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An updated overview of epilepsy that specifically addresses how this condition can affect teens. Epilepsy: The Ultimate Teen Guide, Second Edition gives positive, factual information and explains how young people can take control of their situations by understanding, managing, treating, and living normal lives with epilepsy. This edition includes updated chapters, resource lists, and statistics.

Metabolic modulation of neuronal excitability is becoming increasingly important as an antiepileptic therapy. It was reported that the glycolytic inhibitor 2-deoxy-d-glucose (2-DG) and the activation of the ATP-sensitive potassium ion channel (K sub(ATP) channel) had an antiepileptic effect in models of epilepsy. To explore whether 2-DG exerts an antiepileptic effect through upregulation of the K sub(ATP) channel subunits Kir6.1 and Kir6.2, the expression of these subunits in hippocampus of five groups of mice with pilocarpine-induced status epilepticus (SE) was evaluated. A seizure group with pilocarpine-kindling convulsions (EP) was compared to similar groups treated with high, medium, and low 2-DG concentrations (100-500 mg/kg) and a normal control group (Con). Kir6.1 and Kir6.2 mRNAs and proteins were analyzed at 4 h, 1 days (acute period), 7 days (latent period), 30, and 60 days (chronic period) following SE. In the seizure group (compared to the Con group), hippocampal expression of Kir6.1 and Kir6.2 increased dramatically at 1, 7, and 30 days, and was further increased after treatment with medium and high dose 2-DG (all P < 0.05). Our results suggest that 2-DG may exert an antiepileptic effect through up-regulation of mRNAs and protein levels of Kir6.1 and Kir6.2, which may therefore be used as molecular targets in the treatment of epilepsy with 2-DG.

BackgroundDifferentiating between epileptic seizures (ES) and functional seizures (FS) without video evidence is a common yet challenging presentation in several healthcare environments. Often, the absence of a witnessed collateral history can make this diagnosis even more difficult.Post-ictally, ES classically lead to prolonged lethargy, confusion and headache whilst FS tend to have a much shorter recovery however in practice this may not always be clear.Case reports have anecdotally reported that individuals with FS can sometimes report a sense of relief after their seizures.1 However, this has never been assessed prospectively in a large group of individuals with FS or compared to those with ES.ObjectiveWe aimed to explore the phenomenon of a sense of relief after seizures (paradoxical relief) as a diagnostic tool for FS. We hypothesised that patients with FS may be more likely to feel a sense of relief after seizures than patients with ES.MethodWe prospectively asked 167 patients admitted to a tertiary video telemetry unit if they experienced paradoxical relief. The patients then underwent video telemetry, the gold standard for diagnosis of epileptic and functional seizures.ResultWithin this cohort of 167 patients, 82 patients had events whilst on EEG. 56 patients had FS, and 26 patients had ES. 43 out of the 56 patients with FS described paradoxical relief whereas 2 out of the 26 patients with ES described paradoxical relief. This gives the presence of paradoxical relief in FS a sensitivity of 0.77 and specificity of 0.92. The positive predictive value of presence of paradoxical relief in patients with FS was 0.96. The negative predictive value was 0.65.Some comments made by patients included:It is as if I feel earthed or fused again … whole again.’‘Sometimes it feels like it needed to happen to get my energy back’.‘This strange build up and strange taste has gone ... I am kind of glad it has happened.’ConclusionIn conclusion, paradoxical relief is present in most individuals with FS but not in patients with ES. The single question of presence of paradoxical relief may be valuable in the diagnosis of FS, especially where further investigation or collateral history is not available. The presence of paradoxical relief in patients with FS may be useful to further our understanding of the mechanisms underlying FS.ReferenceStone J, Carson AJ. The unbearable lightheadedness of seizing: wilful submission to dissociative (non-epileptic) seizures. J Neurol Neurosurg Psychiatry 2013;84(7):822–4. doi: 10.1136/jnnp-2012-304842. Epub 2013 Mar 28. PMID: 23538071.

