Comorbidity Of Epilepsy Research Articles

Prevalence and associated factors of psychiatric comorbidities in epilepsy in the Casablanca-Settat region of Morocco: A cross-sectional study.

To determine the estimated prevalence of anxiety, depression, and anxiety-depression syndrome (ADS) and to identify the associated factors in Moroccan people with epilepsy (PWE). A cross-sectional study was conducted among adult PWE (June 2021-December 2022) in the Casablanca-Settat region. PWE were interviewed by completing a questionnaire collecting sociodemographic and clinical data. Anxiety and depression were assessed by the Hospital Anxiety and Depression Scale (HADS). Out of 21 points, a score ≥8 is in favor of considerable anxiety/depression symptoms and a sum of the two scores ≥15 indicates the presence of ADS. Data were analyzed using Statistical Package for Social Sciences (SPSS) 21.0. p-values ≤0.05 were considered statistically significant and logistic regression was performed to determine the associated factors. Among 294 PWE, the median age was 39 years (interquartile range [IQR]: 25.75-54.00). The median anxiety, depression, and ADS scores were 8 (IQR: 5.00-10.00), 7 (IQR: 4.00-10.00), and 15 (IQR: 10.00-20.00), respectively. Anxiety, depression, and ADS were revealed in 51.4%, 44.9%, and 51.0% of PWE, respectively. Depression was the only predictor for anxiety (aOR = 24.20; 95%CI: 12.45-47.01). Antiseizure polytherapy (aOR = 3.35; 95%CI: 1.72-6.54) and anxiety (aOR = 24.04; 95%CI: 12.12-47.67) were the factors associated with depression. The risk of ADS was increased by female gender (aOR = 2.83; 95%CI: 1.68-4.78), antiseizure polytherapy (aOR = 2.75; 95%CI: 1.62-4.65), structural epilepsy (aOR = 1.73; 95%CI: 1.01-2.94), and the presence of concomitant conditions with epilepsy (aOR = 1.96; 95%CI: 1.16-3.31). Our study reports high psychiatric comorbidity prevalence in epilepsy, which supports the bidirectional link hypothesis. Associated factors found are important in the prognosis and prevention. The neural mechanisms underlying epilepsy tend to expose PWE to psychiatric disorders. Our study aims to quantify the rate of psychiatric comorbidities and their predictive factors in Moroccan PWE. The estimated prevalences of significant symptoms of anxiety, depression, and ADS were 51.4%, 44.9%, and 51.0%, respectively. Depression was the predictor of anxiety. Antiseizure polymedication and anxiety were the associated factors with depression. The risk of SAD was increased by female gender, antiseizure polymedication, structural epilepsy, and concomitant diseases with epilepsy. Our results are important for considering the psychiatric aspect of PWE and improving their care and quality of life.

Ficus platyphylla alleviates seizure severity and neurobehavioral comorbidities in pentylenetetrazole–kindled rats via modulation of oxidative stress

PTZ kindling induces oxidative stress, neuronal cell degeneration, and neurobehavioral alterations in rodents that mimic neuropsychiatric comorbidities of epilepsy, which could be initiated or aggravated by some antiepileptic drugs. Here, we investigated the effects of the methanol extract of Ficus platyphylla (FP) on severity scores for seizures, neuronal cell degeneration, and neurobehavioral alterations in rats kindled with pentylenetetrazole (PTZ) and probed the involvement of oxidative stress in these ameliorative effects of FP. FP (50 and 100 mg/kg, p.o.) ameliorated seizure severity, neuronal cell degeneration, depressive behaviors, cognitive dysfunctions, and oxidative stress in rats kindled with PTZ (42.5 mg/kg, i.p.). The findings from this study give additional insights into the potential values of FP in the treatment of persistent epilepsy and major neuropsychiatric comorbidities via modulation of oxidative stress.

Common Ground: We Can Comprehensively Treat Pediatric Epilepsy and Psychiatric Comorbidities.

