPi pallidotomies may be a safe and effective approach to medically refractory generalized dystonias; it can also be speculated that the posttraumatic subgroup may not benefit with this procedure.KEY WORDS: dystonia, pallidotomy, stereotactic surgery. Palidotomia bilateral para distonias generalizadasRESUMO -As distonias generalizadas são freqüentemente um desafio terapêutico, com pobres respostas aos tratamentos farmacológicos. As cirurgias estereotáxicas, como a palidotomia, têm sido utilizadas com êxito no tratamento da doença de Parkinson e estudos recentes relatam importante melhora das distonias generalizadas, refratárias ao tratamento farmacológico, com a palidotomia bilateral. O objetivo dos autores foi avaliar a eficácia e segurança da palidotomia bilateral em cinco pacientes com distonia generalizada. Foram selecionados cinco pacientes com distonia generalizada, predominante axial, refratários ao tratamento farmacológico (quatro idiopáticas e uma pós-traumática). A severidade da distonia foi avaliada através da escala de Burke-Fahn-Marsden (BFM), no 1º, 2º, e 3º dia após a cirurgia e nos dias 30, 60, 90, 120 e 180 do pós-operatório. Quatro pacientes com distonia idiopática tiveram uma progressiva melhora dentro de 3 meses após a cirurgia e o paciente com distonia pós-traumática teve uma piora da distonia após 3 meses da cirurgia. Um dos pacientes teve uma melhora acentuada do quadro de distonia, ficando livre das medicações. Em média ocorreu redução de 52,58 % dos escores da escala de BFM. Um dos...

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Section: Discussionmentioning

confidence: 95%

Bilateral pallidotomy for generalized dystonia

Teive

Sá

Grande

et al. 2001

Arq. Neuro-Psiquiatr.

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“…During movement, most of these neurons were activated, whereas the activation-to-inactivation ratio was reversed for nonparkinsonian monkeys. 99 In dystonia, experimental recordings showed enlarged receptive fields of dystonic joints in the somatosensory cortex, 100 thalamus, 101 and globus pallidus 102,103 (but also see the 2003 article by Hutchison et al 104 ).…”

Section: Effects On Coactivation Of Competing Motor Programsmentioning

confidence: 98%

Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

et al. 2008

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Summary:Chronic electrical stimulation of the brain, known as deep brain stimulation (DBS), has become a preferred surgical treatment for medication-refractory movement disorders. Despite its remarkable clinical success, the therapeutic mechanisms of DBS are still not completely understood, limiting opportunities to improve treatment efficacy and simplify selection of stimulation parameters. This review addresses three questions essential to understanding the mechanisms of DBS. 1) How does DBS affect neuronal tissue in the vicinity of the active electrode or electrodes? 2) How do these changes translate into therapeutic benefit on motor symptoms? 3) How do these effects depend on the particular site of stimulation? Early hypotheses proposed that stimulation inhibited neuronal activity at the site of stimulation, mimicking the outcome of ablative surgeries. Recent studies have challenged that view, suggesting that although somatic activity near the DBS electrode may exhibit substantial inhibition or complex modulation patterns, the output from the stimulated nucleus follows the DBS pulse train by direct axonal excitation. The intrinsic activity is thus replaced by high-frequency activity that is time-locked to the stimulus and more regular in pattern. These changes in firing pattern are thought to prevent transmission of pathologic bursting and oscillatory activity, resulting in the reduction of disease symptoms through compensatory processing of sensorimotor information. Although promising, this theory does not entirely explain why DBS improves motor symptoms at different latencies. Understanding these processes on a physiological level will be critically important if we are to reach the full potential of this powerful tool.

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“…Based on pharmacologic studies, there seems to be a relative increase in the activity of striatal neurons of the direct pathway over those that give rise to the indirect pathway in dystonia [195,196], and single-cell recording studies in patients undergoing functional neurosurgical treatments have demonstrated low discharge rates in both GPe and GPi [197][198][199][200][201][202], in distinction to the aforementioned changes in PD where GPi discharge rates are generally increased. The presence of lowfrequency discharge in the GPi in patients with dystonia is similar to that in other hyperkinetic disorders, including chorea/ ballismus and motor tics [197,203,204].…”

Section: Dystoniamentioning

confidence: 99%

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

2016

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Deep brain stimulation (DBS) is highly effective for both hypo-and hyperkinetic movement disorders of basal ganglia origin. The clinical use of DBS is, in part, empiric, based on the experience with prior surgical ablative therapies for these disorders, and, in part, driven by scientific discoveries made decades ago. In this review, we consider anatomical and functional concepts of the basal ganglia relevant to our understanding of DBS mechanisms, as well as our current understanding of the pathophysiology of two of the most commonly DBS-treated conditions, Parkinson's disease and dystonia. Finally, we discuss the proposed mechanism(s) of action of DBS in restoring function in patients with movement disorders. The signs and symptoms of the various disorders appear to result from signature disordered activity in the basal ganglia output, which disrupts the activity in thalamocortical and brainstem networks. The available evidence suggests that the effects of DBS are strongly dependent on targeting sensorimotor portions of specific nodes of the basal gangliathalamocortical motor circuit, that is, the subthalamic nucleus and the internal segment of the globus pallidus. There is little evidence to suggest that DBS in patients with movement disorders restores normal basal ganglia functions (e.g., their role in movement or reinforcement learning). Instead, it appears that high-frequency DBS replaces the abnormal basal ganglia output with a more tolerable pattern, which helps to restore the functionality of downstream networks.

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Pallidal activity during dystonia: somatosensory reorganisation and changes with severity

Cited by 167 publications

References 11 publications

Bilateral pallidotomy for generalized dystonia

Bilateral pallidotomy for generalized dystonia

Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

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