Acute paraplegia recognized following cesarean section under neuraxial anesthesia is a rare but alarming clinical presentation that requires urgent evaluation. Although neuraxial anesthesia–related complications are important considerations, structural spinal pathologies must be promptly excluded when neurological deficits persist. Hemorrhagic spinal schwannoma presenting acutely in the peripartum period is exceptionally uncommon and may clinically mimic a neuraxial anesthesia–related complication or spinal hematoma. We report a 34-year-old previously healthy woman in whom complete paraplegia was first recognized after emergency cesarean section under spinal anesthesia. Neurological examination revealed complete flaccid paralysis of both lower limbs with a T4 sensory level and urinary retention. Urgent magnetic resonance imaging demonstrated a cervicodorsal intradural extramedullary lesion causing severe spinal cord compression. Emergency surgical decompression was performed. Intraoperatively, a hemorrhagic mass was identified, and histopathological analysis confirmed a schwannoma with extensive intratumoral hemorrhage. Postoperatively, the patient developed fever and inflammatory marker elevation; however, cerebrospinal fluid studies excluded central nervous system infection. Despite adequate surgical decompression, no meaningful neurological recovery was observed during the reported hospitalization, and the patient was referred for comprehensive neurorehabilitation. Hemorrhagic spinal schwannoma is a rare but important cause of acute postpartum paraplegia that may temporally mimic a neuraxial anesthesia–related complication. The temporal association alone should not be interpreted as evidence of causality, particularly when the neurological lesion is anatomically remote from the site of neuraxial puncture. Persistent or atypical neurological deficits after cesarean delivery should prompt urgent spinal imaging to identify structural causes.
Alzheimer’s disease (AD) is increasingly recognized as a major public health concern due to its rising prevalence and the emotional, physical, and economic burdens it imposes. In many communities, AD is often mistaken for normal aging, which delays diagnosis and treatment. This study evaluated the level of public knowledge about AD in the Wadi al Shatii district of the Fezzan region, Libya. A cross-sectional survey using the Arabic-validated Alzheimer’s Disease Knowledge Scale (ADKS) was conducted among 430 respondents (response rate: 84.3
Depression is a frequent comorbidity in Multiple Sclerosis (MS), significantly affecting cases’ quality of life and adherence to treatment. Relapsing-Remitting MS (RRMS), the most prevalent subtype of MS, is notably linked to psychiatric symptoms and impaired functioning resulting from physical disability. This study aimed to assess the relationship between disability severity and depression in RRMS cases, considering neurological symptoms and sociodemographic factors. A cross-sectional study was conducted at the Neuropsychiatry Inpatient and Outpatient MS Clinic, Benha University Hospital, from October to April 2025. Thirty patients with relapsing-remitting multiple sclerosis (RRMS) and 30 age- and sex-matched healthy controls were recruited. Inclusion criteria for RRMS patients were age 18–60 years and diagnosis according to the 2024 Revised McDonald Criteria; participants with significant psychiatric, neurological, or medical comorbidities were excluded. All participants underwent a detailed neuropsychiatric evaluation, including the Expanded Disability Status Scale (EDSS), Beck Depression Inventory-II (BDI-II), and Columbia-Suicide Severity Rating Scale (C-SSRS). Data were analyzed using SPSS v28; quantitative variables were compared with t-tests or ANOVA, categorical variables with Chi-square or Fisher’s exact test, and correlations were assessed using Spearman’s coefficient. Multivariate logistic regression was used to identify predictors of moderate-to-severe depression and suicidal ideation, with P < 0.05 considered significant. Depression was significantly elevated in MS cases than controls (P = 0.001). Moderate to very severe depression affected 73.3
Smart phones emit electromagnetic radiation and blue light which cause many effects on retina and CNS. The aim is to investigate MP usage effect on vision in healthy adults by using VEP and ERG and to correlate these effects with age and previous usage duration. 70 healthy participants were subjected to one hour exposure to a smart phone set at 30 cm distance from eyes. P-VEP and ERG (pattern, full field flash and multifocal) were recorded pre and post exposure. Correlations with age and with prior history of duration of usage were analyzed. Significant P100 latency delay was reported in P-VEP. No effect on P-ERG was observed. F-ERG showed a high statistically significant reduction in b wave amplitude. MF ERG showed a statistically significant P1 amplitude reduction and latency delay. P100 latency increase showed a positive correlation with age and a negative one with prior exposure duration. F-ERG showed significant negative change in (a) wave latency with age but no significant one with MP usage duration. Regarding MF ERG, there was significant negative correlation of P1 wave with age and with the duration of MP usage. Practicing mindful mobile device utilization to minimize possible undesirable effects on vision is advised. These effects were more obvious in central retina. Long duration of previous use of MP increases tolerance of electro-diagnostic tests of vision to acute exposure though impairing basal function. ERG is more affected in young age, but VEP is more impaired in old age after acute MP exposure.
