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European Journal of Neurology logoLink to European Journal of Neurology
. 2023 Nov 7;31(2):e16121. doi: 10.1111/ene.16121

Subthalamic nucleus deep brain stimulation in primary Meige syndrome: motor and non‐motor outcomes

Qing‐Pei Hao 1, Wen‐Tao Zheng 1, Zi‐Hao Zhang 1, Ye‐Zu Liu 1, Hu Ding 2, Jia OuYang 1,3, Zhi Liu 4, Guang‐Yong Wu 1,4,5,, Ru‐En Liu 1,4,
PMCID: PMC11235968  PMID: 37933887

Abstract

Background and purpose

Deep brain stimulation (DBS) has emerged as a promising treatment for movement disorders. This prospective study aims to evaluate the effects of bilateral subthalamic nucleus DBS (STN‐DBS) on motor and non‐motor symptoms in patients with primary Meige syndrome.

Methods

Thirty patients who underwent bilateral STN‐DBS between April 2017 and June 2020 were included. Standardized and validated scales were utilized to assess the severity of dystonia, health‐related quality of life, sleep, cognitive function and mental status at baseline and at 1 year and 3 years after neurostimulation.

Results

The Burke−Fahn−Marsden Dystonia Rating Scale movement scores showed a mean improvement of 63.0% and 66.8% at 1 year and 3 years, respectively, after neurostimulation. Similarly, the Burke−Fahn−Marsden Dystonia Rating Scale disability scores improved by 60.8% and 63.3% at the same time points. Postoperative quality of life demonstrated a significant and sustained improvement throughout the follow‐up period. However, cognitive function, mental status, sleep quality and other neuropsychological functions did not change after 3 years of neurostimulation. Eight adverse events occurred in six patients, but no deaths or permanent sequelae were reported.

Conclusions

Bilateral STN‐DBS is a safe and effective alternative treatment for primary Meige syndrome, leading to improvements in motor function and quality of life. Nevertheless, it did not yield significant amelioration in cognitive, mental, sleep status and other neuropsychological functions after 3 years of neurostimulation.

Keywords: deep brain stimulation, dystonia, Meige syndrome, non‐motor symptoms, subthalamic nucleus

INTRODUCTION

Meige syndrome is a rare form of adult‐onset dystonia characterized by blepharospasm and orofacial‐cervical dystonia, with a higher prevalence in women than in men [1, 2]. Initially, most patients experience ocular symptoms such as dry eyes and photophobia before the onset of blepharospasm [3]. The occurrence of blepharospasm can lead to functional blindness, and over time dystonia may spread to involve the neck and upper extremities. Despite attempts with pharmacological treatments and botulinum toxin injections, achieving adequate relief from movement symptoms is often challenging [4, 5]. Deep brain stimulation (DBS) has emerged as a surgical alternative and is now widely used worldwide [6]. However, most clinical studies evaluating the effects of DBS in treating focal dystonia have focused on the globus pallidus internus (GPi) [7], with the subthalamic nucleus (STN) being less commonly employed for dystonia treatment [8]. Moreover, previous studies on DBS primarily focus on motor symptoms, neglecting the assessment of psychiatric disorders [9, 10].

Therefore, the purpose of this study was to evaluate not only the efficacy and safety of bilateral STN‐DBS in motor performance in patients with primary Meige syndrome, but also to investigate non‐motor features including quality of life, cognitive function, mental status, sleep quality and other neuropsychological functions throughout the entire follow‐up period.

MATERIALS AND METHODS

Study population

Thirty patients with primary Meige syndrome who underwent bilateral STN‐DBS at our institution from April 2017 to June 2020 were recruited. Patients were diagnosed by one neurologist (Dr Hu Ding) who specialized in movement disorders and they had to fulfill the following inclusion criteria: age between 18 years and 75 years; substantial motor impairment; failure of optimal pharmacological treatments; and disease duration of at least 2 years. Exclusion criteria included secondary dystonia; severe cognitive impairment, dementia or psychiatric disorders; and significant comorbidities that increased the risk of anesthesia and surgery. The study was approved by the Ethics Committee of Peking University People's Hospital, and all participants provided written informed consent, in accordance with the Declaration of Helsinki.

