Importance: First-seizure clinics (FSCs) aim to deliver prompt specialist care to patients with new-onset undifferentiated seizure events.
Objective: To determine whether FSC attendance and time to FSC are associated with subsequent health care utilization and mortality and to investigate factors associated with FSC nonattendance.
Design, setting, and participants: This was a record-linkage, retrospective, cohort study of patients who booked appointments at 2 FSCs between 2007 and 2018. Patients' records were linked to state-wide administrative databases between 2000 and 2021. The setting comprised the FSCs of 2 major metropolitan public hospitals in Melbourne, Australia, providing national inpatient and outpatient adult epilepsy services. Of patients who booked appointments at the FSCs, those who were successfully linked for analysis were included in the study. Patients who recorded only canceled appointments were excluded from analysis of outcomes. Study data were analyzed from January 2000 to December 2021.
Exposure: FSC attendance.
Main outcomes and measures: Subsequent all-cause and seizure-related emergency department (ED) presentations and hospital admissions.
Results: Of 10 162 patients with appointments at FSCs, 9392 were linked for analysis, with mean (SD) follow-up time 6.9 (2.8) years after FSC referral. A total of 703 patients were excluded. Among 9392 linked patients, 5398 were male (57.5%; mean [SD] age, 59.7 [11.2] years). FSC attendance was associated with reduced subsequent all-cause emergency presentations (adjusted incidence rate ratio [aIRR], 0.72; 95% CI, 0.66-0.79) and all-cause hospitalization (aIRR, 0.81; 95% CI, 0.75-0.88). Those who attended at the first-scheduled appointment, compared with those who attended only a rescheduled, delayed appointment, had reduced subsequent all-cause emergency presentations (aIRR, 0.83; 95% CI, 0.76-0.91), all-cause hospitalization (aIRR, 0.71; 95% CI, 0.65-0.79), seizure-related presentations (aIRR, 0.40; 95% CI, 0.33-0.49), and mortality (hazard ratio, 0.82; 95% CI, 0.69-0.98). Male sex was associated with nonattendance (adjusted relative risk [aRR], 1.12; 95% CI, 1.03-1.22), as were injury at emergency presentation (aRR, 1.12; 95% CI, 1.01-1.24), psychiatric comorbidity (aRR, 1.68; 95% CI, 1.55-1.81), previous seizure-related presentations (aRR, 1.35; 95% CI, 1.22-1.49), and delays (>14 days) between FSC referral and appointment (aRR, 1.35; 95% CI, 1.18-1.54). Hospitalization at referral was associated with reduced nonattendance (aRR, 0.80; 95% CI, 0.72-0.90), as were non-English language preference (aRR, 0.81; 95% CI, 0.69-0.94), distance greater than 6 mi from home to clinic (aRR, 0.85; 95% CI, 0.76-0.95), and physical comorbidity (aRR, 0.80; 95% CI, 0.72-0.89).
Conclusions and relevance: Results of this cohort study suggest tha
Importance: The discovery of the anti-GQ1b antibody has expanded the nosology of classic Miller Fisher syndrome to include Bickerstaff brainstem encephalitis, Guillain-Barré syndrome with ophthalmoplegia, and acute ophthalmoplegia without ataxia, which have been brought under the umbrella term anti-GQ1b antibody syndrome. It seems timely to define the phenotypes of anti-GQ1b antibody syndrome for the proper diagnosis of this syndrome with diverse clinical presentations. This review summarizes these syndromes and introduces recently identified subtypes.
Observations: Although ophthalmoplegia is a hallmark of anti-GQ1b antibody syndrome, recent studies have identified this antibody in patients with acute vestibular syndrome, optic neuropathy with disc swelling, and acute sensory ataxic neuropathy of atypical presentation. Ophthalmoplegia associated with anti-GQ1b antibody positivity is complete in more than half of the patients but may be monocular or comitant. The prognosis is mostly favorable; however, approximately 14% of patients experience relapse.
Conclusions and relevance: Anti-GQ1b antibody syndrome may present diverse neurological manifestations, including ophthalmoplegia, ataxia, areflexia, central or peripheral vestibulopathy, and optic neuropathy. Understanding the wide clinical spectrum may aid in the differentiation and management of immune-mediated neuropathies with multiple presentations.
Importance: Pediatric obesity is associated with impaired cognitive function; however, the mechanisms underlying this association demand assessment. Sleep may be a relevant moderator, as poor sleep predicts both increased adiposity and impaired cognitive function.
Objective: To determine the effects of adiposity and sleep on adolescent cognitive function.
Design, setting, and participants: This single-blind randomized crossover trial was conducted from September 2020 to October 2022. Parents or caregivers provided demographic information for adolescent participants. Body mass index percentile and bioelectrical impedance analysis assessed adiposity. Adolescents completed 2 actigraphy-confirmed sleep conditions, adequate and restricted, followed by in-person cognitive assessment. No additional follow-up was provided. Data collection for this population-based study took place in a behavioral medicine clinic in Birmingham, Alabama. A total of 323 participants were assessed for eligibility (ages 14-19 years and healthy). Of the 244 eligible adolescents, 157 declined participation. Eighty-seven were randomized and 26 dropped out postenrollment. The final sample included 61 adolescents, 31 with healthy weight and 30 with overweight or obesity. Data were analyzed from April to October 2023.
Interventions: Following a 2-day washout period of adequate sleep, adolescents completed 2 sleep conditions: adequate (mean [SD] duration, 8 hours, 54 minutes [58.0 minutes]) and restricted (mean [SD] duration, 4 hours, 12 minutes [50.7 minutes]).
Main outcomes and measures: The National Institutes of Health Cognitive Toolbox assessed global and fluid cognition, cognitive flexibility, working and episodic memory, attention, and processing speed. The Stroop Task assessed inhibition.
Results: The final sample included 61 adolescents (mean [SD] age, 16.3 [1.6] years; 35 [57.4%] female). Restricted sleep predicted poorer global cognition scores (restricted mean [SD], 98.0 [2.8]; adequate mean [SD], 103.2 [2.9]), fluid cognition scores (restricted mean [SD], 94.5 [3.2]; adequate mean [SD], 102.0 [3.6]), and cognitive flexibility scores (restricted mean [SD], 84.8 [3.0]; adequate mean [SD], 92.8 [3.0]) for adolescents with overweight or obesity. No differences emerged for adolescents with healthy weight. Adolescents with overweight or obesity also had poorer attention scores (mean [SD], 80.0 [2.3]) compared to adolescents with healthy weight (mean [SD], 88.4 [SD, 2.3]) following restricted sleep. No differences emerged following adequate sleep. Findings were similar for total body fat percentage (TBF%); however, for adolescents with TBF% above 42, restricted sleep also predicted poorer processing speed, and the association between sleep and attention did not vary based on TBF%.
Conclusions and relevance: Adolescents wi