Treatment-resistant depression (TRD) is a common and disabling clinical problem associated with persistent symptoms, functional impairment, relapse risk, suicidality, and high health-system burden. Neuromodulation has become an increasingly important treatment pathway because it directly modulates neural circuits implicated in mood regulation rather than relying exclusively on pharmacological mechanisms. To review and critically synthesize current evidence on neuromodulation for TRD, with emphasis on electroconvulsive therapy, repetitive transcranial magnetic stimulation (rTMS), intermittent theta-burst stimulation (iTBS), transcranial direct current stimulation, vagus nerve stimulation, deep brain stimulation, safety, clinical translation, and implementation challenges. We conducted a structured narrative review of clinically relevant literature identified through searches of PubMed/MEDLINE, Scopus, Web of Science, guideline repositories, and reference lists. The search was intended to improve the breadth and transparency of the narrative synthesis and was not conducted as a formal systematic review. No protocol was registered, and no duplicate screening, formal risk-of-bias assessment, certainty-of-evidence evaluation, or quantitative synthesis was performed. The literature supports a provisional multidimensional clinical-positioning framework rather than a head-to-head efficacy hierarchy. Electroconvulsive therapy remains the most established intervention for severe, psychotic, catatonic, suicidal, or life-threatening depression. Repetitive transcranial magnetic stimulation is a validated non-invasive outpatient treatment with favorable tolerability and expanding protocol options. Intermittent theta-burst stimulation provides similar clinical utility with shorter sessions, whereas accelerated and image-guided iTBS protocols are promising but require further replication, durability, and maintenance data. Transcranial direct current stimulation, including supervised home-based models, is being investigated as a potentially scalable approach, but its TRD-specific evidence and real-world implementation remain less established than those of rTMS. Vagus nerve stimulation and deep brain stimulation may benefit selected highly refractory patients, but delayed response, invasiveness, cost, evidentiary heterogeneity, and long-term device-management requirements limit routine use and largely restrict these modalities to specialized services. Neuromodulation may be incorporated as a staged, protocol-based component of multidisciplinary TRD care where appropriate expertise, infrastructure, and follow-up are available, rather than being viewed as a single interchangeable device category. Broader adoption requires standardized definitions, individualized targeting, maintenance planning, adverse-event monitoring, equitable access, and pragmatic implementation research.
Abstract Background Recurrent depressive episodes adversely affect quality of life and treatment outcomes in cases with schizophrenia. This study determined the prevalence of depressive symptomatology among cases with schizophrenia, examined the relationship between sociodemographic and clinical characteristics and the development of depressive symptoms, and compared these characteristics between patients with positive and negative CDSS status. Results No substantial correlations were detected between CDSS scores and sociodemographic characteristics or clinical features, except for duration of illness. CDSS scores showed a statistically marked association with gender and history of suicide attempts (P < 0.05). Male sex was identified as a significant independent protective factor against depression, whereas a duration of schizophrenia of ≥ 8 years was a significant independent risk factor for its development. Conclusions Male sex was independently associated with lower odds of positive CDSS status, while a duration of schizophrenia of ≥8 years was independently associated with higher odds of depressive symptomatology, as defined by positive CDSS status.
