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This study analyzed the neurological manifestation profiles of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection across pandemic waves in pediatric patients. The study collected data on patients aged between 0 and 18 years, diagnosed with acute SARS-CoV-2 infection, admitted to a pediatric tertiary hospital between 1 March 2020 and 28 February 2023. This study included 1677 patients. Neurological manifestations were noted in 10% (n = 168) of patients with a median age of 3.2 years (interquartile range: 1–11.92). Neurological manifestations were significantly associated with the pandemic waves (p = 0.006) and age groups (p < 0.001). Seizures were noted in 4.2% of cases and reached an increasing frequency over time (p = 0.001), but were not associated with age groups. Febrile seizures accounted for the majority of seizures. Headache was reported in 2.6% of cases and had similar frequencies across the pandemic waves and age groups. Muscular involvement was noted in 2% of cases, reached a decreasing frequency over time (p < 0.001), and showed different frequencies among the age groups. Neurological manifestations of acute SARS-CoV-2 infection exhibit distinct patterns, depending on the pandemic wave and patient age group. The Wuhan and Omicron waves involved the nervous system more often than the other waves.

Purpose There is some evidence that trace element and mineral deficiencies may promote the occurrence of febrile seizures. However, the role of these elements in the occurrence of complex seizures in children with FS has not been comprehensively investigated. The present study was conducted to evaluate this issue. Methods In a cross-sectional study, 220 patients including 110 febrile and 110 FS children aged 6–60 months were studied. Blood samples were taken and serum zinc, potassium, sodium, magnesium and calcium levels were measured. Demographic and clinical characteristics were also recorded. Results The patients were similar in age and sex. Higher serum zinc levels decreased the risk of seizure (RR = 0.95, p -value = 0.0001) and complex seizure (OR = 0.96, p -value = 0.03). Higher serum sodium levels decreased the risk of complex seizures (OR = 0.85, p -value = 0.023). Higher serum potassium levels were associated with a lower risk of seizure (OR = 0.55, p -value = 0.035). Serum calcium and magnesium levels were not associated with the risk of seizure and complex seizure. A BMI at the upper end of the normal range decreased the risk of complex seizures (OR = 0.83, p -value = 0.05). Male sex increased the risk of complex seizure (OR = 4.14, p -value = 0.016). Conclusions Low serum levels of zinc, potassium and sodium are risk factors for seizure and complex seizure in febrile children. Male sex is also a risk factor for complex seizures. The time from fever to seizure was shorter in younger children. Children with a BMI at the upper end of the normal range have a lower risk of having a complex seizure.

Traumatic brain injury (TBI) is one of the commonest presentations to emergency departments and is associated with seizures carrying different significance at different stages following injury. We describe the epidemiology of early and late seizures following TBI, the significance of intracranial haemorrhage of different types in the risk of later epilepsy and the gaps in current understanding of risk factors contributing to the risk of post-traumatic epilepsy (PTE). The delay from injury to epilepsy presents an opportunity to understand the mechanisms underlying changes in the brain and how they may reveal potential targets for anti-epileptogenic therapy. We review existing treatments, both medical and surgical and conclude that current research is not tailored to differentiate between PTE and other forms of focal epilepsy. Finally, we review the increasing understanding of the frequency and significance of dissociative seizures following mild TBI.

Albeit primarily a disease of respiratory tract, the 2019 coronavirus infectious disease (COVID-19) has been found to have causal association with a plethora of neurological, neuropsychiatric and psychological effects. This review aims to analyze them with a discussion of evolving therapeutic recommendations. PubMed and Google Scholar were searched from 1 January 2020 to 30 May 2020 with the following key terms: \"COVID-19\", \"SARS-CoV-2\", \"pandemic\", \"neuro-COVID\", \"stroke-COVID\", \"epilepsy-COVID\", \"COVID-encephalopathy\", \"SARS-CoV-2-encephalitis\", \"SARS-CoV-2-rhabdomyolysis\", \"COVID-demyelinating disease\", \"neurological manifestations\", \"psychosocial manifestations\", \"treatment recommendations\", \"COVID-19 and therapeutic changes\", \"psychiatry\", \"marginalised\", \"telemedicine\", \"mental health\", \"quarantine\", \"infodemic\" and \"social media\". A few newspaper reports related to COVID-19 and psychosocial impacts have also been added as per context. Neurological and neuropsychiatric manifestations of COVID-19 are abundant. Clinical features of both central and peripheral nervous system involvement are evident. These have been categorically analyzed briefly with literature support. Most of the psychological effects are secondary to pandemic-associated regulatory, socioeconomic and psychosocial changes. Neurological and neuropsychiatric manifestations of this disease are only beginning to unravel. This demands a wide index of suspicion for prompt diagnosis of SARS-CoV-2 to prevent further complications and mortality.

