A 50-year-old female presented with history of progressive quadriparesis and stiffness of neck for 2 years, dysphagia to liquid for past 3 months. She had visited several doctors without any relief for the said complaints. Magnetic resonance imaging (MRI) of cervical spine was done one year back. On the basis of clinical history and supportive MRI finding, she was previously diagnosed as a case of high cervical compressive myelopathy with cord changes due to thickening of ligamentum flavum and posterior longichudinal ligament extending from foramen magnum up to C4 vertebral level. Corticosteroid was prescribed by her previous physician. Following which her condition deteriorated rapidly.Her neck became so stiff that she was unable to move it, numbness extended to all over her body; she developed dysphagia to liquid and became bed ridden. Physical examination revealed high cervical compressive myelo-radiculopathy with lower cranial nerve palsy and rigid neck. Recent contrast MRI was suggestive of circumferentially, grossly thickened, enhancing dura extending from caudal aspect of posterior fossa up to C7 level with variable compression of cord and emerging nerve roots [Figures 1-4]. Radiological features were in favor of hypertrophic pachymeningitis (HPM). An extensive search was carried out to find out the cause of HPM. Her vital signs and other laboratory data were normal except low hemoglobin level (Hb and Hct, 9 g/dL and 32%, respectively), elevated erythrocyte sedimentation rate (ESR) (patient: 110 mm/h, normal: <25 mm/h) and positive tuberculin skin test. Serologic tests for tuberculous antibody were Immunoglobulin M (IgM) positive indicating persisting infection. The serum was negative for rheumatoid factor, antinuclear antibodies, Venereal disease research laboratory (VDRL) test, hepatitis B surface antigen (HBsAg), and antidouble-stranded DNA. Work up for sarcoidosis such as chest radiograph, serum calcium, and angiotensin converting enzyme were negative. Bone marrow examination and ultrasound scan of the abdomen, to exclude a neoplastic and chronic inflammatory process, were normal. CSF analysis after lumbar puncture revealed 80 lymphocytes/mm3, protein of 90 mg/dl, and sugar of 35 mg/dl. Microbiological evaluation of the CSF for cryptococcal antigen, VDRL, and cultures for acid fast bacilli (AFB) and fungi yielded no positive results. An increase in the adenosine deaminase level in CSF was observed. On basis of radiological, serum analysis, and CSF study, a diagnosis of tuberculous HPM was made. Screening for systemic source of tuberculosis was negative. She was discharged on antituberculosis therapy with regular follow up. At the 3-month follow-up, the patient was able to walk with a cane, neck rigidity vanished, dysphagia and limb spasticity improved. Antitubercular treatment continued for 15 months. At present, she can walk independently with some spasticity.