DOUBLE JEOPARDY: UNTANGLING DEPRESSION, PARKINSON'S DISEASE & FRONTOTEMPORAL DEMENTIA IN CLINICAL PRACTICE WITH BEDSIDE COGNITIVE TESTING

Introduction Progressive supranuclear palsy is a taupathy disorder often mistaken on diagnosis by other neurocognitive disorders such as Parkinson's (PD) and Alzheimer's (AD) disease amongst other. PSP tends to be diagnosed in the later course of the disease and by time of diagnosis, individuals have a median survival of 7?years. PSP is a disease in which a diagnosis and treatment is done in a multidisiplinary approach involving collaboration of Psychiatry and Neurology. As it was seen in this clinical case which describes a patient with undetected progressive supranuclear palsy who were referred to a university hospital psychiatric emergency services facility for treatment of late onset symptoms and signs attributed to primary psychopathology related to behavioral variant of frontotemporal lobar degeneration (FTLDbv). Methods The patient described in the clinical vignette underwent a comprehensive neuropsychiatric assessment, given that the accuracy of the diagnosis of FTLDbv was in doubt. The clinical interview identified no significant prior developmental, medical, neurological, psychiatric, or substance use disorders; no family history of neuropsychiatric disturbance; and no significant psychosocial stressor before the onset of his neuropsychiatric condition at age 59. Bedside cognitive testing showed a Geriatric Depression Scale (GDS) score suggestive of mild symptoms of depression, and would be unlikely to explain his new onset psychosis. His subclinical Executive Interview 25 (EXIT 25) score and normal Mini Mental State Examination (MMSE) were not indicative of a dementia syndrome. Given the strong temporal relationship between the onset of his behavioral changes and perceptual disturbances and the start of levodopa/carbidopa, this medication was discontinued. He was admitted to the inpatient psychiatric service for observation. He was started initially on an atypical antipsychotic, but had this medication discontinued, as he no longer exhibited symptoms of psychosis. His citalopram was titrated to 40mg daily to optimize treatment of his major depressive disorder. Patient was discharge with complete resolution of psychotic symptoms and with diagnosis of Depressive disorder, unspecified and medication-induced psychotic disorder with delusions and hallucinations. A dopamine transporter (DaT) protein scan, a marker for presynaptic terminals in dopaminergic nigrostriatal neuros (marker for PD) and or iodine-123-metaiodobenzylguanadine (MIBG) myocardial scintigraphy (marker for DLB), was not performed. Results CASE REPORT: A 59-year-old, left handed, previously healthy gentleman was brought by police to a university hospital psychiatry emergency services for evaluation of acute safety concerns, regarding behavioral and personality changes. Patient was admitted to the hospital displaying motor symptoms with appearance of jaw tremor, ataxia, and urinary incontinence. After a negative brain MRI and head CT scan, the neurology team concluded that he had Parkinson`s disease and patient was discharged on levodopa/carbidopa (25?mg/?100 mg) QID and citalopram 20?mg daily for associated depressive symptoms with no benefit. After discharge from the hospital, he had become increasingly impulsive, hypersexual and engaging in risky behaviors with firearms. Persistent and progressive change in personality and behavior were the earliest displayed signs and they remained the most prominent features of his condition. All of these disturbances worsened after patient was started on levodopa/carbidopa. After evaluation by the psychiatry consultation and liaison service, a Mental status examination revealed cognitive and neurovegetative symptoms of depression as well as auditory illusions and concerns that a stranger had invaded his home. He denied manic symptoms. No suicidal and homicidal thoughts. Despite extensive neurological and neuropsychological evaluation 10-months later, surprisingly, it was established the diagnosis of progressive supranuclear palsy (PSP), as at that visit the patient presented with predominantly delay axial Parkinsonism, supranuclear gaze palsy, and increased falls due to postural instability. A neuropsychological assessment provided evidence of an executive syndrome of subcortical frontal type. Conclusions Progressive supranuclear palsy is a debilitating taupathy disorder that often is mistaken on diagnosis by other neurocognitive disorders such as Parkinson's dementia, Alzheimer's dementia and Frontotemporal lobar degeneration amongst others. Thus, making PSP diagnosis difficult at initial presentation and often presenting later in life. PSP diagnosis requires a multidisciplinary approach, a collaboration between Psychiatry and Neurology to piece together the complex problems that often manifest in challenging neuropsychiatric syndromes. The possibility of PSP should be considered in the differential diagnosis of late onset psychiatric syndromes. Early PSP diagnosis is imperative for both patients and physicians, as proper treatment will be started without delay to address PSP symptomatology. Thus, reducing the burden of patient and family, as well as reducing unnecessary diagnostic tests, hospitalizations and sub-optimal psychiatric treatment. It is imperative that providers from all specialties be aware of PSP early presentation and how it can be mistaken, specially in early stages, with other neurocognitive disorders in order to make proper referrals for the most effective treatment available. This research was funded by: N/A