Abstract Background Ischemic stroke is a major cause of mortality and long-term neurological disability worldwide. Although conventional vascular risk factors explain a substantial proportion of ischemic stroke burden, genetic susceptibility may contribute to inter-individual and population-level differences in risk. The angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism is a biologically plausible vascular candidate variant because of its relationship with ACE activity, renin-angiotensin system regulation, endothelial function, vascular remodeling, and blood-pressure control. However, findings from Middle Eastern populations remain inconsistent. Objective To systematically evaluate and quantitatively synthesize the association between ACE I/D polymorphism and ischemic stroke susceptibility in populations from the Middle East, with inferences restricted to the countries represented in the eligible evidence—Turkey, Egypt, Iran, and Iraq. Methods This PRISMA 2020–based systematic review and meta-analysis was prospectively registered in PROSPERO (CRD420261406483). PubMed/MEDLINE, Scopus, and Web of Science were searched from inception to May 23, 2026 for observational genetic association studies reporting ACE I/D genotype or allele data in ischemic stroke cases and stroke-free Middle Eastern controls. Two reviewers independently conducted study selection, data extraction, and Newcastle-Ottawa Scale quality assessment. Random-effects ORs with 95% CIs were pooled under allele, dominant, recessive, homozygous, and heterozygous models, with sensitivity analyses excluding studies with HWE deviation, reconstructed counts, historical controls, and other strict-quality concerns. Results Ten studies including 1,317 ischemic stroke cases and 979 controls were included, representing Turkey, Egypt, Iran, and Iraq. Across all primary random-effects models, ACE I/D polymorphism was not significantly associated with ischemic stroke susceptibility. The pooled estimates were: allele contrast D vs. I, OR = 1.16 (95% CI: 0.97–1.38); dominant model DD + ID vs. II, OR = 1.20 (95% CI: 0.91–1.57); recessive model DD vs. ID + II, OR = 1.20 (95% CI: 0.89–1.61); homozygous model DD vs. II, OR = 1.26 (95% CI: 0.94–1.70); and heterozygous model ID vs. II, OR = 1.14 (95% CI: 0.84–1.55). Heterogeneity ranged from low to moderate across most models, with the highest heterogeneity observed in the recessive model. Sensitivity analyses, particularly the exclusion of two studies with control-group Hardy–Weinberg equilibrium deviation, consistently attenuated the pooled estimates toward the null and did not support a robust association. Conclusion Available evidence does not demonstrate a statistically robust association between ACE I/D polymorphism and ischemic stroke susceptibility in the populations studied in Turkey, Egypt, Iran, and Iraq. Although D-allele and DD-genotype carriers showed a weak non-significant trend toward increased risk, this pattern was not stable under sensitivity analyses. Given the null pooled findings, modest evidence base, predominance of unadjusted genotype-derived estimates, and absence of reliable stroke subtype-specific data, the current evidence does not support ACE I/D genotyping for clinical ischemic stroke risk prediction. These findings should not be generalized to Middle Eastern countries for which eligible evidence was unavailable.
Idiopathic epilepsy is often considered mild, yet affected children may experience cognitive and language difficulties, including reading deficits. This study aimed to assess reading abilities and associated cognitive-linguistic skills in Egyptian children with idiopathic epilepsy, and to explore associations between epilepsy-related characteristics and Arabic literacy outcomes. This cross-sectional study included 60 Egyptian children aged 6 years 6 months to 9 years 6 months with idiopathic epilepsy and normal intellectual functioning (IQ > 85). Exclusion criteria included intellectual disability, hearing loss, ADHD, autism spectrum disorder, or other neurological conditions affecting learning. Reading and cognitive-linguistic skills were assessed using eight subtests of the Modified Arabic Dyslexia Screening Test (MADST), measuring phonological processing, rapid naming, working memory, reading fluency, and decoding. Three-quarters (75.0
Abstract Background Emotional and behavioral difficulties among children and adolescents are increasingly recognized worldwide, with significant implications for development, academic performance, and social well-being. In Saudi Arabia, nearly 40% of youth are estimated to experience such challenges, yet parental recognition is often hindered by cultural stigma and limited awareness. Understanding how parents perceive and report these difficulties is critical for early identification and mental health promotion. Objectives To assess Saudi parents’ perceptions and reports of emotional and behavioral difficulties among children and adolescents in Makkah City, examine how sociodemographic factors influence these difficulties, and identify independent predictors. Methods A cross-sectional study was conducted among 434 Saudi parents of children aged 6–18 years, recruited from eight stratified randomly selected schools across Makkah. Data were collected using an online, parent-completed questionnaire that included sociodemographic information and items derived from the validated Arabic version of the Strengths and Difficulties