A case report of long-segment tuberculous myelitis with concomitant tuberculous meningitis
Case Report

A case report of long-segment tuberculous myelitis with concomitant tuberculous meningitis

Mohmed Hussien Ahmed Mohmed1 ORCID logo, Isra Hamed Dafallah Idrees2, Ahmed Mostafa3, Khalid Elfatih Mohammed Ibrahim4, Amna Adnan Ahmad5, Mahmoud H. S. Daoud6 ORCID logo

1Faculty of Medicine, Gezira University, Madani, Sudan; 2Madani Teaching Hospital, Madani, Sudan; 3Radiology Department, Hatta Hospital, Dubai, United Arab Emirates; 4Neurology Department, Hatta Hospital, Dubai, United Arab Emirates; 5Dubai Academic Health Corporation, Dubai, United Arab Emirates; 6Department of Medicine, Faculty of Medicine, University of Gezira, Madani, Sudan

Contributions: (I) Conception and design: MH Ahmed Mohmed, MHS Daoud; (II) Administrative support: MHS Daoud; (III) Provision of study materials or patients: IHD Idrees; (IV) Collection and assembly of data: IHD Idrees, MH Ahmed Mohmed; (V) Data analysis and interpretation: MH Ahmed Mohmed, MHS Daoud; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Mohmed Hussien Ahmed Mohmed, MBBS. Faculty of Medicine, Gezira University, Nobri Street, Madani 21111, Sudan. Email: hussienmohmed93@gmail.com.

Background: Tuberculous myelitis is a form of central nervous system tuberculosis (TB) that can be associated with intracranial involvement but rarely presents with extensive longitudinal involvement of more than one segment. We are reporting a case with tuberculous meningitis and long-segment myelitis in a previously undiagnosed patient with TB.

Case Description: A 53-year-old hypertensive male, presented with subacute lower limbs weakness, sensory level below his nipples, and urine retention. Erythrocyte sedimentation rate (ESR) was above 112 mm/hour. Magnetic resonance imaging (MRI) spine showed a long segment of hyperintense signal seen on the T2-weighted image (T2WI) images in the spinal cord extending from C6 to D3 vertebral segments, with heterogeneous post-contrast enhancement. Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis with high protein and low glucose, and polymerase chain reaction (PCR) for Mycobacterium tuberculosis (MBTB) was positive. The patient received intravenous methylprednisolone daily for 5 days and standard anti-TB medications [rifampicin, isoniazid (INH), pyrazinamide, and ethambutol] for 12 months. However, repeated CSF analysis 3 months after starting anti-TB medications showed a negative PCR for MBTB, normal cell count, and glucose with slightly elevated protein. Still, the patient did not show any clinical improvement.

Conclusions: Long-segment tuberculous myelitis (LSTM) is a rare form of central nervous system TB that can be accompanied by tuberculous meningitis. It must be considered a differential diagnosis of neuromyelitis optica spectrum disorder (NMOSD), especially in endemic areas of TB, as the management approach is completely different.

Keywords: Long-segment tuberculous myelitis (LSTM); tuberculous meningitis; Mycobacterium tuberculosis (MBTB); anti-tuberculous; case report

Received: 03 October 2024; Accepted: 27 February 2025; Published online: 06 June 2025.

doi: 10.21037/acr-24-211

Highlight box

Key findings

• This study reports a rare case of long-segment tuberculous myelitis (LSTM) extending from C6 to D3 vertebral segments accompanied by tuberculous meningitis in a previously undiagnosed tuberculosis (TB) patient. Despite aggressive treatment with intravenous methylprednisolone and standard anti-TB medications, the patient showed no clinical improvement, highlighting the challenges in managing this condition.

What is known and what is new?

• Tuberculous myelitis is a rare form of central nervous system TB, often associated with intracranial involvement. It typically presents with shorter spinal cord segments and is rarely associated with extensive longitudinal involvement.

• This case highlights the rare presentation of LSTM with tuberculous meningitis, emphasizing the need to consider TB in differential diagnoses, especially in TB-endemic regions. It underscores the diagnostic challenges and limited treatment response in such cases, even with appropriate anti-TB therapy.