A trial involving comatose survivors of cardiac arrest tested whether aggressively treating rhythmic and periodic EEG activity would improve neurologic outcomes. Despite suppression of abnormal EEG activity, the incidence of a poor neurologic outcome did not differ significantly from that with standard care, and mortality was high.

The brain is a highly energy-demanding organ and requires bioenergetic adaptability to balance normal activity with pathophysiological fuelling of spontaneous recurrent seizures, the hallmark feature of the epilepsies. Recurrent or prolonged seizures have long been known to permanently alter neuronal circuitry and to cause excitotoxic injury and aberrant inflammation. Furthermore, pathological changes in bioenergetics and metabolism are considered downstream consequences of epileptic seizures that begin at the synaptic level. However, as we highlight in this Review, evidence is also emerging that primary derangements in cellular or mitochondrial metabolism can result in seizure genesis and lead to spontaneous recurrent seizures. Basic and translational research indicates that the relationships between brain metabolism and epileptic seizures are complex and bidirectional, producing a vicious cycle that compounds the deleterious consequences of seizures. Metabolism-based treatments such as the high-fat, antiseizure ketogenic diet have become mainstream, and metabolic substrates and enzymes have become attractive molecular targets for seizure prevention and recovery. Moreover, given that metabolism is crucial for epigenetic as well as inflammatory changes, the idea that epileptogenesis can be both negatively and positively influenced by metabolic changes is rapidly gaining ground. Here, we review evidence that supports both pathophysiological and therapeutic roles for brain metabolism in epilepsy.In this Review, the authors highlight the growing recognition that disruptions in cellular metabolism can be both a cause and a consequence of epileptic seizures and discuss how this emerging science might be exploited to develop innovative therapeutic strategies.

Levels of high mobility group box 1 (HMGB1), an important inflammatory mediator, are high in the serum of febrile seizure (FS) patients. However, its roles in FS and secondary epilepsy after prolonged FS are poorly understood. We demonstrate HMGB1’s role in the pathogenesis of hyperthermia-induced seizures (HS) and secondary epilepsy after prolonged hyperthermia-induced seizures (pHS). In the first experiment, 14–15-day-old male rats were divided into four groups: high-dose HMGB1 (100 μg), moderate-dose (10 μg), low-dose (1 μg), and control. Each rat was administered HMGB1 intranasally 1 h before inducing HS. Temperature was measured at seizure onset with electroencephalography (EEG). In the second experiment, 10–11-day-old rats were divided into four groups: pHS + HMGB1 (10 μg), pHS, HMGB1, and control. HMGB1 was administered 24 h after pHS. Video-EEGs were recorded for 24 h at 90 and 120 days old; histological analysis was performed at 150 days old. In the first experiment, the temperature at seizure onset was significantly lower in the high- and moderate-dose HMGB1 groups than in the control group. In the second experiment, the incidence of spontaneous epileptic seizure was significantly higher in the pHS + HMGB1 group than in the other groups. Comparison between pHS + HMGB1 groups with and without epilepsy revealed that epileptic rats had significantly enhanced astrocytosis in the hippocampus and corpus callosum. In developing rats, HMGB1 enhanced HS and secondary epilepsy after pHS. Our findings suggest that HMGB1 contributes to FS pathogenesis and plays an important role in the acquired epileptogenesis of secondary epilepsy associated with prolonged FS.