Questionnaire–Parent Version (SDQ-P). Emotional and behavioral difficulties were assessed and categorized according to the SDQ Total Difficulties Score (TDS). Statistical analyses included nonparametric Mann–Whitney test and Kruskal–Wallis tests for bivariate associations and multiple linear regression modeling to identify independent sociodemographic predictors. Results The median age of the children was 12 years, with 59% being female. Based on parent-reported TDS, 51.8% of children were within the normal range, 20.7% were borderline, and 27.4% were in the abnormal range. Elevated difficulties were particularly noted in emotional symptoms (26.5%) and conduct problems (27.4%). Bivariate analysis showed that male sex, older age, lower parental education, unemployed fathers, maternal employment, larger family size, separated or widowed parents, and lower household income were significantly associated with higher TDS ( p < 0.05). Multivariate analysis confirmed several of these as independent predictors, with maternal employment (B = 4.437, p < 0.001), low household income (B = 3.761, p < 0.001), and lower parental education (B = 2.801, p = 0.011 for mothers; B = 2.316, p = 0.015 for fathers) showing the strongest associations. Conclusion A substantial proportion of children in Makkah exhibit emotional and behavioral difficulties as reported by their parents using the SDQ-P. These difficulties are significantly influenced by sociodemographic factors, particularly parental education, employment status, and household income. Targeted awareness programs, early school-based screening, and culturally sensitive, family-focused interventions are essential to support child emotional and behavioral health in this setting.
Stroke remains a leading cause of global mortality and disability, necessitating innovative rehabilitation strategies to enhance recovery. Interactions between astrocytes and neurons modulate neural plasticity. This review synthesizes current evidence on the role of astrocytes in stroke recovery, focusing on their contributions to neural plasticity through neurotransmitter homeostasis, gliotransmission, neurotrophic factor release, metabolic support, modulation of inflammation, and extracellular matrix remodeling. Astrocytes regulate synaptic function via glutamate uptake and D-serine release, support neuronal survival through brain-derived neurotrophic factor (BDNF) and glial cell-derived neurotrophic factor (GDNF), and shape the neuroinflammatory response via crosstalk with microglia. While reactive astrocytes form protective glial scars, they also pose barriers to axonal regeneration. We explore astrocyte-targeted therapeutic strategies, including pharmacological interventions (minocycline, celastrol), non-invasive neuromodulation (tDCS, rTMS), stem cell therapy, and cellular reprogramming, highlighting their potential to enhance plasticity and recovery. Challenges such as limited translational models, difficulties isolating astrocyte-specific effects, and methodological constraints in imaging are discussed, alongside future directions involving single-cell transcriptomics to address astrocyte heterogeneity. By elucidating the multifaceted roles of astrocytes, this review highlights their therapeutic potential in stroke rehabilitation and advocates targeted interventions to optimize neuroprotection and circuit rewiring.
Abstract Alzheimer’s disease (AD) is the leading cause of dementia worldwide and poses an increasing challenge for ageing populations. For decades, pharmacologic management has relied on cholinesterase inhibitors and memantine, which provide modest symptomatic benefit without altering the underlying neurodegenerative process. Recent advances in anti-amyloid monoclonal antibodies and investigational therapies targeting tau pathology, neuroinflammation, and metabolic dysfunction have renewed interest in disease-modifying therapies. This PRISMA 2020-guided narrative review critically evaluates current and emerging pharmacotherapies for AD, with emphasis on clinical efficacy, safety, and relevance to geriatric practice. A structured search of PubMed/MEDLINE, Embase, Scopus, Web of Science, CENTRAL, and ClinicalTrials.gov identified 71,663 records published between January 2000 and January 2026. After screening and eligibility assessment, 18 randomized and phase II/III clinical trials were included in the qualitative synthesis. Owing to substantial heterogeneity in study design, patient populations, and outcome measures, findings were synthesized narratively rather than quantitatively. Cholinesterase inhibitors and memantine were associated with small-to-moderate improvements or stabilization in cognition and global function, although limited durability and tolerability may restrict long-term use. Anti-amyloid monoclonal antibodies, particularly lecanemab and donanemab, demonstrated statistically significant slowing of cognitive decline in early AD; however, the absolute clinical benefits remained modest and were accompanied by amyloid-related imaging abnormalities, necessitating careful monitoring with magnetic resonance imaging. Emerging therapies targeting tau pathology, neuroinflammatory pathways, and metabolic dysfunction remain investigational. Overall, symptomatic therapies continue to represent the foundation of AD management, whereas anti-amyloid monoclonal antibodies mark an important, although incremental, transition toward disease modification in carefully selected patients.
