OBJECTIVE:This study was undertaken to determine the incidence of sudden unexpected death in epilepsy (SUDEP) in New Zealand. METHODS:We attempted to prospectively identify all people with epilepsy (PWE) in New Zealand who died from SUDEP after August 1, 2019. Information about the patients' death and epilepsy was recorded in the EpiNet database. Two neurologists (P.S.B. and S.S.) reviewed each case and determined the SUDEP category. The national censuses for 2018 and 2023 were used as the denominator population. RESULTS:Records for 440 PWE who died between August 1, 2019 and July 31, 2021 were reviewed. We concluded that 103 people died from definite, definite plus, probable, probable plus, or resuscitated SUDEP (hereafter referred to as SUDEP). Possible SUDEP was diagnosed in 54. The crude incidence of SUDEP was 10.7 (95% confidence interval [CI] = 8.7-12.9)/1 million person-years. If the prevalence of active epilepsy in New Zealand was 5.49/1000 people, then the incidence of SUDEP in PWE was 1.93 (95% CI = 1.46-2.55) per 1000 person-years. If possible cases are included, the crude incidence of SUDEP was 16.2 (95% CI = 13.8-18.9) per 1 million person-years, and in PWE was 2.94 (95% CI = 2.23-3.89) per 1000 person-years. Sixty-five patients were male, and 38 were female (incidence rate ratio [IRR] = 1.75, 95% CI = 1.18-2.63, p = .005). The rate of SUDEP was lower among Asian people living in New Zealand compared with New Zealand European people (IRR = .33, 95% CI = .10-.83, p = .015). There was a trend toward a higher incidence in Māori and Pacific peoples. Employment status was known for 62 people, of whom 23 were unemployed. SIGNIFICANCE:The incidence of SUDEP in New Zealand in PWE (1.93/1000 person-years) is higher than usually reported for high-income countries, although there is uncertainty regarding the prevalence of epilepsy in New Zealand. We suspect the actual incidence of SUDEP worldwide is higher than is usually reported.

Purpose Epilepsia partialis continua (EPC) is form of focal motor status epilepticus, with limited guidelines regarding effective pharmacological management. This systematic review aimed to describe previously utilized pharmacological management strategies for EPC, with a focus on patient outcomes. Methods A systematic review of the databases PubMed, EMBASE, and SCOPUS was performed from inception to May 2024. The review was conducted and reported in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The review was prospectively registered on PROSPERO. Results Five studies fulfilled the inclusion criteria. All studies were case series, and in total included 51 patients. The mortality rate was 11.8% (6/51). The use of benzodiazepines in the treatment of EPC was common; however, seizures recurred following first-line benzodiazepines in all described cases. Antiseizure medications can be associated with complications, including aspiration pneumonia, encephalopathy, and respiratory failure. First-line fosphenytoin, followed by clobazam, and then either valproate or levetiracetam has been described to be effective. Described cases also support the earlier use of levetiracetam. Other adjunctive treatments have been described, including lacosamide, topiramate, and carbamazepine. Conclusion Despite treatment, EPC typically lasts at least hours, and often days or longer. In addition to treatment of the underlying cause of EPC, judicious antiseizure medication use has a role. However, care should be taken not to cause harm (such as respiratory depression) with antiseizure medications, particularly noting that seizures are likely to be prolonged irrespective of antiseizure medication choice.

Catamenial epilepsy is the best described and most researched sex steroid-specific seizure exacerbation. Yet despite this there are no current evidence-based treatments, nor an accepted diagnostic tool. The best tool we currently have is tracking seizures over menstrual cycles; however, the reality of tracking seizures and menstrual cycles is fraught with challenges. In Part 1 of this two-part review, we outlined the often complex and reciprocal relationship between seizures and sex steroids. An adaptable means of tracking is required. In this review, we outline the extent and limitations of current knowledge on catamenial epilepsy. We use sample data to show how seizure exacerbations can be tracked in short/long and even irregular menstrual cycles. We describe how seizure severity, an often overlooked and underresearched form of catamenial seizure exacerbation, can also be tracked. Finally, given the lack of treatment options for females profoundly affected by catamenial epilepsy, Section 3 focuses on current methods and models for researching sex steroids and seizures as well as limitations and future directions. To permit more informative, mechanism-focused research in humans, the need for both a consistent classification of catamenial epilepsy and an objective biomarker is highlighted.

