Jasmine Wall

ObjectiveDelayed responses to single-pulse electrical stimulation are used during stereo-EEG to localise epileptogenic zone for epilepsy surgery with limited sensitivity. We investigated whether late high-frequency oscillations constitute a previously unrecognised component of the delayed-response spectrum and whether their inclusion improves identification of EZ and seizure propagation networks.MethodsWe analysed Single Pulse Electrical Stimulation responses from 799 contacts across 10 patients. Late responses >300ms post-stimulation were identified with or without accompanying late High Frequency Oscillations (80–500 Hz), and evaluated as epileptogenic zone markers. Distant Late Responses were mapped as markers of seizure propagation network.ResultsLate Responses featured Late High Frequency Oscillations in 49.1% of Late Responses. Including late High Frequency Oscillations improved localisation of epileptogenic zone (Positive Predictive Value 76.0%, Negative Predictive Value 70.3%; McNemar test p=0.046). Distant Late Responses mapped seizure propagation networks with high negative predictive value (92.7%). In a single case, radiofrequency thermocoagulation abolished all local Late Responses, whilst Early Responses remained.ConclusionsLate High Frequency Oscillations form part of a unified spectrum of delayed Single Pulse Electrical Stimulation responses, supporting shared mechanisms of pathological hypersynchrony and the use of late Single Pulse Electrical Stimulation responses as dynamic markers of epileptogenic networks.SignificanceLate HFOs may be considered part of the spectrum of Late Responses which indicate the Epileptogenic Zone.

Background: Stroke is a leading cause of seizures and epilepsy, both of which are linked to increased mortality, disability, and hospital readmissions. Early recognition and management of seizures in acute stroke are crucial for improving outcomes. Electroencephalogram (EEG) is not routinely used for post-stroke seizure monitoring and is typically initiated only after clinical suspicion arises, making bedside recognition essential. This scoping review aimed to map the existing literature on clinical methods used for identifying and observing early post-stroke seizures (EPSSs) at the bedside. Methods: We included literature involving adults with acute ischaemic stroke or primary intracerebral haemorrhage who were diagnosed or suspected of having inpatient EPSS. Searches were conducted in Medline, CINAHL, Embase, and the Cochrane Library for English-language publications up to April 2023. Eligible sources included primary research, case reports, systematic reviews, clinical guidelines, consensus statements, and expert opinion. Reference lists of included articles were also reviewed. Data were charted and synthesised to assess the scope, type, and gaps in the evidence. Results: Thirty papers met inclusion criteria: 17 research studies, six expert opinions, four case reports, and three clinical guidelines. Empirical evidence on clinical methods for seizure recognition and monitoring in acute stroke was limited. No studies evaluated the effectiveness of different approaches, and existing recommendations lacked detail and consensus. Conclusions: Accurate EPSS diagnosis is vital due to its impact on outcomes. This review highlights inconsistency in monitoring methods and a clear need for targeted research into effective clinical identification strategies in acute stroke care.

Background Stroke is one of the commonest cause of seizures and epilepsy and is the leading cause of epilepsy over the age of 60 (1, 2). Post-stroke seizures and epilepsy are associated with increased mortality, disability and recurrent hospital admissions (3, 4). Seizures occurring in the immediate aftermath of the acute stroke can complicate a patient’s stroke diagnosis and management or can even go undiagnosed resulting in increased risk of mortality, disability and hospital readmissions. There is limited evidence on detection, observation, diagnosis and management of early post-stroke seizures as part of acute stroke treatment. Objectives The objective of this series of scoping reviews is to map the extent and type of literature in relation to in-hospital early post-stroke seizures. For this paper, the specific objectives relate to the clinical methods used in the bedside identification and observation, usually performed by nurses, of early post-stroke seizures (EPSS) in adults being treated and managed for acute stroke. Eligibility criteria Participants included adults aged 18 years or older with acute ischaemic stroke or primary intracerebral haemorrhage and a diagnosis, or suspected diagnosis, of post-stroke seizures whilst receiving hospital care for their acute stroke. Sources of evidence Medline, CINAHL, Embase, and the Cochrane Library databases were searched, including papers published up to October 2021, limited to English language. A broad range of published literature was selected comprising of primary research, including case studies/case reports, conference abstracts, systematic reviews/meta-analyses, clinical guidelines and consensus statements. Reference lists of included studies were also searched. Charting methods A data charting table was developed by the reviewers, with key information selected for included articles. Findings have been aggregated to an overview of extent and type of evidence and identify gaps in evidence. Results We included two research papers, two clinical guidelines and four discussion papers. There was limited literature on clinical methods used to identify and observe acute stroke patients for seizures. We found no evaluation of different methods aimed at recognising and observing EPSS, and subsequently recommendations lacking detail and consensus on clinical processes. Conclusion Early post-stroke seizures are important to diagnose due to associated increases in post-stroke complications, mortality, disability and recurrent hospital admissions. Whilst the diagnostic challenge of EPSS is recognised, there is a need for research looking into how to improve the identification and observation of seizure activity in acute stroke settings.