Abstract Background Status epilepticus (SE) has been defined as a seizure that persists for more than 5 min. If SE persists despite benzodiazepine and appropriately dosed antiseizure medications, it could be regarded as refractory SE (RSE). New-onset refractory status epilepticus (NORSE) is a separate syndrome that occurs in individuals without active epilepsy or other preexisting relevant neurological disorders. A small number of neuropathology reports of patients who died of SE, RSE and NORSE are available, revealing hypoxic and ischemic neuronal damage and cortical laminar necrosis (CLN). CLN is a well-known sequela of SE, which has been often suspected radiologically, although its anatomical background is largely unknown. Case presentation An 84-year-old man with a history of malignant lymphoma in complete remission presented with high fever and impaired consciousness. He developed tonic-clonic convulsions, which lapsed into SE. CSF revealed a normal cell count and elevated protein. MRI of the brain showed high signal intensities on diffusion-weighted and FLAIR images in the mid-temporal lobe bilaterally and left insular cortex. EEG showed epileptic discharges on the left side with an extreme delta brush pattern. He was diagnosed with possible autoimmune encephalitis. Despite treatments, he remained comatose and died of pneumonia, 24 days after the onset of seizures. A complete autopsy failed to reveal the presence of malignancy. Neuropathologically, the brain showed atrophic changes involving the insular cortex, orbitofrontal cortex and medial temporal lobe, predominantly on the left side. Histologically, the lesions corresponding to the abnormal MRI images revealed CLN involving the mid- cortical layers. Remarkably, this was associated with perivascular and intraparenchymal infiltration of plasma cells and T lymphocytes, which was also seen in the overlying subarachnoid membrane and in the adjacent intact appearing parenchyma. Conclusion The present case demonstrates that RSE with cortical involvement on MRI could be anatomically associated with CLN, which is accompanied by massive infiltration of plasma cells and T lymphocytes. The novel association of CLN and lympho-plasmacytic infiltration requires further investigation.
Abstract Background To investigate the clinical effectiveness of a custom hand-held endoscopic auxiliary device in assisting unilateral biportal endoscopic lumbar interbody fusion (ULIF) during the treatment of lumbar degenerative diseases. A total of 31 patients with lumbar degenerative diseases who received ULIF treatment between June 2021 and February 2025 were selected for the study. The baseline characteristics, clinical outcomes, complications and radiological data were collected and analyzed. Results The average follow-up time of the 31 patients was 20.65 ± 11.80 months; the average operation time was 305.45 ± 85.39 min; the average intraoperative blood loss was 379.03 ± 213.22 mL; and the average postoperative hospital stay was 21.58 ± 8.68 days. The VAS scores for leg pain and low back pain, as well as the ODI at 1 week, 3 months postoperatively, and the last follow-up, were significantly lower than the preoperative scores ( P < 0.05). The X-ray/CT reexamination conducted 6 months postoperatively showed 15 cases (48.39%) of Bridwell Grade I fusion, 12 cases (38.71%) of Grade II fusion, and 4 cases (12.90%) of Grade III fusion. Based on the modified Macnab criteria at the 6-month postoperative mark, 28 cases (90.32%) were rated as “excellent” and 3 cases (9.68%) as “good”. Conclusion The ULIF procedure, assisted by a custom hand-held endoscope auxiliary device, offers a strategic solution for expanding surgical efficiency in primary hospitals. Its minimally invasive nature makes it an effective, viable option for improving patient care, especially suitable for beginners.