OBJECTIVE:Determination of the real-world performance of a health care system in the treatment of status epilepticus (SE).METHODS:Prospective, multicenter population-based study of SE in Auckland, New Zealand (NZ) over 1 year, with data recorded in the EpiNet database. Focus on treatment patterns and determinants of SE duration and 30-day mortality. The incidence, etiology, ethnic discrepancies, and seizure characteristics of this cohort have been published previously.RESULTS:A total of 365 patients were included in this treatment cohort; 326 patients (89.3%) were brought to hospital because of SE, whereas 39 patients (10.7%) developed SE during a hospital admission for another reason. Overall, 190 (52.1%) had a known history of epilepsy and 254 (70.0%) presented with SE with prominent motor activity. The mean Status Epilepticus Severity Score (STESS) was 2.15 and the mean SE duration of all patients was 44 min. SE self-terminated without any treatment in 84 patients (22.7%). Earlier administration of appropriately dosed benzodiazepine in the pre-hospital setting was a major determinant of SE duration. Univariate analysis demonstrated that mortality was significantly higher in older patients, patients with longer durations of SE, higher STESS, and patients who developed SE in hospital, but these did not maintain significance with multivariate analysis. There was no difference in the performance of the health care system in the treatment of SE across ethnic groups.SIGNIFICANCE:When SE was defined as 10 continuous minutes of seizure, overall mortality was lower than expected and many patients had self-limited presentations for which no treatment was required. Although there were disparities in the incidence of SE across ethnic groups there was no difference in treatment or outcome. The finding highlights the benefit of a health care system designed to deliver universal health care.

PURPOSE:To document the 2-year mortality and seizure recurrence rate of a prospective cohort of patients identified with status epilepticus (SE). METHODS:Patients presenting to any hospital in the Auckland region between April 6 2015, and April 5 2016, with a seizure lasting 10 min or longer were identified. Follow up was at 2 years post index SE episode via telephone calls and detailed review of clinical notes. RESULTS:We identified 367 patients with SE over the course of one year. 335/367 (91.3 %) were successfully followed up at the 2-year mark. Two-year all-cause mortality was 50/335 (14.9 %), and 49/267 (18.4 %) when febrile SE was excluded. Two-year seizure recurrence was 197/335 (58.8 %). On univariate analyses, children (preschoolers 2 to < 5 years and children 5 to < 15 years), Asian ethnicity, SE duration <30 mins and acute (febrile) aetiology were associated with lower mortality, while older age >60 and progressive causes were associated with higher mortality on both univariate and multivariate analyses. Age < 2 years and acute aetiology were associated with lower seizure recurrence, while non convulsive status epilepticus (NCSE) with coma and a history of epilepsy were associated with higher seizure recurrence. On multivariate analyses, a history of epilepsy, as well as having both acute and remote causes were associated with higher seizure recurrence. CONCLUSIONS:All-cause mortality in both the paediatric and adult populations at 2 years was lower than most previous reports. Older age, SE duration ≥30 mins and progressive aetiologies were associated with the highest 2-year mortality, while febrile SE had the lowest mortality. A history of epilepsy, NCSE with coma, and having both acute and remote causes were associated with higher seizure recurrence at 2 years. Future studies should focus on functional measures of outcome and long-term quality of life.

Objectives To determine: the incidence of SUDEP in New Zealand; how this changes over time; risk factors associated with SUDEP. Methods New Zealand coroners and other sources notify us of people with epilepsy (pwe) who die unexpectedly. Cases are reviewed and assessed according to the Devinsky criteria. Results The study commenced on 01/08/2019. We were notified of 159 pwe who died suddenly during the first 2 years of the study. 85 patients died from Definite, Definite-plus, Probable or Probable Plus-SUDEP; (46 in year 1; 39 in year 2); 30 died from Possible SUDEP; 2 further patients died during their first seizure without a formal diagnosis of epilepsy; 40 had an alternative cause of death; the cause of death is still under review in 2 patients. 55 of 85 Definite or Probable SUDEP cases were male. 58% were aged between 20 and 50. New Zealand's estimated population at 30 June 2020 was 5,084,300, giving a crude incidence of SUDEP of at least 8.0/million of population per year. If possible cases are included, then the rate of SUDEP is 10.3/million per year If the prevalence of epilepsy in New Zealand is 5.49/1000 people, then the incidence of SUDEP is between 1.52/1000 pwe and 2.06/1000 pwe (including possible SUDEP cases). Conclusions The estimated incidence of SUDEP for New Zealand is at least 8.0/million per year of population; much higher than determined by retrospective review. We are continuing to collect prospective data, to determine whether changes in epilepsy management reduce the rate of SUDEP.

