Seizure

Data from international studies suggest epilepsy prevalence in people with Intellectual Disability (PwID) is around 22.2% [1] and significantly higher than estimations of 0.8% for the general worldwide population. [2]. UK data shows similar distributions, with 17.9% of PwID having an NHS epilepsy diagnosis, compared to 0.6% of those with no ID. [3] Prevalence increases with severity, with 7.3%-9.8% of people with mild ID and 27%-41.6% with moderate to profound ID diagnosed with epilepsy. [1]

Epilepsy affects almost 1% of the general population [1]. Approximately 30-40% of epilepsy patients do not adequately respond to antiseizure medications (ASMs) [2,3]. They are considered ‘drug-resistant’, defined as failure of two tolerated and appropriately prescribed ASMs to achieve sustained seizure freedom [4]. One proposed mechanism for drug-resistance, relevant for epilepsy and many other CNS disorders, like depression, HIV and cancer, is encapsulated by the ‘transporter hypothesis [5-7], postulating that overactivity of drug efflux transporter(s) at the blood-brain barrier (BBB) ...

Posterior cingulate epilepsy (PCE) is a uncommon variant of focal epilepsy. From a clinical perspective, the identification of patients with PCE based on electroclinical characteristics poses a significant diagnostic challenge, as PCE can closely resemble various other epilepsy types [1]. The complexity of diagnosing PCE can often be attributed to the seizure onset zone (SOZ), which is situated in an anatomically deep and relatively inactive region that quickly disseminates activity to more expressive brain structures closely connected to the posterior ...

Many people with epilepsy (PWE) suffer from cognitive impairments, and neuropsychological investigations are an integral part of comprehensive epilepsy care [1]. Nevertheless, the overlap of subjective cognition (SC) and results of objective tests is often weak [2]. Previous studies found that discordance of SC and objective cognition (OC) occurs in 60-80% of PWE [3–5]. Cognitive dysfunction in PWE may have multifactorial reversible and irreversible causes that may impact SC and OC to different degrees.

Human onchocerciasis is a neglected tropical disease caused by the filarial nematode Onchocerca volvulus. The infection is transmitted by infectious bites of blackflies. Clinical manifestations caused by O. volvulus microfilariae include skin and eye disease (river blindness). In onchocerciasis-endemic regions with ongoing or past O. volvulus transmission, an increased prevalence of epilepsy and nodding syndrome (NS) has been observed [1]. Recent epidemiological studies suggest that onchocerciasis may directly or indirectly induce seizures, called onchocerciasis-associated epilepsy (OAE) [2].

Developmental and epileptic encephalopathies (DEEs) are severe pediatric conditions, characterized by epileptic seizures, frequent epileptiform activity on electroencephalogram (EEG), and psychomotor delay or regression. Heterozygous pathogenic variants in FBXO28 gene, encoding a member of the F-box protein family involved in protein ubiquitination cause a developmental and epileptic encephalopathy type 100 (DEE100) [1,2]. So far, only 10 patients with DEE100 have been described worldwide, all presenting refractory epilepsy and severe developmental impairment.

Functional neurological symptom disorder refers to a state in which the normal functioning of brain networks is affected, rather than any structural abnormalities. One of its manifestations is a condition termed psychogenic non-epileptic seizures (PNES), also known as functional or dissociative seizures [1]. These seizures are characterized by clinically similar events to epileptic seizures, although they do not have characteristically abnormal ictal electroencephalogram activities [2], which supports the theory that their occurrences are psychological in nature rather than epileptic.

Asymmetric index

Children with drug-resistant epilepsy experience regular debilitating seizures despite treatment with multiple antiseizure medications.[1] It is a life-changing diagnosis for the child and their family, requiring an adjustment to a new ‘normal’, characterised by the unpredictability of seizures and the coexistence of comorbidities[2,3] It is widely accepted that chronic illness, such as epilepsy, presents additional burdens and care needs for parents, increasing their anxiety, stress, and depression.[4,5]

Congenital Zika syndrome (CZS) is a severe condition caused by intrauterine exposure to the Zika virus (ZIKV). It is responsible for a 10 times higher mortality rate in children without the syndrome [1]. The phenotype for CZS varies based on neurological impairment [2,3]. It encompasses a wide spectrum of structural [4] and functional [5] alterations or sequelae in neurodevelopment that children with CZS may present in the first years of life [6].