Acute Granulomatous (Tubercular) Myelitis
Amulaya Mishra*, RS Kanwar*, B Santanu*, Ashok Kumar*, RK Dudeja*, AK Jain*, AK Agarwal*

Case Report
AQ 18 year old male patient presented with
inability to move both lower limbs and, loss of
bladder and bowel control for 2 days. There was
history of band like sensation around umbilicus
and tingling sensation in both legs preceding
weakness in lower limbs. No history of root pain.
No history of similar illness or any other significant
complaint in the past. No history of fever,
convulsion, vaccination(s), dog bite, trauma or
diminished vision. The patient was initially taken
to a local hospital where he was catheterized and
given intravenous steroids and referred to our

was reported positive. Skiagram of chest PA view
did not show any abnormality.
A contrast enhanced MRI of the thoracic spine
showed multiple areas of granulomatous
inflammation and surrounding edema affecting
the spinal cord from T3 to T11 level indicative of
granulomatous myelitis (Figures 1, 2 and 3).

General examination of the patient was
unremarkable. No enlargement of lymph nodes
was noticed. On neurological examination the
higher functions and cranial nerves were normal.
Motor system examination revealed hypotonia,
areflexia and grade 0/5 power in both the lower
limbs. Superficial reflexes were absent with plantar
reflex being nonresponsive bilaterally. Motor
examination of upper limbs was normal. There
was sensory loss of all the modalities below T7
dermatome. There was no deformity in the spine
or skull. Examination of other systems was normal.
B/L fundus nad.
Routine haemogram was within normal range. ESR
was 10 mm 1st hour. Serum electrolytes, urea,
sugar, calcium, phosphorus were normal. The
VDRL was non-reactive. CSF examination revealed
150 cell/mm 3 , out of which 60% were
lymphocytes. CSF protein was 600 mg%, chloride
170 mg% and sugar 45 mg%. CSF culture was
reported as sterile after 48 hrs of incubation. CSF
was sent for performing PCR (Polymerase-Chain
Reaction) for Mycobacteriam tuberculosis, which
* Department of Medicine
Dr. Ram Manohar Lohia Hospital
New Delhi-110001

Fig. 1 : Saggital T2 weighted image of dorsal cord : Shows patchy
hyperintensity in the cord region with loss of CSF – cord interphase.
The osseous elements are normal in signal characteristics.

On the basis of above findings he was diagnosed
as a case of acute granulomatous myelitis of
tubercular aetiology and treated accordingly.
Unfortunately response to antitubercular drugs

therapy along with corticosteroids was not clinically
evident when he was discharged after about six
weeks’ stay in the hospital.

Fig. 2 : Axial section through the dorsal region, after administration
of IV Gadodiamide, reveals expanded cord with patchy and focal
intramedullary enhancement.

an uncommon cause of paraparesis in Indian
setting1,2. Tuberculous myelitis generally occurs
when the diagnosis has been delayed and thick
exudates form with spinal blocks. Occasionally,
the infection may begin in the spinal area resulting
in backache and involvement of the spinal cord
and roots at multiple levels. In the early stages,
this may be confused with other forms of viral
myeloradiculopathies, but the evidence of elevated
CSF protein, reduction of sugar, largely
lymphocytic cellular count and presence of acid
fast bacilli should confirm the diagnosis. PCR for
Mycobacterium tuberculosis of the cerebrospinal
fluid is a very specific test in its diagnosis. The
patient should be treated with antituberculous
drugs viz rifampicin, isoniazid, pyrazinamide,
streptomycin and/or ethambutol. Use of steroids
is recommended. Gouri Devi3 has advocated the
use of intrathecal hyaluronidase, for arachnoiditis,
but double blind control studies are needed before
this treatment can be routinely advocated.
With the advent of M.R.I. identification of such
lesions have become much more easier.
Intramedullary tuberculomas are rare and may
cause focal cord enhancement and decreased or
increased signal intensity of T2 – weighted images4.
Gadolinium – DTPA – enhanced MRI is
recommended for evaluation.

The authors are grateful to Dr CP Singh, Medical
Superintendent of the hospital for permission to
report this case.


Fig. 3 : Coronal sections of the spine show expanded dorsal cord
with patchy enhancing areas suggestive of multiple granulomatous


Wadia NH, Dastur DK. Spinal meningitides with
radiculomyelopathy : Clinical and radiological features.
J Neurol Sci 1969; 8: 239-60.


Ahuja GK, Venkataraman S, Roy S et al. Tuberculous
radiculomyelopathy. Neurology (India) 1978; 26: 1359.


Gour Devi M, Satishchandra P. Hyaluronidase as an
adjuvant in the management of tuberculous spinal
arachnoiditis. J Neurol Sci 1991; 102: 105-11.


MacDonell AH, Baird RW, Bronze MS. Intramedullary
tuberculomas of the spinal cord : Case report and review.
Rev Infect Dis 1990; 12: 432-9.

Tuberculous myelitis can occur as a secondary
event in the course of common forms of
tuberculous meningitis. It is an important and not

Journal of Indian Academy of Clinical Medicine 

Vol. 5 

No. 2