Neuropsychiatric‐Led Presentation of Late‐Onset Parkin‐Related Parkinson's Disease

Abstract

Mutations in the Parkin (PRKN) gene represent the most common cause of autosomal-recessive early-onset Parkinson ’ s Disease (PD). 1 Typical age of onset is under 50 with a slowly progressive, 2 symmetric, levodopa-responsive parkinsonism. 1,3 Cognitive function is typically preserved; 4 neuropsychiatric symptoms manifest as depression and anxiety are described in up to two-thirds of patients, 1 usually occurring as a complication of disease progression with additional motor features often limited to hyperre fl exia and early dystonia. 1,3 PRKN-PD represents a distinct clinicopathologic entity from classical idiopathic-PD, where dopaminergic neuronal loss occurs in the absence of Lewy body pathology. 5 A 62-year-old man presented with profound anxiety, somatic preoccupation and social withdrawal ultimately requiring hospital admission for management of agitated depression with electro-convulsive therapy and pharmacologic management with Olanzapine 5 mg BD. An asymmetric, levodopa-responsive par-kinsonism emerged aged 66. Cognitive testing (aged 66) revealed mild frontal-dysexecutive and visuospatial de fi cits (MoCA 25/30). REM-sleep-behavior disorder, although an infrequent occurrence while on a selective-serotonin-reuptake-inhibitor later in the disease course, was absent at presentation. There were no visual hallucinations or cognitive fl uctuations. Low-dose titrations of levodopa provoked dyskinesia and coincided with neuropsychiatric