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An understanding of mechanisms underlying seizure disorders depends critically on the insights provided by model systems. In particular with the development of cellular, molecular, and genetic investigative tools, there has been an explosion of basic epilepsy research. Models of Seizures and Epilepsy brings together, for the first time in 30 years, an overview of the most widely-used models of seizures and epilepsy. Chapters cover a broad range of experimental approaches (from in vitro to whole animal preparations), a variety of epileptiform phenomenology (including burst discharges and seizures), and suggestions for model characterization and validation, such as electrographic, morphologic, pharmacologic, and behavioral features. Experts in the field provide not only technical reviews of these models but also conceptual critiques - commenting on the strengths and limitations of these models, their relationship to clinical phenomenology, and their value in developing a better understanding and treatments. Models of Seizures and Epilepsy is a valuable, practical reference for investigators who are searching for the most appropriate laboratory models for addressing key questions in the field. It also provides an important background for physicians, fellows, and students, offering insight into the potential for advances in epilepsy research. · The first comprehensive description of animal models of epilepsy since the early 1970's· Comprehensive analysis of \"What the models model\" to guide the selection of each model, and what specific questions it will answer· Elegant examples of the use of novel technologies that can be applied in experimental epilepsy research· World expert opinions on the clinical relevance of each model

Functional neurological disorder (FND) is a common cause of persistent and disabling neurological symptoms. These symptoms are varied and include abnormal control of movement, episodes of altered awareness resembling epileptic seizures and abnormal sensation and are often comorbid with chronic pain, fatigue and cognitive symptoms. There is increasing evidence for the role of neurologists in both the assessment and management of FND. The aim of this review is to discuss strategies for the management of FND by focusing on the diagnostic discussion and general principles, as well as specific treatment strategies for various FND symptoms, highlighting the role of the neurologist and proposing a structure for an interdisciplinary FND service.

ObjectiveSome individuals with functional neurological disorder (FND) exhibit motor and affective disturbances, along with limbic hyper-reactivity and enhanced motor-limbic connectivity. Given that the multimodal integration network (insula, dorsal cingulate, temporoparietal junction (TPJ)) is implicated in convergent sensorimotor, affective and interoceptive processing, we hypothesised that patients with FND would exhibit altered motor and amygdalar resting-state propagation to this network. Patient-reported symptom severity and clinical outcome were also hypothesised to map onto multimodal integration areas.MethodsBetween-group differences in primary motor and amygdalar nuclei (laterobasal, centromedial) were examined using graph-theory stepwise functional connectivity (SFC) in 30 patients with motor FND compared with 30 healthy controls. Within-group analyses correlated functional propagation profiles with symptom severity and prospectively collected 6-month outcomes as measured by the Screening for Somatoform Symptoms Conversion Disorder subscale and Patient Health Questionnaire-15 composite score. Findings were clusterwise corrected for multiple comparisons.ResultsCompared with controls, patients with FND exhibited increased SFC from motor regions to the bilateral posterior insula, TPJ, middle cingulate cortex and putamen. From the right laterobasal amygdala, the FND cohort showed enhanced connectivity to the left anterior insula, periaqueductal grey and hypothalamus among other areas. In within-group analyses, symptom severity correlated with enhanced SFC from the left anterior insula to the right anterior insula and TPJ; increased SFC from the left centromedial amygdala to the right anterior insula correlated with clinical improvement. Within-group associations held controlling for depression, anxiety and antidepressant use.ConclusionsThese neuroimaging findings suggest potential candidate neurocircuit pathways in the pathophysiology of FND.

BackgroundDissociative seizures, also known as functional or psychogenic non-epileptic seizures, account for 11%–27% of all emergency seizure presentations. Misdiagnosis as epileptic seizures is common and leads to ineffective and potentially harmful treatment escalations. We assess the potential for diagnostic improvement at different stages of emergency workup and estimate the utility of benzodiazepines.MethodsA retrospective study of all emergency presentations with a discharge diagnosis of acute dissociative seizures seen at a university hospital 2010–2022 was performed to assess clinical characteristics and emergency decision-making.ResultsAmong 156 patients (73% female, median 29 years), 15% presented more than once for a total of 203 presentations. Half of seizures were ongoing at first medical contact; prolonged seizures and clusters were common (23% and 24%). Diagnostic accuracy differed between on-site emergency physicians and emergency department neurologists (12% vs 52%). Typical features such as eye closure, discontinuous course and asynchronous movements were common. Benzodiazepines were given in two-thirds of ongoing seizures, often in high doses and preferentially for major hyperkinetic semiology. Clinical response to benzodiazepines was mixed, with a minority of patients remaining either unaffected (16%) or becoming critically sedated (13%). A quarter of patients given benzodiazepines by emergency medical services were admitted to a monitoring unit, 9% were intubated.ConclusionsImproved semiological assessment could reduce early misdiagnosis of dissociative seizures. Although some seizures seem to respond to benzodiazepines, critical sedation is common, and further studies are needed to assess the therapeutic ratio.