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

IntroductionThe established diagnostic method attempts to produce a unifying diagnosis explaining all of a patient‘s symptoms. In many patients with neuropsychiatric disease however there are multiple coexistent pathologies, making the process of ascribing symptoms to discrete diagnoses difficult. We describe the case of a patient eventually diagnosed with temporal lobe epilepsy and frontotemporal dementia.Case PresentationA 70-year-old man presented with cognitive impairment and a tonic-clonic seizure. He had a background of childhood epilepsy, stopping antiepileptics in his early teens and remaining seizure-free until presentation. His wife reported losses of autobiographical memory, progressive apathy and aphasia. On cognitive assessment there were naming errors/anomia and reduced verbal fluency. On subsequent assessments increasingly frequent unresponsive episodes concerning for subclinical seizures were reported, despite escalating antiepileptic treatment.Serial MRI head scans demonstrated a left amygdala and medial temporal lobe enlargement with T2 hyperintensity but no contrast enhancement. Autoantibody panels demonstrated a modestly raised anti-GAD but were otherwise negative. A trial of immunosuppression for possible autoimmune encephalitis led to neither radiological nor clinical improvement, with worsening behavioural changes and speech.Ambulatory EEG demonstrated subclinical epileptic focal seizures in the left medial temporal area spreading to the left frontal lobe with interictal abnormalities in the left medial temporal area. Further escalation of antiepileptic therapy led to resolution of the patient‘s unresponsive episodes and normalisation of the EEG. A repeat MRI demonstrated resolution of the amygdala asymmetry but progressive cortical atrophy. Despite treatment of the epilepsy the patient continued to deteriorate cognitively. A diagnosis of behavioural variant frontotemporal dementia was made.DiscussionTemporal lobe epilepsy is associated with a range of neuropsychiatric symptoms, complicating the diagnosis of coexistent neuropsychiatric disease. It was only on adequate treatment of the seizures and elimination of temporal lobe epilepsy from the differential diagnosis that frontotemporal dementia was diagnosed. While amygdala pathology is associated with frontotemporal dementia, this generally refers to atrophy rather than enlargement. Amygdala enlargement has been suggested as a distinct subtype of temporal lobe epilepsy, although some have argued that this represents a secondary process in reaction to frequent temporal lobe seizures rather than a primary pathology. A reactive process would explain the resolution of the amygdala asymmetry in this case following epilepsy treatment.ConclusionThis case highlights that clinicians should be vigilant to the possibility of alternate diagnoses when behavioural symptoms do not resolve with treatment of epilepsy. Frontotemporal dementia can mimic the neuropsychiatric comorbidities of epilepsy, complicating the diagnosis of both conditions.

ObjectiveDespite being the subject of many studies over the past two decades, mechanisms underlying psychogenic non-epileptic seizures (PNES) are still poorly understood. We tried to address this issue by utilizing brain functional connectivity analysis to identify brain regions with abnormal activities in patients with PNES. In a case-control study, we performed graph based network analysis, a robust technique that determines the organization of brain connectivity and characterizes topological properties of the brain networks.MethodsTwelve individuals with PNES and twenty-one healthy control subjects were examined. Resting state functional magnetic resonance imaging (rsfMRI) was acquired. All subjects were asked to keep their eyes open during the scanning process. The rsfMRI analysis consisted of pre-processing, extracting the functional connectivity matrix (FCM) based on the AAL atlas, threshold for binary FCM, constructing a graph network from FCM and extracting graph features, and finally statistical analysis. For all cortical and subcortical regions of the AAL atlas, we calculated measures of ‘degree,’ which is one of the features of the graph theory. Results: Our results revealed that, as compared to the healthy control subjects, patients with PNES had a significantly lower degree in some brain regions including their left and right insula (INS), right Putamen (PUT), left and right Supramarginal gyrus (SMG), right Middle occipital gyrus (MOG), and left and right Rolandic operculum (ROL). In contrast, degree was significantly greater in two regions [i.e., right Caudate (CAU) and left Inferior frontal gyrus orbital part (ORBinf)] in patients with PNES compared to that in controls.ConclusionOur findings suggest that functional connectivity of several major brain regions are different in patients with PNES compared with that in healthy individuals. While there is hypoactivity in regions important in perception, motor control, self- awareness, and cognitive functioning (e.g., insula) and also movement regulation (e.g., putamen), there is hyperactivity in areas involved in feedback processing (i.e., using information from past experiences to influence future actions and decisions) (e.g., caudate) in patients with PNES. The observation that individuals with PNES suffer from a wide range of abnormal activities in functional connectivity of their brain networks is consistent with the fact that PNES occur in a heterogeneous patient population; no single mechanism or contributing factor could explain PNES in all patients.

