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Movement Disorders in Central Nervous System Tuberculosis: A Systematic Review

Published online by Cambridge University Press:  29 September 2025

Ravindra Kumar Garg Open the ORCID record for Ravindra Kumar Garg [Opens in a new window] ,
Shweta Pandey ,
Raza Abbas Mahdi  and
Sanjay Singhal
Ravindra Kumar Garg*
Affiliation:
Department of Neurology, Era’s Lucknow Medical College & Hospital, Era University , Lucknow, India
Shweta Pandey
Affiliation:
Department of Neurology, King George’s Medical University, Lucknow, India
Raza Abbas Mahdi
Affiliation:
Department of Nuclear Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India
Sanjay Singhal
Affiliation:
Department of Pulmonary Medicine, Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, India
*
Corresponding author: Ravindra Kumar Garg; Email: garg50@yahoo.com
Rights & Permissions [Opens in a new window]

Abstract

Background:

Tuberculosis (TB) affecting the central nervous system (CNS) can lead to a broad range of movement disorders, which are frequently overlooked in clinical settings. This review explores the various presentations, underlying mechanisms and patient outcomes related to these disorders.

Methods:

We systematically reviewed published case reports, series and cohort studies that described patients with CNS TB who developed movement disorders. Extracted data included patient characteristics, type of CNS TB, imaging and CSF findings, types of movement disorders, treatments used and outcomes.

Results:

A total of 61 patients with CNS TB and associated movement disorders were analyzed. The most common manifestations were ataxia, dystonia, chorea or hemiballismus and parkinsonism. Less frequent symptoms included opsoclonus-myoclonus, segmental myoclonus, tremors, cervical dystonia and stereotypy. TB meningitis was the predominant form, often accompanied by infarcts, hydrocephalus or tuberculomas. Proposed causes included vascular injury, inflammatory lesions, immune mechanisms and drug-related effects. All patients received anti-tuberculosis treatment, and nearly half required corticosteroids or surgical procedures. About 25 patients (41%) fully recovered, 17 (27.9%) had significant improvement, 13 (21.3%) showed partial improvement, 11 (18.0%) had ongoing problems and 1 (1.6%) died. Cohort studies also reveal that movement disorders – particularly tremors, dystonia, parkinsonism and ataxia – are frequent but underrecognized in CNS TB. These typically emerge early, often within three weeks, and are linked to lesions in the basal ganglia or thalamus.

Conclusions:

Movement disorders in CNS TB are more common than generally recognized. Prompt diagnosis through imaging and timely therapy can greatly improve neurological outcomes.

Résumé

RÉSUMÉ

Troubles du mouvement dans la tuberculose du système nerveux central : résultats d’une revue systématique.

Contexte :

La tuberculose (TB) du système nerveux central (SNC) peut se manifester par un large éventail de troubles du mouvement qui, bien souvent, passent inaperçus en clinique. La revue visait à relever les différentes manifestations de la maladie, les mécanismes sous-jacents et l’état de santé des patients en lien avec ces troubles.

Méthode :

L’équipe a procédé à un examen systématique d’exposés de cas, de séries et d’études de cohortes publiés, portant sur des patients atteints de la TB du SNC qui présentaient des troubles du mouvement. Les données extraites comprenaient les caractéristiques des patients, le type de TB du SNC, les résultats des examens par imagerie et des analyses du liquide céphalorachidien, les types de troubles du mouvement, les traitements et les résultats obtenus.

Résultats :

Au total, les dossiers de 61 patients atteints de TB du SNC qui présentaient des troubles du mouvement associés à la maladie ont fait l’objet d’analyse. Les manifestations les plus fréquentes étaient l’ataxie, la dystonie, la chorée ou l’hémiballisme et le syndrome parkinsonien. Des symptômes moins fréquents comprenaient l’opsoclonie-myoclonie, la myoclonie segmentaire, les tremblements, la dystonie cervicale et la stéréotypie. La forme la plus courante était la méningite tuberculeuse, qui s’accompagnait souvent d’infarctus, d’hydrocéphalie ou de tuberculomes. Parmi les causes envisagées, il y avait les lésions vasculaires, les lésions inflammatoires, les mécanismes immunitaires et les effets de certains médicaments. Les patients ont tous été soumis à un traitement antituberculeux, et presque la moitié d’entre eux ont dû recevoir des corticostéroïdes ou être opérés. Environ 25 patients (41 %) ont connu un rétablissement complet; 17 (27, 9 %), une amélioration importante de leur état et 13 (21,3 %), une amélioration partielle; 11 (18,0 %) ont fait face à problèmes persistants, et 1 (1,6 %) est mort. En outre, d’après les études de cohorte, les troubles du mouvement, notamment les tremblements, la dystonie, le syndrome parkinsonien et l’ataxie, sont fréquents, mais ils passent inaperçus dans la TB du SNC. Ces troubles apparaissent généralement tôt, souvent au cours des trois premières semaines de la maladie, et ils sont liés à des lésions des noyaux gris centraux ou du thalamus.

Conclusion :

Les troubles du mouvement dans la TB du SNC sont plus fréquents que ne le laisse croire, en général, leur reconnaissance. Ainsi, la pose rapide d’un diagnostic par l’imagerie et la mise en route d’un traitement en temps opportun peuvent améliorer grandement les résultats neurologiques.

Keywords

Dystoniachoreamyoclonustuberculous meningitistuberculoma

Information

Type
Original Article
Information
Canadian Journal of Neurological Sciences , First View , pp. 1 - 10
Copyright
© The Author(s), 2025. Published by Cambridge University Press on behalf of Canadian Neurological Sciences Federation

Highlights

  • • Movement disorders are frequent but underrecognized in central nervous system tuberculosis.