What is the implication, and what should change now?

• LSTM should be considered a differential diagnosis for neuromyelitis optica spectrum disorder (NMOSD), particularly in TB-endemic areas, as the management strategies differ significantly.

• Increased awareness among clinicians about the rare presentation of LSTM, further research to understand the pathophysiology and improve treatment outcomes for this severe form of central nervous system TB and enhanced diagnostic protocols to differentiate tuberculous myelitis from other demyelinating disorders like NMOSD.

Introduction

Tuberculosis (TB) involving the central nervous system is associated with poor outcomes even when successful treatment is applied (1). Tuberculous myelitis is a rare form of central nervous system TB (2) and can be associated with extensive longitudinal involving more than one segment and intracranial involvement. It is either a primary lesion a downward extension from brain TB or an extension from vertebral TB (3). Central nervous system TB accounts for 1% of all tuberculous infections with 95% presenting as TB meningitis, and half of these cases affecting the spine (4). Long segment myelitis (LSM) is commonly reported as diagnosis of neuromyelitis optica (NMO) but rarely reported due to TB as a possible diagnosis for LSM (5). Tuberculous long-segment myelitis occurs as a result of immune-mediated damage to more than one spinal segment (6). We are reporting a case of tuberculous meningitis and long-segment myelitis in a previously undiagnosed patient with TB. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-24-211/rc).

Case presentation

A 53-year-old Sudanese male with a clear medical background history apart from controlled hypertension was first seen on 26 August 2023 when he presented to the emergency room with acute lower limb weakness to the degree that he could not walk without support. It progressed over a month. The patient reported that his weakness started in his right lower limb first, and then his left lower limb was affected a week later.

He complained of sensory disturbance with hypothesis below the umbilicus, and he had difficulty passing urine 3 weeks prior to admission. He then developed blurring of vision and slurred speech. He has no past medical history of pulmonary TB, no family history or contact with a patient having TB, is not diabetic, has no history of human immunodeficiency virus (HIV), and has no other chronic illnesses, and he is not a smoker or an alcoholic. On examination, he was fully conscious, oriented, and vitally stable, had a convergent squint, and had left ptosis. His upper limb examination revealed normal tone, power, reflexes, coordination, and intact all sensory modalities at both upper limbs. Examination of lower limbs revealed hypotonia, power grade zero in all muscle groups, hyporeflexia, and loss of all sensory modalities below the nipples.

His complete blood count and random blood sugar came normal while his ESR was above 100. Magnetic resonance imaging (MRI) of the whole spine with contrast showed LSM in the lower cervical and the upper thoracic segments extending from C6 to D3, with atrophy at the lower dorsal (Figure 1A,1B), and due to the occurrence of blurred vision and diplopia, basal meningitis was suspected, An MRI of the brain with contrast was also requested. Which revealed marked basal patchy meningeal enhancement (Figure 2A,2B).

Figure 1 MRI of the cervical spine. (A) Sagittal T2-weighted image shows a long segment hyperintense intramedullary signal extending from the C6 to D3 vertebral levels (yellow arrow), consistent with spinal cord edema or inflammation. (B) Axial post-contrast T1-weighted image with fat suppression demonstrates heterogeneous enhancement of the cervical spinal cord (white arrow). MRI, magnetic resonance imaging.
Figure 2 Post-contrast brain MRI. (A) Sagittal and (B) coronal T1-weighted images demonstrate multiple areas of meningeal enhancement (white arrows), indicative of leptomeningeal involvement, suggestive of an inflammatory, infectious, or neoplastic process. MRI, magnetic resonance imaging.

Cerebrospinal fluid (CSF) examination showed a high opening pressure of 27 cmH2O, a high protein of 131.2 mg/dL, low glucose of 12 mg/dL, and a high white cell count (WBC) of 136 cells/mm (polymorphonuclear 35%, mononuclear 65%). Polymerase chain reaction (PCR) (gene-expert) for Mycobacterium tuberculosis (MBTB) was positive. Computed tomography (CT) of the chest, abdomen, and pelvis with contrast revealed no infection or tumor.

