GRAPHICAL ABSTRACT

INTRODUCTION

Tardive dystonia (TD) is a subtype of tardive syndrome characterized by sustained involuntary muscle contractions and abnormal postures that typically emerge after prolonged exposure to dopamine receptor blocking agents (DRBAs), such as antipsychotics or antiemetics. Although less commonly recognized than tardive dyskinesia, TD often causes severe disability and has a substantial effect on quality of life [1,2]. While it shares a common etiology with tardive dyskinesia, TD presents with its own characteristic clinical phenotype and potentially different underlying pathophysiology. Tardive dyskinesia typically presents as choreiform movements of the orofacial region, whereas TD is characterized by sustained, twisting postures, most commonly affecting the craniocervical area. A potential difference in pathophysiology is suggested by their divergent responses to anticholinergic medications, which may worsen dyskinesia but are often used to treat TD [3]. Tardive syndromes as a whole are estimated to occur in approximately 15% to 30% of patients receiving long-term DRBA therapy [4,5]. Among these, TD accounts for approximately 10% to 20%, although this varies depending on diagnostic definitions, clinical settings, and geographic regions [1,5,6]. Initial nonsurgical management prioritizes tapering or discontinuing DRBAs (or switching to lower D2-engaging agents such as clozapine), with adjuncts including anticholinergics, clonazepam, and baclofen; for focal/segmental patterns, botulinum toxin is frequently effective. Younger patients and those treated with high-potency first-generation antipsychotics may have a higher risk of developing TD [5,6]. In a cohort study of patients with tardive syndromes who discontinued the causative agents, only 13% achieved full remission, and only 2.8% recovered without further intervention, indicating the persistent nature of the disorder [1]. Long-term follow-up data also suggest that patients with TD are less likely to respond to pharmacological adjustments alone and often require targeted treatments such as botulinum toxin injection or deep brain stimulation (DBS) [2,6,7]. Although vesicular monoamine transporter-2 (VMAT2) inhibitors (deutetrabenazine and valbenazine) reduce the frequency of abnormal movements in tardive dyskinesia patients, TD-specific evidence remains limited, and approximately 50% of patients do not achieve a ≥50% reduction in abnormal involuntary movement [8]. For those with insufficient response or medically refractory symptoms, options such as DBS remain important therapeutic options. Among surgical targets, the internal segment of the globus pallidus (GPi) has been most frequently used for treating dystonia. Multiple case series and retrospective analyses have demonstrated that bilateral GPi-DBS can lead to substantial and sustained reductions in dystonic symptoms. Reported long-term improvements in Burke–Fahn–Marsden Dystonia Rating Scale (BFMDRS) typically range from approximately 60% to 90% at follow-up of 4–10 years after pallidal DBS, with greater benefits generally observed in younger patients and those with shorter disease duration [9-12]. Additionally, DBS provides the advantages of adjustability and reversibility, making it particularly suitable for managing patients with severe, medically refractory TD [9-12]. In parallel, emerging imaging techniques, including postoperative magnetic resonance imaging (MRI) and computational tools such as Lead-DBS [13], have facilitated the identification of optimal stimulation sites within the GPi. Although these methods have been widely applied in patients with cervical dystonia (CD) and generalized dystonia (GD), systematic analyses specifically focusing on TD remain scarce [14,15].

In this study, we present a retrospective analysis of data from 26 patients with TD who underwent bilateral GPi-DBS at our institution. We evaluated clinical outcomes using BFMDRS scores and examined the relationship between postoperative lead localization and therapeutic response. Our aim is to clarify both the efficacy of GPi-DBS and the precise subregion within the GPi responsible for symptomatic improvement, ultimately guiding more targeted interventions for patients with this challenging disorder.