  • • Common types include ataxia, dystonia, chorea and parkinsonism.

  • • Basal ganglia or thalamic lesions are commonly linked to these disorders.

Introduction

Central nervous system (CNS) tuberculosis (TB) is the most devastating form of extrapulmonary tuberculosis, accounting for approximately 1% of all TB cases and up to 10% of extrapulmonary cases. It remains a significant cause of neurological morbidity and mortality, particularly in endemic regions and among immunocompromised individuals. Reference Garg1,Reference Seddon, Tugume, Solomons, Prasad and Bahr2 CNS TB presents primarily as tuberculous meningitis, intracranial tuberculomas, spinal arachnoiditis or a combination thereof. The pathological processes involved – granulomatous inflammation, vasculitis, infarction, hydrocephalus and immune-mediated injury – can result in a variety of neurological syndromes. Reference Garg1,Reference Seddon, Tugume, Solomons, Prasad and Bahr2

Several case reports and case series have documented a diverse array of movement disorders in patients with CNS TB, particularly tuberculous meningitis, highlighting its complex and often underrecognized neurological manifestations. Reference Alarcón, Dueñas, Cevallos and Lees3–Reference Desai, Yadav, Garg, Schneider and Pal5

Although individual case reports and small series have described diverse movement disorders in CNS TB, the evidence remains fragmented and inconsistent. Cohort studies are limited, and outcome predictors such as lesion location, pathophysiological mechanisms and treatment response have not been systematically synthesized. No prior comprehensive review has pooled available cases and compared them with cohort findings. A systematic review at this time is needed to consolidate dispersed evidence, clarify clinical patterns and identify prognostic factors, thereby addressing a critical gap in the literature and guiding both diagnosis and management.

Methods

This systematic review followed the PRISMA 2020 guidelines for reporting. The review protocol was prospectively registered in the PROSPERO database with the registration number CRD420251075389. Reference Garg, Pandey, Singhal and Mahdi6

Search strategy

A thorough and systematic literature search was conducted across four major databases: PubMed, Embase, Scopus and Google Scholar, to identify all relevant studies reporting movement disorders in patients with CNS TB. We limited Google Scholar screening to the first 50 pages, as results on earlier pages are more relevant, while later ones are largely low-yield or duplicate. The final search was completed on May 31, 2025. Detailed search strategy has been provided in Table 1.

Table 1.

Search strategy

Non-English studies were translated using Google Translate. Critical medical terminology, including diagnoses and outcome measures, was cross-verified against bilingual medical dictionaries, if necessary.

Definitions

CNS tuberculosis was defined as microbiologically, radiologically or histologically confirmed tuberculous infection of the brain or spinal cord, including manifestations such as tuberculous meningitis, intracranial or spinal tuberculomas, abscesses and spinal TB with CNS involvement Reference Dian, Ganiem and van Laarhoven7,Reference Marais, Thwaites and Schoeman8 (Figure 1).

Figure 1.

MRI of the brain showing a ring-enhancing lesion in the left thalamus with surrounding edema on post-contrast T1-weighted coronal image (left). Magnetic resonance spectroscopy from the lesion (right) demonstrates a lipid-lactate peak, reduced N-acetylaspartate and elevated choline, suggestive of a tuberculoma. The patient had right hemichorea.

Movement disorders were defined clinically and classified into hyperkinetic (e.g., chorea, dystonia, myoclonus, tremor) and hypokinetic (e.g., parkinsonism, rigidity) types. Cases with insufficient neurological detail to confirm movement disorders were excluded. 9

Eligibility criteria

We included case reports, case series and cohort studies that provided a confirmed diagnosis of CNS TB, documented the presence of one or more clinically observed movement disorders and offered sufficient clinical, radiological or treatment-related details for meaningful analysis. Studies were excluded if they involved non-human subjects, lacked adequate clinical descriptions or were purely radiological or experimental without clinical correlation.

Study selection

Two reviewers (RKG and SS) independently assessed all titles and abstracts for eligibility. Full texts of potentially relevant articles were retrieved and reviewed. Any disagreements were resolved through discussion or, when necessary, consultation with a third reviewer (SP).

EndNote 21 (Clarivate Analytics, Philadelphia, USA) was used for reference management and to remove duplicates. Duplicate verification was independently performed by HSM, with final adjudication by SS. The selection process was documented in a PRISMA flow diagram.

Data extraction

Data were extracted using a predefined structured format by three reviewers (SP, SS and RAM). The following data were extracted from each included study: patient demographics (including age and sex), subtype of CNS TB (such as tuberculous meningitis or tuberculoma), type of movement disorder observed, time to onset of movement-related symptoms, findings from neuroimaging and CSF analysis and treatment approaches including antitubercular therapy, corticosteroids, symptomatic medications and surgical interventions, as well as clinical outcomes encompassing recovery status, persistence of symptoms, complications or death. All discrepancies were resolved through consensus in consultation with a senior reviewer (RKG). Data were compiled in Microsoft Word tables and verified for accuracy before analysis.

Quality assessment

Case reports and case series were evaluated using the criteria proposed by Murad et al., which assess four key domains: selection, ascertainment, causality and reporting. Records meeting all four domains were rated as “good,” those fulfilling three as “fair” and those satisfying only one or two as “poor.” Cohort studies were appraised using the Newcastle–Ottawa Scale, focusing on three domains: selection, comparability and outcome assessment. Disagreements in scoring were resolved by consensus among the reviewers.