IntroductionPsychogenic nonepileptic seizures (PNES) consist of paroxysmal changes in responsiveness, movements, or behaviour that superficially resemble epileptic seizures.ObjectivesPresentation of a clinical case of a PNES in a patient with a diagnose of secondary epilepsy, illustrating the relevance of an adequate evaluation, differential diagnosis, and intervention.MethodsDescription of the clinical case, with brief literature review and discussion. A search was conducted on PubMed and other databases, using the MeSH terms “nonepileptic seizure”, and “epileptic seizure”.ResultsWe report the case of a 45-year-old female patient, brought to the emergency department because of tonic axial and limb nonsynchronous movements, closed eyes, long duration, with immediate awareness, no desaturation, tongue bite, facial flushing, dyspnoea or sphincter incontinency. She was medicated with clonazepam 1 mg and levetiracetam 1000 mg ev. TC-CE had no acute alteration. Bloodwork had no other major alteration except valproic acid below therapeutic levels (her usual medication, along with other antiepileptic drugs, antidepressant and antipsychotic). The antecedents of the patient: mild intellectual disability and an accidental traumatic brain injury in infancy, with secondary epilepsy. She was transferred to Psychiatry department. No electroencephalogram (EEG) was realized, because she had a recent one confirming PNES, and many other emergency observations with the diagnosis of PNES.ConclusionsThis clinical case showcases the diagnostic difficulties that clinicians face when there is an overlap in symptoms, emphasizing the need to combine patient history, witness reports, clinician observations, and ictal and interictal EEG to help distinguish these different clinical identities.DisclosureNo significant relationships.

IntroductionPsychogenic nonepileptic seizures (PNES), the most common conversion disorder, are episodic alterations in behaviour that resemble epileptic seizures without its characteristic EEG changes. PNES presumably reflect a physical manifestation of underlying psychological distress and can be as disabling as epilepsy. Standardized treatment approaches for PNES care are lacking.ObjectivesOur aim is to review the literature for therapeutic interventions in PNES.MethodsA literature search was conducted in PubMed/MEDLINE database for randomized controlled trials (RCTs) examining the effect(s) of specific intervention(s) in patients with PNES. Search terms were “psychogenic-nonepileptic-seizures” and selection was based on the abstracts of all the studies retrieved. Priority outcome was frequency of PNES.ResultsWe identified 8 eligible RCTs. Samples ranged from 19 to 82 patients. Follow-up periods varied from 6 weeks to 18 months. Regarding reduction of PNES frequency, several interventions were effective: motivational interviewing combined with psychotherapy; cognitive behavioural therapy informed psychotherapy (CBT-ip); combination of CBT-ip and sertraline; immediate withdrawal of antiepileptic drugs after PNES diagnosis; a standardized diagnostic approach associated with psychiatric inpatient consultation. Treatment with sertraline alone and brief educational interventions didn’t reduce PNES frequency significantly. Beside PNES rate reduction, most interventions conveyed some type of benefit such as improvement in quality of life, mood or functionality.ConclusionsThe majority of the beneficial interventions included a structured communicational approach and/or psychotherapeutic treatment. Our analysis highlights the importance of a multidisciplinary strategy that includes psychotherapy. Further studies with larger samples and longer follow-up periods are needed to robustly inform evidence-based treatment for PNES.DisclosureNo significant relationships.