Epilepsy and psychiatric illness have been long studied and today are better accepted as co-occurring than as discrete illnesses that are independent even if associated. Common pathophysiology may not be easily explained, but clearly exists given the significant overrepresentation of psychiatric illness among individuals with epilepsy. Conditions like autism spectrum disorder, anxiety, depression, and attention deficit hyperactivity disorder are prevalent in pediatric epilepsy much more than expected, even in the context of chronic neurologic disease. The interplay between pediatric epilepsy and neuropsychiatric symptoms represents a complex clinical circumstance that is not well subtended by the chasm-like division of labor between psychiatrists and neurologists. The unfortunate result is that children and families often experience care that is fractured and at worst, counterproductive for their quality of life. A neuropsychiatric paradigm is essential to address epilepsy and its intrinsic psychiatric symptoms. Practical strategies will be discussed to address this challenge.

Neuronal Mitochondrial Calcium Uniporter (MCU) Deficiency Is Neuroprotective in Hyperexcitability by Modulation of Metabolic Pathways and ROS Balance.

Epilepsy is one of the most common neurological disorders in the world. Common epileptic drugs generally affect ion channels or neurotransmitters and prevent the emergence of seizures. However, up to a third of the patients suffer from drug-resistant epilepsy, and there is an urgent need to develop new therapeutic strategies that go beyond acute antiepileptic (antiseizure) therapies towards therapeutics that also might have effects on chronic epilepsy comorbidities such as cognitive decline and depression. The mitochondrial calcium uniporter (MCU) mediates rapid mitochondrial Ca2+ transport through the inner mitochondrial membrane. Ca2+ influx is essential for mitochondrial functions, but longer elevations of intracellular Ca2+ levels are closely associated with seizure-induced neuronal damage, which are underlying mechanisms of cognitive decline and depression. Using neuronal-specific MCU knockout mice (MCU-/-ΔN), we demonstrate that neuronal MCU deficiency reduced hippocampal excitability in vivo. Furthermore, in vitro analyses of hippocampal glioneuronal cells reveal no change in total Ca2+ levels but differences in intracellular Ca2+ handling. MCU-/-ΔN reduces ROS production, declines metabolic fluxes, and consequently prevents glioneuronal cell death. This effect was also observed under pathological conditions, such as the low magnesium culture model of seizure-like activity or excitotoxic glutamate stimulation, whereby MCU-/-ΔN reduces ROS levels and suppresses Ca2+ overload seen in WT cells. This study highlights the importance of MCU at the interface of Ca2+ handling and metabolism as a mediator of stress-related mitochondrial dysfunction, which indicates the modulation of MCU as a potential target for future antiepileptogenic therapy.

School Performance and Psychiatric Comorbidity in Juvenile Absence Epilepsy and Juvenile Myoclonic Epilepsy: A Danish Population-based Cohort Study (S8.006)

School Performance and Psychiatric Comorbidity in Juvenile Absence Epilepsy and Juvenile Myoclonic Epilepsy: A Danish Population-based Cohort Study (S8.006)

Post-Ictal Mania: A Case Report with Literature Revue

IntroductionWhile postictal mania is a well-recognized clinical condition, it has received less research attention compared to other postictal manifestations.ObjectivesDrawing upon an analysis of a case report that underscores the clinical and therapeutic challenges associated with comorbid epilepsy and mania, a literature review was carried out to investigate the connection between these two disorders.MethodsWe illustrate a case of comorbidity between mania and epilepsy and provide a concise review of the literature summarizing the key characteristics of this association.ResultsThis case pertains to Mr. M, a 44-year-old male with a history of frontal epilepsy characterized by secondary partial generalization, which was partially controlled with sodium valproate. He was admitted to our service due to acute agitation following a loss of consciousness lasting a few minutes.Upon admission, the patient exhibited symptoms of mental confusion. A neurological examination did not uncover any abnormalities. Brain computed tomography revealed mild frontal atrophy. Video electroencephalography conducted during the interictal period and outside the episodes of confusion did not reveal any abnormalities. The patient was restarted on sodium valproate (20 mg/kg/day) and clonazepam (2 mg/day). Following a lucid interval of ten days, the patient started to manifest psychiatric symptoms, which included irritability, hostility towards his spouse, increased talkativeness, thought pressure, and an unusual sense of familiarity, raising suspicion of post-ictal mania.ConclusionsBased on this clinical case and the existing scientific literature, post-ictal mania occupies a distinct position among the mental disorders observed in the post-ictal period. Therefore, clinicians must be aware of these conditions to facilitate accurate diagnosis and appropriate management.Disclosure of InterestNone Declared

Clinical characteristics and impact of comorbidities on the prognosis of senile epilepsy in Southwest China: a retrospective cohort study