Data synthesis

A descriptive synthesis of data was performed. Categorical variables were reported as frequencies and percentages. Results were grouped by type of movement disorder, type of TB, underlying mechanism (vascular, immune-mediated, compressive), diagnostic modalities, treatments given and clinical outcomes. Structured tables and illustrative figures were developed to present a comprehensive summary of findings and clinical patterns in CNS TB-associated movement disorders. Missing data were extracted as “not reported,” and no imputation was performed. Study authors were not contacted for additional clarification. Only descriptive synthesis was undertaken, as the available evidence consisted solely of case reports, case series and a few heterogeneous cohorts, precluding a meaningful meta-analysis.

Results

This review includes 61 patients with CNS TB who developed movement disorders, with data derived from 56 published reports. Reference Valdes and Sibat12–Reference Jackson67 All included cases were assessed for quality, with each rated as either good or fair (Supplementary Item 1). The PRISMA checklist is available in Supplementary Item 2. Detailed patient-level data are summarized in the tables. Figure 2 presents the PRISMA flow diagram outlining the case selection process. Of 4310 records identified, 3514 were screened after removing 796 duplicates, 158 full texts were retrieved, 131 assessed for eligibility and finally, 60 reports (including 4 cohort studies) met inclusion criteria.

Figure 2.

PRISMA 2020 flow diagram illustrating the study selection process for inclusion in the systematic review. The diagram shows the number of records identified, screened, excluded and included at each stage of the review, along with reasons for exclusions.

The mean age was 26.9 years, with a median of 24 years and a nearly equal male-to-female distribution. The majority of patients were immunocompetent, and most cases were reported from Asia, predominantly India (Table S1 and Table 2). Tuberculous meningitis was the most frequent type of CNS TB, accounting for nearly two-thirds of the cases, often associated with infarcts, hydrocephalus or tuberculomas. Intracranial tuberculomas without meningitis accounted for about one-fifth, and spinal TB, miliary TB and other forms such as cerebritis and demyelination were less frequent. Neuroimaging showed tuberculomas in about half of the patients, hydrocephalus in 44% and infarcts in 34%, particularly involving the thalamus, basal ganglia and brainstem. Leptomeningeal enhancement, basal exudates and arachnoiditis were also commonly noted. CSF findings typically included lymphocytic pleocytosis with elevated protein and low glucose. Microbiological or histopathological confirmation of tuberculosis was obtained in about two-thirds of the cases, most commonly via CSF GeneXpert, culture or biopsy (Table S1 and Table 3).

Table 2.

Summary of demographic characteristics of CNS tuberculosis cases presenting with movement disorders (n = 61)

CNS = central nervous system; HIV = human immunodeficiency virus.

Table 3.

Summary of clinical, neuroimaging and treatment features of CNS TB cases presenting with movement disorders (n = 61)

AFB = acid-fast bacillus; ART = antiretroviral therapy; ATT = anti-tuberculous therapy; BAL = bronchoalveolar lavage; CBNAAT = cartridge-based nucleic acid amplification test; CNS = central nervous system; EVD = external ventricular drainage; GI = gastrointestinal; H = isoniazid; HIV = human immunodeficiency virus; HRZE = isoniazid, rifampicin, pyrazinamide, ethambutol; ICP = intracranial pressure; INH = isoniazid; IQR = interquartile range; IVIG = intravenous immunoglobulin; NA = not available; OMS/OMAS = opsoclonus-myoclonus syndrome/opsoclonus-myoclonus-ataxia syndrome; PAID = paroxysmal autonomic instability with dystonia; PCR = polymerase chain reaction; PMN = polymorphonuclear; R = rifampicin; RIPE = rifampicin, isoniazid, pyrazinamide, ethambutol; TB = tuberculosis; TBM = tuberculous meningitis; VP = ventriculoperitoneal.

The movement disorders observed were diverse and reflected the underlying pathology and lesion location. Ataxia was the most common manifestation, followed closely by dystonia, chorea or hemiballismus and parkinsonism. Less commonly reported were opsoclonus-myoclonus, segmental myoclonus, postural and resting tremors, torticollis, cervical dystonia, blepharospasm, orofacial dyskinesia, stereotypy, trismus and bobble-head doll syndrome. The onset of movement disorders was subacute in most cases, though some occurred acutely or following initiation of anti-tuberculosis therapy, and a few developed after clinical recovery or months to years later. Associated neurological features included motor weakness, cranial nerve palsies, altered consciousness, raised intracranial pressure, autonomic instability, seizures and behavioral or cognitive abnormalities. Anti-tuberculosis therapy was administered in nearly all patients, often with adjunctive corticosteroids. Symptomatic treatment for movement disorders, including agents such as levodopa, trihexyphenidyl, clonazepam, baclofen and midazolam, was provided in nearly half the cases. Neurosurgical interventions, including ventriculoperitoneal shunting, surgical decompression or lesion excision, were performed when indicated.

Among the patients, 25 (41%) achieved full recovery, while 17 (27.9%) showed marked or significant improvement. Partial improvement was observed in 13 (21.3%) cases, and 11 (18.0%) continued to have persistent or serious problems. One patient (1.6%) died (Table S1 and Table 3).

The proposed etiologies of the movement disorders included infarcts and vasculitis affecting the basal ganglia, thalamus or brainstem, compressive effects of tuberculomas, direct basal ganglia involvement, immune-mediated mechanisms, drug-induced neurotoxicity (such as isoniazid toxicity) and complications of hydrocephalus or structural lesions. Outcomes appear less favorable in cases with deep basal ganglia or thalamic infarcts, where persistent parkinsonism, dystonia or hemichorea were commonly reported. Conversely, patients with isolated tuberculomas or cerebellar involvement more often achieved complete or near-complete recovery after anti-TB treatment and adjunctive therapy (Table S1 and Table 4).

