Cerebral toxoplasmosis is a frequent opportunistic infection in patients with HIV. Due to Toxoplasma Gondii’s predilection for basal ganglia structures, movement disorders are a well-recognized complication of cerebral toxoplasmosis.1 We report a case of a 59-year-old female with a background of HIV presenting with complex involuntary movements with markedly different phenomenology on the right and left side of her body. She was diagnosed with cerebral toxoplasmosis 18 months prior, after the onset of the movement disorder and completed antimicrobial treatment with marginal improvement in symptoms. On examination, there was cogwheel rigidity in her right upper limb with accompanying rest tremor and bradykinesia. In contrast, there were prominent hyperkinetic movements of the left side of her body with dystonic posturing of the left upper and lower limb and choreiform movements. Arm swing was reduced on the right (with rest tremor) with dystonic posturing on the left and some subtle patterned movements of left foot while walking (Video). Magnetic resonance imaging of the brain was performed with contrast and it demonstrated multiple ring-enhancing lesions in the right thalamus, left lentiform nucleus, right frontal lobe, and right posterior-temporal lobe (Figure 1). Cerebrospinal fluid (CSF) test result was normal and HIV-1 and -2 were not detected in CSF. HIV viral load was undetectable and CD4 count was 174. Toxoplasma DNA was not detected in serum or CSF. A computerized tomography brain scan was compared with imaging 18 months prior and all lesions were more calcified and felt to be compatible with chronic toxoplasmosis (Figure 2). The left lentiform lesion was felt to be causative for the right-sided hemiparkinsonism, while the right thalamic lesion was felt to be the culprit of the left-sided hemidystonia. A brief trial of risperidone (0.5 mg daily) was not tolerated due to flattened mood and orobuccal dyskinesia and the patient did not wish to pursue further treatment.