BackgroundSenile epilepsy and its comorbidities pose a tremendous burden on patients and the society. This study was aimed to investigate the clinical characteristics and comorbidities of senile epilepsy, as well as the impact of comorbidities on the prognosis of senile epilepsy.MethodsInformation of patients with senile epilepsy was retrospectively collected from three tertiary hospitals in Southwest China between December 2014 and December 2022. A total of 154 patients met the inclusion criteria and were divided into two groups based on the presence or absence of comorbidities. The prevalence, type, characteristics, and impacts of the comorbidities were investigated. The characteristics of patients with and without comorbidities were also compared.ResultsEighty-one percent of patients with senile epilepsy had at least one comorbidity, and 36% had three or more comorbidities. Eighteen different types of comorbidities were identified. The most common comorbidities were neurological (61%), followed by cardiovascular (45%) and psychiatric (26%) comorbidities. More than one-third of patients had bidirectional comorbidities, whereas more than half of the patients had additional causal comorbidities. Among all types of comorbidities, neurological and psychiatric comorbidities were found to be associated with an increased risk of recurrent seizures. Compared to patients without bidirectional comorbidities, those with at least one bidirectional comorbidity had a lower rate of achieving seizure freedom. The higher the number of bidirectional comorbidities, the lower the seizure-free rate. Survival analysis revealed that patients with neurological comorbidities had a higher risk of death.ConclusionsThis study revealed a high comorbidity rate and a low seizure-freedom rate among patients with senile epilepsy. In particular, neuropsychiatric comorbidities can increase the risk of seizures and affect the survival rate of patients with senile epilepsy. Therefore, preventing and managing these comorbidities may improve seizure outcomes and reduce mortality in this special population.

Psychiatric Co-Morbidities of Epilepsy in the University Hospitals of Ouagadougou, Burkina Faso

Psychiatric Co-Morbidities of Epilepsy in the University Hospitals of Ouagadougou, Burkina Faso

Challenging behaviour and epilepsy in patients with intellectual disability: frequency and mutual association.

Comorbid epilepsy and challenging behaviours is quiet common in patients with ID (intellectual disability). This study aims to determine the frequency and mutual association between epilepsy and challenging behaviours. In this cross-sectional analytical study, 252 patients were enrolled through convenient sampling technique. Comorbid epilepsy and CB (challenging behaviour) were seen in 111 (44.6%) and 116 (46.6%) patients, respectively. Epilepsy and severity of intellectual disability (ID) are statistically and significantly associated with challenging behaviour. This study concluded that comorbid epilepsy is more common among people with ID as compared to the general population. The clinical variables, i.e. comorbid epilepsy and severity of ID have statistically significant association with the CB.

Diet composition and sterilization modifies intestinal microbiome diversity and burden of Theiler's virus infection-induced acute seizures.

Brain infection with Theiler's murine encephalomyelitis virus (TMEV) in C57BL/6J mice can induce acquired epileptogenesis. Diet alters acute seizure incidence in TMEV-infected mice; yet it is unclear whether intestinal dysbiosis may also impact acute or chronic behavioral comorbidities. This study thus assessed the impact of diet formulation and sterilization on acute seizure presentation, gut microbiome composition, and epilepsy-related chronic behavioral comorbidities. Baseline fecal samples were collected from male C57BL/6J mice (4- to 5-weeks-old; Jackson Labs) upon facility arrival. Mice were randomized to either autoclaved (AC) or irradiated diet (IR) (Prolab RMH 3000) or IR (Picolab 5053). Three days later, mice underwent intracerebral TMEV or phosphate-buffered saline (PBS) injection. Fecal samples were collected from a subset of mice at infection (Day 0) and Day 7 post-infection. Epilepsy-related working memory deficits and seizure threshold were assessed 6 weeks post-infection. Gut microbiome diversity was determined by 16S rRNA amplicon sequencing of fecal samples. TMEV-infected mice displayed acute handling-induced seizures, regardless of diet: 28 of 57 IR Picolab 5053 (49.1%), 30 of 41 IR Prolab RMH 3000 (73.2%), and 47 of 77 AC Prolab RMH 3000 (61%) mice displayed seizures. The number of observed seizures differed significantly by diet: IR Picolab 5053 diet-fed mice had 2.2 ± 2.8 seizures (mean ± standard deviation), IR Prolab RMH 3000 diet-fed mice had 3.5 ± 2.9 seizures, and AC Prolab RMH 3000 diet-fed mice had 4.4 ± 3.8 seizures during the 7-day monitoring period. Gut microbiome composition differed significantly in TMEV-infected mice fed the AC Prolab RMH 3000 diet, with measured differences in gram-positive bacteria. These mice also displayed worsened long-term working memory deficits. Diet-induced differences in intestinal dysbiosis in the TMEV model are associated with marked changes in acute seizure presentation, symptomatic recovery, and onset of chronic behavioral comorbidities of epilepsy. Our study reveals a novel disease-modifying impact of dietary manipulation on intestinal bacterial species after TMEV-induced acute seizures.