Table 4.

Proposed enteropathogenic mechanisms (n = 61)**

TB = tuberculosis; CV = craniovertebral. **Etiopathogenesis was derived from author reports in original case descriptions where explicitly stated; otherwise, categorization was inferred by the reviewers based on clinical, radiological and treatment details.

We also identified four cohort studies that met the PICO criteria. Reference Alarcón, Dueñas, Cevallos and Lees3,Reference Alarcón, Maldonado and Rivera4,Reference Pandey, Kumar, Malhotra, Kohli, Kumar and Verma68,Reference Netravathi, Pal and Devi69 Cohort studies further substantiated these findings. In a pediatric cohort from North India, tuberculous meningitis accounted for 4.3% of all movement disorder cases and typically presented with ataxia or tremors. In a large prospective adult cohort, secondary movement disorders due to CNS TB commonly manifested as dystonia, parkinsonism and tremors, with imaging frequently showing lesions in the thalamus or basal ganglia. Another study of patients with intracranial tuberculomas highlighted the role of focal or unilateral movement disorders caused by mass lesions affecting motor circuits. A separate prospective study of tuberculous meningitis patients found that 87% developed movement disorders, predominantly tremors, chorea, dystonia and parkinsonism, typically within the first three weeks of illness. These cohort findings emphasized that movement disorders are common, often underrecognized consequences of CNS TB, with early imaging and targeted therapy being crucial for improving neurological outcomes (Table 5).

Table 5.

Summary of four cohort studies on movement disorders in central nervous system (CNS) tuberculosis

Discussion

CNS TB, especially tuberculous meningitis, gives rise to a wide variety of movement disorders driven by inflammation, infarction, hydrocephalus or immune-mediated phenomena. Hyperkinetic forms such as chorea, dystonia, tremor, myoclonus, opsoclonus and stereotypies are commonly associated with basal ganglia or brainstem involvement, whereas hypokinetic syndromes like parkinsonism and akinetic mutism are usually linked to thalamic or frontal lobe injury. From a clinical perspective, early recognition of these disorders is crucial since they may precede or persist despite anti-TB therapy and significantly influence long-term outcomes. Active screening, timely neuroimaging and appropriate use of corticosteroids, surgery or symptomatic drugs can substantially improve prognosis (Table 6).

Table 6.

Key findings of our review (n = 61)

Immune-mediated mechanisms

In some patients, movement disorders arise without visible lesions, suggesting an immune basis. Molecular mimicry and cytokine-driven inflammation may lead to parainfectious syndromes such as opsoclonus-myoclonus or dystonia. These cases often respond to corticosteroids or immunotherapy, reinforcing the immune-mediated pathogenesis. Reference Netravathi, Pal and Devi69

Vascular mechanisms

Vasculitis is one of the most common causes of movement disorders in CNS TB. In tuberculous meningitis, infectious vasculitis frequently produces infarcts involving deep brain structures such as the basal ganglia, thalamus, internal capsule and brainstem. These infarcts disrupt motor circuits, leading to manifestations such as chorea, dystonia, tremor or parkinsonism. Reference Misra, Kalita and Maurya70

Structural and compressive lesions

Tuberculomas can exert a mass effect or cause perilesional edema, particularly when located in motor regions like the basal ganglia, thalamus or brainstem. Reference Alarcón, Maldonado and Rivera4 Hydrocephalus, often due to obstruction of CSF pathways by basal exudates, can compress the thalamus or midbrain and disturb motor relays. Reference Rock, Olin, Baker, Molitor and Peterson71 Involvement of the craniovertebral junction or brainstem in spinal or meningeal tuberculosis may also produce abnormal movements through direct compression or inflammation. Reference Synmon, Siangshai, Nongrum and Wezah17,Reference Lee, Oh, Park and Yoon72

Drug-related toxicity

Anti-TB drug neurotoxicity, particularly from isoniazid, may contribute to reversible encephalopathy involving motor pathways, especially in the absence of pyridoxine supplementation. Reference Holla, Netravathi, Kamble, Saini and Pal24 Clinical presentations can mimic vascular or structural complications.

Delayed sequelae

Rarely, movement disorders appear months to years after the initial CNS TB due to sequelae such as gliosis, cortical atrophy or Wallerian degeneration. Reference Alarcón and Giménez-Roldán73 These delayed complications reflect long-term injury and remodeling of motor pathways after the acute infection has subsided.

Taken together, these mechanisms highlight the complex interplay of vascular, inflammatory, immune and drug-related factors underlying movement disorders in CNS TB (Table 3).

This review has several limitations. Most data come from case reports or small series, risking publication bias toward severe or atypical presentations. Variability in clinical descriptions, imaging and diagnostic criteria hindered meta-analysis. Many studies lacked long-term follow-up, consistent treatment details or microbiological confirmation. Immune, drug-induced and infectious causes were often not clearly differentiated. Additionally, geographic bias – mostly from high TB-burden regions like India – limits global generalizability. Future research should focus on prospective cohorts to define the incidence and course of movement disorders in CNS TB. Advanced MRI can clarify mechanisms, while long-term follow-up may reveal prognostic factors. Studies on immune and drug-induced causes are also needed to improve understanding and management.

Conclusions

This review shows that movement disorders are common yet underrecognized in CNS TB. Ataxia, dystonia, chorea and parkinsonism predominate. Causes include infarcts, tuberculomas, hydrocephalus and immune or drug effects. Early diagnosis, neuroimaging, anti-TB treatment and symptomatic therapy improve outcomes. Clinicians should actively screen for these treatable complications to reduce long-term disability.

