Psychotic depression as initial presentation of Parkinson’s disease: an interdisciplinary case report

Introduction

Affective and psychotic symptoms emerging in later life are increasingly recognised as potential prodromal features of Parkinson’s disease (PD), frequently preceding the onset of cardinal motor symptoms by several years. This temporal dissociation poses a diagnostic challenge in psychiatric settings, particularly when patients are exposed to dopamine receptor-blocking agents, which may induce or unmask parkinsonian features. Distinguishing drug-induced parkinsonism (DIP) from early neurodegenerative parkinsonism is therefore essential, given its implications for treatment selection, prognosis, and functional outcomes. From a neurobiological perspective, early dopaminergic dysfunction within nigrostriatal pathways may underlie both psychiatric and motor manifestations.

Objectives

To describe a case in which Parkinson’s disease was identified during psychiatric follow-up for a severe depressive episode with psychotic features, and to illustrate the clinical reasoning required to differentiate drug-induced parkinsonism from underlying neurodegeneration.

Methods

We report a longitudinal case analysis based on repeated psychiatric and neurological assessments over a 12-month period. Clinical evaluation included detailed psychopathological examination, serial neurological assessments, and systematic review of pharmacological treatments. Diagnostic reasoning focused on the temporal relationship between symptom onset and antipsychotic exposure, progression of motor and non-motor features, and response to therapeutic modifications. Brain magnetic resonance imaging was performed to exclude structural causes. The study was conducted in accordance with local ethical standards, with informed consent obtained from the patient.

Results

A 63-year-old woman with no prior neurological history was admitted for a severe major depressive episode with psychotic features, including nihilistic delusions and marked psychomotor retardation. At discharge, she was prescribed olanzapine, aripiprazole, and sertraline. Within three months, she developed progressive parkinsonian symptoms, initially suggestive of DIP. However, despite gradual withdrawal of antipsychotic medication and optimisation of antidepressant therapy, symptoms persisted and worsened. Clinical features included resting distal tremor, dysarthria, urinary incontinence, cogwheel rigidity, bradykinesia, hypomimia, hypophonia with bitonal quality, and magnetic gait. Neurological examination revealed asymmetric bradykinesia, axial rigidity, reduced arm swing, hypometric saccades, and postural instability. Brain imaging demonstrated mild, nonspecific white matter hyperintensities without focal lesions. The persistence, asymmetry, and progression of symptoms beyond pharmacological withdrawal supported a diagnosis of probable PD. Treatment with levodopa/carbidopa resulted in marked clinical improvement, including reduction in tremor and rigidity, improved gait and mobility, and partial amelioration of bradyphrenia, with significant recovery of functional capacity.

Conclusions

This case supports the hypothesis that late-onset affective and psychotic syndromes may represent early manifestations of Parkinson’s disease rather than independent psychiatric conditions. In patients exposed to dopamine receptor-blocking agents, persistence or progression of parkinsonian features after drug discontinuation should prompt consideration of underlying neurodegeneration. Although DIP remains a common differential diagnosis, clinical features such as asymmetry, non-motor involvement, and sustained response to dopaminergic therapy may aid diagnostic clarification. Early recognition of PD within psychiatric settings is crucial to optimise management and improve outcomes. However, conclusions are limited by the single-case design, highlighting the need for prospective studies investigating the neurobiological substrates of prodromal psychiatric presentations of PD.

References

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