Seizures, antiseizure medications, and the reproductive systems are reciprocally entwined. In Section 2 of this review, we outline how seizures may affect the hypothalamic-pituitary-gonadal axis, thereby altering sex steroids, and changes in sex steroids across the menstrual cycle and changes in pharmacokinetics during pregnancy may alter seizure susceptibility. The literature indicates that females with epilepsy experience increased rates of menstrual disturbances and reproductive endocrine disorders. The latter include polycystic ovary syndrome, especially for females on valproate. Studies of fertility have yielded mixed results. We aim to summarize and attempt to detangle the existing knowledge on these reciprocal interactions. The menstrual cycle causes changes in seizure intensity and frequency for many females. When this occurs perimenstrually, during ovulation, or in association with an inadequate luteal phase, it is termed catamenial epilepsy. There is a clear biophysiological rationale for how the key female reproductive neurosteroids interact with the brain to alter the seizure threshold, and Section 3 outlines this important relationship. Critically, what remains unknown is the specific pathophysiology of catamenial epilepsy that describes why not all females are affected. There is a need for mechanism-focused investigations in humans to uncover the complexity of the relationship between reproductive hormones, menstrual cycles, and the brain.

Circannual status epilepticus (SE) patterns in communities near Earth's poles best test the hypothesis that SE susceptibility varies with light exposure because these communities are routinely subject to large changes in annual light exposure, which may result in changes to daily sleep time. We compared northern hemispheric circannual SE occurrence in Kivalliq, Canada (latitude-62.8° N) to southern hemispheric Auckland, New Zealand (latitude-36.9° S). Instead of peaking at a similar calendar time, SE peaked at a similar solar time during the increasing daylight phase after each region's respective winter solstice. This demonstrates that cumulative effects of increasing light exposure can mediate SE susceptibility.

The study of microglia isolated from adult human brain tissue provides unique insight into the physiology of these brain immune cells and their role in adult human brain disorders. Reports of microglia in post-mortem adult human brain tissue show regional differences in microglial populations, however, these differences have not been fully explored in living microglia. In this study biopsy tissue was obtained from epileptic patients undergoing surgery and consisted of both cortical areas and neurogenic ventricular and hippocampal (Hp) areas. Microglia were concurrently isolated from both regions and compared by immunochemistry. Our initial observation was that a greater number of microglia resulted from isolation and culture of ventricular/Hp tissue than cortical tissue. This was found to be due to a greater proliferative capacity of microglia from ventricular/Hp regions compared to the cortex. Additionally, ventricular/Hp microglia had a greater proliferative response to the microglial mitogen Macrophage Colony-Stimulating Factor (M-CSF). This enhanced response was found to be associated with higher M-CSF receptor expression and higher expression of proteins involved in M-CSF signalling DAP12 and C/EBPβ. Microglia from the ventricular/Hp region also displayed higher expression of the receptor for Insulin-like Growth Factor-1, a molecule with some functional similarity to M-CSF. Compared to microglia isolated from the cortex, ventricular/Hp microglia showed increased HLA-DP, DQ, DR antigen presentation protein expression and a rounded morphology. These findings show that microglia from adult human brain neurogenic regions are more proliferative than cortical microglia and have a distinct protein expression profile. The data present a case for differential microglial phenotype and function in different regions of the adult human brain and suggest that microglia in adult neurogenic regions are "primed" to an activated state by their unique tissue environment.