MATERIALS & METHODS

Study design and patients

We performed a retrospective study of data from 26 consecutive patients with TD who underwent GPi-DBS at the Tokyo Women’s Medical University between January 2008 and December 2024. The inclusion criteria were 1) a diagnosis of TD attributable to prolonged exposure to DRBAs, 2) persistent dystonic symptoms despite adequate medical therapy, and 3) at least 6 months of postoperative follow-up. Patients with other, secondary causes of dystonia (e.g., stroke or traumatic brain injury) were excluded.

Surgical procedures

Under local or general anesthesia, DBS leads were stereotactically implanted into the bilateral GPi using a frame-based system. Commercially available DBS systems from several manufacturers were used; the leads implanted included Medtronic Model 3387, Boston Scientific Vercise Cartesia, or Abbott STJ-6142, which were connected to their corresponding implantable pulse generators (IPGs), such as the Activa SC, Vercise Gevia, or Brio. Target coordinates were determined on the basis of preoperative T1-weighted MRI. After the optimal position was confirmed via intraoperative test stimulation, the leads were connected to IPGs placed in the subclavicular area. Microelectrode recording was not performed as part of our standard procedure. Postoperative programming was initiated within a few weeks after surgery, and the settings (contact configuration, voltage/current, frequency, pulse width) were adjusted over several sessions to achieve optimal clinical benefit with minimal side effects.

Clinical assessment

The main outcome measure was the BFMDRS score, including both total and subscale scores, evaluated preoperatively and at the final follow-up. Complications related to the procedure or stimulation were also reviewed.

Imaging analysis

All patients underwent preoperative high-resolution T1-weighted MRI, along with postoperative computed tomography or T1-weighted MRI scans to accurately localize the DBS leads. Image preprocessing, coregistration, and normalization to the standard Montreal Neurological Institute (MNI) space were performed using the Lead-DBS software package [12], which incorporates advanced normalization tools. Subsequently, Lead-DBS was used to reconstruct the DBS lead trajectories and identify the active stimulation contacts utilized during the final clinical program. For the voxelwise sweet spot analysis, the active stimulation sites were defined on the basis of the programming parameters documented at each patient’s final follow-up visit. These settings were established through an iterative clinical process initiated a few weeks post surgery. Over several programming sessions, stimulation parameters (contact configuration, amplitude, pulse width, and frequency) were individually titrated to achieve the maximal improvement in dystonic symptoms, as assessed by the BFMDRS, with minimal to no stimulation-induced side effects. The volume of tissue activated for these final, optimal settings was then calculated using Lead-DBS for the sweet spot mapping.

Statistical analysis

Statistical analysis was performed using the JMP statistical package, version 15.0.0 (SAS Institute). Given the small sample size, the preoperative and postoperative total scores on the BFMDRS were compared using the Wilcoxon signed-rank test, a nonparametric method. Statistical significance was defined as p<0.05.

Ethical considerations

This study was a retrospective analysis and was approved by the Institutional Review Board of Tokyo Women’s Medical University (Approval No. 2021-0169). In accordance with the ethical guidelines for medical and health research involving human subjects in Japan, the requirement for written informed consent was waived, and consent was instead obtained using an opt-out process. All clinical and imaging data were anonymized prior to analysis.

