Intradural spinal tuberculosis in the absence of vertebral or meningeal tuberculosis: a case report

Journal of Orthopaedic Surgery, Apr 2006 by Harsha, C K Sree, Shetty, A P, Rajasekaran, S

ABSTRACT

We present a patient with spinal intradural tuberculosis in the absence of both vertebral and meningeal tuberculosis. Diagnosis was made based on intra-operative findings and was confirmed by histopathology. Early surgical decompression along with a combination of steroid and antitubercular therapy resulted in a good outcome. At 26-month follow-up, the patient regained bladder control and was able to walk with support. Clinical features, magnetic resonance imaging, and intra-operative findings are described. Pathology and the relevant literature are discussed.

Key words: arachnoiditis; spindl cord diseases; tuberculosis, spinal

INTRODUCTION

Spinal tuberculosis is the most common form of skeletal tuberculosis and accounts for almost 50% of all patients with skeletal tuberculosis.1 Central nervous system tuberculosis, in the form of tuberculomas, accounts for 10% of all extrapulmonary tuberculosis.2 Tuberculomas are one of the most common intracranial space-occupying lesions in the developing world. Asymptomatic spinal arachnoiditis has been reported in 18% of patients with tuberculous meningitis (TBM).3 However, tuberculosis of the spinal cord in the absence of vertebral tuberculosis or TBM is uncommon. This atypical presentation may lead to misdiagnosis of intradural tumour.4 We report a case of intradural tuberculosis in a 25-year-old woman presented with paraparesis.

CASE REPORT

In June 2002, a 25-year-old woman presented to Ganga Hospital, India with a one-month history of progressive weakness in the lower limbs. One week before the onset of weakness, she fell from the bed and developed back pain that was relieved with analgesics. She had had a Caesarian delivery 6 months previously, and had developed severe headache and rapidly progressing weakness in all 4 limbs 6 weeks after delivery. She was diagnosed with postpartum cerebral venous thrombosis, and was treated with anticoagulants. She gradually recovered the power in the lower limbs and was able to walk independently, but persistent weakness in the upper right limb remained.

At presentation, she had dysarthria and was unable to stand without support. She developed urinary incontinence 2 days earlier. There was no deformity or tenderness over the spine. Neurological examination revealed grade 5/5 power in the upper left limb, grade 3/5 power in the proximal muscles, and grade 0/5 power in the intrinsics of the upper right limb. She had grade 4/5 power in the lower left limb and grade 2-3/5 in the lower right limb. Her sensations decreased from L2. Reflexes were absent, and plantar response was extensor. Laboratory examination revealed a normal coagulation profile with international normalised ratio of 1.1, albuminglobulin ratio of 1:2, and erythrocyte sedimentation rate of 76 mm/hour.

Radiographs of the spine and chest were normal. Computed tomography of the brain revealed a communicating hydrocephalus that did not progress in comparison with the earlier scans. Magnetic resonance imaging (MRI) of the spine revealed an intradural mass at L2 to L4 levels. On T1-weighted images, the mass was hypointense with cerebrospinal fluid loculation at the T11 and T12 area associated with clumping of cauda equina nerve roots (Fig. 1). Contrast enhancement revealed multiple peripherally enhancing lesions matted together and bunching of nerve roots in axial section (Fig. 2).

Diagnosis of intradural tumour was made in the absence of definitive clinical and imaging findings. As the patient had hydrocephalus, an external ventricular drain was placed and exploration of the intradural mass was performed through L2-L3 laminectomy. On opening, a lobulated greyish white tissue was encountered within thickened dura. The mass was easily separated from the dura, but was circumferentially adherent to the underlying arachnoid and the nerve roots, requiring microscopic dissection for removal. Pockets of pus were encountered during dissection, indicating a strong possibility of tuberculosis. The mass was excised piece by piece. Histopathology of the mass revealed caseating epithelioid cell granulomas suggestive of tuberculosis (Fig. 3). Culture for tuberculous bacilli was not done because clinical and histopathological features were sufficient to institute anti-tubercular therapy. Treatment was initiated on the first postoperative day using 4 drugs (rifampicin, isoniazid, ethambutol, and pyrazinamide) along with steroids. The patient gradually recovered and was able to walk with support at postoperative day 10. Steroids were continued for one month and then tapered off. At 26-month followup, the patient regained bladder control and was able to walk with support.

DISCUSSION

Contrary to general expectations, the incidence of tuberculosis is on the rise. It is no longer a disease of underdeveloped nations, and increasing incidences are being reported trom the developed nations.5 In the presence of immunosuppression and coexisting diseases, presentation of tubercular lesions may be atypical. This may delay diagnosis and result in irreversible damage and the spread of infection in the community.6