Stroke clinical registries are critical for systems planning, quality improvement, advocacy and informing policy. We describe the methodology and evolution of the Registry of the Canadian Stroke Network/Ontario Stroke Registry in Canada.

At the launch of the registry in 2001, trained coordinators prospectively identified patients with acute stroke or transient ischemic attack (TIA) at comprehensive stroke centers across Canada and obtained consent for registry participation and follow-up interviews. From 2003 onward, patients were identified from administrative databases, and consent was waived for data collection on a sample of eligible patients across all hospitals in Ontario and in one site in Nova Scotia. In the most recent data collection cycle, consecutive eligible patients were included across Ontario, but patients with TIA and those seen in the emergency department without admission were excluded.

Between 2001 and 2013, the registry included 110,088 patients. Only 1,237 patients had follow-up interviews, but administrative data linkages allowed for indefinite follow-up of deaths and other measures of health services utilization. After a hiatus, the registry resumed data collection in 2019, with 13,828 charts abstracted to date with a focus on intracranial vascular imaging, identification of intracranial occlusions and treatment with thrombectomy.

The Registry of the Canadian Stroke Network/Ontario Stroke Registry is a large population-based clinical database that has evolved throughout the last two decades to meet contemporary stroke needs. Registry data have been used to monitor stroke quality of care and conduct outcomes research to inform policy.

Optimal stroke care requires access to resources such as neuroimaging, acute revascularization, rehabilitation, and stroke prevention services, which may not be available in rural areas. We aimed to determine geographic access to stroke care for residents of rural communities in the province of Ontario, Canada.

We used the Ontario Road Network File database linked with the 2016 Ontario Acute Stroke Care Resource Inventory to estimate the proportion of people in rural communities, defined as those with a population size <10,000, who were within 30, 60, and 240 minutes of travel time by car from stroke care services, including brain imaging, thrombolysis treatment centers, stroke units, stroke prevention clinics, inpatient rehabilitation facilities, and endovascular treatment centers.

Of the 1,496,262 people residing in rural communities, the majority resided within 60 minutes of driving time to a center with computed tomography (85%), thrombolysis (81%), a stroke unit (68%), a stroke prevention clinic (74%), or inpatient rehabilitation (77.0%), but a much lower proportion (32%) were within 60 minutes of driving time to a center capable of providing endovascular thrombectomy (EVT).

Most rural Ontario residents have appropriate geographic access to stroke services, with the exception of EVT. This information may be useful for jurisdictions seeking to optimize the regional organization of stroke care services.

Meige syndrome is a movement disorder that includes blepharospasm and oromandibular dystonias. Its etiology may be idiopathic (primary) or it may arise secondary to focal brain injury. Acute respiratory distress as a feature of such dystonias occurs infrequently. A review of the literature on Meige syndrome and the relationship between dystonias and respiratory compromise is presented.

A 60-year-old woman suffered a cerebral anoxic event secondary to manual strangulation. She developed progressive blepharospasm combined with oromandibular and cervical dystonias. Neuroimaging demonstrated bilateral damage localized to the globus pallidus. Years later, she presented to the emergency department in intermittent respiratory distress associated with facial and cervical muscle spasms.

Increasing frequency and severity of the disorder was noted over years. The acute onset of respiratory involvement required intubation and eventual tracheotomy. A partial therapeutic benefit of tetrabenazine was demonstrated.

Stereotyped, repeated transient ischemic attacks manifesting as pure motor hemiparesis are most often attributed to ischemia of the internal capsule or ventral pons resulting from in situ disease of the small penetrating arteries.

We report a 61-year-old man presenting with recurrent episodes of left-sided weakness consistent with the lacunar syndrome of pure motor hemiparesis. Subsequent neuroimaging revealed infarction of the right ventral pons and a critical basilar artery stenosis as the inciting lesion. Despite maximal antithrombotic therapy, he continued to have repeated symptoms. Angioplasty and stenting were attempted but both failed due to plaque recoil and technical difficulties. After the procedure, the patient had no further ischemic episodes and remained symptom-free at two months.

This case illustrates the imprecise and discordant relationship between the mode of presentation of a stroke syndrome and its presumed pathophysiology. The lacunar syndrome of pure motor hemiparesis should be recognized by clinicians as a mode of stroke presentation due not only to small vessel disease, but also to large artery atherosclerotic disease such as basilar artery stenosis. Prompt institution of treatment can lead to a good clinical outcome.

Repinotan is a potent, serotonin (5-HT1A) full receptor agonist that interferes with ischemia-mediated neuronal cell death in animal models. This double-blind, placebo-controlled phase II study examined the safety, tolerability, and dose of repinotan in patients with acute ischemic stroke.

Patients with acute hemispheric ischemia and a National Institutes of Health Stroke Scale of 4 to 25 were randomized to placebo or repinotan 0.5, 1.25, or 2.5 mg/day (d) given by continuous intravenous infusion for 72 hours. Treatment was started within six hours of symptom onset. Evaluations were performed at four weeks and three months.

Among 240 patients in the safety analysis, repinotan was well-tolerated, with adverse events appearing more frequently in the highest dose group (2.5 mg/d). The most common adverse event was headache (21.3% to 35% with repinotan and 24.1% with placebo). Most (75%) adverse events were of mild or moderate severity. The most common severe adverse events were neurological worsening, cerebral hemorrhage, and brain edema. The number of deaths and serious adverse events were similar among placebo and repinotan groups. Compared to the placebo group, the proportion of patients with good outcomes at three months was greatest in the group receiving repinotan 1.25 mg/d, although the difference was not statistically significant.