Abstract Background Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease characterized by progressive neurodegeneration and brain atrophy. Objective To evaluate brainstem and cerebellar volumetric changes in patients with relapsing-remitting multiple sclerosis (RRMS) using 3T MRI and to investigate their relationship with disease duration, lesion burden, and neurological disability. Methods This cross-sectional case-control study included 26 RRMS patients and 26 age- and sex-matched healthy controls. Automated volumetric analysis was performed using the volBrain platform. Brainstem and cerebellar volumes were assessed. Disability was evaluated using the Expanded Disability Status Scale (EDSS). Results RRMS patients demonstrated significantly reduced total brainstem volume and normalized brainstem volume percentage compared with controls ( p = 0.016 and p = 0.01, respectively). Normalized total cerebellar volume and normalized left cerebellar volume were significantly lower in patients ( p = 0.043 and p = 0.02, respectively), whereas absolute cerebellar volumes showed no significant differences. Cerebellar gray matter volumes demonstrated strong negative correlations with disease duration (r ranging from − 0.53 to − 0.63, p ≤ 0.005). Cerebellar white matter volumes were negatively associated with lesion load ( r = − 0.42 to − 0.59, p ≤ 0.035) and EDSS scores ( r = − 0.44 to − 0.54, p ≤ 0.026). Receiver Operating Characteristic (ROC) analysis revealed moderate discriminatory performance for brainstem volume (Area Under the Curve (AUC) = 0.694), brainstem volume percentage (AUC = 0.706), normalized cerebellar volume (AUC = 0.691), and cerebellar gray matter percentage measures (AUC = 0.660–0.689). Conclusion Infratentorial volumetric abnormalities are evident in RRMS, with cerebellar measurements demonstrating stronger associations with disease duration, lesion burden, and disability than brainstem measurements. Cerebellar volumetry, particularly normalized gray matter metrics, may represent a sensitive imaging biomarker of disease burden and progression in MS.
Abstract Background High Mobility Group Box 1 protein functions as a danger-associated molecular pattern and is crucial in the pathophysiology of ischemic damage and ensuing inflammatory responses. Objective To assess the role of HMGB1 as a biomarker for evaluation of the severity and clinical outcome of ischemic stroke. Subjects and methods The study participants were split into two categories: Case group (30) and Control group (30). Every participant underwent a medical history review, along with general and neurological evaluations. All patients were categorized according to The TOAST classification and assessed using the NIHSS and The modified Rankin Scale (mRS). The laboratory evaluation included the assessment of HMGB-1 levels. The radiological evaluation included CT brain, MRI brain, and carotid duplex. Results The levels of HMGB-1 were significantly higher in cases of ischemic stroke compared to controls ( P < 0.001). A substantial rise in HMGB-1 levels was observed from mild to severe stroke. Patients with poor mRS showed a notable rise in HMGB-1 levels compared to those with good mRS ( P = 0.005). HMGB-1 can forecast ischemic stroke with a cutoff above 129.8. The Receiver Operating Characteristic (ROC) curve indicated that HMGB-1 can forecast ischemic stroke at a threshold exceeding 129.8. A cut-off value exceeding 247.3 of HMGB-1 demonstrated considerable predictive capability for adverse outcomes in stroke patients, yielding an AUC of 0.787 for HMGB-1 ( P < 0.001). Conclusion HMGB-1 has a potential role as a biomarker for prediction of severity and functional outcome of ischemic stroke.
Abstract Stroke remains a major global health concern, with persistently high rates of morbidity and disability. While advances in acute reperfusion therapy have improved outcomes, post-stroke complications such as glial scar formation continue to limit recovery. The glial scar, though protective in containing injury, also impedes axonal regrowth and neuroplasticity. Emerging preclinical evidence suggests that metabolic dysfunction exacerbates glial scarring, linking systemic metabolic disturbances to impaired neural repair. This editorial re-examines the glial scar through a metabolic lens and proposes the concept of metabolic surveillance—the continuous, multimodal monitoring of systemic and cerebral metabolic status to identify individuals at risk of maladaptive gliosis. Rather than advocating population-level screening, we argue for targeted translational research integrating molecular biomarkers, imaging techniques, and therapeutic modulation. Such a framework could guide personalized interventions to improve recovery after stroke and minimize long-term neuroinflammatory sequelae.
