Effect on parkinsonian signs and symptoms of bilateral subthalamic nucleus stimulation

Limousin, Patricia; Pollak, Pierre; Benazzouz, Abdelhamid; Hoffmann, D.; Bas, JF Le; Perret, J; Benabid, A.L.; Broussolle, El

doi:10.1016/s0140-6736(95)90062-4

Cited by 1,236 publications

(720 citation statements)

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“…However, after the administration of levodopa, cadence was increased in some reports [19] and not changed in the others [7,34] as in our study. Chronic bilateral STN stimulation improves akinesia, rigidity and tremor in patients with severe PD [21,[24][25][26][27][29][30]. The exact mechanism of STN stimulation is still unknown.…”

Section: Discussionmentioning

confidence: 99%

“…All the patients had bilateral chronic STN stimulation (DBS 3389 electrode, Medtronic, Minneapolis, MN, USA). Electrode implantations were carried out according to a procedure already described [27]. These patients were consecutively chosen on the occasion of a follow up of their STN stimulation in our hospital.…”

Section: Materials and Methods S Patientsmentioning

confidence: 99%

“…Since 1993, clinical reports have shown that subthalamic nucleus (STN) stimulation can greatly alleviate the main motor signs and symptoms of PD, including gait [25][26][27][29][30]. Yokoyama et al [38] focused on the poss Abstract Clinical reports show that bilateral subthalamic nucleus (STN) stimulation is effective in improving parkinsonian gait.…”

Section: Introductionmentioning

confidence: 99%

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Effect of bilateral subthalamic nucleus stimulation on parkinsonian gait

Xie¹,

Krack²,

Benabid

et al. 2001

Journal of Neurology

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Section: Discussionmentioning

confidence: 99%

Section: Materials and Methods S Patientsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of bilateral subthalamic nucleus stimulation on parkinsonian gait

Xie¹,

Krack²,

Benabid

et al. 2001

Journal of Neurology

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“…The early finding that DBS of the STN or GPi results in clinical benefits that are strikingly similar to those of lesioning at these sites for tremor and PD, respectively, suggested initially that DBS may act by inhibiting neurons in the area of stimulation [269][270][271]. This view was supported by the demonstration that some neurons in the vicinity of the stimulation site in STN and GPi in experimental animals and in patients with PD are, indeed, inhibited [272][273][274][275], perhaps by depolarization block or the release of GABA from terminals of afferents to the stimulated area [276][277][278][279][280].…”

Section: Dbs Mechanism Of Actionmentioning

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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“…Choice of the STN as a target for PD arose from studies on the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkey model of PD, which showed increased neuronal activity in the STN [13] and marked amelioration of parkinsonian features following its lesion [14]. This antiparkinsonian effect could be reproduced with DBS of the STN in this model [15] and later in PD patients [16,17]. More recently, DBS has been introduced in the field of psychiatry to modulate neuronal activity in the same areas that were targeted for lesioning in the past [18,19].…”

Section: Introductionmentioning

confidence: 99%