Search Results (601)

Background: Fatal choking is a preventable cause of mechanical asphyxia that occurs more frequently among individuals with psychiatric disorders due to behavioural abnormalities, neurological comorbidities, and medication-related swallowing impairment. This review aims to highlight the clinical and forensic factors contributing to fatal choking and the importance of a multidisciplinary approach to its investigation. Methods: A systematic review was conducted according to PRISMA guidelines by searching PubMed, Scopus, and Web of Science. In total, 25 studies describing fatal choking in adults with psychiatric disorders and including medico-legal investigations were selected and analyzed. Results: Schizophrenia was the most frequently reported psychiatric condition, followed by bipolar disorder, depression, and dementia. Antipsychotics, antidepressants, anxiolytics, and other psychotropic drugs were recurrently associated with dysphagia and reduced airway protective reflexes. Food boluses represented the predominant obstructive material, although several unusual foreign bodies were documented. Virtopsy, autopsy, histological, and toxicological investigations consistently proved essential for confirming airway obstruction, reconstructing the mechanism of death, and identifying contributing clinical and pharmacological factors. Conclusions: Fatal choking in psychiatric patients is a multifactorial event requiring early risk assessment, preventive strategies, and comprehensive forensic evaluation to improve patient safety and ensure accurate determination of the cause of death. Full article

In the post-pandemic era, identifying children who are most susceptible to severe illness and COVID-19-related mortality is essential for guiding public health policies. This study examined the risk factors for COVID-19-related severe illness and mortality from 2023 to mid-2025. We conducted a population-based cohort study using nationwide Brazilian data from patients aged <18 years with laboratory-confirmed SARS-CoV-2 infection between January 2023 and June 2025. The primary outcomes were COVID-19-related severity and death. Separate binary multivariable logistic regression models were developed for each of the outcomes. Among 465,689 children, 1.3% (n = 5963) developed severe illness, and 0.18% (n = 847) died. Factors associated with an increased risk of severe illness included age < 2 years, presence of comorbidities, Indigenous ethnicity, and lack of vaccination. Neurological disorders conferred the highest risk among the clinical conditions (adjusted odds ratio [aOR] = 34.1; 95% CI: 27.9–41.8). Regional differences were also observed; the North and Northeast regions showed higher mortality (aOR = 2.3; 95% CI: 1.8–3.0) than the Central-West region. Compared with White ethnicity, non-White ethnicities had higher mortality: Indigenous (aOR = 23.5; 95% CI: 13.5–39.3), Black (aOR = 1.95; 95% CI: 1.29–2.92), and Brown (aOR = 1.43; 95% CI: 1.18–1.73) ethnicities. Lack of any vaccine dose was associated with a significantly increased risk of severe illness (aOR = 1.39; 95% CI: 1.15–1.67. p < 0.001) and death (aOR = 2.1; 95% CI: 1.3–3.5; p < 0.001). In the post-pandemic era, younger age, comorbidities, sociodemographic disparities, and lack of vaccination were associated with an increased risk of severe illness and COVID-19-related death in the pediatric population. Full article

Background: Myasthenia gravis is an autoimmune disorder of the neuromuscular junction characterized by fluctuating skeletal muscle weakness. Late-onset MG (onset ≥ 50 and <65 years) and very late-onset MG (VLOMG; onset ≥ 65 years) are increasingly recognized subgroups, and diagnosis in very elderly patients remains challenging because symptoms frequently overlap with age-related conditions and comorbidities. Case Presentation: An 88-year-old man with very late-onset myasthenia gravis (symptom onset at approximately age 85) was urgently referred because of a several-day history of rapidly worsening dysphagia and dysarthria, superimposed on fluctuating diplopia, dysphagia, dysarthria, and fatigable bulbar symptoms that had progressively worsened over the preceding three years. Initial diagnostic evaluation was challenging because of advanced age, previous lacunar infarctions, and multiple comorbidities, including pulmonary thromboembolism, chronic kidney disease, and permanent pacemaker implantation (which precluded brain MRI). Neurological examination and the characteristic fluctuation of symptoms raised suspicion of myasthenia gravis. Serological testing confirmed markedly elevated acetylcholine receptor antibodies, whereas MuSK antibodies were negative. Repetitive nerve stimulation was not performed given the high antibody titer and unambiguous clinical presentation. Thoracic computed tomography excluded thymoma. Treatment with pyridostigmine, azathioprine (maintenance dose kept lower than standard due to chronic kidney disease stage IIIB), and low-dose prednisone (selected due to age and comorbidity profile) resulted in early, patient-reported clinical improvement (approximately 60% in speech and swallowing) over eight weeks of follow-up; a validated severity scale (MG-ADL) showed a score of six (scoring range 0–24). Conclusions: Myasthenia gravis should remain an important differential diagnosis in very elderly patients presenting with fluctuating ocular and bulbar symptoms, even in the presence of multiple comorbidities that may obscure the diagnosis. In this patient, early recognition, antibody testing, and individualised initiation of therapy were followed by meaningful short-term improvement; a single case with eight weeks of follow-up cannot establish that such therapy prevents disease progression or myasthenic crisis, and longer follow-up and additional cases are needed. Full article

