Gugliotta, Alessio

Abstract Introduction Clinical hypnosis is among the limited treatment options currently available to mitigate the symptom burden associated with parasomnias; however, there is scant literature regarding its effectiveness. We conducted a retrospective cohort study to examine the efficacy of clinical hypnosis in treating parasomnias. Methods We included all adult patients with research authorization on file who were referred for clinical hypnosis for the management of parasomnias at the Mayo Clinic Center for Sleep Medicine. Data on demographics, type and frequency of parasomnia(s), number of hypnosis sessions, concurrent medication(s), and polysomnographic variables were extracted. Information about the efficacy of treatment, including patient reports of change in intensity and frequency was extracted where available. A Clinical Global Impression-Improvement (CGI-I) score was assigned based on review of the follow up note. Results A total of 134 patients received clinical hypnosis. A majority of the sample was female (65.67%) with a median age of 41.5 years. The most common indications were non-rapid eye movement (REM) parasomnia (33), REM sleep behavior disorder (27), nightmare disorder (24), parasomnia overlap disorder (11), and sleep-related eating disorder (8). Follow up data were available on 76 patients (56.71%). Of these, a total of 47/76 (61.84%) reported subjective improvement in parasomnias following hypnosis. The median CGI-I score was 3.07±1.22; a total of 23/76 (30.26%) reported substantial improvement and 19/76 (25.0%) reported some impovement based on the CGI scores. Conclusion A majority of patients reported improvement in symptoms. Clinical hypnosis was effective for both non-REM and REM parasomnias. Given its relative safety and minimal potential adverse effects, clinical hypnosis remains an effective first-line treatment option for parasomnias. Support (if any)

Abstract Introduction Observational studies have reported associations between hypnotic use and increased risk of cognitive decline. These findings may reflect confounding from insomnia severity, healthcare utilization, and comorbidity burden. We evaluated whether hypnotic exposure is independently associated with incident mild cognitive impairment (MCI) or dementia after rigorous adjustment, including a comprehensive propensity score (PS) and Apolipoprotein E (APOE) ε4 status. Methods We conducted a retrospective cohort study using a biobank sample with linked electronic health records and genetic data. Hypnotic exposure was derived from orders data and categorized as unexposed (n=27,055), single prescription (n=4243), shorter-term use (n=3999), long-term use (≥6 orders for ≥1 year; n=3214), and by drug class: benzodiazepines (n=376), Z-drugs (n=6222), trazodone (n=2395), and mixed exposure (≥2 classes; n=2435). Incident MCI/dementia diagnoses (ICD-9/10) occurring ≥12 months after initial prescription constituted outcomes. The PS modeled likelihood of receiving hypnotics based on demographics; sleep-related conditions; healthcare utilization (record length, visit frequency, diagnostic burden); psychiatric comorbidities; alcohol use and chronic pain. Hypnotic users were 1:2 matched to unexposed individuals on age, sex, healthcare utilization, and PS. Cox proportional hazards models with a 60-month lag tested associations of exposure category, duration, and class with outcomes. Models adjusted for all PS covariates, cardiovascular risk score, and APOE ε4 status. Results Matched but unadjusted analyses suggested slightly higher hazards of MCI/dementia among hypnotic users versus unexposed (HR=1.08; CI=0.99–1.18). However, after PS adjustment and APOE ε4 inclusion, hypnotic users showed significantly lower hazards (HR=0.81; CI=0.74–0.89). Class-specific analyses indicated reduced hazards for Z-drugs (HR=0.83; CI=0.74–0.93), trazodone (HR=0.71; CI=0.60–0.86), and mixed users (HR=0.79; CI=0.68–0.91), with all classes showing lower hazards than benzodiazepine-only users. Long-term hypnotic use was associated with lower hazards than no prescription (HR=0.69; CI=0.61–0.80), single prescription (HR=0.81; CI=0.68–0.97), or short-term use (HR=0.76; CI=0.65–0.90). Conclusion The elevated cognitive risk among hypnotic users appears largely attributable to underlying clinical/utilization factors rather than hypnotic exposure itself. After comprehensive confounding control, all hypnotic classes except benzodiazepines demonstrated lower risk of MCI/dementia. These findings underscore the need for rigorous adjustment in studies of insomnia pharmacotherapy and suggest potential protective effects of certain hypnotics that warrant further investigation. Support (if any) None