Bilateral putamen necrosis in a case of dyskinetic movements and schizophrenia – A case report

Schizophrenia is a chronic psychiatric disorder with heterogeneous genetic and neurobiological basis.[1] Structural brain changes in subcortical regions, including the hippocampus, thalamus and basal ganglia, are common, with the putamen drawing particular attention due to its role in dopaminergic pathways.[2] This case report presents an adult male with schizophrenia and choreo-athetoid movements, where magnetic resonance imaging (MRI) revealed bilateral putaminal necrosis. A 31-year-old unmarried male, unemployed, with no significant past medical and family history, presented with 1-year history of involuntary movements of both shoulders, approximately 3-months later by auditory hallucinations, ambitendency, posturing, sleep disturbances, and impaired self-care. He occasionally consumes about 500 ml of country-made liquor. Mental status examination (MSE) revealed a guarded attitude, increased psychomotor activity—choreo-athetoid movements involving B/L shoulders (right >left), irritable affect, below average intelligence, and impaired judgement and insight of 1/5. Routine investigations including complete blood picture, liver/renal function tests, electrolytes, and electro cardiography were normal. Patient assessed using the abnormal involuntary movements scale (AIMS: 12), Bush Franci’s catatonia rating scale (BFCRS: 0), Positive and negative syndrome scale (PAN-SS: 88) and diagnosed with Schizophrenia (according to ICD-11). He was started on olanzapine (optimized to 20 mg) to avoid extrapyramidal symptoms from typical antipsychotics, given his involuntary movements. MRI brain was done to exclude any organic causes underlying the patient’s involuntary movements, which revealed symmetric CSF intense lesions in bilateral putamen measuring 1.4 × 0.4 cm—suggestive of necrosis [Figures 1a and b]. Neurology and radiology opinion was sought and differential diagnoses of carbon monoxide/methanol poisoning, Wilsons disease and neuroferritinopathy was considered. Kayser–Fleischer ring examination, serum copper and iron studies were normal, ruling out Wilson’s disease and neuroferritinopathy. Genetic testing for other familial causes was advised but could not be pursued due to financial constraints. He was discharged on the same dose of olanzapine (AIMS: 12, PANSS: 79) with improvement in auditory hallucinations, though involuntary movements persisted at follow-up.Figure 1: (a)MRI-T2 weighted image showing hyper intensity lesions in bilateral putamen, (b) MRI-FLAIR image showing hypo intensity lesions in bilateral putamenThis paper presents a rare case of an adult male diagnosed with schizophrenia with choreo-athetoid movements, who was found to have bilateral putaminal necrosis on MRI. The temporal relationship between psychotic symptoms and radiological findings remains unclear: it is uncertain whether the putaminal necrosis contributed to psychosis or whether schizophrenia led to basal ganglia changes. Bilateral Putamen necrosis in schizophrenia suggests a possible link to dopaminergic dysregulation or antipsychotic exposure.[3] However, necrosis of the putamen is associated with conditions such as carbon monoxide poisoning, methanol toxicity, hypoxic-ischemic encephalopathy, and mitochondrial disorders.[4] The absence of identifiable causes and neurological deficits raises the possibility of incidental necrosis or basal ganglia abnormality in psychiatric populations. Similar study described an adult with new-onset psychosis associated with a lacunar infarct in the left putamen, suggesting that psychotic symptoms may result directly from the infarct, linking basal ganglia lesions to psychotic symptoms.[5] A voxel-based morphometric study have linked putaminal and thalamic volume reductions to delusional symptoms.[6] Longitudinal studies also suggest that greater putaminal shrinkage correlates with poorer outcomes.[7] However, involuntary movements are intrinsic to schizophrenia and are present even in antipsychotic-naive patients, suggesting basal ganglia abnormality as a core aspect of the disease. Motor abnormalities reflect cortical-subcortical network disruption, rather than solely a side effect of antipsychotics. Antipsychotic medications can reduce mild involuntary movements early in treatment by balancing dopamine activity, but with long-term use, especially first-generation drugs, can worsen these movements in people who are already vulnerable.[8] A key limitation is the unclear temporal relationship between psychiatric symptoms and radiological findings. Further investigations, including metabolic panels, genetic testing, and advanced imaging like MR spectroscopy or diffusion studies, could provide insights into the underlying pathology. This case adds to the limited literature on basal ganglia abnormalities in schizophrenia and highlights the need for thorough evaluation when neuroimaging shows atypical findings. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.