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LETTER TO EDITOR Table of Contents  
Ahead of print publication
A rare clinical presentation of tuberculous myelitis

 Department of Neurology, Dr. RML Hospital, New Delhi, India

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Date of Submission16-Mar-2020
Date of Decision10-May-2020
Date of Acceptance31-May-2020

How to cite this URL:
Jain R, Anand K S, Juneja A. A rare clinical presentation of tuberculous myelitis. Hamdan Med J [Epub ahead of print] [cited 2023 Mar 30]. Available from: http://www.hamdanjournal.org/preprintarticle.asp?id=289741

Dear Editor,

We report a case of a 25-year-old male patient, farmer by occupation, with weakness of bilateral lower limbs for 2 months, impaired sensation to touch and pain in bilateral lower limbs and urinary retention for 1 month. Initially, he had difficulty holding slippers in bilateral feet. Over next few days, he developed difficulty in climbing stairs and getting up from squatting position. He felt grip weakness in the left hand. He also complained of neck pain radiating down his back. He had urgency with occasional urge incontinence for the last 1 month. He developed complete urinary retention on the day of presentation to emergency room. There was no associated fever, weight loss, seizure, visual impairment; no history of recent travel or vaccination. There was no significant past medical history or contact with tuberculosis in family. The patient did not receive routine vaccination during childhood. On neurological examination, cranial nerves testing was normal. On motor examination, he had Grade 2 spasticity (Modified Ashworth scale) in bilateral lower limbs with Grade 1 spasticity in bilateral upper limbs. He had Grade 4 power (Medical Research Council [MRC]) at bilateral hip while Grade 3 power at bilateral ankle joints. Power in bilateral upper limbs was Grade 5 except mild grip weakness in the left hand. Deep tendon reflexes in bilateral lower limbs were exaggerated; while normal in bilateral upper limbs. Plantar responses were bilaterally extensor. There was pan-sensory loss below L1 dermatome. Touch and pain sensation were reduced to 50%. Rest of the neurological examination was unremarkable. On routine investigations, he had haemoglobin of 12.4 g/dl, total leucocyte count of 7600/mm3 and erythrocyte sedimentation rate of 56 mm/h. Mantoux tuberculin skin test was positive. Human immunodeficiency virus test by enzyme-linked immunosorbent assay was negative. Antinuclear antibody test by indirect immunofluorescence assay was also negative. Chest radiograph was normal. Magnetic resonance imaging (MRI) of spine showed multisegmental diffuse T2 hyperintensity noted in cervical cord (C4–C7 segment) and dorsolumbar cord (D10–L1 segment) with subtle cord swelling and post-contrast enhancement [Figure 1], [Figure 2], [Figure 3]. MRI brain was normal. Cerebrospinal fluid (CSF) examination showed total cell count of 30–40 cells/mm3 (80% mononuclear), with a sugar concentration of 42 mg/dl (corresponding plasma sugar - 116 mg/dl) and protein concentration of 1800 mg/dl. CSF Gram's stain, Ziehl-Neelsen and India Ink stain were negative. CSF mycobacterial culture did not show any growth. CSF oligoclonal bands and neuromyelitis optica (NMO) IgG antibody were negative. Serum myelin oligodendrocyte glycoprotein antibody was also negative. CSF for viral and autoimmune panel was negative. Mycobacterium tuberculosis was detected in CSF using polymerase chain reaction. The patient was started on anti-tubercular therapy (ATT) with steroids. ATT was initiated consisting of rifampicin 600 mg, isoniazid 300 mg, ethambutol 1000 mg and pyrazinamide 1500 mg daily. Corticosteroids were initially given as intravenous pulse therapy of methylprednisolone 1 g daily for 5 days followed by oral prednisolone (60 mg once daily). Motor strength improved to MRC Grade 4 (+) power at hip and 4 (−) at ankle at the time of discharge after 4 weeks of therapy.
Figure 1: Magnetic resonance imaging of spine showing diffuse T2 hyperintensity in cervical cord (C4–C7 segment) and dorsolumbar cord (D10–L1 segment)

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Figure 2: Magnetic resonance imaging of cervical spine T2 axial section showing central cord hyperintensity

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Figure 3: Magnetic resonance imaging of dorsolumbar spine showing post-gadolinium contrast enhancement

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Spinal tuberculosis commonly presents with vertebral body involvement or intraspinal granulomas. It rarely presents as transverse myelitis. It is proposed to be secondary to abnormal activation of immune system against the spinal cord.[1]

Longitudinally extensive transverse myelitis (LETM) extends over three or more vertebral segments in length. Tuberculous myelitis presenting as LETM is rare. The most frequent cause of LETM is NMO.[2] LETM can also occur in other autoimmune and inflammatory diseases involving the central nervous system, such as multiple sclerosis, systemic lupus erythematosus (SLE), or Sjögren syndrome, or in infectious diseases like HIV infection.[3] Jain et al. evaluated 64 patients of LETM. They found NMO as the most common cause of LETM, followed by multiple sclerosis, acute disseminated encephalomyelitis, post-infectious, subacute combined degeneration of spinal cord, tuberculous myelitis and SLE.[4] We ruled out other causes by appropriate investigations. In conclusion, tuberculosis should be kept in mind as a possible aetiology for LETM for prompt diagnosis and treatment.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Putruele A, Legarreta C, Limongi L, Rossi S. Tuberculous transverse myelitis: Case report and review of the literature. Clin Pulm Med 2005;12:46-52.  Back to cited text no. 1
Kitley JL, Leite MI, George JS, Palace JA. The differential diagnosis of longitudinally extensive transverse myelitis. Mult Scler 2012;18:271-85.  Back to cited text no. 2
Feng YQ, Guo N, Huang F, Chen X, Sun QS, Liu JX. Anti-tuberculosis treatment for Devic's neuromyelitis optica. J Clin Neurosci 2010;17:1372-7.  Back to cited text no. 3
Jain RS, Kumar S, Mathur T, Tejwani S. Longitudinally extensive transverse myelitis: A retrospective analysis of sixty-four patients at tertiary care center of North-West India. Clin Neurol Neurosurg 2016;148:5-12.  Back to cited text no. 4

Correspondence Address:
Abhishek Juneja,
A-15, Old Quarters, Ramesh Nagar, New Delhi - 110 015
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/HMJ.HMJ_33_20


  [Figure 1], [Figure 2], [Figure 3]


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