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Introduction: Autoimmune encephalitis (AE) comprises a heterogeneous group of autoantibody‐mediated disorders targeting the brain parenchyma. Therapeutic plasma exchange (TPE), one of several first‐line therapies for AE, is often initiated when AE is suspected, albeit prior to an established diagnosis. We sought to characterize the role of TPE in the treatment of suspected AE. Methods: A single‐center, retrospective analysis was performed of adults (≥18 years) who underwent at least one TPE procedure for "suspected AE." The following parameters were extracted and evaluated descriptively: clinicopathologic characteristics, treatment course, TPE‐related adverse events, outcomes (e.g., modified Rankin scale [mRS]), and diagnosis once investigation was complete. Results: A total of 37 patients (median age 56 years, range 28–77 years, 62.2% male) were evaluated. Autoimmune antibody testing was positive in serum for 43.2% (n = 16) and cerebrospinal fluid for 29.7% (n = 11). Patients underwent a median of five TPE procedures (range 3–16), with 97.3% (n = 36) via a central line and 21.6% (n = 8) requiring at least one unit of plasma as replacement fluid. Fifteen patients (40.5%) experienced at least one TPE‐related adverse event. Compared with mRS at admission, the mRS at discharge was improved in 21.6% (n = 8), unchanged in 59.5% (n = 22), or worse in 18.9% (n = 7). Final diagnosis of AE was determined to be definite in 48.6% (n = 18), probable in 8.1% (n = 3) and possible in 27.0% (n = 10). Six (16.2%) patients were ultimately determined to have an alternate etiology. Conclusion: Empiric TPE for suspected AE is generally well‐tolerated. However, its efficacy remains uncertain in the absence of controlled trials, particularly in the setting of seronegative disease. [ABSTRACT FROM AUTHOR]

BACKGROUND: Obesity is now a leading public health problem affecting 30% of the world's population with increasing prevalence in both developed and developing countries (Neto A, Fernandes A, Barateiro A. The complex relationship between obesity and neurodegenerative diseases: an updated review. Front Cell Neurosci. 2023;17:1294420. doi:10.3389/fncel.2023.1294420). Obesity is associated with low-inflammatory states and is linked to autoimmune conditions including multiple sclerosis, systemic lupus erythematosus, and sarcoidosis. However, an association between body mass index (BMI) and encephalitis has not been reported. OBJECTIVES: Here we aim to determine if BMI has an impact on the clinical features and outcomes in patients with encephalitis. METHODS: We conducted an institutional review board--approved, retrospective chart review of patients diagnosed with encephalitis based on the 2013 International Encephalitis Consortium inclusion criteria between 2005 and 2022 at UTHealth Houston and John Hopkins University School of Medicine. We included 628 patients and collected data on demographic features, presenting signs and symptoms, imaging and serum findings, treatment regimens, and clinical outcomes. A bivariate analysis was used to analyze clinical features that were polychotomous by utilizing Pearson χ2 and Fisher exact test values. Descriptive statistics were also used to analyze the data, including analysis of variance for continuous variables. Variables with P < 0.05 and a reasonable CI were deemed statistically significant. RESULTS: Of 628 patients, 3.8% were underweight (< 18.5), 35.7% had normal weight (18.5-24.9), 29.5% were overweight (25- 29.9), and 31.1% were obese (> 30). Patients who were underweight were more likely to be immunocompromised, HIV+, have a greater mortality risk, have a low Glasgow Outcome Scale (GOS) score at presentation, and have higher rates of inpatient mortality. Patients who were obese were more likely to be female, have inflammatory cerebrospinal fluid (CSF) with white blood count (WBC) > 50, serum WBC > 11K, and experience sleep disturbances. These patients had unfavorable outcomes with a GOS < 4; however, they are more likely to be alive. CONCLUSIONS: There were significant differences in comorbidities, clinical findings at presentation, CSF studies, and clinical outcomes between patients with underweight, normal, overweight, and obese BMI. Future studies may be needed to further elucidate these differences. [ABSTRACT FROM AUTHOR]

Objective: Encephalitis is a serious and potentially life-threatening condition of infectious or autoimmune cause. We aim to characterize the frequency and clinical spectrum of presenting psychiatric symptoms in encephalitis in order to inform earlier recognition and initiation of treatment., Methods: This was a retrospective study of adult patients who met the 2013 International Encephalitis Consortium (IEC) and/or 2016 Graus criteria between February 2005 and February 2023. The study included two hospital systems in Houston, Texas, and Baltimore, Maryland and included a total of 642 patients. Psychiatric manifestations were grouped into five high-level categories: behavior, psychosis, mood, sleep disturbances, and catatonia., Results: In our cohort of 642 patients, 318 (49.6%) had psychiatric symptoms at the time of initial presentation, including 78.2% with autoimmune etiologies and 35.2% with viral etiologies (P < 0.001). Those with psychiatric symptoms were younger (median age 47.5 vs. 51.5; P < 0.001), and more likely to have a history of documented psychiatric disorders, as well as longer lengths of hospital stay, and poorer discharge outcomes. Of patients initially admitted to a psychiatric service (n = 28), most had autoimmune causes, although 3 out of 28 (10.7%) had herpes viral infections; admission to a psychiatric service was associated with substantially longer interval to initiation of antivirals and immunotherapy. Autoimmune and infectious etiologies differed in the spectrum and frequency of psychiatric manifestations., Interpretation: Psychiatric symptoms are common across etiologies of encephalitis and are associated with longer lengths of hospital stay and worse clinical outcomes. Specific patterns and dimensionality of psychiatric symptoms distinguish autoimmune from infectious causes., (© 2025 The Author(s). Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.)

Background: Early diagnosis of encephalitis involves identifying signs of neuroinflammation, including cerebrospinal fluid (CSF) pleocytosis. However, absence of CSF pleocytosis in encephalitis has been described, most notably in autoimmune encephalitis. We examined clinical characteristics and outcomes associated with the absence or presence of CSF white blood cell pleocytosis (≥ 5 cells/µL), to inform timely diagnosis and management of encephalitis., Methods: This retrospective study compares initial CSF profiles in 597 adult patients with all-cause encephalitis., Results: Of the 597 patients, 446 (74.7%) had CSF pleocytosis while 151 (25.3%) did not. CSF pleocytosis occurred more commonly in infectious cases (200/446, 44.8%), along with 59 (13.2%) autoimmune cases, comprised chiefly of anti-NMDAR encephalitis (37/59, 62.7%). Notably, the group without pleocytosis was comprised of similar proportions of infectious (47/151, 31.1%) and autoimmune (38/151, 25.92%; p>0.05) encephalitis. Among those with infectious encephalitis, 47/247 (19%) had absent pleocytosis, including 18/76 (23.7%) with HSV-1 encephalitis. The absence of pleocytosis was associated with a decreased rate of acyclovir administration (47.7% in patients without pleocytosis vs. 71.1% in patients with pleocytosis, p<0.001). Despite pleocytosis being associated with some measures of clinical severity at admission such as a Full Outline of UnResponsiveness (FOUR) score ≤14, it was not associated with mortality or prolonged hospitalization., Conclusion: CSF pleocytosis is an important criterion for encephalitis diagnosis, but 25.3% of patients with all-cause encephalitis and 23.7% of those with HSV-1 encephalitis exhibit absence of pleocytosis on initial LP. Acyclovir initiation should not be delayed in the absence of pleocytosis in patients with suspected encephalitis., (© The Author(s) 2024. Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)