Cerebral emboli are generated by every step of standard carotid angioplasty and stenting. Primary carotid stenting (PCS) is a technique in which the use of balloon angioplasty (BA) is minimized to decrease the embolic load. The primary aim of this study is to establish the number of emboli generated by each step of primary stenting and determine the relationship to new diffusion (DWI) lesions on subsequent magnetic resonance imaging (MRI).

Eighty-five patients with severe, symptomatic carotid stenosis were prospectively recruited and underwent carotid stenting. Intraoperative transcranial Doppler was performed in 77 patients. The number and size of microemboli for each of seven procedural steps were recorded. Correlation was made with the number and location of new DWI lesions.

PCS was performed in 73 patients. BA was required in 12 patients. The mean number of microemboli was 114, and most microemboli were generated by stent deployment, followed by BA. Balloon techniques generated significantly more emboli than primary stenting (p = 0.017). There was a significant relationship between total microemboli and new DWI lesions (p = 0.009), and between new DWI lesions in multiple territories and the severity of pretreatment stenosis (p = 0.002).

During PCS, more emboli are generated by stent deployment than during any other stage of the procedure. When BA is necessary, more malignant emboli are generated but total emboli are unchanged and there is no difference in new diffusion lesions on MRI. PCS is safe and is not inferior to historical controls for the generation of new DWI lesions.

A primary admission of patients with suspected acute ischemic stroke and large vessel occlusion (LVO) to centers capable of providing endovascular stroke therapy (EVT) may induce shorter time to treatment and better functional outcomes. One of the limitations in this strategy is the need for accurately identifying LVO patients in the prehospital setting. We aimed to study the feasibility and diagnostic performance of point-of-care ultrasound (POCUS) for the detection of LVO in patients with acute stroke.

We conducted a proof-of-concept study and selected 15 acute ischemic stroke patients with angiographically confirmed LVO and 15 patients without LVO. Duplex ultrasonography (DUS) of the common carotid arteries was performed, and flow profiles compatible with LVO were scored independently by one experienced and one junior neurologist.

Among the 15 patients with LVO, 6 patients presented with an occlusion of the carotid-T and 9 patients presented with an M1 occlusion. Interobserver agreement between the junior and the experienced neurologist was excellent (kappa = 0.813, p < 0.001). Flow profiles of the CAA allowed the detection of LVO with a sensitivity of 73%, a positive predictive value of 92 and 100%, and a c-statistics of 0.83 (95%CI = 0.65–0.94) and 0.87 (95%CI = 0.69–0.94) (experienced neurologist and junior neurologist, respectively). In comparison with clinical stroke scales, DUS was associated with better trade-off between sensitivity and specificity.

POCUS in acute stroke setting is feasible, it may serve as a complementary tool for the detection of LVO and is potentially applicable in the prehospital phase.

Non-penetrating head and neck trauma is associated with extracranial traumatic vertebral artery injury (eTVAI) in approximately 1–2% of cases. Most patients are initially asymptomatic but have an increased risk for delayed stroke and mortality. Limited evidence is available to guide the management of asymptomatic eTVAI. As such, we sought to investigate national practice patterns regarding screening, treatment, and follow-up domains.

A cross-sectional, electronic survey was distributed to members of the Canadian Neurosurgical Society and Canadian Spine Society. We presented two cases of asymptomatic eTVAI, stratified by injury mechanism, fracture type, and angiographic findings. Screening questions were answered prior to presentation of angiographic findings. Survey responses were analyzed using descriptive statistics.

One hundred-eight of 232 (46%) participants, representing 20 academic institutions, completed the survey. Case 1: 78% of respondents would screen for eTVAI with computed topography angiography (CTA) (97%), immediately (88%). The majority of respondents (97%) would treat with aspirin (89%) for 3–6 months (46%). Respondents would follow up clinically (89%) or radiographically (75%), every 1–3 months. Case 2: 73% of respondents would screen with CTA (96%), immediately (88%). Most respondents (94%) would treat with aspirin (50%) for 3–6 months (35%). Thirty-six percent of respondents would utilize endovascular therapy. Respondents would follow up clinically (97%) or radiographically (89%), every 1–3 months.

This survey of Canadian practice patterns highlights consistency in the approach to screening, treatment, and follow-up of asymptomatic eTVAI. These findings are relevant to neurosurgeons, spinal surgeons, stroke neurologists, and neuro-interventionalists.

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.

Intracerebral abscess is a life-threatening condition for which there are no current, widely accepted neurosurgical management guidelines. The purpose of this study was to investigate Canadian practice patterns for the medical and surgical management of primary, recurrent, and multiple intracerebral abscesses.

A self-administered, cross-sectional, electronic survey was distributed to active staff and resident members of the Canadian Neurosurgical Society and Canadian Neurosurgery Research Collaborative. Responses between subgroups were analyzed using the Chi-square test.

