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 <15 years. 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 Māori (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 >4 weeks 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 10 minutes in duration, or repeated seizures lasting >10 minutes 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 >30 minutes, which is the duration that has previously been used for epidemiological studies of status epilepticus.

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.

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A 44-year-old man presented with 1 year of gradually progressive lower limb weakness and numbness and bowel and bladder incontinence. Neurologic examination revealed a T8 spinal sensory level and spastic paraparesis. Preoperative imaging (figure) of the thoracic spine revealed the scalpel sign, a radiologic entity diagnostic of a dorsal thoracic arachnoid web.1 The lesion was surgically and histologically confirmed as an arachnoid web. Clinical deficits and the cord signal abnormality resolved postoperatively. Arachnoid webs are bands of arachnoid tissue extending to the pial surface, causing focal dorsal indentation of the thoracic cord. Early identification followed by surgery appears to result in good functional recovery.

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Cocaine causes myocardial injury via multiple mechanisms.Aims: (a) To compare clinical and cardiac magnetic resonance (CMR) characteristics of myocardial injury in cocaine-induced ST elevation myocardial infarction (STEMI) versus our institution's general STEMI population and (b) to examine for evidence of silent myocardial injury in asymptomatic cocaine users.Methods/results: Four patients presented with cocaineinduced ST elevation MI over 12 months. All were males with a mean age of 37 years. Three had thrombotic coronary occlusion requiring repeated thrombus aspiration and one, who received lysis for anterior STEMI at a peripheral hospital, had anterior akinesis with no obvious culprit. Peak troponins were 4124 ± 1226 ng/L (mean ± SEM). CMR demonstrated extensive transmural MI with microvascular obstruction (MVO) in all four (100%: figure). In contrast, MVO was observed in ∼50% of our general STEMI population undergoing CMR. Thrombophilia screen was positive in two out of three of the cocaine-induced STEMIs tested. Zero in eighteen asymptomatic heavy cocaine users had late gadolinium enhancement on CMR to suggest silent myocardial injury.Conclusions: In patients with STEMI attributed to cocaine use, we have observed extensive thrombosis, with a high degree of MVO. The high incidence of prothrombotic abnormalities suggests an interactive effect of cocaine with thrombophilic tendency.Background: Pulmonary hypertension (PH) is defined as mean pulmonary artery pressure (mPAP) >25 mmHg. Patients undergoing cardiac surgery have increased mortality if they have significant PH, defined as systolic pulmonary artery pressure (sPAP) >60 mmHg. Our aim was to see if measurement of tricuspid regurgitant velocity (TRVmax) by Doppler echocardiography can exclude PH.Methods: Patients having a transthoracic echocardiogram (TTE) and right heart catheterisation (RHC) within three days of each other were reviewed. TRVmax < 2.8 m/s was used as a cut-off to exclude PH as recommended by ESC guidelines for PH.Results: From January 2004 to February 2011, 693 patients had RHC before cardiac surgery. Out of these, 159 patients had TTE within three days of RHC and were used for analysis. Prevalence of PH was 51% in this group. TRVmax was measured in 99(62%) out of 159 patients. Sensitivity, specificity, negative predictive value (NPV) and positive predictive value (PPV) for diagnosis of PH (mPAP > 25mmHg) were 66%, 83%, 65% and 84% respectively. Sensitivity, specificity, NPV and PPV for diagnosis of significant PH (sPAP > 60 mmHg) were 80%, 64%, 93% and 36% respectively. TRVmax was not measurable in 60 (38%) patients due to no tricuspid regurgitation (TR) or trace TR. Absent/trace TR had a 50% NPV to exclude diagnosis of PH and 93% NPV to exclude significant PH.Conclusion: TRVmax < 2.8 m/s has a low sensitivity (66%) and NPV (65%) for diagnosis of PH, but high sensitivity (80%) and NPV (93%) to exclude significant PH. Absent/trace TR has low NPV (50%) for diagnosis of PH but high NPV (93%) to exclude significant PH.