Epilepsy and childhood psychiatric disorders: a two-sample bidirectional Mendelian randomization study.

Observational studies have indicated that psychiatric disorders are the most common comorbidities in pediatric epilepsy. However, the existence and direction of a causal relationship between the two remains controversial. This study aims to investigate the association between common childhood psychiatric disorders and epilepsy using a two-sample, bidirectional Mendelian randomization (MR) approach. Genetic instruments were obtained from the most recent and largest genome-wide association studies (GWAS), including datasets for epilepsy (N_case = 29,994, N_control = 52,538), attention deficit hyperactivity disorder (ADHD) (N_case = 38,691, N_control = 186,843), autism spectrum disorder (ASD) (N_case = 18,381, N_control = 27,969), and Tourette syndrome (TS) (N_case = 4,819, N_control = 9488). MR analyses were conducted using the inverse variance weighted (IVW) method, weighted median method, and MR-Egger regression. No reliable evidence was found to suggest a causal effect of ADHD, ASD, or TS on epilepsy, nor was there any reliable evidence indicating that epilepsy increases the risk of these three psychiatric disorders. These findings remained consistent across various sensitivity analyses. Although observational studies have highlighted a high comorbidity rate between pediatric epilepsy and psychiatric disorders like ADHD and ASD, the MR analysis did not confirm a causal relationship between them. This suggests that previous studies might have been influenced by confounding biases or other biases, potentially overestimating the true relationship. A deeper understanding of the mechanisms underlying these comorbidities is crucial for refining the treatment of pediatric epilepsy.

Current status and influencing factors of family resilience in families of children with epilepsy: a cross-sectional study.

The study was designed to describe the level of family resilience and identify the protective factors and vulnerability factors of family resilience in families of children with epilepsy. So as to provide theoretical guidance for implementing intervention programs to promote family resilience. From November 2020 to July 2021, 258 parents of children with epilepsy were investigated using a convenience sampling method. The questionnaire included demographic data, Chinese-Family Resilience Assessment Scale, Social Support Rating Scale, and the Beck Depression Inventory. SPSS25.0 was used for descriptive statistical analysis, univariate analysis, and multivariate linear regression analysis. In this study, two hundred and fifty-eight primary caregivers completed the paper questionnaires. The total score of family resilience was (134.97 ± 16.57), which was above the medium level. Multiple linear regression analysis revealed that subjective support (β=0.327, P<0.001), comorbidity (β=0.181, P<0.05), objective support (β=0.117, P<0.05), and parental depression (β=-0.158, P<0.05) were significantly related to family resilience. These variables contribute 31.7% of the variance in family resilience (F=18.07, P< 0.001). The families of children with epilepsy presented appropriate resilience after the children were diagnosed with epilepsy. Family resilience was correlated with multiple factors, subjective and objective support could be protective factors, comorbidity and parental depression could be vulnerability factors of family resilience. Therefore, future psychosocial interventions could focus on enhancing subjective support and objective support, reducing parental depression, and screening for epilepsy comorbidity to promote the family resilience of children with epilepsy.