Baseline and postoperative evaluation

Baseline assessments, conducted within 4 weeks before surgery, and postoperative evaluations at 1 and 3 years after neurostimulation were performed using standardized and validated scales. The severity of dystonia and disability were scored by an independent neurologist (Dr Hu Ding) using the movement and disability subscales of the Burke−Fahn−Marsden Dystonia Rating Scale (BFMDRS) [11]. A neuropsychologist (Dr Zhi Liu), blinded to the preoperative and postoperative conditions of the patients, conducted other neuropsychological assessments. Quality of life, cognitive function, learning and memory, language, attention and executive functions, mental status and sleep quality were evaluated with the Medical Outcomes Study 36‐Item Short‐Form General Health Survey [12], Montreal Cognitive Assessment [13], Digit Span Test [14], Boston Naming Test [15], Symbol Digit Modalities Test [16], Self‐rating Depression Scale and Self‐rating Anxiety Scale [17, 18] and Pittsburgh Sleep Quality Index [19], respectively.

Surgical procedure and programming

Bilateral implantation of quadripolar electrodes (model L301, PINS Medical) into the STN was performed by two neurosurgeons (Dr Guang‐Yong Wu and Ru‐En Liu) at our institution. The target location for the STN was determined to be 2–3 mm behind the midpoint of the anteroposterior commissure, 12–14 mm lateral, and 4–6 mm below the plane of the anteroposterior commissure. All patients underwent magnetic resonance imaging (MRI) scan (3.0 T, General Electric). On the day of the operation, the patient was secured in the Leksall stereotactic headframe (type G, Elekta) and subsequently transferred to the CT scan. Fusion images of CT and MRI (Figure 1a) precisely enable the determination of target localizations and trajectories. Microelectrode recordings (NeuroNav, Alpha and Omega) were used during surgery to confirm the accuracy of the target. The STN was identified based on the relatively irregular neuronal discharge pattern of high‐amplitude and high‐frequency activity observed intra‐operatively (Figure 1b). Efficacy and adverse effect assessments were conducted using a temporary pulse generator in vitro. An implantable pulse generator (IPG) (G102 or G102R, PINS Medical) was then surgically implanted in the subcutaneous region. Postoperative CT (Figure 1c) and preoperative MRI fusion images (Figure 1d) provided detailed visualization of the bilateral electrode positions (Figure 1e) and revealed any asymptomatic hemorrhage. IPG programming was initiated approximately 1 month after surgery, allowing for the selection of optimal contacts and stimulation parameters based on symptom changes and adverse effects. The initial amplitude was set at 1.5–2.0 V, with a pulse width of 60 μs and a frequency of 130 Hz. Each electrode contact was tested separately in monopolar mode with case positive and the optimal contact negative. During the follow‐up period, the active contacts were modified to an amplitude 10%–20% lower than the tolerable threshold for adverse effects (usually 4–5 V). These parameters could also be adjusted incrementally at outpatient follow‐ups or via telemedicine applications, depending on the patient's response to neurostimulation.

FIGURE 1.

FIGURE 1

Lead placement accuracy assessed by MRI‐CT fusion images. (a) Preoperative MRI‐CT fusion images showing the targeted region of the STN. (b) Microelectrode recording of high‐amplitude and high‐frequency discharges from STN neurons. (c) Postoperative CT scans to rule out intracranial hemorrhage. (d) MRI‐CT fusion images demonstrating that electrodes were located bilaterally in the STN. (e) Three‐dimensional reconstruction of implanted electrodes using Lead‐DBS software. MRI, magnetic resonance imaging; CT, computed tomography; STN, subthalamic nucleus; DBS, deep brain stimulation; GPi, globus pallidus internus; GPe, globus pallidus externus; RN, red nucleus.

