Deep Brain Stimulation for Parkinson’s Disease

Limousin, Patricia; Martínez‐Torres, Irene

doi:10.1016/j.nurt.2008.01.006

Cited by 125 publications

(77 citation statements)

References 96 publications

(106 reference statements)

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“…1) (see also other reviews of DBS elsewhere in this issue [128][129][130][131] ). The primary targets of DBS for PD include the sensorimotor STN and GPi, 132 and recent studies suggest that the PPN, 80 GPe, 47 and motor cortex 133 are also effective targets.…”

Section: Why So Many Targets?mentioning

confidence: 99%

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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Section: Why So Many Targets?mentioning

confidence: 99%

Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

et al. 2008

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“…As a consequence, movement initiation disorders are not easily alleviated by standard therapies [4][5][6]. Even worse, they can be aggravated by the treatments, for example worsened akinesia [7] or induced impulsivity [8][9][10]. A prerequisite for current therapeutic strategies is to understand the complexity of the basic mechanisms involved in movement initiation and related dysfunctions.…”

Section: Introductionmentioning

confidence: 99%

Deep Brain Stimulation of the Subthalamic Nucleus, but not Dopaminergic Medication, Improves Proactive Inhibitory Control of Movement Initiation in Parkinson's Disease

et al. 2013

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Slowness in movement initiation is a cardinal feature of Parkinson's disease (PD) that is still poorly understood and unsuccessfully alleviated by standard therapies. Here, we raise this major clinical issue within the framework of a novel theoretical model that allows a better understanding of the basic mechanisms involved in movement initiation. This model assumes that movement triggering is inhibited by default to prevent automatic responses to unpredictable events. We investigated to which extent the top-down control necessary to release this locking state before initiating actions is impaired in PD and restored by standard therapies. We used a cue-target reaction time task to test both the ability to initiate fast responses to targets and the ability to refrain from reacting to cues. Fourteen patients with dopaminergic (DA) medication and 11 with subthalamic nucleus (STN) stimulation were tested on and off treatment, and compared with 14 healthy controls. We found evidence that patients withdrawn from treatment have trouble voluntarily releasing proactive inhibitory control; while DA medication broadly reduces movement initiation latency, it does not reinstate a normal pattern of movement initiation; and stimulation of the STN specifically re-establishes the efficiency of the top-down control of proactive inhibition. These results suggest that movement initiation disorders that resist DA medication are due to executive, not motor, dysfunctions. This conclusion is discussed with regard to the role the STN may play as an interface between non-DA executive and DA motor systems in cortico-basal ganglia loops.

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“…The reader is referred to the article on DBS for PD in this issue, by Limousin et al 60 Here we will address only the few comparison trials that have been published (Table 1). In 1998, Kumar et al 61 examined results in a retrospective review with unequal group sizes and follow-up times.…”

Section: Is Dbs a Safer And More Effective Therapy For Pd?mentioning

confidence: 99%

What Happened to Posteroventral Pallidotomy for Parkinson’s Disease and Dystonia?

Gross

2008

Neurotherapeutics

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Summary: Fifteen years after its resurrection, pallidotomy for Parkinson's disease (PD) and dystonia has once again been supplanted, this time by deep brain stimulation (DBS). Did this occur because pallidotomy was not effective or safe, or because DBS was found to be more effective and safer? This review focuses on the evidence-and its quality-supporting the effectiveness and safety of pallidotomy for PD and dystonia, and the comparative effectiveness and safety of DBS of the subthalamic nucleus (STN) and globus pallidus pars interna (GPi). Discussed first are the determinants of "level 1" recommendations, including the confounding effects on interpretation of randomized clinical trials (RCTs) that fail to control for patient bias (i.e., placebo effects). Although several RCTs have been performed comparing unilateral pallidotomy to medical therapy, GPi DBS, or STN DBS for PD, none controlled for patient bias. Comparison of these trials to estimate the placebo effect, and examination of retrospective case series, suggests that the true effectiveness of unilateral pallidotomy is 20% to 30% reduction of 'off' total motor UPDRS scores, which is similar to the effects of unilateral GPi DBS or STN DBS, but less than bilateral STN DBS. At experienced centers, safety of unilateral pallidotomy appears equivalent to unilateral DBS, but bilateral DBS is likely safer than bilateral pallidotomy. Whereas there have been no RCTs of pallidotomy for dystonia, two doubleblind, sham-controlled RCTs of bilateral GPi DBS were performed. Nevertheless, limited uncontrolled series suggest that bilateral pallidotomy is similar to GPi DBS in effectiveness and safety for dystonia. Thus, pallidotomy was not rejected because of lack of effectiveness or safety, and it remains a viable alternative in situations where DBS is not available or not feasible.

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Deep Brain Stimulation for Parkinson’s Disease

Cited by 125 publications

References 96 publications

Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

Deep Brain Stimulation of the Subthalamic Nucleus, but not Dopaminergic Medication, Improves Proactive Inhibitory Control of Movement Initiation in Parkinson's Disease

What Happened to Posteroventral Pallidotomy for Parkinson’s Disease and Dystonia?

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