Medication use in patients with functional seizures from a public and a private hospital

PurposeCurrently, we have limited knowledge of any potential differences among patients with functional seizures (FS), otherwise known as psychogenic non-epileptic seizures (PNES), from different socioeconomic backgrounds. Investigating medication use among these patients may provide insight into the quality and intensity of medical care they receive. Thus, we aimed to assess and compare the frequency and quantity of antiseizure medications (ASMs), and psychiatric and other medications used among patients with FS from a private and public epilepsy monitoring units (EMUs) in Cape Town, South Africa. MethodsOnly video-electroencephalographically (video-EEG) confirmed patients with FS with no comorbid epilepsy were eligible for the study. For this retrospective case-control study we collected data on patients’ medication-taking histories using digital patient records, starting with the earliest available digital patient record for each hospital. ResultsA total of 305 patients from a private hospital and 67 patients from a public hospital were included in the study (N=372). Patients with FS attending the public hospital had lower odds of taking any ASMs at presentation (aOR=0.39, 95% CI [0.20, 0.75]) and ever taking psychiatric medications (aOR=0.41, 95% CI [0.22, 0.78]) compared to FS patients from the private hospital. They did, however, have higher odds of being discharged with an ASM (aOR=6.60, 95% CI [3.27, 13.35]) and ever taking cardiovascular medication (aOR=2.69, 95% CI [1.22, 5.90]) when compared to the private hospital patients. With every additional presenting ASM (aOR=0.63, 95% CI [0.45, 0.89]) and psychiatric medication (aOR=0.58, 95% CI [0.40, 0.84]) the odds of being from the public hospital decreased. However, they increased with every additional discharge ASM (aOR=3.63, 95% CI [2.30, 5.72]) and cardiovascular medication (aOR=1.26, 95% CI [1.02, 1.55]). ConclusionStandard approaches to pharmacological treatment for patients with FS differed between the public and private hospitals and may indicate a gap in quality of care.

Impairments of GABAergic transmission in hippocampus mediate increased susceptibility of epilepsy in the early stage of Alzheimer’s disease

BackgroundPatients with Alzheimer’s disease (AD) are often co-morbid with unprovoked seizures, making clinical diagnosis and management difficult. Although it has an important role in both AD and epilepsy, abnormal γ-aminobutyric acid (GABA)ergic transmission is recognized only as a compensative change for glutamatergic damage. Neuregulin 1 (NRG1)-ErbB4 signaling can promote GABA release and suppress epileptogenesis, but its effects on cognition in AD are still controversial.MethodsFour-month-old APPswe/PS1dE9 mice (APP mice) were used as animal models in the early stage of AD in this study. Acute/chronic chemical-kindling epilepsy models were established with pentylenetetrazol. Electroencephalogram and Racine scores were performed to assess seizures. Behavioral tests were used to assess cognition and emotion. Electrophysiology, western blot and immunofluorescence were performed to detect the alterations in synapses, GABAergic system components and NRG1-ErbB4 signaling. Furthermore, NRG1 was administrated intracerebroventricularly into APP mice and then its antiepileptic and cognitive effects were evaluated.ResultsAPP mice had increased susceptibility to epilepsy and resulting hippocampal synaptic damage and cognitive impairment. Electrophysiological analysis revealed decreased GABAergic transmission in the hippocampus. This abnormal GABAergic transmission involved a reduction in the number of parvalbumin interneurons (PV+ Ins) and decreased levels of GABA synthesis and transport. We also found impaired NRG1-ErbB4 signaling which mediated by PV+ Ins loss. And NRG1 administration could effectively reduce seizures and improve cognition in four-month-old APP mice.ConclusionOur results indicated that abnormal GABAergic transmission mediated hippocampal hyperexcitability, further excitation/inhibition imbalance, and promoted epileptogenesis in the early stage of AD. Appropriate NRG1 administration could down-regulate seizure susceptibility and rescue cognitive function. Our study provided a potential direction for intervening in the co-morbidity of AD and epilepsy.

Novel and known minor alleles of CNTNAP2 gene variants are associated with comorbidity of intellectual disability and epilepsy phenotypes: a case-control association study reveals potential biomarkers.

