A 45-year-old woman presented to the Medicine Emergency Room with new onset Generalized Tonic Clonic convulsions, tongue bite, and urinary incontinence for 48 hours before admission. The patient had been diagnosed as a case of Parkinson's syndrome two years back and put on anti-Parkinsonian therapy on the basis of clinical suspicion. Thereafter, her Parkinsonian features had improved. She had a medical history of “Goiter” for which she had undergone total thyroidectomy 10 years back. She had been put on calcium supplements and levothyroxine therapy since her surgery, but she had been irregular with her treatment, with no follow-ups for last one and a half years. No family history of similar illness was present. The patient's parents were alive and healthy with no significant medical problems. After initial stabilization of the patient with anticonvulsant therapy, the patient was evaluated better. There was painful spasm of hand on inflating sphygmomanometer cuff above systolic blood pressure (i.e., Trousseau's sign was positive). Chvostek sign was also positive. Intention tremors were present. Examination of neck revealed a scar of past thyroid surgery. The patient had cerebellar signs in the form of truncal ataxia, dysdiadochokinesia, dyssynergia, and past pointing. Tandem walking was impaired. Limbs were hypotonic with diminished tendon reflexes. Investigations revealed: Hemoglobin-11.5 gm%, Total Leukocyte count-10,500/cu.mm (N64, L26, M05, E04, B01), Na-134.5 mEq/L, K-3.54 mEq/L, Fasting blood sugar-92 mg/dL, Urea-24 mg/dL, Creatinine-0.9 mg/dL, serum calcium-6.1 mg/dL, serum albumin-4.1 mg/dL. Serum LDH, Liver function tests, Magnesium, Chest X-ray, and abdominal USG revealed no abnormalities. Serum parathormone levels were inappropriately low for the level of hypocalcemia. ECG revealed a prolonged QT interval (QTc-0.58 s). Brain CT revealed extensive intracranial calcifications. Dense calcium deposits were observed in the paraventricular, cerebellar, and basal ganglia regions. The patient was treated with intravenous (IV) calcium gluconate therapy and shifted to oral calcium and calcitriol therapy. Her symptoms improved markedly. By day 7 of hospital admission, the patient could walk back home. At four months of follow up, the patient had not suffered another episode of seizure and was being gradually weaned off anti-Parkinsonian therapy. Her serum calcium levels were well within normal limits at that time.