This study indicates that the incidence of adverse events was comparable with all doses of repinotan and placebo, and no safety issues were observed. A trend toward better tolerability with evidence of efficacy was observed with the repinotan 1.25 mg/d dose.

Dans cette Étude, l’incidence des incidents thÉrapeutiques Était comparable quelle que soit la dose de repinotan par rapport au placebo et aucun problème reliÉ à la sÉcuritÉ du produit n’a ÉtÉ observÉ. On a observÉ l’efficacitÉ du repinotan à la dose de 1,25 mg/j. et une tendance à une meilleure tolÉrance du mÉdicament.

Thrombolytic therapy with recombinant tissue plasminogen activator (tPA) has been shown to be cost-effective and safe. Thrombolysis for stroke with tPA is now a standard of care in North America. However, it is only used on a small percentage of patients.

The Registry of the Canadian Stroke Network was a consent-based stroke registry from 21 hospital sites across Canada. Using the thrombolysis data in phase 1 and 2 of the Registry, we sought to describe the use of stroke thrombolysis and its outcomes.

A total of 4107 patients were diagnosed with ischemic stroke in phase 1 and 2 of the Registry, of which 8.9% were treated with tPA. In consented tPA patients, the method of tPA administration was 85.8% IV only, 9.0% IA only, and 5.2% IV/IA combined. Patients had a median onset-to-treatment time of 167 minutes [IQR 140-188]. One quarter (25.5%) of eligible candidates (time from onset <150 minutes) were treated with tPA. Protocol violations occurred in 27.7% (67/242) of patients with 14.9% (10/67) mortality. Overall, in-hospital mortality was 11.6%. Lower Canadian Neurological Scale score and higher glucose level were predictive of mortality The symptomatic intracerebral hemorrhage (ICH) rate (phase 2 only) was 4.3%. The mean Stroke Impact Scale-16 score at six months was 73.2, approximately equivalent to a modified Rankin scale score of 2.

At selected hospitals in Canada, thrombolysis use is higher than previously reported rates. Thrombolysis continues to be safe and effective in Canada.

Hyperglycemia is noted in up to 60% of stroke patients. Practice guidelines recommend glucose monitoring following stroke but provide few management recommendations. We examined physician care practices for glucose management in stroke patients.

Emergency physicians, family physicians, general internists, intensive care specialists and neurologists in Ontario comprised the study population. A mailed, self-administered survey inquired about glucose management practices. Proportions of responses for survey questions were determined. Chi-square analysis was used for comparing physician groups.

Surveys were mailed to 2,280 physicians; 26.8% returned surveys. There were 278 respondents who reported providing stroke patient care. For physicians treating glucose in stroke patients, 16.6% targeted glucose 4.0-6.0 mmol/l, 52% targeted 6.1-8.0 mmol/l, 13.6% targeted 8.1-12.0 mmol/l, 0.8% targeted 12.1-15.0 mmol/l, and 7.5% were unsure. Comparing specialties, 32% of intensivists, 17.5% of neurologists, 13% of general internists, 14% of emergency physicians, and 0% of family physicians reported targeting 4.0-6.0 mmol/l (p=0.026). Overall, 44% reported aiming for target glucose within 12 hours and 77% within 24 hours from hospital presentation. Intensive care specialists treated glucose most aggressively, including 20% treating, with insulin infusion, patients with no diabetes and initial glucose 6.0-8.0 mmol/l. Emergency physicians were most conservative when treating glucose in stroke patients.

There is variability in the aggressiveness of glucose management in stroke patients by different physician specialty groups, reflecting the lack of evidence available to guide hyperglycemia management in this setting. These results highlight an important gap in knowledge and recommendations for stroke patient care that must be addressed to ensure optimal patient outcomes.

An estimated 20-25% of all strokes occur during sleep and these patients wake up with their deficits. This study evaluated outcomes among patients who woke up with stroke compared to those who were awake at stroke onset.

Using data from the Registry of the Canadian Stroke Network Phases 1 and 2, we compared demographics, clinical data and six-month outcomes between patients with stroke-on-awakening versus stroke-while-awake. Strokes of all types (ischemic stroke, transient ischemic attack, intracerebral hemorrhage and subarachnoid hemorrhage) were included. Standard descriptive statistics, multivariable logistic regression and general linear modeling were applied to the data to compare variables.

Among 2,585 stroke patients, 349 (13.5%) woke up with stroke and 2,236 (86.5%) did not. Patients with stroke-on-awakening were more likely to have higher blood pressure and to suffer ischemic stroke, but stroke severity, measured by level of consciousness, did not differ. Mortality both at discharge and at six-month follow-up did not differ between the two cohorts. However, patients with stroke-on-awakening were less likely to return home, and their median Stroke Impact Scale-16 scores were 7.0 points lower compared to those with stroke-while-awake.

There are minor demographic and clinical differences between patients with stroke-on-awakening and stroke-while-awake. Functional outcomes are slightly worse among patients with stroke-on-awakening, an effect which was driven by poor outcomes among patients with subarachnoid hemorrhage.