Background/ObjectivesPeople referred to First Seizure Clinics (FSCs) often face long waiting times. Many have seizure mimics. This study aimed to evaluate the impact of an epilepsy nurse (EN) in reducing wait times and minimising seizure mimic referrals. We also aimed to illustrate the range of seizure mimics referred to the FSC and describe diagnostic revisions over time.MethodsWe prospectively collected data from a hundred consecutive individuals seen in FSCs at our centre before and after introduction of a new part-time EN and followed up for a minimum 12 months. Key outcomes included diagnostic revisions over time, changes in referral patterns, characteristics of seizure mimics, and time elapsed between referral and FSC appointment.ResultsPatients (50 male, 50 female) had a median age of 41.4 (range 18–90) years. Fifteen (15%) people had an abnormal MRI and 33% had an abnormal EEG, including eleven (11%) with epileptiform abnormalities. Seizure mimics accounted for 29/50 (58%) diagnoses before the commencement of an epilepsy nurse and reduced to 19/50 (38%) after epilepsy nurse commencement (p<0.05). There was no significant reduction in clinic wait-time post-EN (relative reduction in median wait-time of 39%, p = 0.41). Common seizure mimics included syncope (18%) and PNES (8%). Twelve people (8 pre-EN, 4 post-EN) had a diagnostic change to Epilepsy over the next 12 months after FSC.ConclusionAn EN improved performance of our FSC however wait times remained outside best practice recommendations. Seizure mimics accounted for many FSC referrals and better methods of identifying these are required.

Background/ObjectivesTo validate a novel patient-reported outcome measure, the Seizure-Related Impact Assessment Scale (SERIAS). It captures epilepsy-related disability, and is intended for use in epilepsy clinical trials and practice.MethodsProspective longitudinal study of adults with epilepsy recruited from an Australian Comprehensive Epilepsy Centre. Participants completed SERIAS at baseline, and 3- and 6-months later. SERIAS has 6 self-report items; 5 items record the number of days per month impacted by seizures or treatment-related adverse effects, and 1 item is an epilepsy disability visual analogue scale. Higher SERIAS scores indicate greater disability. SERIAS was completed alongside instruments measuring seizure- and treatment-related adverse effects (WSAS, LAEP), mood disorders (NDDI-E, GAD-7), somatic symptoms (SSS-8), and quality of life (QOLIE-31, EQ-5D).Results90 patients (n=58 females, mean age 43.1 years) completed baseline SERIAS. Greater disability was negatively correlated with QOLIE-31 total score (b=-0.17, 95% CI [-0.27, -0.07]), and positively correlated with scores on EQ-5D-5L (b=0.15, 95% CI [0.04, 0.25]), NDDI-E (b=0.22, 95% CI [0.13, 0.31]), GAD-7 (b=0.21, 95% CI [0.09, 0.32]), SSS8 (b=0.29, 95% CI [0.17, 0.41]), LAEP (b=0.29, 95% CI [0.20, 0.39]), WSAS seizure-related adverse events (b=0.23, 95% CI [0.14, 0.33]), and WSAS treatment-related adverse events (b=0.36, 95% CI [0.26, 0.46]). Higher seizure frequency was associated with higher SERIAS score (b=0.07, 95% CI [0.03, 0.11]). Psychometric reliability for the SERIAS was acceptable (all coefficients >0.70) as was test-retest reliability (n=35 patients, ICC=0.72, 95% CI [0.51, 0.85]).ConclusionThese findings suggest that SERIAS is a valid scale to measure epilepsy related disability.