EpilepsiaVolume 62, Issue 5 p. 1280-1281 GRAY MATTERS Invitation to participate in a prospective case–control study of sudden unexpected death in epilepsy Peter Bergin, Corresponding Author pbergin@adhb.govt.nz orcid.org/0000-0003-0181-1959 Neurology Department, Auckland City Hospital, Auckland, New Zealand Correspondence Peter Bergin, Neurology Department, Auckland City Hospital, Park Rd., Auckland 1148, New Zealand. Email: pbergin@adhb.govt.nzSearch for more papers by this authorYvonne Langan, Department of Clinical Neurophysiology, St. James's Hospital, Dublin, IrelandSearch for more papers by this authorEttore Beghi, orcid.org/0000-0003-2542-0469 Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Milan, ItalySearch for more papers by this authorElizabeth Donner, orcid.org/0000-0003-1126-0548 Comprehensive Epilepsy Program, Hospital for Sick Children, Toronto, Ontario, CanadaSearch for more papers by this authorHannah Cock, orcid.org/0000-0002-5656-0141 Atkinson Morley Regional Epilepsy Network, St. George's University Hospitals National Health Service Foundation Trust, London, UKSearch for more papers by this authorWendyl D'Souza, Department of Medicine, St. Vincent's Hospital Melbourne, University of Melbourne, Fitzroy, Victoria, AustraliaSearch for more papers by this authorRhys Thomas, Translational and Clinical Research Institute, Newcastle University, Newcastle Upon Tyne, UKSearch for more papers by this authorRobert Scragg, School of Population Health, Grafton Campus, University of Auckland, Auckland, New ZealandSearch for more papers by this author Peter Bergin, Corresponding Author pbergin@adhb.govt.nz orcid.org/0000-0003-0181-1959 Neurology Department, Auckland City Hospital, Auckland, New Zealand Correspondence Peter Bergin, Neurology Department, Auckland City Hospital, Park Rd., Auckland 1148, New Zealand. Email: pbergin@adhb.govt.nzSearch for more papers by this authorYvonne Langan, Department of Clinical Neurophysiology, St. James's Hospital, Dublin, IrelandSearch for more papers by this authorEttore Beghi, orcid.org/0000-0003-2542-0469 Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Milan, ItalySearch for more papers by this authorElizabeth Donner, orcid.org/0000-0003-1126-0548 Comprehensive Epilepsy Program, Hospital for Sick Children, Toronto, Ontario, CanadaSearch for more papers by this authorHannah Cock, orcid.org/0000-0002-5656-0141 Atkinson Morley Regional Epilepsy Network, St. George's University Hospitals National Health Service Foundation Trust, London, UKSearch for more papers by this authorWendyl D'Souza, Department of Medicine, St. Vincent's Hospital Melbourne, University of Melbourne, Fitzroy, Victoria, AustraliaSearch for more papers by this authorRhys Thomas, Translational and Clinical Research Institute, Newcastle University, Newcastle Upon Tyne, UKSearch for more papers by this authorRobert Scragg, School of Population Health, Grafton Campus, University of Auckland, Auckland, New ZealandSearch for more papers by this author First published: 01 May 2021 https://doi.org/10.1111/epi.16898 Funding information: Health Research Council of New Zealand, Grant/Award Number: 19/420 Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume62, Issue5May 2021Pages 1280-1281 RelatedInformation

AIM: Sudden unexpected death in epilepsy (SUDEP) is well recognised and widely reported but remains poorly understood. SUDEP in young adults is 27 times more common than sudden death in control populations. The incidence of SUDEP in New Zealand is not known but up to 40 people with epilepsy may die from SUDEP every year. A review of coroner's reports of SUDEP was undertaken to learn more about SUDEP in New Zealand. METHOD: Coroner's reports of all cases of possible SUDEP in New Zealand from 2007-2016 (n=190) were obtained and post-mortem and toxicology results were reviewed. Cases were categorised using published criteria. RESULTS: We obtained reports of 190 cases from the coroner's office. Of these 190 cases, we determined that 123 were definite SUDEP, 40 were definite SUDEP plus, three were probable SUDEP, seven were possible SUDEP and 17 were probably not SUDEP. The number of cases per year varied from 11-26 (2013). Cases were aged 1.5-67 years, with 63% aged 15-45 (mean 37 years). Sixty-one percent were mate. Eightyseven percent of the deaths occurred at home, with 74% found dead in their bed or bedroom. The majority were not employed, with only 33% working or retired at the time of death; 15% were children or students. Information regarding work status was not available for 11%. Toxicology results were available for 155 cases; antiepileptic drug (AED) use was detected in 67% of these cases, with a single AED detected in 44%, two AEDs in 21%, and three AEDs in 3% of samples taken at autopsy. Approximately half who took an AED were taking either sodium valproate or carbamazepine. CONCLUSION: This study suggests that people with epilepsy who die from SUDEP in New Zealand are young and are often compliant with their medication. We plan to establish a nationwide SUDEP registry using the EpiNet database to determine the incidence of SUDEP in New Zealand, and to track changes in SUDEP rates. We are also planning to take part in an international case-control study of SUDEP in the hope that we might learn more about risk factors that predispose people with epilepsy to SUDEP, and factors that might reduce the risk.

