A 50-year-old lady with long-standing hypertension and type 2 diabetes presented to us with a 13-day history of high-grade fever, followed by a recent onset of confusion and drowsiness. The lack of headache, vomiting, or visual symptoms veered us away from meningitis. On admission, she was febrile and sluggish, but oriented, with neck stiffness and other meningeal signs. Investigations revealed hyponatremia, hypokalemia, and hyperglycemia along with a raised C-reactive protein. Cerebrospinal fluid analysis showed lymphocytic predominance (210 cells/mm³), protein 277.2 mg/dL, glucose 54 mg/dL, ADA 17.33 U/L, and LDH 91 U/L, all of which point towards TBM.

MRI of the brain showed diffuse leptomeningeal enhancement and multifocal supra- and infratentorial lesions with evolving obstructive hydrocephalus. We began weight-adjusted antitubercular therapy, corticosteroids, and pyridoxine. Her neurological condition deteriorated over the ensuing few days, and repeat imaging showed multifocal infarcts. We also placed a right ventriculoperitoneal shunt to relieve increased CSF pressure. It resulted in a gradual neurological recovery and she recovered clinically without any residual deficits.

This case highlights unpredictable course of TBM in patients with metabolic illness. A delay in diagnosis occurred due to absence of typical symptoms and rapid progression Prompt awareness, aggressive metabolic correction, and early surgical intervention resulted in recovery. Such presentations expand the spectrum of TBM's clinical picture and reiterate the fact that the infection may mimic a metabolic disturbance until the terminal stages in diabetic patients.