RESULTS

A total of 26 patients (14 men and 12 women) with TD were included in this study. The detailed clinical and demographic characteristics of the patients are summarized in Table 1. The mean age at onset of TD was 40.0±9.4 years, and the mean age at surgery was 45.4±9.4 years. Comorbid psychiatric disorders were present in all patients: 12 had schizophrenia, 8 had depression, 4 had bipolar disorder, 1 had anxiety neurosis, and 1 had panic disorder. The mean follow-up duration after GPi-DBS was 45.6±41.9 months. Of the 26 patients, 25 underwent bilateral GPi-DBS. One patient (Case 8) received unilateral DBS. This patient had previously undergone a lesioning procedure on the contralateral side and chose DBS for the untreated side as an additional therapy. The mean BFMDRS motor score at baseline was 11.9± 6.0, which significantly improved to 2.2±2.5 at the final evaluation, corresponding to an 81.5% reduction in dystonic symptoms (p<0.0001). CD was the most common phenotype and was observed in 26 patients. The mean BFMDRS neck subscore improved from 6.0±1.4 preoperatively to 1.3±1.9 at the final follow-up. Table 2 provides the subscale scores for the affected body regions, which consistently improved across all the domains. Two patients achieved complete remission (100% improvement) following GPi-DBS and showed no recurrence of symptoms after cessation of stimulation. Notably, one of these patients underwent complete explantation of the DBS system and remained symptom-free for 3 years and 9 months. In terms of adverse events, hardware-related infection occurred in two patients. In one of these patients, the system was removed, and the patient subsequently underwent pallidotomy. Stimulation-related adverse effects included dysarthria in four patients and gait imbalance, which was consistent with balance-related issues rather than freezing of gait, in one patient. No hemorrhagic complications were observed. All patients continued to use their preexisting psychiatric medications, including antipsychotics, at stable doses throughout the study’s follow-up period. No dose escalations were performed. All patients remained psychiatrically stable, with no reported worsening of their underlying psychiatric disorders.

Postoperative imaging and lead localization analysis were conducted using the Lead-DBS software package. Voxelwise sweet spot mapping revealed the optimal stimulation region in the posteroventral GPi. The peak efficacy coordinates in MNI space were approximately X=20.5 mm, Y=-10 mm, Z=-6.5 mm on the right and X=-22 mm, Y=-9 mm, Z=-6 mm on the left. The three-dimensional reconstruction of active contacts and the sweet spot cluster is shown in Figure 1, and its axial depiction relative to the AC–PC (anterior commissure–posterior commissure) plane is shown in Figure 2. The final stimulation parameters for each patient are listed in Table 3.

DISCUSSION

Our study demonstrated the significant and sustained efficacy of GPi-DBS in patients with TD, with an average BFMDRS score improvement of 81.5% over an average follow-up period of 45.6 months. Using voxelwise sweet spot mapping analysis, we identified optimal stimulation coordinates in the posteroventral GPi, closely aligning with previously reported targets for primary CD and GD. Although two patients experienced device-related infections, no other severe adverse events were noted. These findings reinforce the clinical value of GPi-DBS in managing TD and support the use of similar targeting strategies across patients with dystonia subtypes.

A crucial aspect in managing this patient population is the handling of antipsychotic medications, a challenge highlighted by the fact that all patients in our cohort remained on DRBAs. Throughout the follow-up period, no patient experienced an exacerbation of their underlying psychiatric disorder, and no dose escalation of DRBA medication was needed. Our clinical approach is to prioritize psychiatric stability by maintaining the optimal medication regimen as determined by the patient’s psychiatrist rather than reducing or discontinuing essential DRBAs for the purpose of treating dystonia. Instead, our strategy is to manage the movement disorder with DBS, while the underlying psychiatric condition is managed pharmacologically. The results of this study support the feasibility of this approach, demonstrating that GPi-DBS can be highly effective for patients with TD even when the causative agents are continued.

Our findings demonstrate substantial and sustained improvement following GPi-DBS treatment in patients with TD, with an average BFMDRS score improvement of approximately 81.5%. Previous reports on GPi-DBS outcomes for TD and dyskinesia patients have shown improvement rates ranging widely from 50% to as high as 90%; however, most studies consistently report high efficacy within a narrow range of approximately 70%–80% [11,16-19]. Moreover, long-term follow-up data from these studies has confirmed that therapeutic benefits from GPi-DBS persist over extensive periods, with some studies reporting sustained improvement up to 10 years or more [11-20]. Our observed improvement of 81.5%, together with an average follow- up of approximately 45.6 months, aligns well with the findings of these existing studies and highlights the robustness and durability of the effects of GPi-DBS treatment. Thus, our results reinforce previous literature findings and further validate the clinical efficacy and longevity of GPi-DBS as a reliable intervention for TD patients.