Objective To determine the incidence, etiology, and outcome of status epilepticus (SE) in Auckland, New Zealand, using the latest International League Against Epilepsy (ILAE) SE semiological classification. Methods We prospectively identified patients presenting to the public or major private hospitals in Auckland (population = 1.61 million) between April 6, 2015 and April 5, 2016 with a seizure lasting 10 minutes or longer, with retrospective review to confirm completeness of data capture. Information was recorded in the EpiNet database. Results A total of 477 episodes of SE occurred in 367 patients. Fifty-one percent of patients were aged SE with prominent motor symptoms comprised 81% of episodes (387/477). Eighty-four episodes (18%) were nonconvulsive SE. Four hundred fifty episodes occurred in 345 patients who were resident in Auckland. The age-adjusted incidence of 10-minute SE episodes and patients was 29.25 (95% confidence interval [CI] = 27.34-31.27) and 22.22 (95% CI = 20.57-23.99)/100 000/year, respectively. SE lasted 30 minutes or longer in 250 (56%) episodes; age-adjusted incidence was 15.95 (95% CI = 14.56-17.45) SE episodes/100 000/year and 12.92 (95% CI = 11.67-14.27) patients/100 000/year. Age-adjusted incidence (10-minute SE) was 25.54 (95% CI = 23.06-28.24) patients/100 000/year for males and 19.07 (95% CI = 16.91-21.46) patients/100 000/year for females. The age-adjusted incidence of 10-minute SE was higher in Maori (29.31 [95% CI = 23.52-37.14]/100 000/year) and Pacific Islanders (26.55 [95% CI = 22.05-31.99]/100 000/year) than in patients of European (19.13 [95% CI = 17.09-21.37]/100 000/year) or Asian/other descent (17.76 [95% CI = 14.73-21.38]/100 000/year). Seventeen of 367 patients in the study died within 30 days of the episode of SE; 30-day mortality was 4.6%. Significance In this population-based study, incidence and mortality of SE in Auckland lie in the lower range when compared to North America and Europe. For pragmatic reasons, we only included convulsive SE if episodes lasted 10 minutes or longer, although the 2015 ILAE SE classification was otherwise practical and easy to use.

The EpiNet project has been commenced to facilitate investigator-led collaborative research in epilepsy. A new Web-based data collection tool has been developed within EpiNet to record comprehensive data regarding status epilepticus and has been used for a study of status epilepticus in Auckland, New Zealand. All patients aged >4weeks who presented to any of the five public hospitals and the major private hospital within Auckland city (population = 1.61 million) with an episode of status epilepticus between April 6, 2015 and April 5, 2016 were identified using multiple overlapping sources of information. For this study, status epilepticus was defined as any seizure exceeding 10minutes in duration, or repeated seizures lasting >10minutes without recovery between seizures. Patients who had either convulsive or nonconvulsive status epilepticus were included. Episodes of status epilepticus were classified according to the 2015 International League Against Epilepsy ILAE status epilepticus classification. A total of 477 episodes in 367 patients were considered as definite or probable status epilepticus; 285 episodes (62%) lasted >30minutes, which is the duration that has previously been used for epidemiological studies of status epilepticus.

Background: The trigeminal autonomic cephalalgias (TACs) are a group of debilitating, pathophysiologically similar headache syndromes characterized by facial pain and autonomic symptoms in areas supplied by the trigeminal nerve. Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) is among the rarest of the TAC syndromes and can be particularly recalcitrant to treatment. Case: We describe the case of a 50-year old woman with difficult-to-control SUNCT whose pain was completely aborted within hours of commencing intravenous lignocaine therapy and was maintained pain-free after transitioning to oral mexiletine. Conclusion: This is the first report of successful transition from intravenous lignocaine to oral mexiletine in SUNCT, and we suggest that this treatment should be tried early in difficult-to-control SUNCT. This therapy is safe, effective and with minimal side effects if administered in an appropriate manner.