Supplementary material

The supplementary material for this article can be found at https://doi.org/10.1017/cjn.2025.10436.

Data availability

All data generated or analyzed during this study are contained within the published article and its supplementary materials.

Author contributions

RKG: Conceptualization; Data curation; Formal analysis; Methodology; Project Software; Supervision; Validation; Visualization; Writing – original draft; Writing – review and editing. SP: Methodology; Writing – original draft; Writing – review and editing. RAM: Data curation; Formal analysis; Methodology; Writing – original draft; Writing – review and editing. SS: Project Software; Supervision; Validation; Writing – original draft; Writing – review and editing.

Funding statement

This research received no external funding.

Competing interests

RKG has received honoraria for preparing clinical summaries and articles for MedLink Neurology and UpToDate. The other authors report no conflicts of interest.

Ethical statement

This study did not involve human or animal subjects; therefore, ethical approval was not required.

Ethics approval and consent to participate

As the study did not involve human participants, ethics approval and informed consent were not applicable.

References

Garg, RK. Tuberculosis of the central nervous system: current concepts in diagnosis and treatment. Curr Opin Neurol. 2025;38(4):406–413. https://doi.org/10.1097/WCO.0000000000001358.Google Scholar
Seddon, JA, Tugume, L, Solomons, R, Prasad, K, Bahr, NC. Tuberculous meningitis international research consortium. The current global situation for tuberculous meningitis: epidemiology, diagnostics, treatment and outcomes. Wellcome Open Res. 2019;4:167. https://doi.org/10.12688/wellcomeopenres.15535.1.Google Scholar
Alarcón, F, Dueñas, G, Cevallos, N, Lees, AJ. Movement disorders in 30 patients with tuberculous meningitis. Mov Disord. 2001;16:890–894. https://doi.org/10.1002/mds.1185.Google Scholar
Alarcón, F, Maldonado, JC, Rivera, JW. Movement disorders identified in patients with intracranial tuberculomas. Neurologia. 2011;26(6):343–350. https://doi.org/10.1016/S2173-5808(11)70080-3.Google Scholar
Desai, S, Yadav, R, Garg, D, Schneider, SA, Pal, PK. Tuberculosis related movement disorders: a systematic scoping review highlighting geographic disparities, phenotypic patterns, treatment responses, and knowledge gaps in global reporting. Mov Disord Clin Pract. 2025;12(8):1043–1052. https://doi.org/10.1002/mdc3.70099.Google Scholar
Garg, RK, Pandey, S, Singhal, S, Mahdi, RA. Movement disorders in central nervous system tuberculosis: a systematic review of case reports, case series, and cohort studies. PROSPERO. 2025 CRD420251075389. https://www.crd.york.ac.uk/PROSPERO/view/CRD420251075389.Google Scholar
Dian, S, Ganiem, AR, van Laarhoven, A. Central nervous system tuberculosis. Curr Opin Neurol. 2021;34(3):396–402. https://doi.org/10.1097/WCO.0000000000000920.Google Scholar
Marais, S, Thwaites, G, Schoeman, JF, et al. Tuberculous meningitis: a uniform case definition for use in clinical research. Lancet Infect Dis. 2010;10(11):803–812. https://doi.org/10.1016/S1473-3099(10)70138-9.Google Scholar
The Movement Disorder Society. About Movement Disorders: View clinical information, resources, tools and education about common movement disorders. Downloaded from (https://www.movementdisorders.org/MDS/About/Movement-Disorder-Overviews.htm) Assessed on 5th May, 2025.Google Scholar
Murad, MH, Sultan, S, Haffar, S, Bazerbachi, F. Methodological quality and synthesis of case series and case reports. BMJ Evid Based Med. 2018;23:60–63. https://doi.org/10.1136/bmjebm-2017-110853.Google Scholar
Della Gatta, AN, Rizzo, R, Pilu, G, Simonazzi, G. Coronavirus disease 2019 during pregnancy: a systematic review of reported cases. Am J Obstet Gynecol. 2020;223:36–41. https://doi.org/10.1016/j.ajog.2020.04.013.Google Scholar
Valdes, LFI, Sibat, HF. Opsoclonus myoclonus ataxia syndrome associates to mixed meningitis responding to drug therapy: case report, new hypotheses and systematic review. J Drug Alcohol Res. 2025;14:162719. https://doi.org/10.4303/JDAR/236427.Google Scholar
Johansen, J. Cerebellar tremor caused by meningoencephalitis tuberculosis in a 17-year-old patient: a case report. Mutiara Med J Kedokt dan Kesehat. 2025;25(1):1–9. https://doi.org/10.18196/mmjkk.v25i1.Google Scholar
Gupta, D, Palayullakandi, A, Sopanam, S, Panda, PK, Sharawat, IK. Opsoclonus myoclonus ataxia syndrome: an atypical presentation of tuberculous meningitis. Am J Trop Med Hyg. 2025;112(4):856–858. https://doi.org/10.4269/ajtmh.24-0664.Google Scholar