Statistical analysis

Categorical variables were presented as counts and percentages, whilst continuous variables were reported as mean ± standard deviation (SD). The Wilcoxon matched‐pairs signed‐rank test was utilized to compare score differences between baseline and serial follow‐up visits for each rating scale. Bonferroni correction was applied to account for multiple pairwise comparisons, and p values <0.017 were considered statistically significant. All statistical analyses were conducted using SPSS version 26.0 statistical software (IBM Corp.).

RESULTS

Patient characteristics

Thirty patients with primary Meige syndrome received bilateral STN‐DBS, and there were no dropouts during the follow‐up period. The male‐to‐female ratio was 9:21, and the mean age at onset was 50.6 ± 8.2 years (range 34–70 years). The mean age at surgery was 56.9 ± 9.6 years (range 36–75 years), and the mean disease duration was 6.3 ± 3.5 years (range 2–15 years). Pharmacological treatments and botulinum toxin injections had shown limited efficacy for all patients. The baseline characteristics are shown in Table 1.

TABLE 1.

Baseline characteristics of participants.

Variables Values
Age 56.9 ± 9.6
Disease duration (years) 6.3 ± 3.5
Sex, n (%)
Female 21 (70)
Male 9 (30)
Motor subtype, n (%)
Blepharospasm 6 (20)
Oromandibular dystonia 2 (6.7)
Blepharospasm, oromandibular dystonia 19 (63.3)
Blepharospasm, oromandibular, cervical dystonia 3 (10)

Note: Values are reported as mean ± SD.

Motor function evaluated by BFMDRS scores

Following neurostimulation, the BFMDRS movement scores showed a significant decrease compared to baseline, from 13.1 ± 4.6 before surgery to 5.0 ± 3.0 (63.0%, p < 0.001) at 1 year and to 4.6 ± 3.0 (66.8%, p < 0.001) at 3 years. Similarly, the BFMDRS disability scores improved significantly by 60.8% at 1 year and 63.3% at 3 years compared to preoperative scores (Figure 2). Furthermore, all motor symptoms, except for neck dystonia, exhibited marked improvements for up to 3 years (Table 2).

FIGURE 2.

FIGURE 2

BFMDRS scores at baseline and at 1 and 3 years after neurostimulation. (a) BFMDRS total scores at baseline and at 1 and 3 years after neurostimulation. (b) BFMDRS movement scores at baseline and at 1 and 3 years after neurostimulation. (c) BFMDRS disability scores at baseline and at 1 and 3 years after neurostimulation. BFMDRS, Burke−Fahn−Marsden Dystonia Rating Scale.

TABLE 2.

BFMDRS scores at baseline and at 1 and 3 years after neurostimulation.

Variable Baseline 1 year Improvement (%) p value* 3 years Improvement (%) p value** p value***
BFMDRS total 21.5 ± 7.6 8.7 ± 5.4 62.0 <0.001 8.2 ± 5.6 65.0 <0.001 0.206
BFMDRS movement 13.1 ± 4.6 5.0 ± 3.0 63.0 <0.001 4.6 ± 3.0 66.8 <0.001 0.198
BFMDRS disability 8.4 ± 3.5 3.7 ± 2.8 60.8 <0.001 3.6 ± 3.3 63.3 <0.001 0.795
BFMDRS movement subitem
Eye 6.7 ± 1.6 1.9 ± 1.0 70.9 <0.001 1.8 ± 1.2 73.9 <0.001 0.438
Mouth 3.8 ± 2.3 1.7 ± 1.4 51.4 <0.001 1.4 ± 1.3 58.9 <0.001 0.273
S&S 2.4 ± 2.7 1.3 ± 1.3 37.0 0.015 1.2 ± 1.3 36.1 0.010 0.948
Neck 0.2 ± 0.7 0.1 ± 0.6 12.5 0.326 0.1 ± 0.6 12.5 0.326 1.000

Note: Scores are reported as mean ± SD. Significant p values are in bold.

Abbreviations: BFMDRS, Burke−Fahn−Marsden Dystonia Rating Scale; S&S, speech and swallowing.

