This review highlights recent advances in neuro-vestibular rehabilitation, with emphasis on vestibular adaptation and emerging mobile technologies. It summarizes developments in promoting vestibular plasticity and discusses novel tools such as virtual reality, wearable sensors, and telehealth platforms that enhance access, engagement, and outcomes. The scope is broad, focusing on general principles rather than specific populations. New methods to enhance vestibulo-ocular reflex (VOR) adaptation include incremental adaptation devices and gamified exercises. Inducing VOR gain-down adaptation temporarily increases postural sway, which normalizes via sensory reweighting, demonstrating central compensation. Portable tools like StableEyes show promise in boosting VOR gain with brief sessions. Concurrently, technology-driven approaches are gaining traction. Gamified mobile applications and wearable sensors allow home-based rehabilitation with remote supervision and monitoring, showing promising results in conditions like multiple sclerosis. Virtual reality interventions and telehealth models accelerated during the COVID-19 era, expanding therapy delivery to underserved populations. Adjunctive methods such as vibrotactile feedback and galvanic vestibular stimulation are emerging as complementary therapies. Recent developments are advancing vestibular rehabilitation by refining adaptive training techniques and leveraging digital tools to overcome barriers in access and adherence. These innovations point to a more personalized, technology-enabled approach to optimizing neuro-vestibular recovery.

Ischemic stroke remains a leading cause of death and disability worldwide, with carotid atherosclerosis as a major underlying mechanism. For decades, treatment decisions were based primarily on luminal stenosis, overlooking the biological complexity of plaque instability. This review summarizes recent progress in the imaging-based identification and risk stratification of unstable cerebrovascular plaque, emphasizing the transition from geometric to biological evaluation. Advances in CT, MRI, and ultrasound have enabled in vivo visualization of key features associated with plaque vulnerability, including intraplaque hemorrhage, fibrous cap rupture, neovascularization, inflammation, and perivascular fat alterations. Dual-energy and photon-counting CT now provide spectral and spatial information capable of tissue differentiation at submillimeter scales. MRI offers superior soft-tissue characterization, while contrast-enhanced ultrasound reveals microvascular activity and flow dynamics. The recent introduction of standardized interpretative systems, such as Plaque-reporting and data system (RADS), allows integration of multimodal findings into a unified risk framework. Contemporary imaging has transformed the assessment of carotid atherosclerosis from a static measurement of stenosis into a dynamic, biology-driven discipline. The combination of advanced imaging, quantitative analysis, and emerging molecular and genetic correlates promises to refine individualized risk prediction and guide targeted prevention strategies for cerebrovascular disease.

Three functional neurological disorders are encountered in neuro-otologic practice, persistent postural-perceptual dizziness (PPPD), which is the commonest cause of chronic vestibular and balance symptoms, mal de debarquement (MdDS), a rarer but potentially debilitating disorder, and functional gait disorder, an often overlooked but treatable condition. Recent investigations of PPPD suggested that there may be subtypes or subthreshold variants that merit further investigation. Studies of pathological mechanisms continue to offer new insights into the complex processes that initiate and sustain the disorder, which will require nuanced models to bring together disparate findings. Evidence continues to accumulate in support of vestibulo-ocular reflex readaptation therapy for MdDS, with pilot studies offering refinements and possible alternatives. Functional gait disorder is one of the commonest manifestations of functional neurological disorder, often presenting with other functional neurological symptoms including PPPD. Specialized methods of physical and occupational therapy continue to mature. Optimal outcomes may require short and focused periods of intensive treatment. Evolving theories and continuing emergence of new data are beginning to make functional vestibular and gait disorders a manageable part of neuro-otologic practice.