Neuropsychiatric toxicity related to 5-fluorouracil (5-FU) chemotherapy is an uncommon but clinically significant adverse effect that is frequently underrecognized. This narrative review summarizes the clinical spectrum, proposed mechanisms, diagnostic features, management strategies, and outcomes of 5-FU–associated neuropsychiatric complications. A literature search of PubMed/MEDLINE and EMBASE identified English-language case reports and case series published between 1960 and 2023 describing neuropsychiatric manifestations temporally related to 5-FU or its prodrugs. Symptoms typically emerged within 2–4 days following administration of 5‑FU, primarily manifesting as acute encephalopathy or changes in mental status including toxic leukoencephalopathy, manic or psychotic symptoms, seizures, and cerebellar dysfunction. Hyperammonemia was the most consistent biochemical abnormality, and brain MRI frequently demonstrated reversible bilateral white-matter changes, often involving the corpus callosum. Management centred on immediate cessation of 5-FU and supportive care, including hydration, ammonia-lowering therapy, and thiamine supplementation, with most patients achieving favorable neurological recovery. Early recognition and prompt intervention are critical to optimal outcomes. However, the absence of standardized diagnostic criteria, limited prospective data, and uncertainty regarding safe rechallenge strategies underscore the need for pharmacogenetically informed approaches and larger multicentre observational studies.
Drug-resistant epilepsy (DRE) is defined by International League Against Epilepsy (ILAE) as continued occurrence or persistence of seizures despite treatment with at least two syndrome-adapted antiseizure drugs (ASD) used at an adequate daily dose. This study aims to perform a network meta-analysis to identify and compare the relative contribution of various risk factors to psychiatric comorbidities among patients with DRE. This is a network meta-analysis study using 6 databases for searching the articles with certain PICO criterias. The risk of bias was assessed using ROBINS-E. The final results were analyzed using SUCRA analysis to rank the risk factors’ list. Four included studies were retrospective cohort and cross-sectional, with sample sizes ranging from 50 to 272 participants. Among the evaluated factors, “Onset age < 18 years” demonstrated the highest OR at 1.81 [95
Abstract Background Multimodal Intraoperative neurophysiological monitoring (mIONM) has been involved in spinal and brain surgeries, to localize and monitor important neural structures. Also to maintain their structural integrity throughout the operation, minimizing deficits both during and postoperative complications. Several modalities are used in modern IONM, each modality offers a special means of monitoring the performance of the nervous system during surgery. These modalities include Somatosensory-evoked potential, Motor-evoked potential, Electromyography, and others. This study was conducted to evaluate the usefulness of (mIONM) in complex brain and spinal surgeries, through calculating specificity, sensitivity, negative predicted value, and positive predictive value of combined mIONM modalities for postoperative neurological deficit occurrence. Methods This prospective observational cohort study included 50 patients aged ≥ 12 years who underwent cranial or spinal surgery with planned (mIONM). Monitoring included somatosensory evoked potentials, transcranial motor evoked potentials, and free-running and triggered electromyography, according to the surgical indication and neural structures at risk. The primary outcome was new postoperative neurological deficit within 72 h. Results The study revealed high sensitivity (97.73%), specificity (83.33%), and predictive value for combined SSEP, MEP and EMG monitoring in forecasting neurological outcomes. Conclusions The value of (mIONM) in enhancing the safety and effectiveness of intricate surgical procedures is affirmed by this study.
Wilson disease (WD) is an autosomal recessive disorder of copper metabolism caused by pathogenic variants in the ATP7B gene. Impaired biliary copper excretion leads to progressive accumulation in the liver, brain, and other organs. Despite prevalence estimates of 1:30,000 to 1:50,000, WD remains significantly underdiagnosed due to heterogeneous clinical manifestations and the absence of pathognomonic markers. This comprehensive review aimed to describe the current evidence on WD epidemiology, molecular pathogenesis, clinical manifestations, diagnostic strategies, and therapeutic approaches, with particular emphasis on neuropsychiatric presentations that contribute substantially to diagnostic delay and disability. We searched PubMed/MEDLINE, EMBASE, and the Cochrane Library from inception to July 2025 using MeSH terms and free-text keywords including ‘Wilson disease’, ‘ATP7B’, ‘copper metabolism’, ‘neuropsychiatric manifestations’, ‘ceruloplasmin’, ‘exchangeable copper’, ‘relative exchangeable copper’, ‘liver biopsy’, and ‘chelation therapy’. Priority was given to systematic reviews, randomized trials, clinical guidelines (EASL-ERN 2025, AASLD 2022), and large prospective or retrospective cohort studies. Clinical presentations encompass hepatic dysfunction (40–60
