Oxytocin for Frontotemporal Dementia: A Systematic Review

Oxytocin for Frontotemporal Dementia: A Systematic Review

2017 AAGP Annual Meeting Poster Number: EI 21 Oxytocin for Frontotemporal Dementia: A Systematic Review Rajesh Tampi, MD, MS1; Deena Tampi, MSN, MBA-...

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2017 AAGP Annual Meeting Poster Number: EI 21

Oxytocin for Frontotemporal Dementia: A Systematic Review Rajesh Tampi, MD, MS1; Deena Tampi, MSN, MBA-HCA, RN2; Silpa Balachandran, MD1; Michael Maksimowski, MD1; Mohsina Ahmed, MD1 1

Case Western Reserve University School of Medicine, Cleveland, OH Saint Francis Hospital and Medical Center, Cleveland, OH

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Introduction: The aim of this systematic review is to identify published randomized controlled trials (RCTs) that evaluated the use of oxytocin in individuals with frontotemporal dementia. Methods: A literature search was conducted of PubMed, MEDLINE, EMBASE, PsycINFO and Cochrane collaboration databases for randomized controlled trials (RCTs) in any language that evaluated the use of oxytocin in individuals with FTD. Bibliographic databases of published articles were also searched for additional studies. Results: A total of two RCTs that evaluated the use of oxytocin in individuals with FTD were identified. In one study, the use of oxytocin in individuals with FTD produced a reduction in identification of negative facial expressions (anger and fear) which can be hypothesized to improve trust and increase cooperation in these individuals. Both studies noted oxytocin was well tolerated and showed short term benefits on behavioral symptoms in individuals with FTD. Conclusions: Oxytocin appears to improve social aspects of cognition and behavioral symptoms in individuals with FTD and is well tolerated. However, positive data from larger and longer duration RCTs are needed before the routine use of oxytocin in individuals with FTD can be recommended. This research was funded by: None. Poster Number: EI 22

Akathisia or Anxiety: What is the Difference? Patricia Serrano, MD; Priya Musunuri, MD Einstein Medical Center, Philadelphia, PA Introduction: Akathisia is a medication-induced movement disorder often described by patients as restlessness or an inability to stay still. It is often interpreted as anxiety and insomnia. If the symptoms are severe enough, the agitation that it causes may be treated with neuroleptic medication that can worsen the condition if it hasn’t been properly identified. Methods: Review of patient’s chart and Pubmed and Ovid searches were conducted using the terms akathisia, anxiety, and denosumab. Results: We present the case of a 64-year-old female hospitalized in the geriatric psychiatric ward for severe anxiety. She had no psychiatric history prior to the start of the symptoms she presented with. She endorsed multiple symptoms of depression, including suicidal ideation, decreased sleep and appetite, severe anxiety, and restlessness. Symptoms had started rather acutely 6 months prior with insomnia and anxiety. Her physical examination was relevant for tremor in her upper extremities that worsened when she was expressing her distress. She had been given multiple combinations of medications by outpatient providers and her restlessness only increased. At the time of admission she was taking mirtazapine, olanzapine, and buspirone. The initial impression was that she had akathisia, and her medications were tapered. She was then started on propanolol and ativan. After several days her symptoms had not changed. In her personal history there were no identifiable triggers at the time symptoms started. Medical causes were ruled out with assistance of the geriatrics and neurology teams after an extensive laboratory work-up and head tomography. The patient was unable to tolerate an MRI because of her symptoms. After a thorough medication review with the help of her outpatient pharmacy and provider, denosumab was identified as the only different medication the patient received days prior to the start of her symptoms. After a literature search, one case report was obtained reporting a woman with organic anxiety after denosumab administration. Even though denosumab was administered 3 days prior to the start of symptoms and there were no other triggers, it is unknown if this is the cause of the patient’s symptoms because she was given only one dose and several months later her symptoms had only worsened. In the one case described in the literature, hypocalcemia as a secondary effect was identified in the patient who developed anxiety after several doses. Our patient’s symptoms and presentation were attributed to akathisia after antipsychotic treatment, but even after the treatment was stopped, and she was provided with benzodiazepines and beta blockers, she did not improve. After over 20 days in the unit she did not improve with optimal pharmacological management. Medical reasons were exhausted and ECT was offered as treatment, but the patient and her family requested discharge.

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Am J Geriatr Psychiatry 25:3S, Supplement 1