Background: Objective gait speed, self-rated walking pace, and self-reported walking difficulty are consistently associated with mortality. Far less is known about the prognostic meaning of perceiving, or being told, that one has recently become slower in both walking and everyday activities. We examined whether reported slowing was associated with long-term all-cause mortality in older adults. Methods: The Neurological Disorders in Central Spain (NEDICES) study is a prospective population-based cohort of 5278 adults aged 65 years or older. At baseline (1994–1995), participants were asked whether they noticed, or had been told, that lately they walked or did things more slowly; the item was available for 3994 participants. Vital status was ascertained through 31 December 2017 by linkage to the Spanish National Population Register. Kaplan–Meier methods and Cox regression were used. The primary model included the Carey-based comorbidity score and adjusted for demographic, movement-disorder, musculoskeletal, and lifestyle covariates. Results: Reported slowing was present in 1516 participants (38.0%); 3426 deaths occurred. In the primary complete-case model (n = 3858; 3311 deaths), reported slowing was associated with mortality after multivariable adjustment (hazard ratio 1.10, 95% confidence interval 1.02–1.18; p = 0.012). The item changed Harrell’s C-index from 0.7046 to 0.7048. The estimate was attenuated after excluding deaths within five years (1.08, 0.99–1.17; p = 0.087) and after exploratory adjustment for the Pfeffer Functional Activities Questionnaire score (1.08, 1.00–1.16; p = 0.055). Conclusions: Reported slowing in walking and everyday activities was associated with a modest increase in mortality after multivariable adjustment. It may serve as a simple indicator of slightly higher mortality risk, although its incremental contribution to individual-level prognostication was limited. Full article

Primary dystrophin deficiency, caused by X-chromosome mutations within the DMD gene, encompasses a continuous clinical spectrum of neurological, muscular, and cardiac disorders known as dystrophinopathies that exhibit profound phenotypic variability driven by specific mutation profiles and epigenetic factors. This comprehensive review analyzes the clinical and molecular characteristics of seven primary classifications: Duchenne muscular dystrophy (DMD), a severe childhood myopathy caused by a complete absence of the protein that leads to loss of ambulation and fatal cardiorespiratory failure in youth; Becker muscular dystrophy (BMD), a milder variant with partial protein deficiency that preserves walking capabilities into adulthood and prolongs life expectancy; pseudometabolic dystrophinopathic syndrome, featuring exercise intolerance, cramps, and recurrent rhabdomyolysis that mimics metabolic diseases; asymptomatic dystrophinopathy, representing the mild end of the spectrum identified incidentally through chronically elevated creatine kinase levels; brain dystrophin-related syndrome, where the disruption of distal isoforms like Dp140 and Dp71 results in neurodevelopmental and neuropsychiatric comorbidities such as ADHD, autism, and intellectual disability; X-linked dilated cardiomyopathy (XLDCM), a cardiac-selective condition causing severe heart failure and arrhythmias while sparing skeletal muscle function; and female dystrophin-related syndrome, distinguishing between familial carriers—who can manifest symptoms due to skewed X-chromosome inactivation—and rare sporadic females who develop an exceptional, severe, Duchenne-like phenotype due to cytogenetic accidents such as Turner syndrome or chromosomal translocations. Ultimately, advancements in molecular testing (NGS and WGS) have significantly optimized diagnostic precision, proving essential for implementing early cardioprotective care, accurate genetic counseling, and the development of future tissue-specific targeted gene therapies. The present study also discusses the psychosocial impact that the disease has on patients. Full article