Our study identified the optimal stimulation sites in patients with TD using voxelwise sweet spot mapping analysis with Lead-DBS software, with coordinates of X=20.5 mm, Y=-10 mm, and Z=-6.5 mm on the right and X=-22 mm, Y=-9 mm, and Z=-6 mm on the left. These results are highly consistent with previously reported optimal coordinates for CD patients, such as those described by Horn et al. [15] (X=±20.4 mm, Y=-12.4 mm, Z=-5.2 mm) and Reich et al. [14] (X=-19.4 mm, Y=-10.1 mm, Z=-5.9 mm). Notably, the similarity between our sweet spot coordinates and those reported for CD patients suggests that the substantial improvement observed in our patient cohort, particularly reflected by the total BFMDRS score, may be predominantly driven by improvement in CD symptoms. This interpretation is supported by our patient cohort demographics, in which the cervical spine was the most frequently affected body region, significantly contributing to the overall dystonia burden. In contrast, the optimal stimulation sites reported for GD patients by Horn et al. [15] (X=±21.1; mm Y=-9.1 mm; Z=-0.14 mm) and Reich et al. [14] (X=-20.5 mm; Y=-7.1 mm; Z=-1.0 mm) show greater differences, especially in the vertical (Z-axis) dimension, indicating a more dorsal target for GD patients. The proximity of our coordinates to those reported for CD rather than GD highlights the potential specificity of the identified stimulation sites for CD phenotypes. Given the notable similarity in optimal stimulation coordinates between TD and other primary dystonias, it is reasonable to apply similar GPi targeting strategies across these subtypes. It is important to consider these findings in the context of the known anatomy of the GPi. While the motor territory of the GPi has a well-defined somatotopic organization, with representations for the face, arm, and leg arranged along a ventrolateral-to-dorsomedial gradient [21], our results demonstrate that targeting a standardized, common sweet spot region led to significant symptom improvement across our heterogeneous patient cohort, without the need for individualized targeting on the basis of each patient’s specific symptom topography. These findings are consistent with the influential work by Starr et al. [22], who similarly reported that effective electrode contacts for a diverse group of dystonia patients were clustered within a common posterolateral region of the GPi. This suggests that stimulation of this core motor region may modulate a wider basal ganglia–thalamocortical network subserving various dystonic manifestations. Future studies with diverse patient populations and symptom distributions are warranted to validate these findings and clarify the relationship between stimulation site location and specific dystonia subtypes.

An intriguing observation in our series was that two patients maintained complete (100%) relief of TD even after GPi-DBS was unintentionally or deliberately stopped: one preferred to leave the pulse-generator switched off, while the other proceeded to full hardware explantation and has now remained symptom-free for 3 years 9 months. While such outcomes could reflect spontaneous remission or placebo effects, this “DBS-independent” remission echoes a small but growing body of literature, suggesting that it may be a genuine, albeit rare, phenomenon. In the longest follow-up to date, Krause et al. [11] reported continued benefit in three of seven TD patients who had discontinued stimulation after 3–10 years of chronic GPi-DBS; the mean BFMDRS motor improvement at the final review was 90%, and their active contacts clustered around X=21.0 mm lateral, Y=+2.3 mm anterior, Z=-3.1 mm inferior to the mid-commissural point. Krause et al. [11] proposed that long-term GPi- DBS could induce durable neuroplastic changes within the basal ganglia and related cortical circuits, suggesting potential disease-modifying effects. These coordinates align closely with the sweet spot in our cohort, underscoring the likelihood that precise posteroventral GPi targeting is crucial for inducing durable network reorganization. Additional single-case and small-cohort reports converge on the same phenomenon across etiologies. Wolf et al. [23] described a patient with acquired GD who remained markedly improved for several years after battery depletion following 6.5 years of GPi-DBS. In terms of inherited forms, Ruge et al. [24] reported that several DYT1-positive patients exhibited unchanged clinical scores 48 hours after stimulation was turned off more than 4.5 years post-implantation, accompanied by normalized corticomotor plasticity on transcranial magnetic stimulation. They suggested that low-intensity DBS might induce enduring synaptic plasticity, although such low-intensity parameters were specifically highlighted in their study and not broadly applicable across other reports [22]. Earlier, Hebb et al. [25] reported a Meige-syndrome case with stable remission for >1 year after 5 years of GPi-DBS were stopped, and Cheung et al. [26] noted only mild, partial recrudescence during several-month OFF periods in two young patients with primary GD. Collectively, these findings support the notion that GPi-DBS may trigger sustained neuroplasticity, although the mechanisms underlying this effect, such as stimulation intensity and duration, may vary across patients. Consequently, GPi-DBS might act as a disease-modifying intervention in select patients. Nevertheless, the rarity of such cases and the well-documented risk of precipitous worsening or status dystonicus when stimulation is interrupted mandate cautious, individualized consideration before deliberate weaning protocols are contemplated.