Garg, RK, Rizvi, I, Kumar, N, et al. Acute hemichorea–hemiballismus in patients with tuberculous meningitis: an atypical manifestation of stroke. Neurol India. 2025;73(1):165–169. https://doi.org/10.4103/0028-3886.380255.Google Scholar
Vidhale, TA, Jaya, RP, Pande, M, Ganiyani, MA. A middle-aged patient living with HIV (PLHIV), presented with persistent hiccups, imbalance, and multifocal myoclonus secondary to disseminated tuberculosis. J Pediatr Neurol. 2024;21(2):103–105. https://doi.org/10.1055/s-0044-1783393.Google Scholar
Synmon, B, Siangshai, F, Nongrum, H, Wezah, W. CV junction drug-resistant tuberculosis presenting as acquired torticollis: a rare case presentation. Neurol India. 2024;72(3):687–688. https://doi.org/10.4103/neurol-india.Neurol-India-D-24-00062.Google Scholar
Qavi, A, Maurya, PK, Singh, AK, Kulshreshtha, D, Thacker, AK, Sikand, TS. Tongue tremor: a rare manifestation of disseminated central nervous system tuberculosis. Ann Mov Disord. 2024;7(2):147–148. https://doi.org/10.4103/aomd.aomd_34_23.Google Scholar
Jha, S, Tiwari, M, Chatterjee, D, Datta, A, Shobhana, A. Stereotypy and parkinsonism in tubercular meningitis: expanding the spectrum. Ann Mov Disord. 2024;7(2):125–127. https://doi.org/10.4103/aomd.aomd_20_23.Google Scholar
Garcia, JJB, Tecson-Delos Santos, CMA. Dancing out of step: a case of tuberculous meningitis presenting as childhood chorea. Tremor Other Hyperkinet Mov (N Y). 2024;14(1):17. https://doi.org/10.5334/tohm.871.Google Scholar
Sajjad, F, Baloch, MF, Ashraf, M, et al. Focal dystonia and ataxic hemiparesis as the initial presentation of a thalamic tuberculoma: a diagnostic challenge in an immunocompetent pediatric patient. Surg Neurol Int. 2023;14:350. https://doi.org/10.25259/SNI_581_2023.Google Scholar
Saishoji, Y, Mori, H, Izumi, Y. Cerebellar Ataxia caused by central nervous system tuberculosis with pulmonary tuberculosis: a case report. Cureus. 2023;15(1):e33493. https://doi.org/10.7759/cureus.33493.Google Scholar
Mukherjee, D, Mukherjee, A, Bhattacharya, S, Chakraborty, A, Pandit, A. Clinico-radiological evolution of CNS tuberculosis presenting as parkinsonism-predominant movement disorder. Acta Neurol Belg. 2023;123(1):319–321. https://doi.org/10.1007/s13760-022-02106-z.Google Scholar
Holla, VV, Netravathi, M, Kamble, N, Saini, J, Pal, PK. “Face of the giant panda” sign and bilateral thalamic hyperintensity in isoniazid-induced Ataxia. J Mov Disord. 2024;17(1):99. https://doi.org/10.14802/jmd.23112.Google Scholar
Dichoso, LP, Pagaling, G, Jamora, RDG, Anlacan, VMM. Case report: paroxysmal autonomic instability with dystonia syndrome: a rare complication of tuberculous meningitis. F1000Res. 2023;12:725. https://doi.org/10.12688/f1000research.132201.1.Google Scholar
Saini, AG, Hassan, I, Sharma, K, et al. Status dystonicus in children: a cross-sectional study and review of literature. J Child Neurol. 2022;37(6):441–450. https://doi.org/10.1177/08830738221079811.Google Scholar
Mahale, R, Pon, AG, Sandeep, M, Padmanabha, H, Mailankody, P, Pavagada, M. Levodopa non-responsive parkinsonism in tuberculous cerebral arteritis: a rare occurrence. Ann Indian Acad Neurol. 2022;25(3):519–520. https://doi.org/10.4103/aian.aian_1214_21.Google Scholar
Kalita, J, Misra, UK, Vibhute, A. Movement disorder in tuberculous meningitis. Neurol India. 2022;70(5):2196–2199. https://doi.org/10.4103/0028-3886.359206.Google Scholar
Dimal, NPM, Santos, NJC, Reyes, NGD, Astejada, MN, Jamora, RDG. Hemichorea-hemiballismus as a presentation of cerebritis from intracranial toxoplasmosis and tuberculosis. Tremor Other Hyperkinet Mov (N Y). 2021;11:2. https://doi.org/10.7916/d8-tfsy-bt19.Google Scholar
Alharbi, A, Khairy, S, Al Sufiani, F, Alkhani, A. Intracranial tuberculomas: a case report of clinical, radiological, and pathological characteristics. Int J Surg Case Rep. 2021;88:106477. https://doi.org/10.1016/j.ijscr.2021.106477.Google Scholar
Saini, AG, Sharma, R, Aneja, S, Sankhyan, N, Singhi, P. Infection-associated opsoclonus in children: a case series and review of the literature. J Neurovirol. 2020;26(3):338–47. https://doi.org/10.1007/s13365-020-00845-6.Google Scholar
Chouksey, A, Pandey, S. Blepharospasm with photophobia secondary to Midbrain tuberculoma and thalamic infarct. Neurologist. 2020;25(3):78–81. https://doi.org/10.1097/NRL.0000000000000265.Google Scholar
Boussetta, R, Zairi, M, Ben Sami, S, et al. Torticollis as a sign of spinal tuberculosis. Pan Afr Med J. 2020;36:277. https://doi.org/10.11604/pamj.2020.36.277.22977.Google Scholar