Neurodevelopmental disorders are heterogeneous due to underlying multiple shared genetic pathways and risk factors. Intellectual disability, epilepsy and autism spectrum disorder phenotypes overlap which indicates the diverse effects of common genes. Recent studies suggested the probable contribution of CNTNAP2 gene polymorphisms to the comorbidity of these neurological conditions. This study was conducted to investigate the role of CNTNAP2 polymorphisms rs147815978 (G>T) and rs2710102 (A>G) as a risk factor for comorbidity of intellectual disability and epilepsy in a group of 345 individuals including 170 patients and 175 healthy controls recruited from various ethnic groups of Pakistani population. Our case-control study group was genotyped by tetra primer ARMS-PCR technique and results were analysed to know the effects of CNTNAP2 rs147815978 (G>T) and rs2710102 (A>G) polymorphisms in the group. The frequency of risk allele T (rs147815978) and risk allele G (rs2710102) for homozygous recessive genotypes (TT/GG) in our study group was 36.47% while odds ratios for risk allele T (rs147815978) was 5.45 (3.90-7.61: 95% CI, P = 0.000) and that for risk allele G (rs2710102) was 2.39 (1.76-3.24: 95% CI, P = 0.0001). Homozygous recessive genotypes (TT/GG) appeared only in cases and not in control group which indicated these as suspected risk genotypes and the significant association (p < 0.05%) of CNTNAP2 gene polymorphisms rs147815978 (G>T) and rs2710102 (A>G) with co-occurrence of intellectual disability and epilepsy phenotypes in our study group which is in HWE (χ2 = 174, P < 0.0001). Logistic regression analysis shows additive (p < 0.0001) and multiplicative (p < 0.001) models which confirms significant association of both the polymorphisms in our data, which are closely located on same haplotype (D' = -0.168). We propose that CNTNAP2 rs147815978 (G>T) and rs2710102 (A>G) polymorphisms are possible risk loci for overlapping neurodevelopmental disorders in Pakistani population. We propose the role of a previously reported common SNP rs2710102 (A>G) with a rarely reported novel SNP rs147815978 (G>T) for CNTNAP2 gene association with neurodevelopmental disorders in our data. Our study has expanded the knowledge of CNTNAP2 gene polymorphisms as probable biomarkers for susceptibility of co-occurrence of intellectual disability and epilepsy phenotypes in Pakistani population. We hope that our study will open new horizons of CNTNAP2 gene variants research to cure the neurological conditions in Pakistani population where consanguinity is a tradition and prevalence of neurodevelopmental disorders has increased from 1 to 2% during last 5 years.

Epilepsy and psychiatric comorbidities: A bidirectional mendelian randomization study

Study objectivesPsychiatric comorbidities are relatively common among patients with epilepsy; however, the underlying mechanisms of this association remain largely unknown. The objective of this Mendelian randomization (MR) study was to analyze the genetic correlations and causality underlying these reciprocal associations. MethodsSingle-nucleotide polymorphisms associated with epilepsy (29,677 controls and 15,212 cases) and seven psychiatric comorbidities (485,436 controls and 269,495 cases) were identified from genome-wide association studies. Causal significance was estimated using inverse variance weighting. Sensitivity analyses included the weighted median, MR-Egger, and MR-PRESSO. The psychiatric comorbidities analyzed in this study included attention deficit hyperactivity disorder (ADHD), autism spectrum disorder, major depressive disorder, bipolar disorder, schizophrenia, obsessive-compulsive disorder (OCD), and anorexia nervosa. ResultsBoth forward and reverse genetic associations were observed for the selected psychiatric disorders. Notably, ADHD was significantly associated with an increased risk of generalized epilepsy (odds ratio [OR], 1.09; 95 % confidence interval [CI], 1.01–1.18; p = 0.013). However, MR-PRESSO detected the existence of pleiotropy (p = 0.001). Additionally, focal epilepsy was significantly associated with a higher risk of OCD (OR, 1.44; 95 % CI, 1.08–1.92; p = 0.013), and all sensitivity tests yielded favorably nonsignificant results. There was no significant genetic association between epilepsy and other examined psychiatric disorders. However, due to the detection of pleiotropy by MR-Egger and considerations related to the threshold for genetic instruments, a cautious approach is warranted in interpreting some of the results. ConclusionsThis study revealed significant genetic causality between focal epilepsy and OCD, as well as between ADHD and generalized epilepsy. However, no casual significance was observed with other psychiatric comorbidities examined. Considering the inherent limitations of MR studies, further research is warranted to definitively clarify these genetic causal associations.

Behavioral and Cognitive Comorbidities in Genetic Rat Models of Absence Epilepsy (Focusing on GAERS and WAG/Rij Rats).

