"I Can Be Anything I Want" – A Rare Case of Tuberculous Arachnoiditis Mimicking as Peripheral Sensory Neuropathy

Abstract INTRODUCTION: Central nervous system (CNS) tuberculosis represents approximately 10% of extra pulmonary tuberculosis. Tuberculous arachnoiditis is a rare complication of CNS tuberculosis that can result in debilitating peripheral neurological deficits and varying atypical symptoms presenting a challenging diagnosis. We present a case of Tuberculous Arachnoiditis without prior history of pulmonary or CNS TB symptoms. CASE DESCRIPTION: A 60-year-old male with Type 2 Diabetes Mellitus presented with bilateral lower limb weakness and inability to stand for 10 days, impacting daily activities. Examination showed hypotonia, 1/5 motor power in proximal muscles, 3/5 in distal muscles, knee hyporeflexia, and absent ankle reflexes. Sensory testing indicated absent touch sensation in the soles. There was no history of slipping footwear or bowel/bladder involvement, leading to a diagnosis of sensory motor polyneuropathy. CSF analysis revealed 70 WBC/uL, glucose 25 mg%, proteins 90 mg%, and 70% lymphocyte predominance, indicating CNS tuberculosis. TB diagnosis was confirmed by CSF Nucleic Acid Amplification Test. Chest X-ray was normal, and MRI showed spinal arachnoiditis and nerve root enhancement. Nerve conduction studies confirmed axonal sensory neuropathy, diagnosing TB Arachnoiditis. The patient received the RIPE antitubercular regimen, IV steroids, and insulin for hyperglycemia. He progressively improved, regaining motor strength and eventually walking independently. RIPE regimen to be continued for 12 months until full recovery. DISCUSSION: Tuberculous arachnoiditis typically arises from a primary TB lesion in the spine, downward spread from the meninges or secondary lesions from adjacent vertebrae. Our case presents an atypical instance without any identifiable primary TB focus. If untreated or misdiagnosed, spinal tuberculous arachnoiditis can lead to permanent neurological deficits. Therefore, it is crucial to consider this condition even in the absence of pulmonary or extrapulmonary TB to ensure timely diagnosis and prevent debilitating complications. Our case highlights the importance of considering tuberculous arachnoiditis even without identifiable primary tuberculosis lesions especially in TB Endemic regions.The atypical presentation in our patient underscores the need for a thorough evaluation of neurological deficits. Early diagnosis and prompt treatment with the RIPE regimen resulted in significant recovery. This case reinforces the risks of untreated spinal tuberculous arachnoiditis, emphasizing the need for awareness among healthcare providers regarding this condition in patients with unexplained neurological symptoms.