Background: Migraine is a leading cause of disability worldwide and is frequently associated with psychiatric comorbidities that may influence pain perception and treatment response. Anti-CGRP monoclonal antibodies represent an effective preventive treatment, although response variability remains poorly understood, particularly in patients with complex neuropsychiatric profiles. Case Presentation: We report the case of a 49-year-old woman with migraine with a previously chronic course and psychiatric comorbidity, including bipolar disorder and obsessive–compulsive disorder, treated with galcanezumab. The clinical course was characterized by an “on-off-on” pattern, with marked worsening after treatment discontinuation and subsequent improvement after treatment reintroduction. Results: The patient presented with severe emotional distress (BDI-II = 59; STAI = 77–80), a very high self-reported burden of central sensitization-related symptoms (CSI = 100/100) and reduced performance on cognitive screening measures (MoCA = 19/30; BCSE = 18/58). MMPI-3 findings indicated a high level of self-reported psychological distress; however, substantial elevations in symptom-validity indicators required cautious interpretation of the substantive scales. Conclusions: This case illustrates that complex neuropsychiatric comorbidity and psychotropic polypharmacotherapy did not preclude an apparent clinical benefit from galcanezumab. Treatment discontinuation and reintroduction were temporally associated with worsening and subsequent improvement in headache frequency, although causality cannot be established from a single uncontrolled observation. The case also highlights the potential value of coordinated neurological and psychiatric monitoring in patients with migraine and complex neuropsychiatric profiles. Full article

Background/Objectives: Endovascular thrombectomy (EVT) has transformed the treatment of acute ischaemic stroke due to large-vessel occlusion, yet peri-procedural haemodynamic instability may compromise penumbral perfusion and neurological recovery. We assessed the frequency, determinants and clinical consequences of post-procedural hypotension after EVT. Methods: We retrospectively reviewed 201 consecutive adults who underwent endovascular thrombectomy for anterior-circulation large-vessel occlusion at a single tertiary centre over a period of eight years, from 1 January 2017 to 31 January 2025. Post-procedural hypotension was defined as hypotension requiring initiation of a continuous noradrenaline infusion within 24 h of the procedure. Comorbidities, anaesthetic modality (general anaesthesia [GA] or conscious sedation [CS]), National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS) scores, and in-hospital mortality were recorded. Logistic regression identified independent predictors of hypotension. Results: Fifty-five patients (27.4%) developed post-procedural hypotension. They presented with more severe strokes (NIHSS 16.0 ± 5.0 vs. 13.7 ± 5.0; p = 0.002), had higher NIHSS scores at day 2 (14.0 ± 6.9 vs. 9.4 ± 6.7; p < 0.001) and day 7 (p = 0.003), and displayed markedly higher in-hospital mortality (50.9% vs. 20.5%; p < 0.001). In an ordinal analysis of the day 7 modified Rankin Scale with death coded as 6, hypotension was associated with a shift towards greater disability (common OR 2.57, 95% CI 1.40–4.72; p = 0.002). In an exploratory model, each additional 10 min of door-to-groin time was independently associated with hypotension (adjusted OR 1.10, 95% CI 1.03–1.18; p = 0.003). Independent predictors of hypotension were baseline NIHSS (adjusted OR 1.11 per point, 95% CI 1.04–1.19; p = 0.003) and active malignancy (adjusted OR 2.90, 95% CI 1.04–8.09; p = 0.042). Hypotension occurred with similar frequency under GA and CS (28.6% vs. 24.6%; adjusted OR 1.12, 95% CI 0.54–2.34; p = 0.766). Conclusions: Post-EVT hypotension is common and associated with poorer early neurological recovery and a more than two-fold higher in-hospital mortality rate. Its independent predictors were baseline stroke severity and active malignancy. Patients with severe stroke or active cancer may warrant intensified haemodynamic surveillance after thrombectomy. Procedural delay emerged as the only modifiable predictor identified and warrants prospective evaluation. Full article

