D’Souza, Caitlin E.

Abstract Despite substantial advances in stroke care, vascular cognitive impairment remains a prominent source of disability. Unlike sensorimotor impairments, cognition often continues to decline after stroke. An aging population will increase the prevalence of vascular cognitive impairment, with stroke playing an important role. Ten percent of patients presenting with stroke have pre-stroke dementia; an additional 10% will develop incident dementia with a first stroke, and 30% with a recurrent stroke. While stroke increases the risk of cognitive impairment, the presence of cognitive impairment also impacts acute stroke treatment and increases risk of poor outcome by nearly twofold. There is substantial overlap in the clinical and pathological aspects of vascular and degenerative dementias in many patients. How they relate to one another is controversial. The treatment of vascular cognitive impairment remains supportive, focusing on treating vascular risk factors. Cognitive rehabilitation after stroke is an area of active research, and existing pharmacologic treatments have limited benefit. Heightened awareness of cognitive impairment in the setting of stroke is imperative for prognostication and management, impetus for research and, ultimately, the discovery of efficacious treatments.

Background: With increasing demand for neurologists, nontraditional health care delivery mechanisms have been developed to leverage this limited resource. Introduction: Telemedicine has emerged as an effective digital solution. Over the past three decades, telemedicine use has steadily grown; however, neurologists often learn on the job, rather than as part of their medical training. The current literature regarding telestroke training during neurology training is sparse, focusing on cerebrovascular fellowship curricula. We sought to enhance telestroke training in our neurology residency by incorporating real-life application. Materials and Methods: We implemented a formal educational model for neurology residents to use telemedicine for remote acquisition of the National Institutes of Health Stroke Scale (NIHSS) for patients with suspected acute ischemic stroke (AIS) before arrival at our comprehensive stroke center. This three-phase educational model involved multidisciplinary classroom didactics, simulation exercises, and real-world experience. Training and feedback were provided by neurologists experienced in telemedicine. Results: All residents completed formal training in telemedicine prehospital NIHSS acquisition and had the opportunity to participate in additional simulation exercises. Currently, residents are gaining additional experience by performing prehospital NIHSS acquisition for patients in whom AIS is suspected. Our preliminary data indicate that resident video encounters average 10.6 min in duration, thus saving time once patients arrive at our hospital. Discussion: To our knowledge, this is the first report of a telestroke-integrated neurology residency program in a comprehensive stroke center resulting in shortened time to treatment in patients with suspected AIS. Conclusions: We present a model that can be adopted by other neurology residency programs as it provides real-world telemedicine training critical to future neurologists.

ABSTRACTAntibodies against the 65‐kDa isoform of the intracellular enzyme, glutamate decarboxylase (GAD65), have been found in patients with limbic encephalitis and drug‐resistant autoimmune epilepsy. We report a 22‐year‐old female who presented with new‐onset seizures and neuropsychiatric symptoms. Video‐EEG captured unique, independent bitemporal‐onset focal seizures with impaired awareness and ictal asystole. An autoimmune epilepsy panel revealed elevated GAD65 antibodies in the serum (225 nmol/l) and CSF (2.78 nmol/l), while [18F]‐fluoro‐deoxy‐glucose positron emission tomography showed bitemporal hypometabolism (left > right). The patient was diagnosed with GAD65 antibody‐associated autoimmune epilepsy. Our observation adds to the spectrum of neurocardiac syndromes associated with autoimmune epilepsy.

Objective: To perform a feasibility pilot study comparing the usefulness of EEG electrode cap versus standard scalp EEG for acquiring emergent EEGs in emergency department, inpatient, and intensive care unit patients. Background: Nonconvulsive status epilepticus (NCSE) is a neurological emergency diagnosed exclusively by EEG. Nonconvulsive status epilepticus becomes more resistant to treatment 1 hour after continued seizure activity. EEG technologists are alerted “stat” when there is immediate need for an EEG during oncall hours, yet delays are inevitable. Alternatively, EEG caps can be quickly placed by in-house residents at bedside for assessment. Design/Methods: EEG caps were compared with standard-of-care “stat” EEGs for 20 patients with suspected NCSE. After the order for a stat EEG was placed, neurology residents were simultaneously alerted and placed an EEG cap prior to the arrival of the on-call out-of-hospital technologist. Both EEG cap recordings and standard EEG recordings were visually reviewed at 10 and 20 minutes in a blinded manner by two electroencephalographers. The timing, accuracy of interpretation, and diagnosis between the two techniques were then compared. Results: Of the 20 adult patients, 70% (14 of 20) of EEG cap recordings were interpretable, whereas 95% (19 of 20) standard EEGs were interpretable; three had findings consistent with NCSE on both the EEG cap and standard EEG recordings. In the time analysis, 16 patients were included. EEG cap placement was significantly more time efficient than an EEG performed by technologist using the usual “stat” EEG protocol, with the median EEG cap electrode placement occurring 86 minutes faster than standard EEG (22.5 minutes vs. 104.5 minutes; P < 0.0001; n = 16). Conclusions: New rapid EEG recording using improved EEG caps may allow for rapid diagnosis and clinical decision making in suspected NCSE.

