Antipsychotics and Seizure Risk in Patients with Brain Tumors: Mechanisms, Modifiers, and Clinical Insights

The Impact of Recurrent Seizures on Cognitive Functions in Epilepsy: A Literature Review

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.

Pharmacological Insights in to Schizophrenia: Neurochemical Dysregulation, Disease Mechanisms and Future Therapeutic Strategies

Current understanding of the clinical features, etiological factors, biological mechanisms, and pharmacological management of schizophrenia is summarized, while emerging therapeutic targets that may guide future research and drug development are outlined.

Pediatric Epilepsy: Current Perspectives and Emerging Therapies

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.

Astroglial dysregulation and gliotransmitter imbalance in schizophrenia.

Autoimmune Epilepsy: Insights into Pathophysiology, Diagnostic Strategies and Treatment

Abstract Autoimmune epilepsy, once regarded as a rare and poorly understood subset of seizure disorders, has now emerged as a clinically significant and potentially reversible cause of epilepsy. Advances in neuroimmunology have substantially broadened the spectrum of neural autoantibodies implicated in epileptogenesis—particularly those directed against neuronal cell surface and synaptic proteins, such as the N-methyl-D-aspartate receptor (NMDAR), leucine-rich glioma-inactivated protein 1 (LGI1), contactin-associated protein-like 2 (CASPR2), and glutamic acid decarboxylase 65 (GAD65). Distinct autoantibody profiles are now recognized to correlate with characteristic clinical syndromes, facilitating earlier and more targeted diagnosis. For instance, faciobrachial dystonic seizures are highly suggestive of LGI1 antibody-mediated encephalitis, while neuropsychiatric manifestations and movement disorders are typical of NMDAR antibody encephalitis, and chronic temporal lobe epilepsy frequently accompanies GAD65 autoimmunity. Early identification of these immune-mediated forms is critical, as antibody-mediated epilepsies involving cell surface antigens often respond favorably to immunotherapy, leading to substantial recovery. In contrast, epilepsies associated with intracellular antigen targets or cytotoxic T-cell–driven mechanisms, such as Rasmussen encephalitis, typically show poor therapeutic response due to irreversible neuronal injury. Some autoimmune encephalitides also occur as paraneoplastic syndromes, underscoring the importance of comprehensive oncological evaluation in affected patients. Moreover, immune dysregulation has been implicated in catastrophic epileptic conditions such as new-onset refractory status epilepticus and febrile infection-related epilepsy syndrome, further broadening the clinical spectrum of autoimmune-mediated seizures. Although seizures may arise from diverse etiologies, immune mechanisms have gained increasing recognition as an important and potentially modifiable contributor to epileptogenesis. This recognition has been formally endorsed by the International League Against Epilepsy, which classifies autoimmune epilepsy as a distinct diagnostic entity. Nevertheless, true autoimmune epilepsy, in which seizure susceptibility persists after resolution of encephalitic activity, remains relatively uncommon. In most cases, seizures associated with autoimmune encephalitis are acute and reversible with timely immunotherapy. Thus, precise terminology—differentiating acute symptomatic seizures from chronic autoimmune-associated epilepsy—is essential for appropriate management, prognostication, and research standardization.

First-episode psychosis and mood disorder onset in individuals with epilepsy.

BACKGROUND Psychiatric disorders represent a major burden for patients with epilepsy (PwE). This study examined how demographic, epilepsy-related, and clinical risk factors contribute to the onset of mood and psychotic disorders in epilepsy. METHODS In this retrospective cohort, we intersected a hospital structured database with results from direct text mining in all available documentation from each patient to include PwE without prior psychiatric history. Logistic regression evaluated age, sex, epilepsy type, treatment resistance, histories of status epilepticus and febrile seizures, neurological and neurodevelopmental comorbidities as risk factors of psychotic and mood disorders. A five-fold cross-validated logistic regressor tested their predictive performance. Pairwise comparisons examined psychiatric outcomes across monotherapy treatments. RESULTS We screened 4269 individuals ; 1709 were excluded for lack of an established epilepsy diagnosis or anti-epileptic medication ; 696 already had a psychiatric history at the time of first antiseizure medication. In 1864 PwE without prior psychiatric history, psychiatric disorders occurred in 25% of cases (15.8% mood, 2.9% psychosis, 3.4% mood and psychosis). Risks for mood disorders included female sex, focal epilepsy, drug resistance, a history of febrile seizures, neurological comorbidities, and neurodevelopmental disorders. Risk factors for psychotic disorders included drug resistance, a history of febrile seizures and neurodevelopmental disorders. Supervised analyses significantly predicted outcomes for mood disorders (AUC = 0.70, p < 0.001) and psychosis (AUC = 0.61, p < 0.001). Pairwise treatment comparisons found no significant differences. DISCUSSION Identification of these risk factors to psychosis and mood disorder onset provides clinicians with red flags that will facilitate timely psychiatric referral and intervention, as well as integrated care between neurologists and psychiatrists.