Thoracoabdominal aortic aneurysm (TAAA) is a complex vascular disorder involving both thoracic and abdominal segments of the aorta and remains associated with substantial morbidity and mortality. One of the most serious complications after thoracoabdominal aortic aneurysm (TAAA) repair is spinal cord ischemia (SCI), which may progress to spinal cord infarction and result in irreversible neurologic deficits including paraplegia, neurogenic bladder dysfunction, and bowel dysfunction. The incidence of SCI after TAAA repair varies with the extent of aneurysmal involvement, operative duration, and patient comorbidities. The primary pathophysiologic mechanism involves interruption of radiculomedullary arterial flow, compounded by systemic hypotension and limited collateral circulation. Because SCI profoundly affects functional recovery and long-term quality of life, prevention and early recognition are central to perioperative management. Established neuroprotective strategies emphasize maintenance of spinal cord perfusion through meticulous hemodynamic optimization, cerebrospinal fluid (CSF) drainage, and temperature modulation. Intraoperative neuromonitoring using motor and somatosensory-evoked potential facilitates early detection, while newer modalities such as near-infrared spectroscopy and CSF lactate monitoring may offer additional insight. When SCI occurs despite prophylaxis, rapid initiation of rescue measures including CSF drainage, hemodynamic augmentation, and other discussed treatments may improve neurologic outcomes. Long-term care focuses on rehabilitation, symptom management, and psychological support. Therefore, this review aims to consolidate medical evidence to improve the prevention, detection, and treatment of spinal cord infarction associated with thoracoabdominal aortic aneurysm repair. Full article

Stroke remains one of the leading causes of death and long-term neurological disability worldwide, while currently available therapeutic strategies are limited by narrow treatment windows and incomplete neuroprotection. In this context, plant-derived polyphenols have attracted increasing attention as potential adjunctive agents because of their multimodal biological activity. This review focuses on resveratrol and curcumin, two of the most extensively investigated polyphenols, and evaluates their potential role in the prevention and treatment of ischaemic and haemorrhagic stroke. Evidence from in vitro studies, animal models, and early clinical trials indicates that both compounds may attenuate key mechanisms involved in stroke-related brain injury, including oxidative stress, neuroinflammation, mitochondrial dysfunction, apoptosis, autophagy dysregulation, blood–brain barrier disruption, and microglial activation. Emerging evidence further suggests that interactions with the gut microbiota and modulation of the gut–brain axis may contribute to their biological effects by influencing intestinal barrier integrity, microbial metabolite production, systemic inflammation, and vascular risk. Preclinical studies show that resveratrol and curcumin can reduce infarct volume, limit cerebral oedema, preserve neuronal viability, promote angiogenesis and neurogenesis, and improve neurological and cognitive outcomes. Their beneficial effects have been reported both when administered before stroke onset and after cerebral injury, suggesting potential relevance for both prevention and post-stroke therapy. However, interpretation of these findings requires consideration of the translational limitations of experimental stroke models, which do not fully reproduce the heterogeneity, comorbidities, age profile, and variable reperfusion patterns characteristic of human stroke. Although commonly used models such as middle cerebral artery occlusion provide important mechanistic and therapeutic insights, preclinical efficacy should therefore not be regarded as a direct predictor of clinical benefit. Resveratrol and curcumin may also complement established and emerging treatment strategies, including thrombolysis, endovascular interventions, antihypertensive therapy, and stem cell-based approaches. Nevertheless, their clinical translation remains limited by poor solubility, low bioavailability, rapid metabolism, and insufficient clinical evidence. Novel formulations, including nanoparticles, exosome-based delivery systems, and structurally modified analogues, may help overcome these barriers by improving brain targeting and therapeutic efficacy. Overall, resveratrol and curcumin represent promising but still investigational candidates for adjunctive stroke therapy, requiring further well-designed clinical trials to define their optimal dosing, timing, safety, and clinical value. Full article

Peripheral neuropathy constitutes a prevalent, albeit underrecognized, extraglandular manifestation of Sjögren’s disease (SjD). Carpal tunnel syndrome (CTS) commonly coexists with SjD; however, the efficacy of standard CTS treatments in this population remains insufficiently characterized. This study evaluated the clinical and biological response to local corticosteroid injection in CTS patients with and without SjD and explored factors potentially associated with treatment outcomes. Twenty patients with SjD and CTS diagnosed based on typical clinical symptoms and supportive ultrasonographic findings and 19 control subjects with idiopathic CTS underwent ultrasound-guided corticosteroid injection. Median nerve cross-sectional area (CSA), the Boston Carpal Tunnel Questionnaire (BCTQ), and the Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire were assessed before treatment and 4 weeks after injection. Patients with SjD additionally underwent comprehensive clinical, laboratory, neurophysiological, and patient-reported outcome assessments. Patients with SjD appeared to demonstrate a significantly greater reduction in median nerve CSA following corticosteroid injection compared with controls (mean reduction: 0.46 vs. 0.31 mm²; p = 0.006, Cohen’s d = 0.96, CI90% [0.51, 1.49]). Despite this favorable biological response, clinical improvement was significantly smaller in the SjD group. Patients without SjD exhibited greater improvement in both the BCTQ Symptom Severity Scale (p = 0.021) and Functional Status Scale (p = 0.033), whereas changes in DASH scores did not differ significantly between groups. Patients with concomitant peripheral neuropathies experienced significantly poorer BCTQ improvement than those with isolated CTS, suggesting that neurological comorbidity may contribute to treatment resistance. No significant associations were identified between treatment response and fibromyalgia status or ESSPRI domains. Among quality-of-life measures, only the SF-36 General Health domain differed significantly between neuropathy types. Patients with SjD and CTS exhibit a dissociation between structural improvement of the median nerve and subjective symptom relief after corticosteroid injection. These findings suggest that mechanisms beyond local nerve compression, including coexisting peripheral neuropathy and potentially altered pain processing, may contribute to persistent symptoms. Comprehensive neurological assessment and multidimensional outcome evaluation may improve identification of SjD patients at risk of suboptimal response to conventional CTS therapies. Full article

