Jul 2026· Journal of Society Medicine· Vol 5, pp. 259-263· 0 citations
TL;DR
The evidence indicates that epilepsy management should extend beyond seizure control to incorporate routine cognitive surveillance, and practical screening tools such as the Montreal Cognitive Assessment demonstrate higher sensitivity than the Mini-Mental State Examination for detecting mild impairment.
Abstract
Epilepsy is among the most prevalent chronic neurological disorders, affecting more than 50 million people worldwide and contributing substantially to the global burden of neurological disease. Beyond the seizures themselves, recurrent epileptic activity is increasingly recognized as a driver of progressive cognitive decline; however, cognitive comorbidity remains under-addressed in routine clinical management. This literature review synthesizes current evidence on the mechanisms, clinical manifestations, and assessment of cognitive impairment associated with recurrent seizures. Recurrent seizures arise from an imbalance between excitatory (glutamate) and inhibitory (GABA) neurotransmission, producing neuronal hyperexcitability and hypersynchronization. During and after seizure episodes, cyclooxygenase-2–dependent cerebral vasoconstriction induces localized hypoperfusion and hypoxia; when repeated, these events accumulate, causing structural and functional brain injury. The hippocampus, essential for memory, is particularly vulnerable to hypoxic-ischemic damage, whereas temporal- and frontal-lobe involvement disrupts memory, language, attention, and executive function. Approximately 60–70% of patients with chronic epilepsy experience cognitive impairment, the severity of which is modulated by age at onset, seizure frequency, duration, and antiepileptic drug use. Practical screening tools such as the Montreal Cognitive Assessment (MoCA), including its validated Indonesian version (MoCA-Ina), demonstrate higher sensitivity than the Mini-Mental State Examination for detecting mild impairment, while brain-derived neurotrophic factor represents a promising biomolecular marker of cognitive dysfunction. Collectively, the evidence indicates that epilepsy management should extend beyond seizure control to incorporate routine cognitive surveillance. Early detection through sensitive screening instruments enables comprehensive, individualized treatment planning and may ultimately improve the long-term quality of life for people living with epilepsy.
0.5–1% of children worldwide suffer from epilepsy, a widespread neurological condition that affects people of all genders and demographics. It is a collection of disorders rather than a single illness that is typified by frequent, erratic seizures brought on by aberrant brain activity. These seizures can take many different forms, such as convulsions, sensory or behavioral abnormalities, or loss of consciousness. Recurrent unprovoked seizures, a high likelihood of recurrence, or an epileptic syndrome are the criteria used by the International League Against epileptic (ILAE) to describe epilepsy. Patients' neurological, emotional, and social well-being are greatly impacted by epilepsy, which is caused by neuronal hyperexcitability. Seizure type, EEG results, and related neurological characteristics determine classification. All things considered, epilepsy is a complicated condition with a wide range of causes and symptoms. In children, epilepsy and Attention Deficincy Hyperactivity Disorder (ADHD) often co-occur; approximately 30–40% of children with epilepsy also have ADHD. There are two types of epileptic seizures: focal and generalized. Automatisms, atonic or tonic episodes, clonic jerks, spasms, hyperkinetic movements, or myoclonus are examples of motor symptoms that can accompany focal seizures. Non-motor symptoms include autonomic changes, behavior arrest, cognitive disturbances, emotional changes, or sensory abnormalities. Absence seizures, myoclonic seizures, atonic seizures, tonic seizures, and tonic-clonic seizures are examples of generalized seizures that affect both hemispheres of the brain. This categorization aids in the diagnosis, management, and comprehension of epileptic seizure patterns. A common neurological condition in children, epilepsy is most common in the first year of life and is more common in low- and middle-income nations, where the majority of cases go untreated. The six main categories of its causes are structural, genetic, infectious, metabolic, immunological, and unknown. An imbalance between neuronal excitation and inhibition causes aberrant electrical activity during seizures, which can extend to different parts of the brain. Ion channel malfunction, neurotransmitter imbalance, and altered neuronal circuitry are some of the factors that lead to epileptogenesis and can have long-term repercussions on cognition, particularly following protracted or frequent seizures. When assessing epilepsy, a physical examination is crucial. This includes measuring blood pressure, looking for signs of neurocutaneous syndromes on the skin, and looking for anomalies in the skull that can point to underlying neurological conditions. Electroencephalography (EEG), neuroimaging, and genetic testing are used to diagnose epilepsy in children. Sleep EEG is crucial for focal epilepsies and epileptic encephalopathies. EEG is an easy-to-use method for identifying aberrant cortical excitability. While genetic testing, including next-generation sequencing, has identified over 265 genes associated with epilepsy, increasing the identification of genetic epilepsies, neuroimaging detects structural abnormalities in the brain. Antiepileptic medications including carbamazepine, ethosuximide, and levetiracetam are used in treatment; each is customized for a particular type of seizure and age group while taking side effects and effectiveness into account. An alternate strategy is offered by dietary therapy, especially the ketogenic diet, which lowers seizure frequency by altering neurotransmitter activity and brain metabolism. Together, these therapeutic and diagnostic approaches allow children with epilepsy to be Effecetiveiy managed.