In total, 101 respondents (57.7%) completed the survey. The majority (60.0%) were staff neurosurgeons working in an academic, adult care setting (80%). We identified a consensus that abscesses >2.5 cm in diameter should be considered for surgical intervention. The majority of respondents were in favor of excising an intracerebral abscess over performing aspiration if located superficially in non-eloquent cortex (60.4%), located in the posterior fossa (65.4%), or causing mass effect leading to herniation (75.3%). The majority of respondents were in favor of reoperation for recurrent abscesses if measuring greater than 2.5 cm, associated with progressive neurological deterioration, the index operation was an aspiration and did not include resection of the abscess capsule, and if the recurrence occurred despite prior surgery combined with maximal antibiotic therapy. There was no consensus on the use of topical intraoperative antibiotics.

This survey demonstrated heterogeneity in the medical and surgical management of primary, recurrent, and multiple brain abscesses among Canadian neurosurgery attending staff and residents.1

The Calgary Postoperative Pain after Spine Surgery (CAPPS) score was developed to identify patients at risk of experiencing poorly controlled pain after spine surgery. The goal of this study was to independently validate the CAPPS score on a prospectively collected patient sample.

Poor postoperative pain control was defined as a mean numeric rating scale (NRS) for pain >4 at rest in the first 24 hours after surgery. Baseline characteristics in this study (validation cohort) were compared to those of the development cohort used to create the CAPPS score. Predictive performance of the CAPPS score was assessed by the area under the curve (AUC) and percentage misclassification for discrimination. A graphical comparison between predicted probability vs. observed incidence of poorly controlled pain was performed for calibration.

Fifty-two percent of 201 patients experienced poorly controlled pain. The validation cohort exhibited lower depression scores and a higher proportion using daily opioid medications compared to the development cohort. The AUC was 0.74 [95%CI = 0.68–0.81] in the validation cohort compared to 0.73 [95%CI = 0.69–0.76] in the development cohort for the eight-tier CAPPS score. When stratified between the low- vs. extreme-risk and low- vs. high-risk groups, the percentage misclassification was 21.2% and 30.7% in the validation cohort, compared to 29.9% and 38.0% in the development cohort, respectively. The predicted probability closely mirrored the observed incidence of poor pain control across all scores.

The CAPPS score, based on seven easily obtained and reliable prognostic variables, was validated using a prospectively collected, independent sample of patients.

Youth hockey is a high-impact sport and can cause concussions with lasting effects. We hypothesized that important injury prevention information would accrue from longitudinal tracking of concussed players with persisting concussion symptoms (PCS).

This case series comprised 87 consecutive concussed ice hockey players aged 10–18 including 66 males and 21 females referred to our Concussion Clinic from 1997 to 2017 and followed longitudinally by clinic visits and questionnaires.

PCS occurred in 70 (80.4%) of 87 concussed players and lasted 1–168 months in males and 3–26 months in females. Bodychecking was the most common concussion mechanism in 34 (39.1%) players and caused PCS in 24 (70.6%) with symptom duration 4.00 [2.75, 14.50] months (median [IQR]). The remaining 53 players had other concussion mechanisms with PCS in 86.8% (p = 0.113) with similar duration (p = 0.848).

This is the first longitudinal study of concussion with PCS in youth hockey and showed that symptoms can last for several years. Bodychecking was the commonest mechanism of prolonged disability from concussion in boys and girls’ hockey with average PCS duration of 12.3 months but several years in some players. The injury prevention message is to raise the age of permitted bodychecking to 18 in boys’ hockey from age 13 to 14 where it is currently. In this case series, this change could have prevented the majority of the bodycheck concussions and several years of suffering from PCS and is strong evidence for raising the permitted age for bodychecking in boys’ ice hockey to age 18.

To characterize Parkinson’s disease (PD) symptoms based on the presence, onset time, and severity of rapid eye movement sleep behavior disorder (RBD) and their association with impulse control disorders (ICD).

RBD is a frequent non-motor symptom in PD, usually described as prodromal. The severity of RBD according to the start time and its relationship with ICD in PD needs further clarification.

A survey-based study was performed to determine the presence of RBD symptoms, their severity, and the temporal relationship with the PD onset. The survey included RBD1Q, the Mayo Sleep, and the RBDQ-HK questionnaires and questions about clinical characteristics, including ICD. Only PD patients with care partners spending night hours in the same room were included.

410 PD patients were included: 206 with RBD (50.2%) and 204 non-RBD (49.8%). The PD-RBD patients were younger and their daily levodopa dose was higher than the non-RBD group. Most of these patients developed RBD symptoms after the onset of clinical PD were younger at motor symptom onset and had higher scores in the hallucinations and psychosis subsection of MDS-UPDRS-I. RBD group had a more severe non-motor phenotype, including more ICD than those without RBD, mainly due to higher compulsive eating.

In our study, most patients recognized RBD symptoms after the onset of the PD motor symptoms and the clinical features of PD with and without RBD were distinctive, supporting the hypothesis that PD-RBD might represent a variant pattern of neurodegeneration.

Neuroimaging studies in Wilson’s disease (WD) have identified various alterations in white matter (WM) microstructural organization. However, it remains unclear whether these alterations are localized to specific regions of fiber tracts, and what diagnostic value they might have. The purpose of this study is to explore the spatial profile of WM abnormalities along defined fiber tracts in WD and its clinical relevance.