*

p, 1 year versus baseline.

**

p, 3 years versus baseline.

***

p, 3 years versus 1 year.

Assessment of non‐motor functions

Significant improvements were observed in many components of the Medical Outcomes Study 36‐Item Short‐Form General Health Survey related to physical functioning, role‐physical, general health, vitality and social functioning at 1 year, and these improvements were sustained at 3 years (Table 3). Therefore, STN‐DBS not only alleviated dystonic symptoms but also improved the overall quality of life for patients in their daily lives. However, no significant differences were found in cognitive function, learning and memory, language, attention and executive functions, mental status and sleep quality at 1 year and 3 years compared to baseline (Table 4).

TABLE 3.

SF‐36 scores at baseline and at 1 and 3 years after neurostimulation.

Variable Baseline 1 year p value* 3 years p value** p value***
Physical functioning 64.5 ± 12.3 69.5 ± 9.3 0.003 70.2 ± 10.1 0.002 0.555
Role‐physical 62.3 ± 19.3 72.3 ± 16.5 0.008 70.8 ± 18.7 0.020 0.612
Bodily pain 77.0 ± 13.4 78.3 ± 12.3 0.394 78.3 ± 10.9 0.564 1.000
General health 68.7 ± 11.0 72.7 ± 7.0 0.013 73.8 ± 5.6 0.011 0.319
Vitality 70.2 ± 12.4 74.3 ± 11.0 0.006 76.2 ± 9.0 0.009 0.239
Social functioning 65.0 ± 16.2 72.9 ± 11.9 0.001 72.9 ± 10.9 0.012 1.000
Role‐emotional 60.0 ± 20.4 66.7 ± 17.5 0.050 66.7 ± 17.5 0.058 1.000
Mental health 66.5 ± 12.0 68.0 ± 11.1 0.307 68.3 ± 9.5 0.211 0.820

Note: Scores are reported as mean ± SD. Significant p values are in bold.

Abbreviation: SF‐36, Medical Outcomes Study 36‐Item Short‐Form General Health Survey.

*

p, 1 year versus baseline.

**

p, 3 years versus baseline.

***

p, 3 years versus 1 year.

TABLE 4.

Non‐motor scores at baseline and at 1 and 3 years after neurostimulation.

Variable Baseline 1 year p value* 3 years p value** p value***
Global cognition
MoCA 27.6 ± 1.1 27.7 ± 1.0 0.581 27.8 ± 1.1 0.386 0.797
Mood
SDS 58.7 ± 8.0 58.5 ± 7.8 0.370 58.5 ± 7.8 0.403 0.975
SAS 56.2 ± 7.2 56.1 ± 6.7 0.602 55.9 ± 6.7 0.272 0.302
Sleep
PSQI 5.8 ± 4.2 5.6 ± 3.5 0.888 5.7 ± 4.6 0.721 0.952
Language
BNT 26.2 ± 2.4 26.2 ± 2.6 0.745 26.5 ± 2.3 0.125 0.174
Learning and memory
DSFT 6.1 ± 1.3 6.2 ± 1.2 0.688 6.3 ± 1.2 0.476 0.753
DSBT 4.9 ± 1.4 5.1 ± 1.1 0.611 5.0 ± 0.9 0.829 0.711
Attention and executive
SDMT 48.8 ± 10.2 50.1 ± 11.2 0.185 49.6 ± 10.6 0.401 0.529

Note: Scores are reported as mean ± SD.

Abbreviations: BNT, Boston Naming Test; DSBT, Digit Span Backward Test; DSFT, Digit Span Forward Test; MoCA, Montreal Cognitive Assessment; PSQI, Pittsburgh Sleep Quality Index; SAS, Self‐rating Anxiety Scale; SDMT, Symbol Digit Modalities Test; SDS, Self‐rating Depression Scale.

*

p, 1 year versus baseline.

**

p, 3 years versus baseline.

***

p, 3 years versus 1 year.