Stroke is one of the leading causes of acquired epilepsy in adults. An instrument to predict whether people are at high risk of developing post-stroke seizures is not available. We aimed to develop and validate a prognostic model of late (>7 days) seizures after ischaemic stroke. In this multivariable prediction model development and validation study, we developed the SeLECT score based on five clinical predictors in 1200 participants who had an ischaemic stroke in Switzerland using backward elimination of a multivariable Cox proportional hazards model. We externally validated this score in 1169 participants from three independent international cohorts in Austria, Germany, and Italy, and assessed its performance with the concordance statistic and calibration plots. Data were complete for 99·2% of the predictors (99·2% for Switzerland, 100% for Austria, 97% for Germany, and 99·7% for Italy) and 100% of the outcome parameters. Overall, the risk of late seizures was 4% (95% CI 4–5) 1 year after stroke and 8% (6–9) 5 years after stroke. The final model included five variables and was named SeLECT on the basis of the first letters of the included parameters (severity of stroke, large-artery atherosclerotic aetiology, early seizures, cortical involvement, and territory of middle cerebral artery involvement). The lowest SeLECT value (0 points) was associated with a 0·7% (95% CI 0·4–1·0) risk of late seizures within 1 year after stroke (1·3% [95% CI 0·7–1·8] within 5 years), whereas the highest value (9 points) predicted a 63% (42–77) risk of late seizures within 1 year (83% [62–93] within 5 years). The model had an overall concordance statistic of 0·77 (95% CI 0·71–0·82) in the validation cohorts. Calibration plots indicated high agreement of predicted and observed outcomes. This easily applied instrument was shown to be a good predictor of the risk of late seizures after stroke in three external validation cohorts and is freely available as a smartphone app. The SeLECT score has the potential to identify individuals at high risk of seizures and is a step towards more personalised medicine. It can inform the selection of an enriched population for antiepileptogenic treatment trials and will guide the recruitment for biomarker studies of epileptogenesis. None.

Purpose of ReviewIn this review, we summarize the recent literature regarding the incidence and treatment of seizures arising after ischemic and hemorrhagic strokes. Additionally, we identify open questions in guidelines and standard clinical care to aid future studies aiming to improve management of seizures in post-stroke patients.Recent FindingsStudies demonstrate an increasing prevalence of seizures following strokes, probably a consequence of advances in post-stroke management and expanding use of continuous EEG monitoring. Post-stroke seizures are associated with longer hospitalization and increased mortality; therefore, prevention and timely treatment of seizures are important. The standard of care is to treat recurrent seizures with anti-epileptic drugs (AEDs) regardless of the etiology. However, there are no established guidelines currently for prophylactic use of AEDs following a stroke.SummaryThe prevalence of post-stroke seizures is increasing. Further studies are needed to determine the risk factors for recurrent seizures and epilepsy after strokes and optimal treatment strategies.

Background Seizures are an important comorbidity in Alzheimer’s disease (AD). Conflicting results regarding clinical parameters associated with seizures in AD were previously reported. Data on seizure recurrence risk, a crucial parameter for treatment decisions, are lacking. Methods National Alzheimer’s Coordinating Center data were analyzed. Seizure prevalence in AD and an association with disease duration were investigated. Associations of seizures with age of AD onset and with cognitive and functional performance, and seizure recurrence risk were studied. Results 20,745 individuals were investigated. In AD dementia, seizure recurrence risk was 70.4% within 7.5 months. Seizure history was associated with an earlier age of onset of cognitive symptoms (seizures vs. no seizures: 64.7 vs. 70.4 years; p  < 0.0001) and worse cognitive and functional performance (mean MMSE score: 16.6 vs. 19.6; mean CDR-sum of boxes score: 9.3 vs. 6.8; p  < 0.0001; adjusted for disease duration and age). Seizure prevalence increased with duration of AD dementia (standardized OR = 1.55, 95% CI = 1.39–1.73, p  < 0.0001), rising from 1.51% at 4.8 years to 5.43% at 11 years disease duration. Seizures were more frequent in AD dementia compared to normal controls (active seizures: 1.51% vs. 0.35%, p  < 0.0001, OR = 4.34, 95% CI = 3.01–6.27; seizure history: 3.14% vs. 1.57%, p  < 0.0001, OR = 2.03, 95% CI = 1.67–2.46). Conclusion Seizures in AD dementia feature an exceptionally high recurrence risk and are associated with a poor course of cognitive symptoms. AD patients are at an increased risk for seizures, particularly in later disease stages. Our findings emphasize a need for seizure history assessment in AD, inform individual therapeutic decisions and underline the necessity of systematic treatment studies of AD-associated epilepsy.