Faculty Bibliography

OBJECTIVE:The primary aim of this qualitative study was to delineate psychological mechanisms of change in the first randomized controlled trial of psilocybin-assisted psychotherapy to treat alcohol use disorder (AUD). Theories regarding psychological processes involved in psychedelic therapy remain underdeveloped. METHOD/METHODS:Participants (N = 13) mostly identified as non-Hispanic and White, with approximately equal proportions of cisgender men and women. Participants engaged in semistructured interviews about their subjective experiences in the study. Questions probed the nature of participants' drinking before and after the study as well as coping patterns in response to strong emotions, stress, and cravings for alcohol. Verbatim transcripts were coded using Dedoose software, and content was analyzed with interpretive phenomenological analysis. RESULTS:Participants reported that the psilocybin treatment helped them process emotions related to painful past events and helped promote states of self-compassion, self-awareness, and feelings of interconnectedness. The acute states during the psilocybin sessions were described as laying the foundation for developing more self-compassionate regulation of negative affect. Participants also described newfound feelings of belonging and an improved quality of relationships following the treatment. CONCLUSION/CONCLUSIONS:Our results support the assertion that psilocybin increases the malleability of self-related processing, and diminishes shame-based and self-critical thought patterns while improving affect regulation and reducing alcohol cravings. These findings suggest that psychosocial treatments that integrate self-compassion training with psychedelic therapy may serve as a useful tool for enhancing psychological outcomes in the treatment of AUD. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

PURPOSE OF REVIEW/OBJECTIVE:Patients diagnosed with HIV can now survive well into their old age. Aging with HIV is not only associated with comorbid medical illnesses but also with neuropsychiatric conditions that can range from cognitive changes to severe behavioral manifestations. This paper reviews mood, anxiety, and cognitive changes in older patients with HIV, as well as some of the treatment challenges in this population. RECENT FINDINGS/RESULTS:Most recent findings show that untreated HIV illness over a long period of time may further worsen both preexisting neuropsychiatric illness and may cause new onset behavioral and cognitive symptoms. HIV induces immune phenotypic changes that have been compared to accelerated aging Low CD 4 counts and high viral counts are indicative of poor prognosis. Evaluation for potential HIV infections may be overlooked in older adults and require screening. Older adults experience accelerated CD4 cell loss. Older adults endorsing new onset mood or cognitive changes must be screened for HIV infection. New onset neurobehavioral symptoms should be carefully screened for and treated simultaneously in patients with HIV infection.

Background/Significance: Catatonia is common in anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis (Espinola-Nadurille, 2019). The glutamate NMDAR antagonists amantadine and memantine are effective in catatonia (Beach, 2017), but data on their use in anti-NMDAR encephalitis is limited. We describe three patients with catatonia due to anti-NMDAR encephalitis treated with NMDAR antagonists and propose a possible mechanism underlying differential outcomes. Case 1: A 20-year-old woman presented with catatonic symptoms after successful treatment of anti-NMDAR encephalitis with immunotherapy and salpingo-oopherectomy for ovarian teratoma. Initial Bush-Francis Catatonia Rating Scale (BFCRS) score was 22. Lorazepam 2.5 mg three times daily was partially effective, but increased doses caused sedation. Memantine was titrated to 10 mg twice daily with complete resolution of catatonia over two weeks. Case 2: A 26-year-old woman presented with catatonic with BFCRS score of 25, after successful immunotherapy for anti-NMDAR encephalitis. Lorazepam 2 mg four times daily was partially effective, but further increase caused respiratory depression. Memantine 10 mg daily resulted in further improvement. Lorazepam titration to 4 mg four times daily was then possible, with complete resolution of catatonia over two weeks. Case 3: A 31-year-old woman with anti-NMDAR encephalitis presented with catatonic symptoms with BFCRS score of 22, after a hospital course significant for limited response to immunotherapy with persistently elevated serum anti-NMDAR antibody titers. Lorazepam 2 mg three times daily was partially effective, but further increase caused sedation. Both amantadine 100 mg twice daily and memantine 10 mg were trialed but were discontinued due to agitation. Mutism and negativism persisted, with a discharge BFCRS score of 12.
Discussion(s): Memantine was effective for catatonia and well tolerated in two patients with successfully treated anti-NMDAR encephalitis, but both amantadine and memantine caused agitation in a third patient with active disease. NMDARs are reversibly internalized in the presence of anti-NMDAR antibodies, leading to a compensatory increase in downstream glutamatergic tone. We hypothesize that NMDAR reemergence after successful treatment, in the context of excess extracellular glutamate, creates a state of excitotoxicity contributing to catatonic signs for which NMDAR blockade can be effective. In the third case, where NMDARs presumably remained internalized in the presence of persistent anti-NMDAR antibodies and a state of NMDAR hypofunction persisted, further NMDAR blockade caused clinical worsening. Conclusion/Implications: NMDAR antagonists can be safe and effective in patients with residual catatonia following successful treatment of anti-NMDAR encephalitis but may be less useful during active disease. More work is needed to clarify best practices for patients with catatonia due to anti-NMDAR encephalitis. References: 1. Espinola-Nadurille M, Flores-Rivera J, Rivas-Alonso V, et al. Catatonia in patients with anti-NMDA receptor encephalitis. Psychiatry Clin Neurosci. 2019;73(9):574-580. 2. Beach SR, Gomez-Bernal F, Huffman JC, Fricchione GL. Alternative treatment strategies for catatonia: A systematic review. Gen Hosp Psychiatry. 2017;48(June):1-19.
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