N. P. Patil, Divakar. R. Patil, Akash S. Jain et al.· Research Journal of Pharmaco...· 0 citations
Neuropsychiatric symptoms including agitation, delirium, and psychosis are common in patients with primary or metastatic brain tumors and frequently necessitate antipsychotic treatment. Brain tumors create a hyperexcitable cortical environment characterized by glutamatergic excess, impaired inhibitory signaling, peritumoral edema, network disruption, and treatment-related neurotoxicity, all of which lower seizure threshold. Emerging data further implicates impaired astrocytic glutamate regulation, neuroligin-3–mediated neuron–glioma synaptic signaling, and IDH-mutant–associated oncometabolite accumulation as contributors to cortical instability. Neuropsychiatric symptoms often localize to frontal and temporal networks that are also highly epileptogenic, amplifying vulnerability. Brain tumor–related epilepsy further compounds this risk through recurrent seizures, interictal dysfunction, and antiseizure medication effects that contribute to cognitive and behavioral disturbance. In general psychiatric populations, second-generation antipsychotics have low intrinsic seizure liability. However, these data largely exclude patients with structural brain disease. In neuro-oncology, seizure risk is context-dependent and reflects the interaction of tumor biology, antiseizure medication exposure, metabolic instability, and dynamic treatment effects. Clozapine and low-potency first-generation antipsychotics confer the greatest seizure risk, whereas risperidone and aripiprazole are associated with lower risk. Commonly used antiseizure medications, particularly levetiracetam, may exacerbate irritability and behavioral dysregulation, increasing the need for antipsychotic treatment within an already unstable neurophysiologic environment. This review synthesizes evidence on tumor-associated hyperexcitability, antipsychotic-specific seizure liability, and clinical modifiers of risk in brain tumor populations. We propose a seizure-informed, interdisciplinary framework that integrates tumor biology, antiseizure medication selection, and psychiatric indication to guide antipsychotic prescribing in neuro-oncology.
F. Taj, H. Newton, Y. Alici· Current Psychiatry Reports· 0 citations
Paediatric epilepsy is one of the most common chronic neurological disorders of childhood, characterised by recurrent unprovoked seizures resulting from abnormal neuronal activity. Accurate diagnosis is essential and is based on a detailed clinical history, seizure semiology, neurological examination, and electroencephalography (EEG), with neuroimaging such as magnetic resonance imaging (MRI) used to identify structural abnormalities. Classification according to seizure type and underlying aetiology genetic, structural, metabolic, immune, infectious, or unknown—guides appropriate management strategies. The primary goal of treatment is to achieve optimal seizure control while minimising adverse effects and supporting normal neurodevelopment. First-line management typically involves antiseizure medications (ASMs) selected according to seizure type, patient age, comorbidities, and potential drug interactions. Approximately two-thirds of affected children achieve seizure remission with pharmacological therapy. However, a significant proportion develop drug-resistant epilepsy (DRE), requiring alternative approaches such as ketogenic diet therapy, vagus nerve stimulation, or epilepsy surgery. Early identification of DRE is critical to reduce the risk of cognitive, behavioural, and psychosocial impairment. Comprehensive care extends beyond seizure management and includes addressing developmental, educational, and psychosocial needs. A multidisciplinary, family-centred approach involving neurologists, dietitians, psychologists, and educators is essential. Advances in genetic testing and precision medicine are improving diagnostic accuracy and enabling more personalised treatment strategies in (PE).
