Despite the high proportion of stroke patients with a pre-existing impairment, patients with disabilities are often excluded from stroke treatment trials. Trials are designed for “perfect patients”: patients who are functionally independent and thus generally younger with fewer comorbidities; ironically, such patients are less likely to experience stroke than those with premorbid disability. Exclusionary practices in trials may translate into disparities in stroke care in practice. Through a review of literature, our purpose is to illuminate how people with disabilities are treated across the care continuum following a stroke.

We completed a qualitative systematized review of articles pertaining to the care of patients with premorbid disability and stroke and their outcomes. Using a critical disability studies' theoretical lens, we analyzed inequity across the stroke care continuum.

Among 24 included studies, we found evidence that people with disabilities did not receive equitable access to treatment ranging from being admitted to stroke units to receiving post-stroke rehabilitation. However, observational studies suggest that stroke therapies may be beneficial in selected patients with disabilities when measures of success are framed more achievable (e.g. return to pre-stroke status). This leaves us concerned about how people with pre-existing impairments might be structurally disabled within current systems of stroke care.

We use our critical disability studies' theoretical lens to argue that an intersectional approach to stroke treatment is much needed if we are to remedy structural inequities embedded throughout the care continuum.

Hyperacute treatment of acute stroke may lead to thrombolysis in stroke mimics (SM). Our aim was to determine the frequency of thrombolysis in SM in primary stroke centers (PSC) dependent on telestroke versus comprehensive stroke centers (CSC).

Retrospective review of prospectively collected data from the Quality improvement and Clinical Research (QuICR) registry, the Discharge Abstract Database (DAD), and The National Ambulatory Care Reporting System (NACRS) of consecutive patients treated with intravenous thrombolysis for acute ischemic stroke in Alberta (Canada) from April 2016 to March 2021.

A total of 2471 patients who received thrombolysis were included. Linking the QuICR registry to DAD 169 (6.83%) patients were identified as SM; however, on our review of the records, only 112 (4.53%) were actual SM. SMs were younger with a mean age of 61.66 (±16.15) vs 71.08 (±14.55) in stroke. National Institute of Health Stroke Scale was higher in stroke with a median (IQR) of 10 (5–17) vs 7 (5–10) in SM. Only one patient (0.89 %) in SM groups had a small parenchymal hemorrhage versus 155 (6.57%) stroke patients had a parenchymal hemorrhage. There was no death among patients of thrombolysed SM during hospitalization versus 276 (11.69%) in stroke. There was no significant difference in the rate of SM among thrombolysed patients between PSC 27 (5.36%) versus CSC 85 (4.3%) (P = 0.312). The most responsible diagnosis of SM was migraine/migraine equivalent, functional disorder, seizure, and delirium.

The diagnosis of SM may not always be correct when the information is extracted from databases. The rate of thrombolysis in SM via telestroke is similar to treatment in person at CSC.

Accurate anti-aquaporin-4 (AQP4) and anti-myelin oligodendrocyte glycoprotein (MOG) autoantibody assays are needed to effectively diagnose neuromyelitis optica spectrum disorder and MOG antibody-associated disease. A proportion of patients at our centre have been tested for anti-AQP4 and anti-MOG autoantibodies locally, followed by an outsourced test as part of real-world practice. Outsourced testing is costly and of unproven utility. We conducted a quality improvement project to determine the value of outsourced testing for anti-AQP4 and anti-MOG autoantibodies.

All patients seen by Calgary neurological services who underwent cell-based testing for anti-AQP4 and/or anti-MOG autoantibodies at both MitogenDx (Calgary, AB) and Mayo Clinic Laboratories (Rochester, MN, USA) between 2016 and 2020 were identified from a provincial database. The interlaboratory concordance was calculated by pairing within-subject results collected no more than 365 days apart. Retrospective chart review was done for subjects with discordant results to determine features associated with discordance and use of outsourced testing.

Fifty-seven anti-AQP4 and 46 anti-MOG test pairs from January 2016 to July 2020 were analyzed. Concordant tests pairs comprised 54/57 (94.7%, 95%CI 88.9–100.0%) anti-AQP4 and 41/46 (89.1%, 95%CI 80.1–98.1%) anti-MOG results. Discordant anti-AQP4 pairs included two local weak positives (negative when outsourced) and one local negative (positive when outsourced). Discordant anti-MOG pairs were all due to local weak positives (negative when outsourced).

Interlaboratory discordant results for cell-based testing of anti-AQP4 autoantibodies were rare. Local anti-MOG weak positive results were associated with discordance, highlighting the need for cautious interpretation based on the clinical context. Our findings may reduce redundant outsourced testing.

Despite its effectiveness, surgery for drug-resistant epilepsy is underutilized. However, whether epilepsy surgery is also underutilized among patients with stroke-related drug-resistant epilepsy is unclear. Therefore, our objectives were to estimate the rates of epilepsy surgery assessment and receipt among patients with stroke-related drug-resistant epilepsy and to identify factors associated with these outcomes.

We used linked health administrative databases to conduct a population-based retrospective cohort study of adult Ontario, Canada residents discharged from an Ontario acute care institution following the treatment of a stroke between January 1, 1997, and December 31, 2020, without prior evidence of seizures. We excluded patients who did not subsequently develop drug-resistant epilepsy and those with other epilepsy risk factors. We estimated the rates of epilepsy surgery assessment and receipt by March 31, 2021. We planned to use Fine-Gray subdistribution hazard models to identify covariates independently associated with our outcomes, controlling for the competing risk of death.

We identified 265,081 patients who survived until discharge following inpatient stroke treatment, 1,902 (0.7%) of whom subsequently developed drug-resistant epilepsy (805 women; mean age: 67.0 ± 13.1 years). Fewer than six (≤0.3%) of these patients were assessed for or received epilepsy surgery before the end of follow-up (≤55.5 per 100,000 person-years). Given that few outcomes were identified, we could not proceed with the multivariable analyses.

Patients with stroke-related drug-resistant epilepsy are infrequently considered for epilepsy surgery that could reduce morbidity and mortality.

Quantitative susceptibility mapping (QSM) demonstrates elevated iron content in Parkinson’s disease (PD) patients within the basal ganglia, though it has infrequently been studied in relation to gait difficulties including freezing of gait (FOG). Our purpose was to relate QSM of basal ganglia and extra-basal ganglia structures with qualitative and quantitative gait measures in PD.

This case–control study included PD and cognitively unimpaired (CU) participants from the Comprehensive Assessment of Neurodegeneration and Dementia study. Whole brain QSM was acquired at 3T. Region of interests (ROIs) were drawn blinded manually in the caudate nucleus, putamen, globus pallidus, pulvinar nucleus of the thalamus, red nucleus, substantia nigra, and dentate nucleus. Susceptibilities of ROIs were compared between PD and CU. Items from the FOG questionnaire and quantitative gait measures from PD participants were compared to susceptibilities.

Twenty-nine participants with PD and 27 CU participants were included. There was no difference in susceptibility values in any ROI when comparing CU versus PD (p > 0.05 for all). PD participants with gait impairment (n = 23) had significantly higher susceptibility in the putamen (p = 0.008), red nucleus (p = 0.01), and caudate nucleus (p = 0.03) compared to those without gait impairment (n = 6). PD participants with FOG (n = 12) had significantly higher susceptibility in the globus pallidus (p = 0.03) compared to those without FOG (n = 17). Among quantitative gait measures, only stride time variability was significantly different between those with and without FOG (p = 0.04).

Susceptibilities in basal ganglia and extra-basal ganglia structures are related to qualitative measures of gait impairment and FOG in PD.