Tapiero, B, Décarie, JC, Crevier, L, Altit, G. An unexpected disease presenting as a pediatric cerebellar mass. Radiol Infect Dis. 2019;6(2):83–86. https://doi.org/10.1016/j.jrid.2019.06.001.Google Scholar
Gavigan, P, Hysmith, ND, Bagga, B. Case 2: Lethargy and ataxia in a 3-year-old girl. Pediatr Rev. 2019;40(4):194–196. https://doi.org/10.1542/pir.2017-0183.Google Scholar
Aasfara, J, Regragui, W, El Ouardi, L, Ben Haddou, EHA, Benomar, A, Yahyaoui, M. A case of bilateral thalamic infarct complicating tuberculous meningoencephalitis. Pan Afr Med J. 2019;33:2. https://doi.org/10.11604/pamj.2019.33.2.13327.Google Scholar
Franzini, A, Franzini, A, Levi, V, Cordella, R, Messina, G. An unusual surgical indication for cerebral tuberculosis: status dystonicus. Case report. Acta Neurochir (Wien). 2018;160:1355–1358. https://doi.org/10.1007/s00701-018-3555-0.Google Scholar
Pandey, S, Singh, AS. Unilateral parkinsonism: symptomatic of brain tuberculoma. Neurologist. 2017;22(3):80–81. https://doi.org/10.1097/NRL.0000000000000114.Google Scholar
Deepesh, A, Pendharkar, HS. Isoniazid toxicity presenting as bilateral dentate hyperintensities. Neurol India. 2017;65(5):1193. https://doi.org/10.4103/neuroindia.NI_249_17.Google Scholar
Parralo, A, Lopez, A, Giraldo, N, Bravo, JJ, Valencia, C, Hernandez, A. Cerebral and cerebellar tuberculomas in a 78-year-old woman: a case report. Eur J Neurol. 2015;22:510. https://doi.org/10.1111/ene.12808.Google Scholar
Pinto, MV, Aguiar, T, Nogueira, R, Dias, AC, Rosso, AL. Hemichorea in tuberculous meningitis. Arq Neuropsiquiatr. 2014;72(2):160. https://doi.org/10.1590/0004-282X20130230.Google Scholar
Sahu, R, Patil, TB, Kori, P, Shukla, R. Isolated thalamic tuberculoma presenting as ataxic hemiparesis. BMJ Case Rep. 2013;2013:bcr2013009100. https://doi.org/10.1136/bcr-2013-009100.Google Scholar
Singh, DK, Singh, N. Paroxysmal autonomic instability with dystonia in a child: rare manifestation of an interpeduncular tuberculoma. Pediatr Neurosurg. 2011;47(4):275–278. https://doi.org/10.1159/000334276.Google Scholar
Garg, RK, Singh, SK, Malhotra, HS, Singh, MK. Bobble-head doll syndrome in a patient with tuberculous meningitis. BMJ Case Rep. 2012;2012:bcr2012006663. https://doi.org/10.1136/bcr-2012-006663.Google Scholar
Chakor, RT, Rajadhyaksha, GC. A young adult with progressive limb shaking and slowness. J Postgrad Med. 2011;57(3):231–6. https://doi.org/10.4103/0022-3859.85221.Google Scholar
Ashraf, VV, Praveenkumar, Sureshkumar, EK, Anand, R, Kuruvilla, S, Girija, AS. Segmental myoclonus and marked ataxia in a patient of pulmonary tuberculosis. Neurol India. 2011;59(6):904–906. https://doi.org/10.4103/0028-3886.91376.Google Scholar
Prashantha, DK, Pal, PK, Bharath, RD. Hyperventilation-induced painful tonic spasms secondary to a structural lesion of the pons. Parkinsonism Relat Disord. 2010;16(9):618–619. https://doi.org/10.1016/j.parkreldis.2010.07.005.Google Scholar
Krygowski, JD, Brennen, DF, Counselman, FL. Intracranial tuberculomas: an unusual cause of altered mental status in a pediatric patient. J Emerg Med. 2010;38(3):323–327. https://doi.org/10.1016/j.jemermed.2007.12.040.Google Scholar
Gujjar, A, Al-Mamari, A, Jacob, PC, Jain, R, Balkhair, A, Al-Asmi, A. Extrapontine myelinolysis as presenting manifestation of adrenal failure: a case report. J Neurol Sci. 2010;290(1–2):169–171. https://doi.org/10.1016/j.jns.2009.11.012.Google Scholar
Donmez, FY, Coskun, M, Guven, G. Medulla oblongata tuberculoma mimicking metastasis presenting with stroke-like symptoms. Neurol Sci. 2009;30(4):349–352. https://doi.org/10.1007/s10072-009-0099-6.Google Scholar
Avila, A, Berrade, J. Tuberculosis involving bilateral middle cerebellar peduncles and the brainstem. AJNR Am J Neuroradiol. 2009;30(8):E119. https://doi.org/10.3174/ajnr.A1682.Google Scholar
Mridula, KR, Alladi, S, Varma, DR, et al. Corticobasal syndrome due to a thalamic tuberculoma and focal cortical atrophy. J Neurol Neurosurg Psychiatry. 2008;79(1):107–108. https://doi.org/10.1136/jnnp.2007.131532.Google Scholar
Ozer, F, Meral, H, Aydemir, T, Ozturk, O. Hemiballism–hemichorea in presentation of cranial tuberculoma. Mov Disord. 2006;21(10):1771–1773. https://doi.org/10.1002/mds.21055.Google Scholar
Alkhani, A, Al-Otaibi, F, Cupler, EJ, Lach, B. Miliary tuberculomas of the brain: case report. Clin Neurol Neurosurg. 2006;108(4):411–414. https://doi.org/10.1016/j.clineuro.2005.04.012.Google Scholar
Tey, HL, Seet, RCS, Lim, ECH. Tuberculomas causing cervical dystonia. Intern Med J. 2005;35(4):261–262. https://doi.org/10.1111/j.1445-5994.2005.00708.x.Google Scholar
Poonnoose, SI, Singh, S, Rajshekhar, V. Giant cerebellar tuberculoma mimicking a malignant tumour. Neuroradiology. 2004;46(2):136–139. https://doi.org/10.1007/s00234-003-1100-z.Google Scholar