Finally, the patient was diagnosed with tuberculous meningitis and long-segment myelitis. He received intravenous methylprednisolone 1,000 mg infusion for 5 days, then oral prednisolone 40 mg per day with tapering over 2 months, anti-tuberculous (isoniazid 300 mg, rifampicin 600 mg, pyrazinamide 1,000 mg, and ethambutol 1,600 mg daily in a poly pill formulation) for 2 months, then he continued with (isoniazid 300 mg, rifampicin 600 mg) for another ten months. In addition, the patient received subcutaneous low molecular weight heparin 4,000 IU, then after discharge 10 mg rivaroxaban daily as a prophylaxis from deep vein thrombosis and he did physiotherapy.

The patient came for a follow-up in November (Table 1); still, he had dense weakness, was catheterized, sensory loss for all modalities up to his chest, superficial sacral ulcers, and also had a convergent squint indicating bilateral 6th cranial nerve palsy. He also documented difficulty in opening his jaw. The patient repeated CSF analysis 3 months after starting anti-TB medications, CSF PCR for MBTB was negative, cell count and glucose were in the reference range, and protein was slightly high 85 mg/dL. The patient admitted he was taking the medication regularly as prescribed, but still, there was no obvious improvement. Also, due to the patient’s low socioeconomic status, no further imaging was ordered to reassess the condition. All aspects of this study, including data collection, analysis, and reporting, were conducted in accordance with the ethical standards of the institutional and/or national research committees, and in compliance with the principles of the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and any accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Table 1

Timeline

Date Event
26 August 2023 The patient presented to the emergency room with lower limb weakness, sensory loss below the umbilicus, and urinary difficulty, symptoms progressed over a month earlier, associated with blurred vision and slurred speech. On examination, he has convergent squint, left ptosis with lower limbs hypotonia, grade zero power, hyporeflexia, sensory loss below nipples, and upper limbs were normal. All investigations came normal except for ESR, which was high. CNS tuberculosis was suspected and CSF analysis including MBTB gene-expert with brain and whole spinal MRI was ordered
31 August 2023 MRI spine: myelitis (C6–D3). MRI brain: basal meningeal enhancement. CSF: high protein, low glucose, high WBC, PCR positive for TB. The patient was diagnosed as LSTM with tuberculous meningitis, he received intravenous steroids, anti-TB drugs, DVT prophylaxis, and physiotherapy. He was discharged on oral steroids and oral DVT prophylaxis
November 2023 The patient came for follow-up with persistent weakness, sensory loss, sacral ulcers, cranial nerve palsy, and no significant improvement. The patient could not afford a follow-up MRI, but CSF was ordered
November 2023 CSF: PCR negative, and slightly high protein

CNS, central nervous system; CSF, cerebrospinal fluid; DVT, deep vein thrombosis; ESR, erythrocyte sedimentation rate; LSM, long segment myelitis; LSTM, long segment tuberculous myelitis; MBTB, Mycobacterium tuberculosis; MRI, magnetic resonance imaging; PCR, polymerase chain reaction; TB, tuberculosis; WBC, white cell count.

Discussion

TB is an infectious disease with an estimated 10.4 million new cases and 1.8 million deaths in 2016 globally (7); TB of the central nervous system is an extrapulmonary TB with resultant morbidity and mortality (1). Spinal cord TB is usually manifested as intramedullary tuberculoma, extradural TB, leptomeningitis, but rarely as transverse myelitis (TM) (8).

TM is an uncommon neurological disorder that occurs due to inflammation of the spinal cord with an incidence range between 1.34 and 4.6 per million per year (9). LSM is a common finding of neuromyelitis optica with occurrence to other etiologies like infections, paraneoplastic and metabolic disturbances (10), but is rarely manifested as a complication of central nervous system TB (5), as in this case of LSM accompanied with tuberculous meningitis in a patient with no history TB.

The pathogenesis of tuberculous myelitis is an inflammatory reaction to MBTB resulting in inflammatory demyelination of the spinal cord (11). It usually manifests as lower limb weakness, sensory disturbance with a certain level, and sphincter disturbances (12). Our case presented with lower weakness, sensory disturbance below the nipple, and urine retention.