Endovascular treatment (EVT) has dramatically improved outcomes of patients suffering from acute ischemic stroke due to large vessel occlusion (LVO), becoming the standard of care. However, up to one-third of ischemic strokes are caused by distal medium vessel occlusions (DMVO), which are beyond the LVO territory. Medical management, including intravenous thrombolysis, leaves more than half of DMVO patients disabled at 3 months, with mortality exceeding 10%. In face of this grim prognosis, expanding EVT to DMVO has gained considerable interest. This review summarizes the clinical, anatomical, and imaging features of DMVO stroke, discusses recent EVT trial results and their interpretation, and outlines future directions for establishing safe and effective reperfusion strategies in this population. Recent randomized trials investigating EVT for DMVO stroke yielded neutral results overall. However, they provided important insights about patient subgroups likely to benefit from intervention and set key challenges to improving the management of patients with DMVO. While current evidence does not support routine EVT for DMVO stroke, the field is evolving rapidly. Ongoing advances in device technology, patient selection, and trial design hold promise for refining treatment and improving outcomes in carefully selected patients.

Moyamoya vasculopathy is a progressive cerebrovascular steno-occlusive disease with variable presentation. As revascularization techniques, antiplatelet therapies, and imaging-based artificial intelligence (AI) diagnostics continue to advance, there is an emerging opportunity to refine patient stratification by integrating genetic profiling, neuroimaging phenotypes, and circulating biomarkers. The RNF213 locus (particularly p.R4810K) represents the primary susceptibility allele in East Asian cohorts, with secondary contributors including ACTA2 and GUCY1A3 showing incomplete penetrance. Emerging. data reveal dysregulated lipid metabolism, impaired arginine-arginine-nitric oxide (NO) and methionine signaling, heightened oxidative stress, and ferroptotic pathways. Proteomic studies identify disrupted angiogenic and cytoskeletal programs with potential biomarker utility in cerebrospinal fluid and serum. Current diagnostic standards employ MRI/MRA and digital subtraction angiography. Observational data support antiplatelet agents, including cilostazol, in reducing stroke recurrence and mortality. Direct and combined bypass approaches demonstrate superior outcomes in adult hemorrhagic disease, whereas indirect revascularization predominates in pediatric populations. Emerging AI-integrated diagnostic algorithms incorporating imaging and multiomic data exhibit promising diagnostic accuracy. Systematic integration of genotypic and multiomic profiling with hemodynamic assessment could enhance prognostic precision, optimize surgical timing, and guide antiplatelet selection in Moyamoya. Next step priorities include studying ethnically diverse multicenter registries and rigorous trials evaluating targeted and regenerative therapeutic strategies. Digital subtraction angiography (DSA)-guided diagnosis and individualized revascularization strategies remain the clinical standard.

This review provides an update on recent advances in molecular and imaging biomarker discovery for the diagnosis and prognosis of vestibular schwannoma (VS), with the goal of accelerating their validation and clinical adoption. A panel of nine circulating plasma biomarkers - TNF-R2/MIF/CD30/MCP-3/IL-2R/BLC/TWEAK/eotaxin/S100B - shows strong discriminatory power between patients with VS and healthy controls, with MCP-3 and S100B correlating with hearing loss and tumor size, respectively. A ~40-fold elevation of CFHR2 levels in the perilymph of patients with severe VS-induced hearing loss implicates complement activation in cochlear inflammation. Tumor-secreted TNF-α and TWEAK reach the inner ear and exhibit synergistic ototoxicity. Tissue profiling identified two distinct biomarker panels: one comprising ANGPTL1/IL17RC/LTBR/OLR1/TGFBR1, which associates with tumor cell proliferation and migration; and another including MMP-2/MMP-14/CD80/CD163/CD45, which accurately predicts peritumoral adhesion. Several tumor-derived miRNAs, including miR-431-5p, miR-7, miR-142-3p/5p, miR-155, and hypoxamiRs, are associated with hearing outcomes and tumor growth. MRI biomarkers from dynamic contrast-enhanced and diffusion-weighted imaging, as well as perilymph signal intensity ratio correlate with tumor growth, surgical outcomes, and auditory decline, respectively. This review outlines emerging circulating, tissue-derived and imaging biomarker candidates in VS that may complement MRI and support more precise diagnosis, monitoring, and individualized management.