Kalita, J, Ranjan, P, Misra, UK, Das, BK. Hemichorea: a rare presentation of tuberculoma. J Neurol Sci. 2003;208(1-2):109–111. https://doi.org/10.1016/S0022-510X(02)00417-3.Google Scholar
Alarcón, F, Tolosa, E, Munoz, E. Focal limb dystonia in a patient with a cerebellar mass. Arch Neurol. 2001;58(7):1125–1127. https://doi.org/10.1001/archneur.58.7.1125.Google Scholar
Chaudhary, N, Ravat, SH, Shah, PU. Phenytoin induced dyskinesia. Indian Pediatr. 1998;35(3):274–276.Google Scholar
de la Fuente-Aguado, J, Bordón, J, Moreno, JA, Sopeña, B, Rodriguez, A, Martínez-Vázquez, C. Parkinsonism in an HIV-infected patient with hypodense cerebral lesion. Tuberc Lung Dis. 1996;77(2):191–192. https://doi.org/10.1016/S0962-8479(96)90013-1.Google Scholar
Tang, PS, Low, LCK. Radiological and clinical features of basal ganglia infarction in tuberculous meningitis. Aust Paediatr J. 1989;25(6):361–362. https://doi.org/10.1111/j.1440-1754.1989.tb02237.x.Google Scholar
Verma, A, Tandon, PN, Maheshwari, MC. Trismus caused by paradoxical activity of jaw-closing muscles in brain stem tuberculoma. Oral Surg Oral Med Oral Pathol. 1988;65(6):675–678. https://doi.org/10.1016/0030-4220(88)90007-2.Google Scholar
Babikian, VL, Heydemann, PT, Swisher, CN. Extrapyramidal movements in a patient with tuberculous meningitis: an early clue to diagnosis. Clin Pediatr (Phila). 1985;24(2):113–115. https://doi.org/10.1177/000992288502400208.Google Scholar
Sandyk, R. Hemifacial spasm in tuberculous meningitis. Postgrad Med J. 1983;59(695):570–571.Google Scholar
Riela, A, Roach, ES. Choreoathetosis in an infant with tuberculous meningitis. Arch Neurol. 1982;39(9):596. https://doi.org/10.1001/archneur.1982.00510210028008.Google Scholar
Slot, GJ, Morris, D. Erythema nodosum associated with chorea and tuberculous meningitis. Lancet. 1939;233(6028):571–572. https://doi.org/10.1016/S0140-6736(00)73744-5.Google Scholar
Jackson, JH. On choreal movements and cerebellar rigidity in a case of tubercular meningitis. Br Med J. 1875;1(750):636–637. https://doi.org/10.1136/bmj.1.750.636.Google Scholar
Pandey, CS, Kumar, R, Malhotra, HS, Kohli, N, Kumar, C, Verma, SK. Movement disorders in children: an observational study in a tertiary care center in North India. J Pediatr Neurol. 2019;17(3):131–138. https://doi.org/10.1055/s-0039-1693030.Google Scholar
Netravathi, M, Pal, PK, Devi, BI. A clinical profile of 103 patients with secondary movement disorders: correlation of etiology with phenomenology. Eur J Neurol. 2012;19(2):226–233. https://doi.org/10.1111/j.1468-1331.2011.03469.x.Google Scholar
Misra, UK, Kalita, J, Maurya, PK. Stroke in tuberculous meningitis. J Neurol Sci. 2011;303(1–2):22–30. https://doi.org/10.1016/j.jns.2010.12.015.Google Scholar
Rock, RB, Olin, M, Baker, CA, Molitor, TW, Peterson, PK. Central nervous system tuberculosis: pathogenesis and clinical aspects. Clin Microbiol Rev. 2008;21(2):243–261. https://doi.org/10.1128/CMR.00042-07.Google Scholar
Lee, JK, Oh, CH, Park, HC, Yoon, SH. Grisel’s syndrome induced by mycobacterium tuberculosis. Korean J Spine. 2015;12(2):84–87. https://doi.org/10.14245/kjs.2015.12.2.84.Google Scholar
Alarcón, F, Giménez-Roldán, S. Systemic diseases that cause movement disorders. Parkinsonism Relat Disord. 2005;11(1):1–18. https://doi.org/10.1016/j.parkreldis.2004.10.003.Google Scholar
Figure 0

Table 1. Search strategy

Figure 1

Figure 1. MRI of the brain showing a ring-enhancing lesion in the left thalamus with surrounding edema on post-contrast T1-weighted coronal image (left). Magnetic resonance spectroscopy from the lesion (right) demonstrates a lipid-lactate peak, reduced N-acetylaspartate and elevated choline, suggestive of a tuberculoma. The patient had right hemichorea.

Figure 2

Figure 2. PRISMA 2020 flow diagram illustrating the study selection process for inclusion in the systematic review. The diagram shows the number of records identified, screened, excluded and included at each stage of the review, along with reasons for exclusions.

Figure 3

Table 2. Summary of demographic characteristics of CNS tuberculosis cases presenting with movement disorders (n = 61)

Figure 4

Table 3. Summary of clinical, neuroimaging and treatment features of CNS TB cases presenting with movement disorders (n = 61)

Figure 5

Table 4. Proposed enteropathogenic mechanisms (n = 61)**

Figure 6

Table 5. Summary of four cohort studies on movement disorders in central nervous system (CNS) tuberculosis

Figure 7

Table 6. Key findings of our review (n = 61)

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