Tuberculous myelitis accounts for 1% of all extrapulmonary cases with various presentations, and many cases were reported associated with intracranial involvement (3), as in our case, which developed features of meningeal involvement.

MRI is considered to be a valuable diagnostic tool for TM and usually appears as high signal intensity on T2-weighted image (T2WI) extending longitudinally over more than one segment (13). In this case, MRI showed a long segment hyperintense signal seen on the T2WI images in the spinal cord more prominent from C6 to D3 vertebral segments, the post-contrast images showed heterogenous enhancement of the cervical spinal cord and MRI brain showing multiple areas of meningeal enhancement on the viewed areas of the brain. As well presence of mycobacterium TB in the CSF helps confirm the etiology (14), besides other CSF findings like high opening pressure of 27 cmH2O, high protein 1.5 grams, WBC more than 500 mainly lymphocytes and CSF low sugar.

A high dose of corticosteroids is the first line of therapy for TM as it occurs due to an inflammatory response with concomitant anti-tuberculous drugs, to prevent subsequent morbidity and mortality (15), the patient received intravenous methylprednisolone 1,000 mg infusion for 5 days then oral prednisolone 40 mg per day. Contrary to the study of Fang et al. (16) which showed a good response to high-dose and short-period steroid therapy (500 mg of methylprednisolone intravenously per day for 5 continuous days, then halve the dose and stop it after 2 days) and intravenous immunoglobulins (400 mg/kg per day for 5 continuous days) and anti-tuberculous. Unfortunately, this patient showed poor response to treatment and no evidence of clinical improvement in his follow-up, as many studies revealed spinal involvement of TB associated with poor prognosis (11,12,17).

In many cases, it was reported that the absence of meningeal involvement was associated with a good outcome and greater improvement of disability (18,19); our case has meningeal involvement, and that might contribute to the poor outcome in our case, similar to a case reported in Vietnam with meningeal involvement (15). In previous studies, a 19-year-old Indian male and another case were reported in China; both cases were diagnosed as long-segment extensive myelitis and pulmonary TB, and both cases showed a good response to anti-tuberculous medications and corticosteroids (20,21). The absence of a previous diagnosis of pulmonary TB in our case might be the cause that previous physicians made tuberculous myelitis unlikely, which resulted in a delay in the diagnosis and poor outcome as the pathology progressed.

The prevalence of TB in Sudan was 30.72%, with extrapulmonary involvement accounting for 13.95% (22). The incidence of TB is much higher among HIV patients with a range of 10–20% (5), but the patient tested negative for HIV and has no chronic illnesses, leaving his presence in an endemic area is the only risk factor for TB.

Our case highlights the importance of considering tuberculous myelitis as a possible etiology of LSM, testing for MBTB even in formerly undiagnosed patients, especially in endemic areas of TB, and indicates the necessity of further studies to evaluate the mechanism of poorer outcomes as well as guidelines for management.

Conclusions

Long-segment tuberculous myelitis (LSTM) is a rare form of central nervous system TB that can be accompanied by tuberculous meningitis in a patient with a history of TB; therefore, it must be considered as a differential diagnosis of neuromyelitis optica spectrum disorder (NMOSD) especially in endemic areas of TB, as the management approach is completely different. LSTM has a poor response to treatment, which can result in serious morbidity.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-24-211/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-24-211/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-24-211/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All aspects of this study, including data collection, analysis, and reporting, were conducted in accordance with the ethical standards of the institutional and/or national research committees and in compliance with the principles of the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and any accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