Objectives In this first large-scale analysis of neurological emergency admissions in England, we determine the number and types of emergency admissions with neurological emergency diagnostic codes, how many are under the care of a neurologist or neurosurgeon and how such admissions vary by levels of deprivation. Design Retrospective empirical research employing a derived list of neurological emergency diagnostic codes Setting This study used the Hospital Episode Statistics data set for the financial year 2019/2020 based on 17 million in-year inpatient admissions in England including 6.5 million (100%) emergency admissions with any diagnosis codes. Results There were 1.4 million (21.2%) emergency inpatient admissions with a mention of any neurological code, approx. 248 455 (3.8%) with mention of a specific neurological emergency code from the derived list, and 72 485 (1.1%) included such a code as the primary reason for admission. The highest number of in-year admissions for adults was for epilepsy (145 995), with epilepsy as the primary diagnostic code in 15 945 (10.9%). Acute nerve root/spinal cord syndrome (41 215), head injury (29 235) and subarachnoid haemorrhage (18 505) accounted for the next three highest number of admissions. 3230 (1.4%) in-year emergency hospital admissions with mention of a neurological emergency code were under the care of a neurologist or neurosurgeon, with only 1315 (0.9%) admissions with mention of an epilepsy code under a neurologist. There was significant variation for epilepsy and functional neurological disorders (FNDs) in particular by Index of Multiple Deprivation decile. The association between deprivation and epilepsy and FND was significant with p-values of 2.5e-6 and 1.5e-8, respectively. Conclusions This study has identified important findings in relation to the burden of neurological emergency admissions but further work is needed, with greater clinical engagement in diagnostic coding, to better understand the implications for workforce and changes to service delivery needing to be implemented.

Late-onset epilepsy (LOE) is closely associated with cerebrovascular disease. LOE also appears to be a harbinger of dementia. We performed a systematic review of observational studies, clinical studies and radiological studies relating to LOE. We conducted a meta-analysis of 5 observational studies and have found that patients presenting with LOE experience an increased risk of subsequent stroke, weighted OR 3.88 (95% CI 2.76 - 5.46). Above the age of fifty, incidence of new onset epilepsy is approximately 400/100,000 person years. Of these, 9.8–11.9% will have a stroke in the decade following epilepsy onset, translating to an incidence of «pre-stroke epilepsy» of 25–55/100,000 person years. The additional studies demonstrated clinical and radiological evidence to support the premise that LOE is likely to reflect underly- ing cerebrovascular disease. Cerebrovascular risk factors convey increased risk of LOE, and LOE can act as a «harbinger» for stroke and dementia, with various proposed pathophysiological mechanisms. The onset of LOE may represent a potential point for intervention, with the aim of stroke prevention. Current data supports the need for prospective research in order to better understand the natural history of LOE, disease mechanisms and opportunities for intervention to reduce the apparent sequelae of stroke and dementia. jasminewall@googlemail.com

