Neurological dysfunction following epileptic seizures is a well-recognized phenomenon. Several potential mechanisms have been suggested to explain postictal dysfunction, with alteration in cerebral blood flow being one possibility. These vascular disturbances may be long lasting and localized to brain areas involved in seizure generation and propagation, as supported by both animal and human studies. Therefore, measuring perfusion changes in the postictal period may help localize the seizure onset zone. Arterial spin labelling is a non-invasive, rapid and reproducible magnetic resonance imaging technique that measures cerebral perfusion. To this end, we measured postictal perfusion in patients with drug resistant focal epilepsy who were admitted to our seizure-monitoring unit for presurgical evaluation. Twenty-one patients were prospectively recruited and underwent arterial spin labelling scanning within 90 min of a habitual seizure. Patients also underwent a similar scan in the interictal period, after they were seizure-free for at least 24 h. The acquired scans were subtracted to identify the areas of significant postictal hypoperfusion. The location of the maximal hypoperfusion was compared to the presumed seizure onset zone to assess for concordance. Also, the localizing value of this technique was compared to other structural and functional imaging modalities. Postictal perfusion reductions of >15 units (ml/100 g/l) were seen in 15/21 patients (71.4%). In 12/15 (80%) of these patients, the location of the hypoperfusion was partially or fully concordant with the location of the presumed seizure onset zone. This technique compared favourably to other neuroimaging modalities, being similar or superior to structural magnetic resonance imaging in 52% of cases, ictal single-photon emission computed tomography in 60% of cases and interictal positron emission tomography in 71% of cases. Better arterial spin labelling results were obtained in patients in whom the seizure onset zone was discernible based on non-invasive data. Thus, this technique is a safe, non-invasive and relatively inexpensive tool to detect postictal hypoperfusion that may provide useful data to localize the seizure onset zone. This technique may be incorporated into the battery of conventional investigations for presurgical evaluation of patients with drug resistant focal epilepsy.

Objective:Since the strongest risk factor for sudden unexpected death in epilepsy (SUDEP) is frequent bilateral tonic-clonic seizures (BTCSs), our aim was to determine whether postictal hypoperfusion in brainstem respiratory centres (BRCs) is more common following tonic-clonic seizures.Methods:We studied 21 patients with focal epilepsies who underwent perfusion imaging with arterial spin labeling (ASL) MRI. Subtraction maps of cerebral blood flow were obtained from the postictal and baseline scans. We identified six regions of interest in the brainstem that contain key BRCs. Patients were considered to have postictal BRC hypoperfusion if any of the six regions of interest were significantly hypoperfused.Results:All six patients who experienced bilateral tonic-clonic seizures during the study had significant clusters of postictal hypoperfusion in BRCs compared to seven who had focal impaired awareness seizures (7/15). The association between seizure type studied and the presence of BRC hypoperfusion was significant. Duration of epilepsy and frequency of bilateral tonic-clonic seizures were not associated with postictal brainstem hypoperfusion despite also being associated with risk for SUDEP.Conclusion:Postictal hypoperfusion in brainstem respiratory centres occurs more often following bilateral tonic-clonic seizures than other seizure types, providing a possible explanation for the increased risk of SUDEP in patients who regularly experience bilateral tonic-clonic seizures.

BackgroundAt hospital discharge, care is handed over from providers to patients. Discharge encounters must prepare patients to self-manage their health, but have been found to be suboptimal. Our study objectives were to describe and determine the correlates of perceived discharge quality and to explore the association between perceived discharge quality and postdischarge outcomes.MethodsWe conducted a prospective cohort study in medical inpatients admitted to a tertiary care hospital in Calgary, Canada. Perceived discharge quality was measured by the Care Transitions Measure (CTM). Linkage to administrative databases provided data for the composite outcome—90-day hospital readmission or emergency department visit. Logistic regression modelling was used to determine the association between global CTM scores, and the individual CTM components, and the composite outcome.ResultsA total of 316 patients were included in the analysis. The median CTM score was 80.0 (IQR 66.6–100.0). The distribution of CTM scores were significantly different based on comorbidity burden, with the median and maximum CTM scores being lower and the IQR being narrower, for those with six or more comorbidities compared with those with fewer comorbidities. CTM scores were not associated with the composite outcome, though a single CTM item—not understanding warning signs and symptoms—was (adjusted OR 3.46 (95% CI 1.02 to 11.73)).ConclusionPerceived quality of discharge varies based on patient burden of comorbidities. While global perceived discharge quality was not associated with postdischarge outcomes, lack of patient understanding of warning symptoms was. Discharging healthcare teams should pay special attention to these priority patient groups and specific discharge process components.

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Epilepsy is at times a fatal disease. Sudden unexpected death in epilepsy (SUDEP) is the leading cause of mortality in people with intractable epilepsy and is defined by exclusion; non-accidental, non-toxicologic, and non-anatomic causes of death. While SUDEP often follows a bilateral tonic-clonic seizure, the mechanisms that ultimately lead to terminal apnea and then asystole remain elusive and there is a lack preventative treatments. Based on the observation that discrete seizures lead to local vasoconstriction, resulting in hypoperfusion, hypoxia and behavioural disturbances in the forebrain (Farrell et al., 2016 eLife), we reasoned that similar mechanisms may play a role in SUDEP when seizures invade the brainstem. Here we tested this neurovascular-based hypothesis of SUDEP in awake non-anesthetized mice by pharmacologically preventing seizure-induced vasoconstriction, with cyclooxygenase-2 or L-type calcium channel antagonists. In both acute and chronic mouse models of SUDEP, ibuprofen and nicardipine extended life. We also examined the potential role of spreading depolarization in the acute model of SUDEP. These data provide a proof of principle for the neurovascular hypothesis of SUDEP and the use of currently available treatments to prevent it.