About 4 months back, a 25-year-old young man had high-grade fever, headache and vomiting for 5 days and later developed altered sensorium. He was admitted in the intensive care unit of a nearby hospital for 10 days. Investigations revealed a positive dengue NS1 antigen test. He was treated symptomatically and over the next 15 days, the sensorium gradually improved. During the recovery phase, the patient was found to have dysarthria and reduced speech output. Two months following encephalitis, he developed slowness while walking and a feeling of stiffness in both lower limbs. He required one-person support to walk and had toe walking with bent knees. In addition, he developed snapping of fingers of left-hand which was repetitive, purposeless and non-goal directed. It was present for most of the day and was partially suppressible. There was no feeling of discomfort or urge to perform these movements on voluntary suppression. It was sometimes associated with tremulousness of left index finger. The patient was aware of the symptoms but could not control them completely. These movements would subside during sleep. There was no progression in the severity of these snapping movements till the time he presented to us. He was born to a non-consanguineous parentage with normal birth and developmental history. There was no history of neurological illness, movement disorders (dystonia/parkinsonism) or psychiatric illness in the family. There was no history of psychiatric illness in the past and he was never treated with dopamine blockers or other medications. There was no history of alcohol or substance abuse. Our patient hails from north Karnataka state in the southern part of India which is endemic for dengue. He was working in a grocery shop and there was no history of exposure to alcohol or chemicals/solvents. On examination, the patient was conscious, alert and responsive to commands. His vital parameters were within normal limits. On neurological examination, he had mild up-gaze restriction along with jerky pursuits and normal saccades. He also had reduced facial expression. His speech was severely hypophonic with palilalia. Examination of other cranial nerves was normal. Paratonia was observed in both the upper limbs and spasticity in lower limbs. There was a mild head flexion to left with dystonic posturing of right hand. Hand grip of both sides were normal. Lower limb movements were restricted due to spasticity; however, he was able to lift against gravity. All deep tendon reflexes were brisk with bilateral extensor plantar responses. Sensory examination was normal. He had repetitive, coordinated and patterned snapping movements involving the left thumb and middle finger which were partially suppressible. In addition, there was slow and coarse tremor of the left index finger (). Generalized bradykinesia was present along with micrographia. He had a stooped posture with knees flexed, severe freezing of gait and needed one-person support to walk, (). Other systemic examinations were unremarkable. His routine blood investigations- complete hemogram, liver and kidney function tests were normal. Serum IgM antibodies against dengue virus were detected. Antibodies against chickungunya and Japanese encephalitis infections were negative. Screening for HIV, Hepatitis B, hepatitis C and valuations for autoimmune encephalitis were negative. Serum copper/ceruloplasmin were within normal limits. CSF was acellular and normal protein and glucose. Ultrasound abdomen was normal. Brain MRI showed atrophy with bilateral basal ganglia T2/FLAIR hyperintensities without any contrast enhancement (). He was treated symptomatically with combination of levodopa-carbidopa (400 mg/day), baclofen (30 mg/day), pramipexole (0.75 mg/day), amantadine (100 mg/day), tolperisone (50 mg/day) and diazepam (6 mg/day). In addition, the patient also underwent physiotherapy, neurorehabilitation and speech therapy. There was minimal improvement in parkinsonism symptoms with no improvement in stereotypy.