Absence epilepsy is a non-convulsive type of epilepsy characterized by the sudden loss of awareness. It is associated with thalamo-cortical impairment, which may cause neuropsychiatric and neurocognitive problems. Rats with spontaneous absence-like seizures are widely used as in vivo genetic models for absence epilepsy; they display behavioral and cognitive problems similar to epilepsy in humans, such as genetic absence epilepsy rats from Strasbourg (GAERS) and Wistar Albino rats from Rijswijk (WAG/Rij). Depression- and anxiety-like behaviors were apparent in GAERS, but no anxiety and depression-like symptoms were found in WAG/Rij rats. Deficits in executive functions and memory impairment in WAG/Rij rats, i.e., cognitive comorbidities, were linked to the severity of epilepsy. Wistar rats can develop spontaneous seizures in adulthood, so caution is advised when using them as a control epileptic strain. This review discusses challenges in the field, such as putative high emotionality in genetically prone rats, sex differences in the expression of cognitive comorbidities, and predictors of cognitive problems or biomarkers of cognitive comorbidities in absence epilepsy, as well as the concept of "the cognitive thalamus". The current knowledge of behavioral and cognitive comorbidities in drug-naive rats with spontaneous absence epilepsy is beneficial for understanding the pathophysiology of absence epilepsy, and for finding new treatment strategies.

What is the role of screening instruments in the management of psychiatric comorbidities in epilepsy? Tools and practical tips for the most common comorbidities: Depression and anxiety

Depression and anxiety are the most common psychiatric comorbidities in epilepsy and are known to increase healthcare utilization, the risk of refractory epilepsy, and anti-seizure medication intolerability. Despite this, depression and anxiety continue to be underrecognized and undertreated in people with epilepsy (PWE). Several barriers to the identification of depression and anxiety in PWE exist, including reliance on unstructured interviews rather than standardized, validated instruments. Moreover, there is a dearth of behavioral health providers to manage these comorbidities once identified. The use of validated screening instruments in epilepsy clinics can assist with both the identification of psychiatric symptoms and monitoring of treatment response by the epilepsy clinician for PWE with comorbid depression and/or anxiety. While screening instruments can identify psychiatric symptoms occurring within a specified time, they are not definitively diagnostic. Screeners can be time efficient tools to identify patients requiring further evaluation for diagnostic confirmation.This article reviews recent literature on the utility of depression and anxiety screening instruments in epilepsy care, including commonly used screening instruments, and provides solutions for potential barriers to clinical implementation. Validated depression and anxiety screening instruments can increase identification of depression and anxiety and guide epilepsy clinician management of these comorbidities which has the potential to positively impact patient care.

Psychiatric comorbidities in epilepsy: population co-occurrence, genetic correlations and causal effects

BackgroundPsychiatric comorbidities are common in patients with epilepsy. Reasons for the co-occurrence of psychiatric conditions and epilepsy remain poorly understood.AimWe aimed to triangulate the relationship between epilepsy and psychiatric conditions...

Do psychotropic drugs cause seizures?

Patients with epilepsy often present with concurrent psychiatric disorders, posing unique challenges for healthcare providers. This review explores the intricate relationship between psychiatric comorbidities, epilepsy, and psychotropic medications to inform clinical decision-making. The bidirectional association between epilepsy and psychiatric conditions complicates treatment, with psychiatric symptoms preceding or following seizure onset. The review discusses the seizure risks associated with antidepressants, CNS stimulants, and antipsychotics, shedding light on both historical perspectives and recent empirical evidence. Antidepressants, particularly tricyclic antidepressants (TCAs), are known to pose seizure risks, while newer agents like selective serotonin reuptake inhibitors (SSRIs) exhibit lower incidences and even potential anticonvulsant effects. Contrary to common beliefs, CNS stimulants used in attention-deficit/hyperactivity disorder (ADHD) treatment show efficacy without significantly increasing seizure risk. However, the association between ADHD and seizures warrants careful consideration. Among antipsychotics, clozapine stands out for its heightened seizure risks, especially during titration and at high doses, necessitating close monitoring and individualized approaches. Understanding the nuanced seizure risks associated with different psychotropic medications is crucial for optimizing patient care and minimizing iatrogenic seizures in this vulnerable population. By recognizing the complexities of psychiatric comorbidities in epilepsy and considering the unique challenges they pose, healthcare providers can make informed decisions to enhance patient safety and treatment outcomes. This review offers practical insights to guide clinicians in navigating the intricate landscape of managing psychiatric comorbidities in patients with epilepsy.