Alessandro Zilioli

Objective: Treatment strategies for non‐convulsive status epilepticus (NCSE) are largely extrapolated from convulsive SE, despite biological and clinical differences. NCSE arises from heterogeneous etiological substrates that may influence treatment response and prognosis. We examined the association between treatment sequence, anti‐seizure medication (ASM) adequacy, etiological context, and clinical outcomes in NCSE. Methods: We analyzed 189 adult non‐anoxic NCSE patients from a 6‐year ambispective registry. Treatment variables included first‐line benzodiazepine (BDZ) use, ASM underdosing, and escalation to continuous intravenous anesthetic drugs (CIVADs). Etiology was classified according to International League Against Epilepsy (ILAE) categories and further stratified as potentially fatal v non‐fatal and as primary vs secondary central nervous system (CNS) pathology. Outcomes were failure of NCSE cessation, in‐hospital mortality, and functional worsening at discharge. Associations between treatment patterns and outcomes were evaluated using univariate and multivariable logistic regression analyses, with exploratory pre‐specified subgroup analyses across etiological categories. Results: ASM underdosing occurred in 73 of 189 episodes (38.6%) and was independently associated with failure of NCSE cessation (odds ratio [OR] 6.56, 95% confidence interval [CI] 1.98–21.78) and in‐hospital mortality (OR 4.38, 95% CI 2.01–9.54). Lack of first‐line BDZs (93/189, 49.2%) and escalation to CIVADs (41/189, 21.7%) were not independently associated with outcome. In subgroup analyses, the association between ASM underdosing and adverse outcomes was observed more consistently in acute primary CNS pathology and non‐fatal etiologies. Significance: In NCSE, outcome appears more closely associated with ASM dosing adequacy than strict adherence to a pre‐defined treatment sequence, particularly in clinical contexts where epileptic activity is likely to contribute substantially to prognosis. Pending future prospective, ideally randomized, investigations, optimal therapeutic strategies across heterogeneous NCSE subtypes remain to be clearly established.

Background: Up to half of patients with acute ischemic stroke (AIS) achieving successful reperfusion after endovascular thrombectomy (EVT) remain dependent. Although global atrophy may influence recovery, the prognostic value of regional atrophy patterns and white matter (WM) lesions remains uncertain. Methods: We retrospectively included consecutive AIS patients achieving successful reperfusion (modified Thrombolysis in Cerebral Infarction (mTICI) 2b–3) after EVT at a comprehensive stroke center (2015–2023). Baseline CT was used to rate medial temporal atrophy (MTA), parietal atrophy (Koedam; antero-posterior index (API)), global cortical atrophy-frontal (GCA-F), and white matter lesions (Fazekas scale). The primary outcome was a composite measure of futile recanalization: functional dependence (modified Rankin Scale (mRS) >2), mRS worsening if premorbid mRS>2, or death. The secondary outcome was the ordinal shift across the mRS distribution. Associations between visual rating scales and outcomes were assessed using multivariable logistic and proportional-odds models, with sex-stratified and interaction analyses. Results: A total of 450 AIS patients (mean age 73.6±14.0 years; 53.8% females; n=406 anterior circulation) were included. In anterior circulation stroke, parietal and frontal atrophy scales were independently associated with poor outcome: Koedam (adjusted OR (aOR) 2.19, 95% CI 1.32 to 3.63), GCA-F (aOR 1.90, 95% CI 1.11 to 3.26), and API-positivity (aOR 2.27, 95% CI 1.36 to 3.81). Periventricular and basal ganglia Fazekas scores were associated with poor outcome in univariate analyses but lost significance after multivariable adjustment. Conclusions: Parietal and frontal atrophy are independently associated with the risk of futile recanalization after EVT. CT-based regional atrophy ratings could enhance individualized risk stratification and support treatment selection.

The intricate connection between eating behaviors and sleep habits is often overlooked in clinical practice, despite their profound interdependence. Sleep plays a key role in modulating psychological, hormonal and metabolic balance and exerting an influence on food choices. Conversely, various eating disorders may affect sleep continuity, sometimes promoting the development of sleep pathologies. Neurologists, nutritionists and psychiatrists tend to focus on these issues separately, resulting in a failure to recognize the full extent of the clinical conditions. This detrimental separation can lead to underestimation, misdiagnosis and inappropriate therapeutic interventions. In this review, we aim to provide a comprehensive understanding of the tangled relationship between sleep, sleep pathologies and eating disorders, by incorporating the perspective of sleep experts, psychologists and psychiatrists. Our goal is to identify a practical crossroad integrating the expertise of all the involved specialists.

Wernicke's encephalopathy is an under-recognized life-threatening disease caused by thiamine (vitamin B1) deficiency. It has historically been related to chronic alcoholic intake but other causes of malnutrition, such as invasive gastric surgery and hyperemesis, have been linked to the onset of this illness over the years, often presenting with atypical clinical manifestations. Herein we report a case of a young obese woman affected by non-alcoholic Wernicke's Encephalopathy following a minimally invasive gastrointestinal surgery. She showed an unusual clinical profile characterized by prominent subacute neuro-ophthalmological involvement which combined to her juvenile age, overweight condition and brain lesions, have made diagnosis challenging due to similarities with Neuromyelitis Optica Spectrum Disorder. Our case underscores the relevance of prompt diagnosis in order to prevent the development of irreversible neuropathological changes and to avoid the use of a long-term immunosuppressive treatment.

Purpose: The pleiotropic effect of gliomas on the development of cognitive disorders and structural brain changes has garnered increasing interest in recent years. While it is widely accepted that multimodal therapies for brain cancer can foster cognitive impairment, the direct effect of gliomas on critical cognitive areas before anti-tumor therapies is still controversial. In this study, we focused on the effect of IDH1 wild-type glioblastoma on the human hippocampus volume. Methods: We carried out a case-control study using voxel-based morphometry assessment, analyzed with the Computational Anatomy Toolbox software. Glioblastoma diagnosis was performed according to the latest 2021 WHO classification. Due to stringent inclusion criteria, 15 patients affected by IDH1 wild type glioblastoma were included and compared to 19 age-matched controls. Results: We observed a statistically significant increase in the absolute mean hippocampal volume (p = 0.017), as well as in the ipsilateral (compared to the lesion, p = 0.027) and the contralateral hippocampal volumes (p = 0.014) in the group of patients. When the data were normalized per total intracranial volume, we confirmed a statistically significant increase only in the contralateral hippocampal volume (p = 0.042). Conclusions: To the best of our knowledge, this is the first study to explore hippocampal volumetric changes in a cohort of adult patients affected by IDH1 wild-type glioblastoma, according to the latest WHO classification. We demonstrated an adaptive volumetric response of the hippocampus, which was more pronounced on the side contralateral to the lesion, suggesting substantial integrity and resilience of the medial temporal structures before the initiation of multimodal treatments.