Jayesh S. Patil, Hitendra S. Chaudhari, S. Pawar et al.· Research and reviews : a jou...· 0 citations
Refractory epilepsy remains a significant clinical challenge, affecting over a third of patients with epilepsy and drastically increasing their risk of sudden unexpected death in epilepsy (SUDEP). Furthermore, psychiatric comorbidities - such as depression and anxiety disorders - are highly prevalent among patients with epilepsy. As neuromodulatory therapeutic approaches evolve, it is paramount that novel targets for stimulation are explored that may concomitantly reduce seizure burden, ameliorate psychiatric comorbidities, and/or reduce SUDEP risk. Here, we review physiological factors that are thought to contribute to SUDEP and which may reduce risk of SUDEP if addressed therapeutically, then we describe how the bed nucleus of the stria terminalis (BNST) represents a forebrain limbic region that concurrently influences many of these physiological processes. We conclude by synthesizing recent findings regarding the BNST in patients and preclinical models of epilepsy and propose that this evidence positions the BNST as a promising extra-thalamic target for therapeutic neurostimulation in patients with refractory epilepsy.
Jackson G. Murray, Eunyoung Hong, S. Mulloy et al.· Frontiers in Network Physiol...· 0 citations
Late-onset epilepsy (LOE) remains of unknown aetiology (LOEU) in around 20% of cases. Longitudinal studies have demonstrated the presence of early cognitive impairment at seizure onset, progressive memory decline and a substantially elevated risk of dementia within a decade of diagnosis, with an increased risk of subsequent neurodegenerative disorders, particularly Alzheimer's disease (AD). LOEU is associated with cognitive network alterations and epileptiform activity, although links remain unclear. Further emerging data suggest that neurodegenerative processes related to β-amyloid and tau pathology may precede the onset of epilepsy. Although epilepsy is highly prevalent among older adults, its impact on quality of life remains unclear, with affective symptoms and sleep disturbances as key determinants of subjective well-being. These findings suggest that LOEU should be reconceptualised as a multidimensional neurological condition. This protocol advocates an integrated approach, combining neuropsychological assessment, advanced biomarkers, neurophysiological measures and systematic sleep evaluation to identify high-risk phenotypes and define optimal windows for neuroprotective interventions in LOEU. This strategy could improve the early detection of cognitive decline, guide personalised management, and ultimately enhance quality of life, while contributing to the long-term sustainability of healthcare systems in an ageing population, focusing on LOEU as a model for dementia prevention.
G. Bergamo, M. Fernandes, S. Maio et al.· Mechanisms of Ageing and Dev...· 0 citations
Pediatric occipital lobe epilepsy (OLE) comprises syndromes with seizures originating from the posterior cerebral cortex. Previously "benign", recent International League Against Epilepsy (ILAE) updates reclassified these as self-limited or structural focal epilepsies, reflecting their complex causes and morbidity potential. The 2017 ILAE guidelines shifted from syndromic recognition to an etiology-driven approach. High-resolution magnetic resonance imaging is crucial to differentiate self-limited genetic syndromes from structural OLE (e.g., focal cortical dysplasia), as the latter often requires surgery. Self-limited epilepsy with autonomic seizures (formerly Panayiotopoulos syndrome) presents with prolonged nocturnal autonomic seizures. Childhood occipital visual epilepsy (previously Gastaut type) manifests as frequent, brief daytime visual hallucinations. Despite high seizure freedom rates with monotherapy, patients face neurocognitive challenges in visuospatial processing and academic performance. For drug-resistant structural cases, surgery offers high seizure freedom rates, though with risk of visual deficits. Accurate differentiation between idiopathic and structural OLE is essential for improving outcomes. The shift from "benign" to "self-limited" terminology emphasizes the need to monitor cognitive comorbidities and syndrome evolution. Early diagnosis is critical to avoid clinical mimics and enhance neurodevelopmental outcomes. This review examines the evolving landscape of pediatric OLE, highlighting the shift from syndromic to etiological classification and management strategies.
Preeti Srivastava, D. Nag, Shikha Swaroop et al.· World Journal of Clinical Pe...· 0 citations