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Objectives: Virtual Reality-based interventions have become an important element of digital mental health, offering accessible and scalable treatment options. However, studies on VR-based approaches in elderly patients are scarce. This explorative study examined the feasibility of using Virtual Reality (VR) for elderly patients with psychiatric illness, focusing on the sense of presence as the primary outcome., Methods: The study included N = 30 patients between the ages of 59-92 years who were currently in geriatric psychiatric inpatient and day clinic treatment. Participants were assessed before, during and after a relaxing ten-minute VR experience. Attitude towards digital media and VR, subjective digital competence, and previous experience were examined using questionnaires. Motion sickness was measured repeatedly during the VR experience using the Fast Motion Sickness Scale (FMS). Patients rated their motion sickness and their general well-being in the virtual environment. Sense of presence in the virtual environment was quantified with the Igroup Presence Questionnaire (IPQ)., Results: Participants reported a notable sense of presence (M = 0.41 ± 1.4) in the virtual environment, particularly in terms of spatial presence. Motion sickness was reported by a minority of patients. Three patients terminated the VR application before it was finished. The average well-being during the VR experience was reported as high (70/100). Sense of presence and motion sickness showed a significant negative correlation. Presence, motion sickness and well-being were not significantly correlated with age, nor did they differ significantly between groups., Conclusions: This study underscores the potential of VR-based experiences in the treatment of elderly psychiatric patients and highlights their willingness and ability to engage with VR technology. While the results are promising, future research should explore more interactive VR scenarios and assess their safety and feasibility in elderly populations., (© 2024 The Authors. International Journal of Geriatric Psychiatry published by John Wiley & Sons Ltd.)

Introduction: The increasing identification of specific autoantibodies against brain structures allows further refinement of the group of autoimmune-associated epilepsies and affects diagnostic and therapeutic algorithms. The early etiological allocation of a first seizure is particularly challenging, and the contribution of cerebrospinal fluid (CSF) analysis is not fully understood., Methods: In this retrospective study with a mean of 7.8 years follow-up involving 39 well-characterized patients with the initial diagnosis of new-onset seizure or epilepsy of unknown etiology and 24 controls, we determined the frequency of autoantibodies to brain proteins in CSF/serum pairs using cell-based assays and unbiased immunofluorescence staining of unfixed murine brain sections., Results: Autoantibodies were detected in the CSF of 30.8% of patients. Underlying antigens involved glial fibrillary acidic protein (GFAP) and N-methyl-D-aspartate (NMDA) receptors, but also a range of yet undetermined epitopes on neurons, glial and vascular cells. While antibody-positive patients had higher frequencies of cancer, they did not differ from antibody-negative patients with respect to seizure type, electroencephalography (EEG) and cranial magnetic resonance imaging (cMRI) findings, neuropsychiatric comorbidities or pre-existing autoimmune diseases. In 5.1% of patients with seizures or epilepsy of initially presumed unknown etiology, mostly CSF findings resulted in etiological reallocation as autoimmune-associated epilepy., Discussion: These findings strengthen the potential role for routine CSF analysis. Further studies are needed to understand the autoantibody contribution to etiologically unclear epilepsies, including determining the antigenic targets of underlying autoantibodies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Schulz, Lütt, Stöcker, Teegen, Holtkamp and Prüss.)

The recent discovery of neuronal cell-surface antibodies profoundly expanded the clinical spectrum of paraneoplastic neurological syndromes. Many of these syndromes are associated with impaired cognitive function, a clinical symptom that is of increasing concern in cancer patients. However, the frequency of these antibodies in cancer patients and their relation to clinical syndromes is currently unknown. Here, we investigated the prevalence of neuronal cell-surface antibodies and associated paraneoplastic neurological syndromes in 323 patients with different cancer types and in 105 controls. Cerebrospinal fluid and serum samples were analysed for a large panel of anti-neuronal antibodies and all patients were screened for cognitive deficits. Blood-brain barrier integrity was assessed using the age-normalized albumin cerebrospinal fluid/serum ratio. Anti-neuronal autoantibodies were observed in 24.5% of cancer patients (in contrast to 3.1% in neurological control patients without cancer and 2.5% in healthy controls) and were almost exclusively detected in serum. The majority of antibodies were directed against cell-surface antigens (75.9%), most frequently IgA/IgM isotypes targeting the N-methyl-D-aspartate (NMDA) receptor. Cognitive deficits and cerebellar syndromes were significantly more prevalent in antibody-positive in comparison with antibody-negative patients (21 vs. 7%, p = 2.7 × 10 -4 ; 11 vs. 2%, p = 3.0 × 10 -3 ). Antibody-positive patients with cognitive deficits had a significantly increased albumin cerebrospinal fluid/serum ratio in comparison with antibody-positive patients with other neurological deficits, indicating blood-brain barrier dysfunction (49.1 × 10 -3 vs. 12.0 × 10 -3 ; p = 0.036). Our results show that anti-neuronal antibodies have a high prevalence in a wide range of different tumour types and are associated with distinct neurological deficits. Specifically, the results suggest a so far undefined cognitive paraneoplastic syndrome in patients with antibodies targeting neuronal surface antigens and concurrent blood-brain barrier dysfunction. Anti-neuronal antibodies might thus serve as a biomarker for potentially treatment-responsive cognitive impairments in cancer patients.