Stimulation variables

Electrode active contacts were distributed as follows: on the left side, there were three cases with contact 1, 20 cases with contact 2, five cases with contact 3 and two cases with contact 4; on the right side, there were five cases with contact 1, 18 cases with contact 2, six cases with contact 3 and one case with contact 4. It is important to note that “Contact 1” designates the most ventral contact, whilst “Contact 4” denotes the most dorsal one. Electrode active contacts were primarily located within the dorsal STN. The activation or programming of IPGs resulted in an instantaneous response for the majority of patients, typically occurring within a few minutes to a few hours. Voltage, pulse width and frequency were adjusted based on clinical response and individual tolerance during follow‐up visits. These beneficial effects consistently improved over several months to 3 years and remained stable even after reprogramming. Specifically, 1 year after neurostimulation the amplitude was 3.1 ± 1.2 V, pulse width was 85.5 ± 41.3 μs and frequency was 138.6 ± 32.1 Hz. At the 3‐year mark, the voltage was 3.3 ± 1.1 V, pulse width was 90.8 ± 37.5 μs and frequency was 141.7 ± 26.8 Hz.

Adverse events

Eight adverse events were reported in six patients during the study period. One patient experienced a procedure‐related adverse event; the patient developed an infection at the site of the IPG within a week of surgery, which was successfully resolved by temporarily removing the IPG and administering antibiotics. Five patients experienced stimulation‐related adverse events, with two reporting dysarthria and five experiencing dizziness. Most of these transient stimulation‐related adverse events could be effectively managed by adjusting the stimulation settings. No serious adverse events, such as death or persistent neurological sequelae, were observed.

DISCUSSION

This cohort study shows the efficacy and safety of bilateral STN‐DBS for patients with primary Meige syndrome and indicates that it can decrease the severity of dystonia and restore the impaired quality of life. The study reveals that bilateral STN‐DBS leads to a 63.0% and 66.8% reduction in the BFMDRS movement scores at 1 and 3 years after neurostimulation, respectively, which aligns with previous reports showing improvements ranging from 56% to 93% [7, 9, 20]. The BFMDRS disability scores also showed significant improvement, with a mean 60.8% reduction at 1 year and 63.3% reduction at 3 years. Collectively, these results are consistent with previous reports and further advance our knowledge and understanding of STN‐DBS. Notably, the most prominent improvement was in blepharospasm (73.9%, p < 0.001), followed by oromandibular dystonia (58.9%, p < 0.001), speech and swallowing (36.1%, p = 0.010) and cervical symptoms (12.5%, p = 0.326) at 3 years. However, contrary to previous reports [21, 22], no noticeable improvement in cervical symptoms was observed, possibly due to the study's small sample size of patients with cervical dystonia. Moreover, the symptomatic benefit translated into a significant improvement in all activities of daily living [23, 24], particularly in walking difficulties. Patients with severe blepharospasm tended to suffer functional blindness and visual deprivation before surgery, causing them to lose their ability to obtain external information. After neurostimulation, with the marked improvement of blepharospasm, they could independently ambulate without assistance, as reflected by the improvement (73.9%, p < 0.001) of the ‘gait’ item in the BFMDRS disability scale [25]. Likewise, the quality of life also significantly improved across various components, including physical functioning, role‐physical, general health, vitality and social functioning, which is attributed to the dramatic improvement of dystonic symptoms, as previously reported [26, 27].