To review progress in developing new pharmacological treatments for epilepsy, focusing on agents in clinical development. Over 30 different treatments are currently in clinical development, including novel small molecules, nucleic acid-based therapies, stem cells, microbiome-targeting bacteria, and repurposed drugs originally approved for other indications. Most of these treatments target rare epilepsies, particularly the developmental and epileptic encephalopathies, reflecting a development shift from common epilepsies to rare drug-resistant syndromes where unmet therapeutic needs are greatest. Most compounds are still in early development, and publicly accessible data consist mainly of conference reports and congress abstracts. For only two compounds (the Kv7 activator azetukalner and the inhaled emergency treatment Staccato alprazolam) has evidence of efficacy been obtained from relatively large, well designed randomized placebo-controlled trials. New paradigms in drug discovery have brought to development innovative treatments with diverse targets and mechanisms of action. Many of these treatments are etiology-targeting and have the potential for disease-modifying effects. Although high-quality evidence is awaited, there is hope that over the next few years, much needed life-changing therapies will be widely available for millions of people with disabling, drug-resistant epilepsies.

Alzheimer's disease (AD) is commonly defined by its hallmark brain pathologies, yet mounting evidence shows that metabolic impairment particularly linked to mitochondrial dysfunction, is a central and systemic feature of the disease. This review highlights consistent abnormalities in mitochondrial function, and turnover (mitophagy) across multiple AD-derived peripheral cells, including skin fibroblasts, lymphocytes, platelets, and peripheral blood mononuclear cells. We also report on potential peripheral AD biomarkers linked to mitochondria dysfunction in AD. Mitochondrial abnormalities in peripheral cells from individuals with AD robustly correlate with disease development. These mitochondrial dysfunctions mostly include reduced respiratory chain activity, increased accumulation of reactive oxygen species (ROS), altered mitochondrial membrane potential, and consequently decreased ATP production. Studies have also identified a complex pattern of mitochondrial hyperactivity and hypoactivity in peripheral cells of AD patients that appears to depend on the stage of AD and whether the disease is sporadic or familial. Furthermore, multiple steps of the mitophagy pathway are disrupted in peripheral cells as AD progresses. Finally, biochemical and proteomic analyses of peripheral fluids further support the loss of mitochondrial homeostasis in AD patients. Collectively, the reviewed findings support mitochondrial homeostasis disruption as a core pathophysiological component of AD and a promising target for biomarker development and therapeutic intervention.

One in five patients with epilepsy has idiopathic generalized epilepsy (IGE). Novel definitions of seizure types, recent data on pharmacotherapy, and new studies on psychiatric and cognitive comorbidities will be critically discussed. Epileptic seizures have been re-classified by the International League Against Epilepsy (ILAE), acknowledging absence-to-tonic-clonic seizures and generalized negative myoclonic seizures. Differing from the classical ILAE definition of IGE subtypes, current evidence underlines that IGEs represent rather a neurobiological continuum than separate syndromes. Valproate is still the most efficacious compound to suppress myoclonic and tonic-clonic seizures, but novel data confirm the high risk for both anatomical and neurodevelopmental teratogenicity. However, switching from valproate to other antiseizure medications commonly results in seizure recurrence or worsening. As compared to the general population, persons with IGE have a two- to fourfold increased risk of psychiatric disorders, the lifetime risk is 30-50%. Bidirectional associations between IGE and psychiatric conditions suggest that the latter are integral components of a broader IGE endophenotype. Valproate continues to be the most efficacious treatment for IGE but also the most teratogenic, leaving women who plan to become pregnant in a dilemma. Psychiatric comorbidities are frequent in IGE and thus require special attention and a holistic treatment approach.