Introduction: Psychosis is a prominent neuropsychiatric symptom of Parkinson’s disease (PD) and is associated with negative outcomes, such as poorer quality of life and greater rate of functional impairment. Early identification of patients with PD at risk of developing psychosis facilitates appropriate management to improve outcomes. However, this phenomenon has not been examined locally. This study aimed to examine the prevalence of PD-associated psychosis in the local setting, identify any associated risk factors, as well as characterise the cognitive trajectory of patients with PD with psychosis. Methods: A retrospective cohort of 336 patients with PD, who presented to the National Neuroscience Institute, Singapore, in 2006 and 2007 and attended follow-up visits through to 2013 was analysed. The data analysed included scores from clinician assessments of cognitive function, disease severity and presence of psychotic symptoms, conducted when clinically appropriate during patients’ medical visits. Survival analysis and logistic and linear regression analysis were performed. Results: Psychosis was diagnosed in 63 patients with PD, indicating a prevalence of 18.8% for PD-associated psychosis. Incidence of psychosis in PD was calculated to be 40 per 1,000 person-years. No significant association was found between demographic variables and the odds of developing psychosis in PD. Regression analyses found that the presence of psychosis significantly predicted greater cognitive decline and disease severity. Conclusion: Psychosis has a significant presence among the PD population in Singapore, possibly serving as an indicator of more rapid cognitive decline and progression of PD severity.

Abstract:Background:Antidepressant-induced hyponatremia/syndrome of inappropriate antidiuretic hormone (SIADH) can cause significant morbidity and mortality. Antidiuretic hormone release due to stimulation of central serotonin 5HT1C, 5HT2 and α-1 adrenergic receptors is thought to cause this adverse effect (Spigset, 1995). Evidence on which antidepressants are more likely to cause hyponatremia is inconsistent (Coupland, 2011; Leth-Moller, 2016). Owing to its uncommon use, there is limited and conflicting data on the risk of hyponatremia with Moclobemide, a reversible inhibitor of monoamine oxidase A (Mercier, 1997; Mazhar, 2019). There are few reports of hyponatremia induced by multiple antidepressant classes in the same patient.Objective:To add to the literature on risk of hyponatremia with Moclobemide and other antidepressants.Methods:We report a case of hyponatremia sequentially induced by multiple different antidepressant classes who was treated with Moclobemide with no recurrence of hyponatremia. We review existing literature on antidepressant-induced hyponatremia.Results:A 67-year-old man with a history of hypertension, dyslipidemia and gout was first diagnosed with major depressive disorder at age 50 after presenting with pervasive depressed mood, anhedonia, insomnia, poor concentration and feelings of worthlessness. Investigations found no medical causes of depression. His depression remitted on Venlafaxine 75mg/day with no hyponatremia induced. During a second depressive episode 4 years later, his serum sodium (Na) dropped from a normal baseline to 122mmol/L after Venlafaxine was restarted. He appeared euvolemic on physical examination. Investigations found no other causes of hyponatremia and were consistent with SIADH, which was attributed to Venlafaxine. His depression later remitted on Mirtazapine 30mg/day with no hyponatremia induced. During his third depressive episode at age 67, he developed hyponatremia (serum Na 123mmol/L) a week after restarting Mirtazapine. His clinical picture was consistent with SIADH. He later developed hyponatremia after initiating the following antidepressants sequentially: Fluvoxamine, Agomelatine, Nortriptyline, Bupropion. Hyponatremia resolved with fluid restriction and cessation of the implicated antidepressant each time before the next was initiated. He eventually tolerated Moclobemide 300mg/day with no recurrence of hyponatremia.Conclusions:Agomelatine, Nortriptyline and Bupropion are reported to have a low risk of hyponatremia but were implicated in this case. Venlafaxine and Mirtazapine did not cause hyponatremia when first taken but were implicated when restarted after a period of cessation, underscoring the idiosyncratic nature of antidepressant-induced hyponatremia. Moclobemide can be considered for depressed patients with recurrent antidepressant-induced hyponatremia. Serum Na should be regularly monitored in patients taking antidepressants who are at high risk of hyponatremia.

IntroductionAn eighty-one-year-old lady presented with mood changes within days of the commencement of prednisolone eye drops, which was prescribed following a cataract operation. She had a history of chronic schizophrenia, with one previous episode of hypomania in the early1990s. She was admitted to our institution on this occasion, with symptoms including elated mood, disinhibition, insomnia, pressured speech, flight of ideas and grandiose ideation. This was a distinctly different presentation from her previous relapses and the duration of this episode was prolonged. Her symptoms persisted despite an aggressive titration of psychotropic medications. After a review of her medication, the possible causal relationship between the prednisolone eye drops and manic episode was made. As the steroid eye drops were necessary following her eye operation, we allowed the completion of its course. Within days of its discontinuation, we saw a dramatIc improvement in her mental state and she was discharged. She currently remains in remission two months from the cessation of prednisolone.DiscussionThe postulation that the prednisolone eye drops triggered this manic episode can be substantiated by the clear observation that her symptoms completely resolved after the steroid course was completed. This appeared to be the one single factor which coincided with the emergence, maintenance and termination of her symptoms. Steroid-induced psychiatric symptoms are a well documented phenomenon, but are typically seen with higher doses and systemic administration of corticosteroids. This case report is of a rare presentation, and to our knowledge there are no similar cases described.

Background: Donepezil is a reversible, centrally-acting acetylcholinesterase inhibitor used in the treatment of mild to moderate symptoms of dementia associated with Alzheimer's disease. In recent years, there has been emerging evidence of its use in other conditions, such as Lewy Body dementia and autism. However, there have been few reports of the use of Donepezil to treat depression in the absence of cognitive impairment. Methods: This is a case report of a 62-year old female with a long-standing history of major depressive disorder with no history of cognitive impairment, who failed to respond to antidepressants with augmentation therapy including antipsychotics , lithium and methylphenidate; but eventually improved on Donepezil. Results: A then-56-year old Chinese lady diagnosed with major depressive disorder, was treated with several antidepressants with poor response. Despite augmentation with dual antidepressants, antipsychotics, methylphenidate and lithium, her symptoms of avolition, depressed mood and irritability persisted. After 4 years of antidepressant treatment, she was started on donepezil 5mg. Within a month of augmentation, significant improvement in symptoms were reported, notably in mood and volition, and the patient was able to engage in an active and meaningful lifestyle of semblance to her pre-morbid mental state. Conclusion: This case highlights the possibility of Donepezil being used as an adjunctive therapy in major depressive disorder, even in the absence of cognitive impairment. Future studies to investigate the use of Donepezil may therefore be worthwhile to explore its use in this population of patients.

Although many persons with severe dementia (PWSDs) are cared for at home by their family caregivers, few studies have assessed end of life (EOL) care experiences of PWSDs. We present the protocol for the PISCES study