Hypoglossal nerve stimulation (HNS) is an established treatment for selected patients with obstructive sleep apnoea (OSA) who cannot tolerate or benefit adequately from positive airway pressure. Insomnia symptoms are common in this population. This review examines how insomnia should be assessed and managed before and after implantation. Observational evidence is heterogeneous. A large international registry found similar respiratory response and adherence across baseline insomnia-severity groups, although questionnaire-defined insomnia was far more prevalent than insomnia recorded by clinical history. Smaller cohorts have reported reduced nightly use, lower stimulation levels, less favourable respiratory response or poorer patient-reported outcomes with insomnia. Associations appear more consistent for device use and patient-reported benefit than for respiratory efficacy. No insomnia intervention has been evaluated in a controlled study of HNS recipients. Clinicians should distinguish chronic insomnia disorder from respiratory-event-related awakenings and identify circadian, restless legs and medication contributors. Cognitive behavioural therapy for insomnia remains first-line for established chronic insomnia. When insomnia persists after activation, stimulation timing and intensity should be reviewed alongside objective confirmation of respiratory control. A questionnaire score should not be treated as an automatic contraindication. Insomnia should inform, rather than determine, candidacy for hypoglossal nerve stimulation (HNS). We favour clinical assessment before implantation to distinguish chronic insomnia from respiratory-event-related awakenings and identify relevant comorbidities. The Insomnia Severity Index can quantify symptom severity and monitor treatment response, supplemented by a sleep diary where appropriate. Cognitive behavioural therapy for insomnia (CBT-I) remains first-line treatment for chronic insomnia. We propose considering it before implantation or activation, particularly in patients with persistent sleep-onset insomnia or conditioned arousal, without routinely delaying otherwise appropriate HNS treatment. Whether this approach improves HNS outcomes remains untested. If insomnia develops or worsens after activation, respiratory control, device use and stimulation tolerability should be assessed together. Individualised adjustments to start delay or stimulation parameters may improve tolerability, provided effective airway treatment is maintained. Persistent sleep disturbance despite adequate respiratory control warrants assessment of non-respiratory causes. Pharmacotherapy may be considered selectively, recognising the limited HNS-specific evidence and the importance of respiratory safety.
To critically review the literature on bidirectional pharmacokinetic interactions between antiseizure medications (ASMs) and hormonal contraception and provide practical contraceptive guidance for women with epilepsy (WWE), as well as to summarize evidence for hormonal treatment of catamenial epilepsy. To review current data on fertility and assisted reproductive technology (ART), and to provide a practical counseling framework to optimize preconception care and reproductive outcomes in WWE. Intrauterine devices (IUDs) are first-line recommendation for contraception for women with epilepsy due to high efficacy, long lasting effect, and minimal interaction with antiseizure medications. Enzyme-inducing ASMs accelerate estrogen and progestin metabolism, reducing the efficacy of combined oral contraceptives (COCs), the patch, ring, progestin-only pills, and subdermal implants. Conversely, estrogen-containing contraception accelerates lamotrigine clearance through glucuronidation, lowering serum concentrations and risking breakthrough seizures in the absence of adequate adjustments. Depot medroxyprogesterone acetate is a reliable alternative, though enzyme induction may lower its concentrations in some patients. Because many newer ASMs, including lamotrigine and levetiracetam, are non-enzyme-inducing, hormonal contraception, particularly COCs (used by nearly a quarter of WWE), remains a reasonable option for many women. Of note, catamenial epilepsy affects at least one-third of WWE and hormonal therapies (continuous COCs, progestins and cyclic progesterone) may be beneficial for a subgroup of these WWE. Regarding fertility, a Danish registry found that 30.7
This article reviews current prospects for disease-modifying therapy in Parkinson’s Disease, with a focus on genotype-targeted treatments for the condition. Over 100 genes and loci are implicated in the pathogenesis of PD. They have varied cellular functions and studies of these roles have yielded insights into the mechanisms underlying PD pathogenesis, with this in turn leading to the identification of multiple possible targets for disease modification. Some of the most promising developments so far have been with GBA1, LRRK2, PINK1/PRKN and SNCA, and therapeutic strategies employing molecular chaperones, antisense oligonucleotides, small molecule inhibitors/activators, and gene therapies among others have been proposed. There remain no currently licensed medications to slow or prevent the progression of Parkinson’s Disease, the second most common neurodegenerative disease worldwide. However, multiple potential genotype-targeted therapeutic options have been developed and have progressed through pre-clinical and clinical phase work, with many trials expected to report shortly.
Adults with intellectual disability (ID) experience a disproportionate burden of sleep disorders with major impacts on physical, neuropsychiatric and behavioural health, yet evidence to guide practice has lagged behind the general population. This review updates our 2024 narrative synthesis, focusing on clinically actionable advances in sleep health for adults with ID. Recent observational data in adults with Down syndrome indicate that obstructive sleep apnoea is associated with adverse cardiometabolic, mortality and Alzheimer disease outcomes. Positive airway pressure can be feasible with individualised support, while retrospective studies of surgical treatment suggest possible benefits in selected patients, although residual OSA and confounding by treatment selection remain important considerations. Emerging diagnostic technologies, including home-based acoustic sensors, wearables, cardiorespiratory algorithms and three-dimensional facial biomarkers, represent promising developments that require further evaluation against established diagnostic pathways. Meta-analytic and cohort studies describe aetiology-related sleep phenotypes and persistent sleep and circadian disruption in autistic adults; a small uncontrolled case series provides preliminary evidence that daridorexant may be tolerated and associated with improved sleep in selected adults with intellectual disability. Despite recent advances, major inequalities persist, highlighting the need for accessible diagnostics, population‑specific instruments and adult‑focused guidelines embedding sleep management within lifelong care for people with ID.
Global warming is intensifying exposure to extreme heat, creating a growing but under-recognised threat to brain health in later life. Older adults, particularly those with or at risk of neurodegenerative disease, are uniquely susceptible because ageing and neuropathology can impair thermoregulation, sleep, vascular and inflammatory homeostasis, and the capacity to recognise and respond to heat stress. This vulnerability may be greatest at night, when elevated temperatures can disrupt sleep architecture, limit physiological recovery, and prolong thermal strain. In this narrative review, we (1) describe mechanisms of heat vulnerability in normative and pathological ageing (2) synthesise epidemiological studies linking ambient temperature, heatwaves, and warm nights with dementia-related mortality, hospitalisation, emergency care, and cognitive outcomes, while noting limitations in exposure assessment, confounding, diagnostic specificity, and causal inference (3) propose a “hotter nights–sleep disruption–neurodegeneration” pathway as a plausible framework for future research (4) outline management implications, including targeted sleep and heat advice, medication review, caregiver planning and cooling strategies. Testing this proposed pathway will require bedroom-level exposure assessment and longitudinal designs that measure heat, sleep and brain health together, rather than the outdoor-temperature proxies and siloed studies that dominate current evidence. Night-time heat warrants anticipatory, function-based clinical care alongside housing, urban-cooling and heat-health policy measures that protect sleep and cognitive resilience as the climate warms.
