RESUMO
The percentage of individuals who are functionally bilingual in the United States has grown substantially in the last 3 to 4 decades. Nevertheless, bilingual mental health providers remain relatively scarce and bilingualism in psychosis or schizophreniaspectrum disorders remains relatively unexplored. Here, we present a clinical case study of a man with schizophrenia who presented his psychotic symptoms differently in his primary and secondary languages. We also consider this case in the context of other published cases with similar themes. Based on our review, we hypothesize that the presentation of psychotic symptoms may be influenced by the language a person uses, and more specifically, by their cognitive abilities to speak that language and/or their emotional attachment to that language. We outline the importance of obtaining a thorough language background of each patient with psychosis and investigate the ways in which a second language could serve as a protective factor against functional decline in psychotic and healthy populations. We suggest that attempts to engage bilingual patients with psychosis clinically in each language could lead to a more holistic evaluation of psychotic and disorganized symptoms and thus lead to more multidimensional intervention strategies.
Assuntos
Multilinguismo , Transtornos Psicóticos , Esquizofrenia , Masculino , Humanos , Idioma , Transtornos Psicóticos/complicações , Transtornos Psicóticos/diagnóstico , Esquizofrenia/complicações , CogniçãoRESUMO
INTRODUCTION: People with psychotic disorders may be disproportionately affected by the traumatic effects of the COVID-19 pandemic. Childhood trauma, which also increases vulnerability to subsequent stressors, is common in individuals with psychosis. In this study, we investigated the intersection of the pandemic, childhood trauma, and psychotic and trauma-related symptoms in individuals with psychotic disorders. METHODS: We administered a cross-sectional survey to 151 participants [47 schizophrenia (SZ), 53 psychotic bipolar disorder (BP)], 51 healthy control (HC)] during the COVID-19 pandemic. Participants were asked about exposure to the pandemic's impacts, childhood trauma, and post-traumatic stress, dissociative, and psychotic symptoms. RESULTS: BP reported greater negative impacts to emotional health than SZ and HC and to non-COVID physical health than HC. SZ reported less impact on work and employment during the pandemic. There were no other group differences in pandemic-related adversities. We also found that cumulative exposure to the pandemic's negative impacts was significantly associated with PTSD symptoms but not psychotic or dissociative symptoms. Moreover, the number of adversities an individual experienced during the pandemic was strongly associated with the cumulative number of traumatic experiences they had in childhood. DISCUSSION: Our results suggest that having a psychotic disorder does not, in and of itself, increase susceptibility to the pandemic's negative impacts. Instead, we provide evidence of a graded relationship between cumulative exposure to the pandemic's negative impacts and PTSD symptom severity, as well as a graded relationship between cumulative childhood traumatic experiences and the number pandemic adversities, across diagnoses.
RESUMO
OBJECTIVES: 1) to assess generalizability of neurocognitive deficits reported in previous Western clinical high-risk (CHR) for psychosis studies in a prodromal program in Shanghai, China; and 2) to investigate neurocognition in CHR subjects in relation to a broader range of clinical outcomes (e.g. remission) than presence or absence of psychosis. METHOD: Baseline neurocognitive assessments of CHR (nâ¯=â¯217) and healthy control (HC; nâ¯=â¯133) subjects were compared based on 1-year follow-up clinical status using MANOVA. CHR subjects were first divided into 'converter' (CHR-C; nâ¯=â¯41) and 'non-converter' (CHR-NC; nâ¯=â¯155) to psychosis groups and compared to HC and to each other. CHR subjects were then divided into 'remission' (i.e. achieved remission; nâ¯=â¯102), 'symptomatic' (persistent positive symptoms in the absence of conversion; nâ¯=â¯37) and 'poor-outcome' (converted and symptomatic subjects who did not respond to treatment; nâ¯=â¯57) groups. RESULTS: CHR neurocognitive performance was broadly impaired compared to HC; CHR-C subjects showed lower performance in processing speed and visual learning than CHR-NC. CHRs with poor clinical outcomes showed lower performance on most MCCB tasks compared to HC, particularly in learning and processing speed, as clinical outcome worsened from remission to symptomatic to poor outcome groups. CONCLUSIONS: Level and pattern of baseline neurocognitive weaknesses in SHARP CHR subjects were similar to those in NAPLS-2. Outcome stratification into remission, symptomatic and poor groups was associated with increasing cognitive deficits in learning and processing speed. These findings support cross-cultural generalizability and advance understanding of CHR neurocognitive heterogeneity associated with 1-year clinical outcomes.