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Endgames Case Review

An intramedullary mass

BMJ 2021; 374 doi: (Published 01 September 2021) Cite this as: BMJ 2021;374:n1948
  1. Jun-Song Yang, consultant1,
  2. Lei Chu, attending doctor2,
  3. Liang Yan, chief physician1,
  4. Ding-Jun Hao, chief physician,, professor1
  1. 1Department of spinal surgery, Honghui Hospital, Xi’an Jiaotong University, Xi’an, China
  2. 2Department of Orthopaedics, the Second Affiliated Hospital Chongqing Medical University, Chongqing, China
  1. Correspondence to D-J Hao dingjun.hao{at}

A man in his 30s presented with one month of progressive bilateral numbness and paralysis in the lower extremities. He had a history of pulmonary tuberculosis two years earlier, which resolved after treatment with isoniazid, rifampicin, and ethambutol. Physical examination showed hypoesthesia below the level of T10; grade I strength in the bilateral iliopsoas, quadriceps femoris, and tibialis anterior muscles; and bilateral lower extremity hyperreflexia. Gadolinium enhanced magnetic resonance imaging (MRI) detected a mass in the thoracic canal (fig 1).

Fig 1
Fig 1

Gadolinium enhanced MRI of the thoracic spine (sagittal plane) showing a “target” sign—a ring enhancing intramedullary lesion with a clear border measuring 0.8 cm×3.0 cm×0.8 cm (red arrows) and central hypointensity (black arrow)


  • 1. What is the most likely diagnosis?

  • 2. How is the diagnosis confirmed?

  • 3. What is the management for this condition?


1. What is the most likely diagnosis?

Intramedullary tuberculoma: a form of intraspinal tuberculosis1 in which only the spinal cord is compromised, without vertebral narrowing, disc space collapse, or extraspinal abscess.

It mainly occurs in the thoracic spinal cord via blood dissemination of active tuberculosis foci, or by cerebrospinal fluid dissemination.234

MRI shows dynamic evolution (homogenous enhancement in the early stage and ring enhancement in the late stage). When caseous necrosis appears in the lesion centre, the characteristic “target sign” of intramedullary tuberculomas may be seen (and can help distinguish it from other intramedullary lesions).

Intramedullary lesions can cause varying degrees of spinal cord compression and neurological deficit. Subacute spinal cord compression from intramedullary tuberculoma has been shown to have a mean duration of 2.3 months, and causes progressive lower limb weakness in up to 94% of untreated patients.4

Tumours, vascular diseases, granulomatous diseases, and demyelinating diseases are the main differential diagnoses.

2. How is the diagnosis confirmed?

Rapid nucleic acid testing for Mycobacterium tuberculosis complex, acid-fast bacilli staining smear, and mycobacterial culture of cerebrospinal fluid (CSF).

If surgery is required (for example, for deteriorating neurological dysfunction), histopathology samples taken during surgery can enable a definitive diagnosis.

3. What is the management for this condition?

No consensus exists on treatment. Evidence from some case reports suggests that conventional anti-tuberculosis therapy can enable complete recovery.25 However, other reports show that early surgical decompression is more effective in patients with spinal cord compression, worsening neurological function, or lesion enlargement despite standard drug treatment.6789

Learning point

Consider intraspinal tuberculosis in patients with a history of tuberculosis infection and neurological symptoms.

Patient outcome

Despite treatment with isoniazid, rifampicin, and ethambutol for 10 days, strength in the patient’s left lower limb decreased to 0, and he developed urinary retention. CSF tests were not performed because of the reduced strength and urinary retention.

Urgent decompression surgery was performed. The intramedullary lesion was identified and totally excised via intraspinal exploration, and the diagnosis was confirmed by histopathology.

At 3 month follow-up, the muscle strength in the bilateral lower limbs recovered to 3/5, and the urinary retention was improved. Within two years, the patient was able to walk independently, and his sensory impairment and urinary dysfunction were completely resolved. He had no recurrence of symptoms.