IntroductionPsychogenic Nonepileptic Seizures (PNES) refer to the dissociative condition which resembles seizures but does not involve epileptic synchronous cortical activity (Huff, 2021). 20% of people visiting epilepsy clinics have PNES (Huff, 2021). Depression, anxiety, and personality disorders predispose towards PNES (Ekanayake, 2018).ObjectivesTo present a case of PNES in a patient with dependent personality disorder (DPD) and to discuss the sociocultural aspects.MethodsA case study.ResultsA 23-years old, married female presented with 20 days history of episodes of ‘falling down, rolling on ground, and involuntary movements of her head.’ The episodes typically lasted from 20-25 minutes. During the episodes, patient closed her eyes but remained conscious and expressed her distress with gestures, and tearfulness was also observed. Her condition improved when she was offered water. The clinical picture of these episodes evolved with time. Her EEG and serum prolactin levels following the episodes were normal. Accordingly, a diagnosis of PNES was made. No acute stressor was present. The patient also fulfilled the criteria of Dependent Personality Disorder (DPD) (American Psychiatric Association, 2013). During communication with the patient, it appeared that the patient and her attendants perceived the train of questioning as investigational rather than therapeutic. Efforts were made towards a more empathetic understanding of their point of view, and the tailoring of long-term management in accordance with their sociocultural context.ConclusionsThe socio-cultural context is important in the management of PNES and a sensitive, and collaborative approach is recommended. Assessment of personality should be considered in patients presenting with PNES.DisclosureNo significant relationships.

Background and purpose Cognitive complaints are common in functional neurological disorder (FND), but it is unclear whether objective neurocognitive deficits are present. This systematic review summarized validated/standardized cognitive test performance in FND samples across cognitive domains. Methods Embase, PsycInfo and MEDLINE were searched from inception to 15 May 2023, combining terms for FND and cognitive domains (e.g., attention, memory, executive functioning). Studies included a range of FND phenotypes (seizures, motor, cognitive disorder, mixed), compared to healthy or clinical controls. Risk of bias was assessed with the modified Newcastle–Ottawa Scale and a qualitative synthesis/narrative review of cognitive performance in FND was conducted. Test performance scores were extracted, and random effects meta‐analyses were run where appropriate. This review was registered on PROSPERO, CRD42023423139. Results Fifty‐six studies including 2260 individuals with FND were eligible. Although evidence for some impairments emerged across domains of executive functioning, attention, memory and psychomotor/processing speed, this was inconsistent across studies and FND phenotypes. Common confounds included group differences in demographics, medication and intellectual functioning. Only 24% of studies objectively assessed performance validity. Meta‐analyses revealed higher scores on tests of naming (g = 0.67, 95% confidence interval [CI] 0.50, 0.84) and long‐term memory (g = 0.43, 95% CI 0.13, 0.74) in functional seizures versus epilepsy, but no significant differences in working (g = −0.08, 95% CI −0.44, 0.29) or immediate (g = 0.25, 95% CI −0.02, 0.53) memory and cognitive flexibility (g = −0.01, 95% CI −0.29, 0.28). Conclusions There is mixed evidence for objective cognitive deficits in FND. Future research should control for confounds, include tests of performance validity, and assess relationships between objective and subjective neurocognitive functioning.

We investigated the association between the glucocorticoid receptor (GR) gene, also known as the nuclear receptor subfamily 3, group C, member 1 (NR3C1), rs41423247 polymorphism, and functional seizures (psychogenic nonepileptic seizures/attacks) in a case-control study. We hypothesized that the tested polymorphism has significant associations with functional seizures (psychogenic nonepileptic seizures/attacks) independent from comorbid depression. Seventy patients with functional seizures (psychogenic nonepileptic seizures/attacks), 70 with major depressive disorder (MDD), and 70 healthy controls (HCs) were studied. Their DNAs were analyzed for NR3C1 rs41423247 polymorphism. Genotype and allele frequencies of rs41423247 were different between the three groups. G allele carriers were more frequent in patients with functional seizures (psychogenic nonepileptic seizures/attacks) and those with MDD compared to HCs (p = 0.0001). However no significant difference was observed with respect to allele distributions between functional seizures (psychogenic nonepileptic seizures/attacks) and MDD groups (p = 0.391). CC genotype was less often associated with functional seizures (psychogenic nonepileptic seizures/attacks) versus HC: Codominant model; p = 0.001, OR = 0.11, 95% CI = 0.05-0.24, and -2loglilkelihood = 231.7. In comparison between functional seizures (psychogenic nonepileptic seizures/attacks) group and other (MDD + HC) groups, we observed a significant association between CG genotype and functional seizures (psychogenic nonepileptic seizures/attacks) (Codominant model; p = 0.001, OR = 5.63, 95% CI = 2.60-12.40 and -2loglikelihood = 245.99). Patients with functional seizures (psychogenic nonepileptic seizures/attacks) and those with MDD were significantly more often G allele carriers in rs41423247 compared with HCs. We observed a significant association between CG genotype and functional seizures (psychogenic nonepileptic seizures/attacks). However, we could not exclude the possibility of confounding effects of depression. Future genetic studies of patients with functional seizures (psychogenic nonepileptic seizures/attacks) should include a comparison group with depression in addition to a comparison group of HCs.