OBJECTIVE:Previous studies have shown moderate agreement between physicians when diagnosing epilepsy, but have included small numbers. The EpiNet study group was established to undertake multicentre clinical trials in epilepsy. Before commencing trials, we wanted to determine levels of agreement between physicians from different countries and different health systems when diagnosing epilepsy, specific seizure types and etiologies. METHODS:30 Case scenarios describing six children and 24 adults with paroxysmal events (21 epileptic seizures, nine non-epileptic attacks) were presented to physicians with an interest in epilepsy. Physicians were asked how likely was a diagnosis of epilepsy; if seizures were generalised or focal; and the likely etiology. For 23 cases, clinical information was presented in Step 1, and investigations in Step 2. RESULTS:189 Participants from 36 countries completed the 30 cases. Levels of agreement were determined for 154 participants who provided details regarding their clinical experience. There was substantial agreement for diagnosis of epilepsy (kappa=0.61); agreement was fair to moderate for seizure type(s) (kappa=0.40) and etiology (kappa=0.41). For 23 cases with two steps, agreement increased from step 1 to step 2 for diagnosis of epilepsy (kappa 0.56-0.70), seizure type(s) (kappa 0.38-0.52), and etiology (kappa 0.38-0.47). Agreement was better for 53 epileptologists (diagnosis of epilepsy, kappa=0.66) than 56 neurologists with a special interest in epilepsy (kappa=0.58). Levels of agreement differed slightly between physicians practicing in different parts of the world, between child and adult neurologists, and according to one's experience with epilepsy. CONCLUSION:Although there is substantial agreement when epileptologists diagnose epilepsy, there is less agreement for diagnoses of seizure types and etiology. Further education of physicians regarding semiology of different seizure types is required. Differences in approach to diagnosis, both between physicians and between countries, could impact negatively on clinical trials of anti-epileptic drugs.

Surely the most interesting finding in the debate among Campbell, Weijer, and colleagues is that the authors all agree on the benefits of doctors participating in pragmatic research.1 Even those who don’t think that doctors should be forced to participate agree that participation benefits society. The issue of “duty” or “obligation” misses the point: we need a …

SummaryObjectiveEpiNet was established to encourage epilepsy research. EpiNet is used for multicenter cohort studies and investigator‐led trials. Physicians must be accredited to recruit patients into trials. Here, we describe the accreditation process for the EpiNet‐First trials.MethodsPhysicians with an interest in epilepsy were invited to assess 30 case scenarios to determine the following: whether patients have epilepsy; the nature of the seizures (generalized, focal); and the etiology. Information was presented in two steps for 23 cases. The EpiNet steering committee determined that 21 cases had epilepsy. The steering committee determined by consensus which responses were acceptable for each case. We chose a subset of 18 cases to accredit investigators for the EpiNet‐First trials. We initially focused on 12 cases; to be accredited, investigators could not diagnose epilepsy in any case that the steering committee determined did not have epilepsy. If investigators were not accredited after assessing 12 cases, 6 further cases were considered. When assessing the 18 cases, investigators could be accredited if they diagnosed one of six nonepilepsy patients as having possible epilepsy but could make no other false‐positive errors and could make only one error regarding seizure classification.ResultsBetween December 2013 and December 2014, 189 physicians assessed the 30 cases. Agreement with the steering committee regarding the diagnosis at step 1 ranged from 47% to 100%, and improved when information regarding tests was provided at step 2. One hundred five of the 189 physicians (55%) were accredited for the EpiNet‐First trials. The kappa value for diagnosis of epilepsy across all 30 cases for accredited physicians was 0.70.SignificanceWe have established criteria for accrediting physicians using EpiNet. New investigators can be accredited by assessing 18 case scenarios. We encourage physicians with an interest in epilepsy to become EpiNet‐accredited and to participate in these investigator‐led clinical trials.

Microglia, the resident macrophages of the central nervous system play vital roles in brain homeostasis through clearance of pathogenic material. Microglia are also implicated in neurological disorders through uncontrolled activation and inflammatory responses. To date, the vast majority of microglial studies have been performed using rodent models. Human microglia differ from rodent counterparts in several aspects including their response to pharmacological substances and their inflammatory secretions. Such differences highlight the need for studies on primary adult human brain microglia and methods to isolate them are therefore required. Our procedure generates microglial cultures of >95% purity from both biopsy and autopsy human brain tissue using a very simple media-based culture procedure that takes advantage of the adherent properties of these cells. Microglia obtained in this manner can be utilised for research within a week. Isolated microglia demonstrate phagocytic ability and respond to inflammatory stimuli and their purity makes them suitable for numerous other forms of in vitro studies, including secretome and transcriptome analysis. Furthermore, this protocol allows for the simultaneous isolation of neural precursor cells during the microglial isolation procedure. As human brain tissue is such a precious and valuable resource the simultaneous isolation of multiple cell types is highly beneficial.