Background Patients with Type 2 Diabetes Mellitus (T2DM) are at a relatively higher risk of severe stroke. Glucagon like peptide-1 receptor agonists (GLP-1RAs) are licensed for the management of T2DM. Cardio- vascular outcome trials (CVOTs) have demonstrated that GLP-1RAs can be safely administered to T2DM patients but have also indicated a trend towards a reduction in non-fatal stroke incidence compared to placebo. Methods We searched the literature to identify all GLP-1RA CVOTs. We performed a meta-analysis of the incidence of non-fatal stroke and presented the outcomes by Odds Ratio (OR) with 95% confidence intervals (CI). Results We identified 7 GLP-1RA studies. SUSTAIN-6 and REWIND reported statistically significant reductions in non-fatal stroke incidence, whilst LEADER demonstrated a similar, non-significant trend. ELIXA, EXSCEL, HARMONY and PIONEER-6 did not report a reduction in stroke incidence. Meta-analysis of 7 studies, totalling 56,004 participants yielded a significant reduction in non-fatal stroke incidence in patients receiving GLP-1RAs when compared with placebo (OR 0.85, 95% CI 0.76 – 0.94). Conclusions This data supports the value of GLP-1RAs in reducing stroke incidence in patients with T2DM. There is potential value in prospective, randomised controlled trials adequately powered to establish the value of GLP-1RAs in stroke prevention in T2DM patients. mark.maskery@doctors.org.uk|ABN Bursary

Reports of Guillain-Barré syndrome (GBS) have emerged during the Coronavirus disease 2019 (COVID-19) pandemic. This epidemiological and cohort study sought to investigate any causative association between COVID-19 infection and GBS. The epidemiology of GBS cases reported to the UK National Immunoglobulin Database was studied from 2016 to 2019 and compared to cases reported during the COVID-19 pandemic. Data were stratified by hospital trust and region, with numbers of reported cases per month. UK population data for COVID-19 infection were collated from UK public health bodies. In parallel, but separately, members of the British Peripheral Nerve Society prospectively reported incident cases of GBS during the pandemic at their hospitals to a central register. The clinical features, investigation findings and outcomes of COVID-19 (definite or probable) and non-COVID-19 associated GBS cases in this cohort were compared. The incidence of GBS treated in UK hospitals from 2016 to 2019 was 1.65–1.88 per 100 000 individuals per year. GBS incidence fell between March and May 2020 compared to the same months of 2016–19. GBS and COVID-19 incidences during the pandemic also varied between regions and did not correlate with one another (r = 0.06, 95% confidence interval: −0.56 to 0.63, P = 0.86). In the independent cohort study, 47 GBS cases were reported (COVID-19 status: 13 definite, 12 probable, 22 non-COVID-19). There were no significant differences in the pattern of weakness, time to nadir, neurophysiology, CSF findings or outcome between these groups. Intubation was more frequent in the COVID-19 affected cohort (7/13, 54% versus 5/22, 23% in COVID-19-negative) attributed to COVID-19 pulmonary involvement. Although it is not possible to entirely rule out the possibility of a link, this study finds no epidemiological or phenotypic clues of SARS-CoV-2 being causative of GBS. GBS incidence has fallen during the pandemic, which may be the influence of lockdown measures reducing transmission of GBS inducing pathogens such as Campylobacter jejuni and respiratory viruses.

Background: Clinical frailty is an important syndrome for clinical care and research, independently predicting mortality and rates of institutionalisation in a range of medical conditions. However, there has been little research into the role of frailty in stroke. Objective: This study investigates the effect of frailty on 28-day mortality following ischaemic stroke and outcomes following stroke thrombolysis. Methods: Frailty was measured using the Clinical Frailty Scale (CFS) for all ischaemic stroke admissions aged ≥75 years. Stroke severity was measured using the National Institutes of Health Stroke Scale (NIHSS). 28-day mortality and clinical outcomes were collected retrospectively. Analysis included both dichotomised measures of frailty (non-frail: CFS 1–4, frail: 5–8) and CFS as a continuous ordinal scale. Results: In 433 individuals with ischaemic stroke, 28-day mortality was higher in frail versus non-frail individuals (39 (16.7%) versus 10 (5%), P < 0.01). On multivariable analysis, a one-point increase in CFS was independently associated with 28-day mortality (OR 1.03 (1.01–1.05)). In 63 thrombolysed individuals, median NIHSS reduced significantly in non-frail individuals (12.5 (interquartile range (IQR) 9.25) to 5 (IQR 10.5), P < 0.01) but not in frail individuals (15 (IQR 11.5) to 16 (IQR 16.5), P = 0.23). On multivariable analysis, a one-point increase in CFS was independently associated with a one-point reduction in post-thrombolysis NIHSS improvement (coefficient 1.07, P = 0.03). Conclusion: Clinical frailty is independently associated with 28-day mortality after ischaemic stroke and appears independently associated with attenuated improvement in NIHSS following stroke thrombolysis. Further research is needed to elucidate the underlying mechanisms and how frailty may be utilised in clinical decision-making.