Introduction: White matter hyperintensities (WMH) is the most prominent neuroimaging feature of small vessel disease (SVD). SVD is thought to be a result of arteriolosclerosis, chronic hypoperfusion of white matter, selective oligodendrocyte death and degeneration of myelinated fibers. The risk of ischemic stroke is significantly increased with the presence of WMH. The presence of intracranial collaterals is a strong predictor of salvageable neurological function in acute stroke; however, the factors affecting the ability to recruit collaterals are poorly understood. We wanted to study if the presence and severity of small vessel white matter disease had an adverse effect on cerebral collateral flow in acute embolic large vessel stroke. Methods: We identified a consecutive series of adult subjects with acute embolic large vessel strokes confirmed on CT angiography (CTA) from a 10-year institutional database. Patients without a brain MRI within six months of CTA were excluded. Collateral scores of the affected hemisphere were calculated on CTA using the modified Tan scale (0-4) by two independent trained reviewers and confirmed by a neuroradiologist. The WMH was quantified using the Fazekas scale (0-3) incorporating both deep and periventricular components. Areas of restricted diffusion on brain MRI in the peri-stroke period were eliminated from the assessment of Fazekas score. Spearman’s correlation tests were performed for the association between collateral scores and WMH. Results: A total of 234 patients (mean age 70±14 years, 47% [110/234] women) satisfied the inclusion criteria. The prevalence of periventricular and deep WMH was 83% and 87% respectively. Aging had a significant impact on periventricular WMH (r=0.48, p <0.001) and deep WMH (r=0.47, p <0.001). However, collateral scores exhibited no statistically significant relationship with the presence or severity of periventricular scores (r=0.08, p=0.17) or deep WMH scores (r=0.01, p=0.77). Conclusions: Our results indicate that the presence of SVD does not affect cerebral collateral flow. The vascular niche and risk factors of SVD appear to be distinct from that of intracranial vessels responsible for collateral reperfusion of ischemic territory in acute large vessel embolic stroke.

Introduction: Poor leptomeningeal collateral flow is related to worse neurological outcome in acute ischemic stroke. The increased release of stress hormones during the first hours of acute stroke leads to inhibition of insulin secretion and increase insulin resistance, thus inducing stress hyperglycemia, which is often evident on blood glucose levels at admission. While admission hyperglycemia, independent of diabetes mellitus (DM) is associated with poor clinical outcome in ischemic stroke, studies on its effect on collateral circulation after acute cerebral embolism are largely inconclusive. Methods: We identified a consecutive series of patients aged 18 years and older from 2008 to 2018 with acute embolic large vessel stroke confirmed on CT angiography (CTA) using an institutional database. Individual CTAs were over-read, and collateral scores of the affected hemisphere were calculated using a modification of the Tan scale (0-4), by two trained readers. We reviewed the electronic medical records for presenting NIHSS, admission glucose and HbA1C levels, and prior history of DM. Spearman’s ρ, odds ratios (OR), and their 95% confidence intervals (CI) were analyzed. All tests were considered significant when P<0.05. Results: Of the 405 patients identified through the database (mean age 70 years [range, 55-85], 45% [183/405] women), 35% (142/405) had a prior history of DM. Mean admission glucose was 134±51 mg/dL, and median NIHSS at presentation was 17. Blood glucose level at admission was negatively correlated with collateral scores (ρ= -0.23, P=0.008). Specifically, glucose levels above 120 mg/dL were significantly associated (OR 1.68 CI 1.13-2.5) with poor collateral scores (≤1). However, collateral scores exhibited no statistically significant relationship with HbA1c (ρ=-0.08, P=0.15) or prior history of DM (P=0.73). Conclusions: Patients with higher admission glucose levels have poor collateral scores, while HbA1c and prior DM do not have a similar effect on collateral flow. Our results suggest that poor collateral flow may explain adverse outcomes associated with hyperglycemia in acute ischemic stroke. Determining if there is a benefit of aggressive glycemic control within the first few hours of embolic stroke warrants further study.

Introduction: Good collateral flow is associated with improved outcomes in acute embolic stroke. There is compelling data linking smoking to all types of stroke, with current smokers at a higher risk than former or never smokers. Smoking has, however, been shown to promote collaterals in coronary vascular bed in humans. It is unknown if there is a similar effect in cerebral collateral flow. We aimed to investigate if cigarette smoking was positively associated with collateral blood flow in a homogenous cohort of patients with acute large vessel occlusive embolic stroke. Methods: We identified all patients aged ≥18 with acute ischemic stroke showing embolic occlusion of ICA terminus/M1 MCA on admission CT angiography (CTA), between 2008 to 2018, through an institutional database. Patients with chronic occlusions and stenotic lesions were excluded. Individual CTAs were independently reviewed by two trained investigators to calculate collateral scores of the affected hemisphere using the modified Tan scale (0-4) as a reference. Details of cigarette smoking history were obtained from the electronic medical records. Patients were grouped into smokers (former and current smokers) and never smokers. Odds ratios (OR) and their 95% confidence intervals (CI) were estimated, and all tests were considered significant when P<0.05. Results: Of the 612 patients identified through the database, 429/612 patients (mean age 71±16 years, 45% [194/429] women) satisfied the inclusion criteria. 64.8% (278/429) had a positive history of smoking with an average of 47±12 pack-years. There was a significant association between good collateral scores (≥2) with smoking history (OR 1.74 CI 1.17-2.61, P=0.006). This trend remained significant even after comparing raw collateral scores (0-4) ( P=0.006, Spearman’s ρ=0.22). However, number of pack-years and collateral scores exhibited no statistically significant relationship (P=0.6). Conclusions: Our study shows that patients who have ever smoked have higher intracranial collateral vessel scores in the event of an acute embolic stroke. Increased impedance and reduced cerebral blood flow resulting from cigarette smoking may stimulate collateral recruitment in cerebral pial circulation, similar to the effect in coronary bed.