Several limitations of this study should be acknowledged. First, our findings are constrained by the study design and patient cohort. The retrospective design, small sample size (n=26), and significant heterogeneity in dystonia phenotypes and severity may limit the generalizability of our findings and the internal validity of subgroup analyses. Furthermore, while the diagnosis of TD was based on clear clinical criteria, the absence of systematic genetic testing to definitively exclude rare inherited forms is a formal limitation to diagnostic certainty. Second, the scope of our assessments was limited. The absence of a control or sham-stimulation group prevents definitive conclusions regarding placebo effects, particularly in interpreting cases of sustained improvement after stimulation cessation. We also did not include patient-reported outcomes, such as quality-of-life assessments, which are crucial for evaluating the full impact of the treatment on patient well-being. Finally, there are technical limitations to our imaging analysis. Despite the use of robust sweet spot mapping analysis, individual anatomical variability and image normalization issues can affect the precision of target localization. Therefore, the group-level coordinates we identified should serve as a probabilistic guide and should not be interpreted as absolute surgical targets for individual patients. Prospective, controlled, multicenter studies are needed to validate these results and further refine the optimal targeting strategy for GPi-DBS in TD patients.

In conclusion, our study supports bilateral GPi-DBS as a highly effective and durable therapeutic option for TD. The identified optimal stimulation coordinates in the posteroventral GPi are consistent with those of previously reported targets for primary CD and GD patients, suggesting that similar targeting strategies may be beneficial across dystonia subtypes. The observation of sustained improvement even after stimulation cessation highlights the potential for DBS to induce lasting neuroplastic changes. Further research is warranted to confirm these findings and refine DBS treatment strategies for TD.

Notes

Conflicts of Interest

The authors have no financial conflicts of interest.

Funding Statement

None

Acknowledgments

None

Author Contributions

Conceptualization: Shiro Horisawa. Data curation: Taku Nonaka, Shiro Horisawa, Kilsoo Kim, Masato Murakami, Masahiko Nishitani, Takaomi Taira. Formal analysis: Taku Nonaka, Shiro Horisawa. Investigation: Taku Nonaka, Shiro Horisawa. Methodology: Shiro Horisawa. Project administration: Shiro Horisawa. Resources: Shiro Horisawa, Takakazu Kawamata, Takaomi Taira. Software: Shiro Horisawa. Supervision: Shiro Horisawa. Validation: Shiro Horisawa. Visualization: Shiro Horisawa. Writing—original draft: Taku Nonaka. Writing—review & editing: all authors.

Figure 1.

Three-dimensional reconstruction of GPi leads and group level sweet spot in MNI space. A: Reconstruction of DBS leads and active contacts. B: Voxel-wise clinical sweet-spot map. GPi, globus pallidus internus; DBS, deep brain stimulation; MNI, Montreal Neurological Institute.

Figure 2.

Axial depiction of the optimal stimulation cluster relative to the AC-PC plane. A: Right side. B: Left side. AC, anterior commissure; PC, posterior commissure.

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