Bilateral vestibular weakness (BVW), while uncommon, causes significant disability. We review the epidemiology, etiologies, and diagnostic techniques for BVW, followed by a discussion of established and investigative therapeutics. Recent research increasingly suggests that some BVW cases previously designated as idiopathic may be due to RFC1 mutations. While the standard of care for BVW remains vestibular rehabilitation therapy, promising investigative therapeutics include noisy galvanic vestibular stimulation and prosthetic vestibular implants; research on vestibular hair cell regeneration is ongoing. Bilateral vestibular weakness (BVW) refers to pathological reduction of vestibular signals from one or more labyrinthine inputs on each side due lesions of the end organelles, or their afferent pathways, or some combination thereof. There are many etiologies of BVW. Symptoms include oscillopsia and unsteadiness. The diagnosis can be suspected from bedside examination techniques, but requires confirmation from instrumented vestibular testing. Potential mechanisms for recovery include healing of damaged (but not dead) vestibular hair cells, central compensation and sensory substitution. Vestibular rehabilitation therapy is the standard of care for BVW, and emphasizes adaptive techniques thought to improve gain of the vestibulo-ocular reflex, and sensory substitution. Investigational therapeutics include noisy galvanic vestibular stimulation, vestibular implantation, and vestibular hair cell regeneration. Prognosis is unfavorable.

Magnetic resonance imaging-guided laser interstitial thermal therapy (LITT) has emerged as a minimally invasive alternative to open surgical resection for drug-resistant epilepsy, with increasing adoption in advanced epilepsy centers over the past decade. This review provides a comprehensive overview of LITT applications and outcomes in treating various epilepsy etiologies. Stereotactic laser amygdalohippocampectomy (SLAH) via LITT for temporal lobe epilepsy achieves Engel Class 1 outcomes in 58% of patients, which is comparable to anterior temporal lobectomy, while demonstrating less neurocognitive morbidity and fewer visual field deficits. LITT has shown favorable seizure outcomes across multiple epilepsy etiologies, including corpus callosotomy, cavernous malformations, focal cortical dysplasia, and epilepsy associated tumors. The minimally invasive nature of LITT has expanded treatment options for lesions traditionally associated with significant operative morbidity, including hypothalamic hamartomas and periventricular nodular heterotopias. While much of the current data consists of retrospective case series, there is growing evidence to support the use of LITT as an effective treatment option across diverse drug-resistant epilepsy indications. Its combination of acceptable seizure outcomes with reduced surgical morbidity positions LITT as a valuable tool in the epilepsy surgery armamentarium.

Abstract Purpose of Review This narrative review synthesises emerging evidence on the neurophysiological underpinnings of sleep disturbances across psychiatric disorders. Historically regarded as secondary symptoms, sleep disruptions are now increasingly conceptualised as mechanistic drivers of psychopathology. We advance a transdiagnostic framework for understanding how alterations in sleep microstructure and circadian regulation intersect with neural circuits implicated in major psychiatric syndromes. Recent Findings Electroencephalographic markers such as reduced sleep spindle density, slow-wave activity, increased cyclic alternating pattern rate, and changes in aperiodic slope, have demonstrated relevance across mood, anxiety, psychotic, and neurodevelopmental disorders. These sleep EEG phenotypes show associations with disrupted thalamocortical and frontolimbic circuitry, and may function as candidate biomarkers for diagnosis, prognosis, and treatment response. Neuroimaging and genomic studies further support a convergence of sleep-related mechanisms with affective and cognitive dysfunction. Targeted interventions, ranging from cognitive behavioural therapy for insomnia (CBT-I), to neuromodulation and circadian-phase shifting agents increasingly show promise in modulating sleep architecture and ameliorating psychiatric symptoms. Summary Sleep dysfunction constitutes a mechanistically embedded, transdiagnostic substrate in psychiatric illness. Integrating sleep metrics into precision psychiatry may facilitate early detection, stratification, and tailored interventions. We advocate for the routine inclusion of sleep assessments and biomarker-guided sleep interventions as essential components of psychiatric care. Such a shift holds promise not only for symptom relief but also for prevention and long-term functional recovery.

Purpose of ReviewIncreased understanding of the pathophysiology of Alzheimer’s disease (AD) has led to development of disease modifying therapies. The therapies primarily target measures of cognitive decline since AD has been thought of as a cognitive disorder. However, the non-cognitive symptoms seen in AD contribute to overall quality-of-life. This scoping review was undertaken to further our understanding of the non-cognitive features of AD.Recent FindingsThe non-cognitive symptoms in AD range from changes in sensory perception, systemic changes, and neuropsychiatric manifestations. We targeted the following non-cognitive domains: vision, olfaction, GI, muscle, sleep, circadian rhythm, immune and behavioral symptoms as it relates to AD for this review. Non-cognitive features impact the ability of individuals to perform their activities of daily living, have safety implications and lead to increased caregiver burden. The review explores non-pharmacological and pharmacological measures targeted at the non-cognitive changes in AD.SummaryNon-cognitive symptoms contribute to significant disease burden in Alzheimer’s disease. It is important to screen for and provide supportive care for these symptoms to help improve clinical care. Incorporation of non-cognitive features of AD in clinical trials will help ascertain the true societal and economic impact of AD and that of potential therapeutics.Opinion StatementAlzheimer’s disease (AD) is primarily recognized as a disorder of cognition; however, non-cognitive symptoms significantly contribute to disease burden and clinical presentation. These manifestations particularly behavioral symptoms and systemic changes beyond the central nervous system impact patients’ quality of life and increase caregiver stress. Often, such symptoms necessitate a transition from home-based care to more intensive settings, such as memory care facilities. As AD prevalence rises alongside an aging population, the shortage of dedicated memory care providers in community settings challenges access and quality of care. Improved awareness and early recognition of non-cognitive features among healthcare professionals can aid identification of modifiable systemic issues and allow timely behavioral management during clinical encounters. Treatment of these symptoms requires a multifaceted approach, incorporating pharmacological and non-pharmacological strategies. Non-pharmacological interventions, including tailored behavioral approaches and environmental modifications, can enhance quality of life for individuals with AD and reduce caregiver burden especially where specialized medical resources are limited.

Purpose of ReviewWe performed a narrative review of the current knowledge in epidemiology, mechanisms, clinical presentation, and treatment of sleep disorders in adults with intellectual disability.Recent FindingsAdults with Intellectual disability face significant mental and physical health disparities, including in sleep medicine. Despite sleep disorders having been identified as adversely affecting the health and quality of life of both adults with intellectual disabilities and their caregivers, the evidence base for assessment, diagnosis and treatment in this population remains under developed when compared to that of the general population. This review summarises the existing literature on insomnia, sleep disordered breathing, and other common sleep disorders in adults with intellectual disability. Emphasising the existing gaps in our understanding of sleep disorders in adults with intellectual disabilities, we propose strategies to address and mitigate these gaps.SummarySleep disorders are common, yet frequently ignored in adults with intellectual disabilities. To address sleep health inequality gaps, future research should adopt tailored approaches, considering the heterogeneity within the intellectual disability population, including stratification by aetiology and health comorbidities. This is essential to improve the diagnostic accuracy and treatment of sleep disorders in adults with intellectual disability.