Due to the microlesion effect (MLE), 26 patients (86.7%) experienced immediate symptomatic improvements after electrode placement. MLE may be associated with local microglial proliferation caused by secondary microscopic hematoma and edema after lead placement. However, the improvement induced by MLE diminished over time, which may be related to the healing process of the damaged brain tissue [28, 29, 30]. Additionally, most patients responded immediately to stimulation after programming, enabling the rapid selection of the most effective individualized stimulation parameters. For some patients, neurostimulation therapy typically reaches its peak therapeutic effects between 6 and 12 months after initiation, which tend to remain stable for up to 3 years [7, 26]. Our observations indicated a predominant distribution of active electrode contacts within the dorsal STN in STN‐DBS patients. As widely recognized, the dorsal STN is linked to motor function. Consequently, stimulating the dorsal STN, specifically the sensory‐motor function area, holds the potential to terminate abnormal neuronal activity and afferent fibers, leading to improvements in dystonic symptoms [31]. Consequently, our findings support the notion that the most effective contacts are those positioned dorsally, in line with prior reports advocating dorsal contact selection within the STN [32]. Precise electrode placement and postoperative programming are notably crucial to ensure the effectiveness of bilateral STN‐DBS in dystonia. In this study, various techniques were employed, including intra‐operative microelectrode recordings, temporary IPG tests and MRI‐CT fusion images, to enhance the accuracy of lead placement. By assessing symptomatic improvement and side effects, optimal contacts and programming settings were identified for chronic stimulation.

Recent studies have unveiled non‐motor features of dystonia, including sleep disorders and depression [27, 33], which may play a vital role in the unknown pathophysiology of the disease. In our study, 23.3% of patients with Meige syndrome had sleep disorders, and 55% of those cases preceded the onset of focal dystonia, such as blepharospasm, by an average duration of 9.8 ± 6.6 years. Persistent sleep disorders after neurostimulation can also contribute to worsening symptoms, although no direct correlation was observed between sleep disorders and the severity of dystonia. Nocturnal polygraphic studies on focal dystonia showed a correlation between impaired sleep efficiency, reduced rapid eye movement sleep, increased awakenings and disease severity, suggesting the potential involvement of some part of the basal ganglia in sleep regulation and thus in the pathophysiology of movement disorders [34, 35, 36, 37]. Depression is common in various primary generalized and segmental dystonia, including Parkinson's and Huntington's disease [38, 39]. Some previous studies reported that STN‐DBS affects mental health [23, 40], whilst no changes in depressive status associated with neurostimulation were observed. This finding contrasts with the decline in mental health after DBS treatment despite relatively stable motor outcomes [41, 42], probably because of disease progression in non‐motor domains. Primary Meige syndrome is a complex disorder encompassing both motor and non‐motor symptoms, rather than being solely movement‐related. Our study found no significant correlation between depression severity and the severity of dystonia. However, dystonic symptoms can seriously impact the quality of life and aggravate depression. Whilst sleep disturbances and depression have not yet been established as crucial features of Meige syndrome, psychological interventions should still be considered in the management of dystonia [43].

The underlying mechanisms of DBS for primary Meige syndrome remain unclear, but insights can be gained from the functional and anatomical divisions within the STN. High‐frequency stimulation of the STN directly inhibits its excitatory output to the GPi and substantia nigra pars reticulata, regulating dysfunction in the basal ganglia‐thalamus‐cortical circuit [28, 44]. Neuroimaging and neurophysiological studies have identified hyperactivity in the motor circuit [42, 45], suggesting that cortical or subcortical network plasticity may also play another role in the efficacy of DBS on this form of dystonia [46]. The gradual symptom improvement and delayed recurrence of dystonia after turning off the IPG provide additional evidence for this mechanism. Our clinical experience indicates that optimal therapeutic outcomes are achieved with electrode contacts located in the dorsal STN, which has a high density of interconnecting fibers, including the pallidothalamic, pallidosubthalamic and subthalamopallidal fibers [10]. Stimulation of these fibers upsets afferent and efferent connectivity with the STN, resulting in outcomes similar to pallidal DBS. GPi and STN are widely acknowledged as crucial targets in the treatment of primary dystonia. Current literature indicates no significant difference in the effects of GPi and STN for dystonia treatment [6, 47]. According to Lin et al. [48], STN‐DBS has been reported to effectively alleviate dystonic symptoms within 1 month of surgery, surpassing the outcomes of GPi‐DBS. Moreover, STN‐DBS proves to be more cost‐effective due to its lower battery consumption, leading to delayed battery replacement [49].