  1. Thwaites GE, Tran TH. Tuberculous meningitis: many questions, too few answers. Lancet Neurol 2005;4:160-70. [Crossref] [PubMed]
  2. Hristea A, Constantinescu RV, Exergian F, et al. Paraplegia due to non-osseous spinal tuberculosis: report of three cases and review of the literature. Int J Infect Dis 2008;12:425-9. [Crossref] [PubMed]
  3. Garg RK, Malhotra HS, Gupta R. Spinal cord involvement in tuberculous meningitis. Spinal Cord 2015;53:649-57. [Crossref] [PubMed]
  4. Sahu SK, Giri S, Gupta N. Longitudinal extensive transverse myelitis due to tuberculosis: a report of four cases. J Postgrad Med 2014;60:409-12. [Crossref] [PubMed]
  5. Cherian A, Thomas SV. Central nervous system tuberculosis. Afr Health Sci 2011;11:116-27. [PubMed]
  6. West TW. Transverse myelitis--a review of the presentation, diagnosis, and initial management. Discov Med 2013;16:167-77. [PubMed]
  7. Thwaites G, Fisher M, Hemingway C, et al. British Infection Society guidelines for the diagnosis and treatment of tuberculosis of the central nervous system in adults and children. J Infect 2009;59:167-87. [Crossref] [PubMed]
  8. Coclitu C, Mergeani A, Parvu T, et al. An Uncommon Cause of Longitudinally Extensive Transverse Myelitis. Maedica (Bucur) 2016;11:245-9. [PubMed]
  9. Bhat A, Naguwa S, Cheema G, et al. The epidemiology of transverse myelitis. Autoimmun Rev 2010;9:A395-9. [Crossref] [PubMed]
  10. Kitley JL, Leite MI, George JS, et al. The differential diagnosis of longitudinally extensive transverse myelitis. Mult Scler 2012;18:271-85. [Crossref] [PubMed]
  11. Khan MI, Garg RK, Rizvi I, et al. Tuberculous myelitis: a prospective follow-up study. Neurol Sci 2022;43:5615-24. [Crossref] [PubMed]
  12. Beh SC, Greenberg BM, Frohman T, et al. Transverse myelitis. Neurol Clin 2013;31:79-138. [Crossref] [PubMed]
  13. Murthy JM, Reddy JJ, Meena AK, et al. Acute transverse myelitis: MR characteristics. Neurol India 1999;47:290-3. [PubMed]
  14. Van Tuan N, Van Tuan B, Ung HT, et al. Longitudinally extensive transverse myelitis combined with tuberculosis meningitis: Case reports. Medicine Case Reports and Study Protocols 2021;2:e0114. [Crossref]
  15. Frohman EM, Wingerchuk DM. Clinical practice. Transverse myelitis. N Engl J Med 2010;363:564-72. [Crossref] [PubMed]
  16. Fang L, Gong Y, Han K, et al. Longitudinally extensive transverse myelitis with mycobacterium tuberculosis infection. Acta Neurol Belg 2023;123:243-6. [Crossref] [PubMed]
  17. Jiang Y, Xu X, Guo Z, et al. Myelitis: A Common Complication of Tuberculous Meningitis Predicting Poor Outcome. Front Neurol 2022;13:830029. [Crossref] [PubMed]
  18. Jain RS, Kumar S, Tejwani S. A rare association of tuberculous longitudinally extensive transverse myelitis (LETM) with brain tuberculoma. Springerplus 2015;4:476. [Crossref] [PubMed]
  19. Ortega-Rosales A, Delgado-Torres N, Burneo-Rosales C. A rare neurological complication of tuberculosis: Transverse myelitis. IDCases 2019;17:e00564. [Crossref] [PubMed]
  20. Zhang Y, Zhu M, Wang L, et al. Longitudinally extensive transverse myelitis with pulmonary tuberculosis: Two case reports. Medicine (Baltimore) 2018;97:e9676. [Crossref] [PubMed]
  21. Ramineni KK, Jakkani RK, Swamy BVG, et al. Pulmonary Tuberculosis with Longitudinally Extensive Transverse Myelitis. J Neurosci Rural Pract 2020;11:178-82. [Crossref] [PubMed]
  22. Badawi MM. Tuberculosis in Sudan: systematic review and meta analysis. BMC Pulm Med 2024;24:51. [Crossref] [PubMed]
doi: 10.21037/acr-24-211
Cite this article as: Mohmed MHA, Idrees IHD, Mostafa A, Ibrahim KEM, Ahmad AA, Daoud MHS. A case report of long-segment tuberculous myelitis with concomitant tuberculous meningitis. AME Case Rep 2025;9:76.

Article Options

Download Citation

Share