Baqai Medical University

Multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein-associated disease (MOGAD) are the major types of demyelinating disorders of the central nervous system (CNS). Demyelinating disorders impact women disproportionately and frequently present during reproductive years. These conditions can cause significant neurological disability and psychosocial challenges, especially for women. Because they often present during reproductive years, clinicians frequently manage contraception, pregnancy, and the postpartum period alongside disease control. Sex-specific evidence, therefore, becomes especially important for treatment decisions. Despite this, sex-specific differences in epidemiology, immunopathology, clinical features, and therapeutic response remain inconsistently addressed in both clinical practice and research. In this review, we synthesize current evidence on the factors underlying the female predominance observed in MS, NMOSD, and MOGAD, and discuss the clinical consequences of these findings. We investigate the influence of sex hormones, X-chromosome–mediated immune regulation, and immunological changes associated with pregnancy and the postpartum period, as well as disease-specific mechanisms. We also examine how these factors affect diagnosis, prognosis, therapeutic decision-making, pregnancy management, and quality of life. Finally, we highlight important gaps in knowledge and underscore the necessity for a sex-informed approach to the diagnosis, management, and research of autoimmune demyelinating diseases.

Temporal Lobe Epilepsy with Hippocampal Sclerosis (TLE-HS) presents a significant therapeutic challenge, primarily due to pharmacoresistance and progressive hippocampal neurodegeneration. Since current anti-seizure therapies often provide limited seizure control in TLE-HS, there is increasing interest in exploring alternative and complementary treatment approaches. Chinese herbal medicine (CHM) or Traditional Chinese medicine (TCM) has gained attention for its multifaceted therapeutic potential, particularly its neuroprotective and anticonvulsant effects. This review explores preclinical and emerging clinical evidence supporting the efficacy of TCM in modulating key molecular targets involved in epileptogenesis. Several TCM-derived bioactive compounds exhibit anti-inflammatory properties by downregulating proinflammatory cytokines and damage-associated molecular patterns. Additionally, TCMs promote neurotrophic factor expression and enhance synaptic plasticity, thereby supporting neuronal survival. By balancing excitatory (glutamatergic) and inhibitory (GABAergic) neurotransmission, TCM may reduce seizure susceptibility and progression. Notably, herbs such as Gastrodia elata and Uncaria rhynchophylla demonstrate promising mechanistic effects. Although encouraging, these findings necessitate further pharmacological validation and clinical trials to substantiate TCM as a complementary, evidence-based intervention for patients with pharmacoresistant TLE-HS.

INTRODUCTION:Ischemic stroke, comprising nearly 85% of all strokes, remains a leading cause of death and disability worldwide. Annually, about 795,000 individuals in the United States (US) experience a new or recurrent stroke. Despite advancements in diagnosis, treatment, and prevention, significant disparities and geographic variability persist, highlighting the need for targeted strategies to address these ongoing challenges. METHODS:We analyzed US death certificate data from Centers for Disease Control and Prevention Wide-ranging Online Data for Epidemiologic Research (1968-2023) for ischemic stroke mortality using International Classification of Diseases (ICD-8, ICD-9, and ICD-10) codes. Demographics included age, sex, and race/ethnicity. Crude and age-adjusted mortality rates (AAMRs), annual percent change (APC), and average annual percent changes (AAPC) were calculated using joinpoint regression, and a p-value less than 0.05 defined significance. RESULTS:From 1968 to 2023, ischemic stroke mortality declined substantially, with 1,363,668 total deaths and the AAMR decreasing from 76.2 to 10.0 per 100,000 (AAPC: -3.59%). Early steep declines occurred from 1968 to 1982 and continued through 2014, followed by pronounced increases between 2014-2017 (APC 38.69) and 2017-2023 (APC 7.48). Men consistently exhibited higher AAMRs than women, with long-term declines, yet both experienced recent upward trends. Racial disparities persisted, with Black adults declining from 85.9 to 14.2 (AAPC: -3.30%) and White from 75.5 to 9.8 (AAPC: -3.63%), but both showed reversals after 2014. Older adults (≥65 years) bore the greatest burden (AAPC: -3.91%), while younger age groups exhibited smaller reductions. CONCLUSION:Despite long-term declines in mortality, recent increases and persistent disparities by age, sex, and race underscore the need for targeted prevention and equitable healthcare interventions in particularly high-risk populations.

[This corrects the article DOI: 10.7759/cureus.88238.].

Introduction Sleep deprivation is an escalating public health concern among young adults, as it impairs cognitive function and increases the risk of cardiovascular disease (CVD). Existing studies have linked chronic sleep deficiencies to mental confusion, reduced cognitive performance, and early signs of cognitive decline. Research also indicates that inadequate sleep contributes to metabolic dysregulation and autonomic system instability, both of which elevate cardiovascular risk. However, the overall effects of sleep deprivation on cognitive function and cardiovascular markers in young adults require further exploration. This study aims to examine the relationship between sleep deprivation, brain fog, early cognitive decline, and cardiovascular risk factors in this population. Methods This cross-sectional study involved 300 participants aged 18-30 from Pakistan and various other countries. Participants were selected using non-probability purposive sampling. Data were collected using four validated instruments: the Pittsburgh Sleep Quality Index, the Cognitive Failures Questionnaire, the Mini-Mental State Examination, and the Perceived Stress Scale. Data analysis was conducted using IBM SPSS Statistics for Windows, Version 26.0 (Released 2019; IBM Corp., Armonk, NY, USA), applying chi-square tests, independent sample t-tests, ANOVA, Pearson correlation, and logistic regression to assess associations between sleep deprivation, cognitive performance, and cardiovascular outcomes. Results Participants with shorter sleep durations had significantly higher scores in cognitive failures (p < 0.01) and perceived stress (p < 0.01). Poor sleep quality was associated with reduced cognitive performance (r = -0.114, p < 0.05), and it also increased the likelihood of developing cardiovascular risk factors. Participants with a family history of CVD exhibited significantly higher cognitive failure scores (t = 5.540, p < 0.001). Furthermore, a decline in sleep quality was associated with increased cardiovascular risk (B = 0.035, p = 0.019), although sleep disorders were not significantly influenced by sleep quality deterioration (B = 0.012, p = 0.400). Employment status and smoking habits were also found to impact both sleep quality and cognitive function (p < 0.01). Conclusions This study highlights the adverse impact of insufficient sleep on cognitive function and cardiovascular health in young adults aged 18-30. Poor sleep quality is associated with increased cognitive errors, heightened stress levels, and a greater risk of cardiovascular issues. These findings emphasize the importance of targeted health interventions aimed at improving sleep hygiene and lifestyle behaviors to reduce the risk of early cognitive decline and cardiovascular conditions. Future research should employ longitudinal designs and objective sleep tracking to strengthen causal inferences.