Background/Objectives: Micronutrient deficiencies are common in inflammatory bowel disease (IBD) and contribute to anemia, impaired wound healing, neurologic injury, and adverse disease outcomes. Major societies, including ESPEN, ACG, and ECCO, recommend nutritional and micronutrient assessment in patients with IBD, yet few studies describe how comprehensively these recommendations are applied during hospitalization. This study aimed to characterize inpatient testing practices for vitamins B1, B6, B12, and zinc in hospitalized IBD patients, quantify deficiency frequency among those tested, and identify gaps between guideline-recommended and actual micronutrient assessment. Methods: A retrospective chart review was performed on adults with Crohn’s disease (CD) or ulcerative colitis (UC) hospitalized for an IBD flare at a tertiary care center. Demographics, comorbidities, and deficiency-associated clinical features were recorded. Yield was defined as the proportion of tested patients meeting institutional deficiency thresholds. Yield for each non-B12 micronutrient was compared with B12 as an internal benchmark. Results: Among 356 patients (285 CD, 71 UC), inpatient micronutrient testing was markedly imbalanced: B12 was tested in 97.2%, whereas B6, B1, and zinc were tested in only 34.8%, 30.6%, and 18.8%, respectively. Among those tested, deficiencies were common: B6 40.3%, zinc 32.8%, B1 22.9%, and B12 9.0%. Each non-B12 micronutrient yielded deficiency significantly more often per test than B12 (all p < 0.001), a testing-yield mismatch interpreted cautiously given selective testing of non-B12 nutrients. Deficiency frequencies did not differ significantly between CD and UC. Clinical contexts included tachycardia and edema (B1); elevated inflammatory markers and thromboembolism history (B6); anemia and neuropathy (B12); and diarrhea and hypoalbuminemia (zinc). Conclusions: Inpatient micronutrient assessment in IBD is heavily skewed toward B12, with B1, B6, and zinc under-tested despite a substantially higher yield of identified deficiency per test. This testing-yield mismatch represents a measurable implementation gap between guideline-recommended comprehensive assessment and actual inpatient practice; whether systematic panel-based assessment improves clinical outcomes warrants prospective evaluation. Full article

Background: Temporomandibular disorders (TMD), bruxism, and occlusal dysfunction have traditionally been managed as localized orofacial conditions. Emerging evidence suggests, however, that the stomatognathic system may interact with broader neuromusculoskeletal and central pain-processing networks, with potential systemic and neurological implications. Methods: A structured narrative literature search was conducted using PubMed, Google Scholar, and Web of Science, with the final targeted search performed in June 2026. Original research articles, systematic reviews, meta-analyses, and relevant pilot studies were considered. No formal risk-of-bias or certainty-of-evidence assessment was performed. Results: The reviewed literature indicates that TMD and bruxism are associated with musculoskeletal pain beyond the orofacial region, cervical musculoskeletal dysfunction, and headache comorbidity, with relatively stronger evidence derived from systematic reviews and meta-analyses. Emerging neuroimaging evidence suggests alterations in central pain-modulatory networks, including the default mode network, which may be relevant to central sensitization, although this evidence remains preliminary. Clinically accessible parafunctional signs may prompt further orofacial assessment, and individualized intraoral splint therapy has been investigated for effects beyond local symptom relief, although the evidence remains heterogeneous across domains. Conclusions: TMD and occlusal dysfunction may be better understood within a broader neuromusculoskeletal framework. Multidisciplinary assessment and management may warrant consideration in selected patients. Future research should incorporate standardized TMD diagnostic criteria and, where relevant, neuroimaging and posturographic outcomes. Full article