This study demonstrates that STN‐DBS is a safe and well‐tolerated surgical treatment for Meige syndrome. Eight adverse events were reported in six patients in this cohort, but none of these events was considered serious, and all cases were resolved without permanent sequelae. The most commonly reported adverse event was stimulation‐induced dizziness, which was successfully resolved by adjusting the parameters.

Our study presents two significant advantages. First, a prospective study was conducted with a sample size of 30 subjects, avoiding the weakness of a retrospective study and making it one of the most extensive studies on bilateral STN‐DBS with primary Meige syndrome, resulting in more robust conclusions. Additionally, a greater emphasis was placed on evaluating the depressive state, sleep quality and other neuropsychological functions, as well as the efficacy of the treatment. Finally, the data for this study were collected from a single institution where all procedures and assessments were performed by the same neurosurgeons and an unaware neuropsychologist, ensuring consistency of data capture and avoiding potential bias. However, the main limitations of our study are described below. Only the efficacy and safety of STN‐DBS at the 1‐year and 3‐year follow‐ups were reported, whilst extended follow‐up studies are necessary to assess the long‐term outcomes of the treatment. Moreover, the single‐center, uncontrolled design of this study may potentially introduce selection bias on our local practice patterns or the population of DBS patients in our region, and the placebo effect cannot be ruled out since the patients were not blinded to the surgery or stimulation parameters. Therefore, it is essential to carry out randomized controlled multicenter studies to provide more reliable evidence of the efficacy of STN‐DBS in primary Meige syndrome.

CONCLUSIONS

In summary, bilateral STN‐DBS, an alternative to the GPi, is a highly effective and relatively safe therapeutic option for patients with primary Meige syndrome. It markedly reduces the severity of dystonia and alters the overall quality of life. Furthermore, it is crucial to acknowledge that non‐motor features such as sleep and depression are vital components of Meige syndrome, which deserve greater attention in its diagnosis and management.

AUTHOR CONTRIBUTIONS

Qing‐Pei Hao: Conceptualization; data curation; formal analysis; methodology; investigation; writing – review and editing; writing – original draft. Wen‐Tao Zheng: Conceptualization; data curation; software; investigation; writing – review and editing; visualization. Zi‐Hao Zhang: Data curation; formal analysis; methodology; investigation; writing – original draft. Ye‐Zu Liu: Data curation; formal analysis; methodology; investigation; resources. Hu Ding: Data curation; methodology; investigation; formal analysis. Jia Ouyang: Data curation; formal analysis; methodology; validation. Zhi Liu: Methodology; investigation; data curation; validation. Guang‐yong Wu: Conceptualization; investigation; resources; supervision; writing – review and editing. Ru‐En Liu: Conceptualization; funding acquisition; project administration; resources; supervision; writing – review and editing.

FUNDING INFORMATION

This study was funded by grants from Peking University People's Hospital (2017‐T‐01) and partly supported by the Beijing Municipal Health Commission (SHOUFA‐202224085).

CONFLICT OF INTEREST STATEMENT

None declared.

ETHICS STATEMENT

All participants provided a written informed consent and the study was approved by the Ethics Committee of the Peking University People's Hospital (approval number 2017PHB066‐03), in accordance with the Declaration of Helsinki.

ACKNOWLEDGEMENTS

The authors appreciate all cohort individuals and their families for their participation in this study.

Hao Q‐P, Zheng W‐T, Zhang Z‐H, et al. Subthalamic nucleus deep brain stimulation in primary Meige syndrome: motor and non‐motor outcomes. Eur J Neurol. 2024;31:e16121. doi: 10.1111/ene.16121

Qing‐Pei Hao, Wen‐Tao Zheng and Zi‐Hao Zhang contributed equally to this work.

Contributor Information

Guang‐Yong Wu, Email: wgy614@163.com.

Ru‐En Liu, Email: liuruen@pku.edu.cn.

DATA AVAILABILITY STATEMENT

Data used for the analysis are available upon reasonable request to the corresponding author.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

Data used for the analysis are available upon reasonable request to the corresponding author.


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