Pediatric obesity is a complex, multifactorial pandemic with serious early-onset comorbidities, including prediabetes, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD), and cardiovascular disorders. While lifestyle modifications and the Mediterranean diet remain primary interventions, artificial intelligence (AI) is emerging as a critical tool for early diagnosis and personalized management. This review evaluates the current role of AI in predicting and treating childhood obesity and its complications. A literature search was conducted on PubMed and Google Scholar for English-language articles published from 2015 onward. Search terms included combinations of keywords related to “obesity”, “pediatric”, “comorbidities” (e.g., MASLD, diabetes), and “artificial intelligence” (e.g., machine learning, deep learning, multi-omics). Eligible study types ranged from original articles to systematic reviews and clinical guidelines. By integrating multi-omic data (genome, epigenome, transcriptome, metabolome, microbiota) with socio-psychological metrics, AI can predict obesity risk and early complications. Machine learning (ML) and deep learning have successfully identified specific metabolites, gut flora alterations, neurological pathways, and metabolic SNPs linked to obesity susceptibility. Furthermore, ML-driven prognostic models enable risk assessment for MASLD or diabetes progression, while specialized software supports remote lifestyle monitoring and tailored dietary interventions. AI has the potential to revolutionize pediatric obesity management through precision medicine. However, challenges regarding data privacy, digital literacy, and equitable access persist. Because current evidence relies heavily on limited and heterogeneous pediatric datasets, large-scale, well-characterized, and externally validated cohorts are essential to establish the clinical applicability of AI models before routine implementation. Full article

Background/Objectives: Autism spectrum disorder (ASD) is currently singularly described as a behaviourally defined neurodevelopmental diagnosis with symptoms affecting social communication and social understanding alongside the presence of restricted patterns of behaviour. Wide, and often very personal, variations in symptom intensities and differing developmental trajectories, reflective of large heterogeneity, are an important feature of the label. ASD carries enhanced risks for multiple over-represented, sometimes overlapping, comorbidities spanning behavioural, psychiatric and somatic domains. Said comorbidities often have numerous and far-reaching effects on quality of life by way of their impacts and, in extreme cases, their potential effects on life expectancy. It is of paramount importance that data on the risks of such comorbidities are available and, where possible, screening, preventive and/or treatment options implemented. Methods: In this narrative review, the authors searched databases (PubMed/Medline, ScienceDirect, Google Scholar) for papers published between 1 January 2015 and 16 February 2026 that were pertinent to comorbidity and autism. Results: We present data on the frequency of various somatic (gastrointestinal, immunological, metabolic, neurological, motor-sensory disorders), psychiatric (anxiety, mood, schizophrenia spectrum, personality, substance abuse, trauma, feeding and eating, sleeping, self-harm, neurocognitive disorders) and neurodevelopmental comorbidities (intellectual, attentional, speech and language, motor disorders) that can present alongside a diagnosis of ASD. We provide accompanying data on the magnitude of potential risk and, where available, information on comorbidity risks according to sex and age. Conclusions: This review paper deals with an extremely broad field. Limitations of the narrative review strategy are discussed alongside how the variable risk of comorbidity mimics the heterogeneity present in autism, thus inviting further investigations. Full article

Autism spectrum disorder (ASD) and epilepsy are complex, frequently co-occurring neurodevelopmental and neurological disorders that share key mechanisms, such as altered neurotransmission, oxidative stress, neuroinflammation, and gut–brain axis disruption. Despite pharmacological advances, current treatments often provide only partial relief and are associated with significant side effects. The comorbidity of ASD and epilepsy, affecting millions worldwide, remains under-recognised and poorly addressed, imposing a profound burden on patients, families, and healthcare systems through reduced quality of life, increased caregiving demands, and substantial social and economic costs. This review highlights the convergent pathways shared between ASD and epilepsy, including immune dysregulation, synaptic dysfunction, and metabolic imbalance, which create opportunities for unified therapeutic strategies. Marine algae have emerged as a sustainable source of bioactive compounds offering a unique potential to address these overlapping pathologies. Algal polyunsaturated fatty acids, carotenoids, polyphenols, polysaccharides, and vitamins have antioxidant, anti-inflammatory, neuroprotective, and microbiota-modulating activities. By addressing both the biological underpinnings and clinical burden of ASD–epilepsy comorbidity, algae-based strategies represent a novel and ecologically sustainable direction for mitigating ASD–epilepsy comorbidity and advancing marine-inspired neurotherapeutics. Full article