Ninety-nine patients with WD (62 men and 37 women) and 91 age- and sex-matched controls (59 men and 32 women) were recruited to take part in experiments of diffusion-weighted imaging with 64 gradient vectors. The data were calculated by FMRIB Software Library (FSL) software and Automated Fiber Quantification (AFQ) software. After registration, patient groups and normal groups were compared by Mann–Whitney U test analysis.

Compared with the controls, the patients with WD showed widespread fractional anisotropy reduction and mean diffusivity, radial diffusivity elevation of identified fiber tracts. Significant correlations between diffusion tensor imaging (DTI) parameters and the neurological Unified Wilson’s Disease Rating Scale (UWDRS-N), serum ceruloplasmin, and 24-h urinary copper excretion were found.

The present study has provided evidence that the metrics of DTI could be utilized as a potential biomarker of neuropathological symptoms in WD. Damage to the microstructure of callosum forceps and corticospinal tract may be involved in the pathophysiological process of neurological symptoms in WD patients, such as gait and balance disturbances, involuntary movements, dysphagia, and autonomic dysfunction.

To measure regional cerebral metabolic rate of glucose (CMRGlu) in patients with chronic disorders of consciousness (DOCs) using 18F-fluorodeoxyglucose positron emission tomography (FDG-PET).

This retrospective cohort study examined 50 patients (mean age: 40.9 ± 20.1 years) with traumatic brain injury (TBI)-induced chronic DOCs [minimally conscious state (MCS)+, n = 20; MCS−, n = 15 and vegetative state (VS), n = 15]. We measured FDG-PET-based CMRGlu values in 12 regions of both brain hemispheres and compared those among MCS+, MCS − and VS patients.

In both hemispheres, the regional CMRGlu reduced with consciousness deterioration in 11 of 12 regions (91.7%). In seven right hemisphere regions, CMRGlu values were markedly higher in MCS+ patients than in MCS− patients. Furthermore, CMRGlu was suggestively higher in the left occipital region in MCS− patients than in VS patients.

Functional preservation in the left occipital region in patients with chronic DOCs might reflect an awareness of external environments, whereas extensive functional preservation in the right cerebral hemisphere might reflect communication motivation.

We investigated the change in limbic structure volumes and intrinsic limbic network in patients with obstructive sleep apnea (OSA) compared to healthy controls.

We enrolled 26 patients with OSA and 30 healthy controls. They underwent three-dimensional T1-weighted magnetic resonance imaging (MRI) on a 3 T MRI scanner. The limbic structures were analyzed volumetrically using the FreeSurfer program. We examined the intrinsic limbic network using the Brain Analysis with Graph Theory program and compared the groups' limbic structure volumes and intrinsic limbic network.

There were significant differences in specific limbic structure volumes between the groups. The volumes in the right amygdala, right hippocampus, right hypothalamus, right nucleus accumbens, left amygdala, left basal forebrain, left hippocampus, left hypothalamus, and left nucleus accumbens in patients with OSA were lower than those in healthy controls (right amygdala, 0.102 vs. 0.113%, p = 0.004; right hippocampus, 0.253 vs. 0.281%, p = 0.002; right hypothalamus, 0.028 vs. 0.032%, p = 0.002; right nucleus accumbens, 0.021 vs. 0.024%, p = 0.019; left amygdala, 0.089 vs. 0.098%, p = 0.007; left basal forebrain, 0.020 vs. 0.022%, p = 0.027; left hippocampus, 0.245 vs. 0.265%, p = 0.021; left hypothalamus, 0.028 vs. 0.031%, p = 0.016; left nucleus accumbens, 0.023 vs. 0.027%, p = 0.002). However, there were no significant differences in network measures between the groups.

We demonstrate that the volumes of several limbic structures in patients with OSA are significantly lower than those in healthy controls. However, there are no alterations to the intrinsic limbic network. These findings suggest that OSA is one of the risk factors for cognitive impairments.

Leber hereditary optic neuropathy (LHON) is a rare but bilaterally blinding disease. Three characteristic disease-causing point mutations, and other less common mutations, are most often found on the mitochondrially encoded genes of NADH-ubiquinone oxidoreductase core subunits (MT-ND). The purpose of this study is to provide an overview of LHON mutations in Southwestern Ontario and to describe the associated demographic and clinical characteristics.

A retrospective genetic and clinical chart review was performed from January 2015 to 2020. Patients were identified within a mitochondrial mutation database and included if a mutation was detected on the MT-ND1, -ND4, or -ND6 genes. A clinical chart review was done on all available patients.

Forty-five of 63 patients identified had classic disease-causing mutations (6.7% m.3460G>A, 44.4% m.11778G>A, and 48.9% m.14484T>C). Several of the remaining 18 patients had rare mutations previously documented in association with LHON. Of the 14 patients with clinical charts accessible for review, 12 had symptomatic disease, and all but one had bilateral optic neuropathies. Nine patients had classic LHON mutations and 3 had possible novel mutations; 7 were males; 9 had final visual acuity ≤ 20/200 in at least one eye; and 6 of those had ≤20/400 in both eyes.

This study adds to the literature on LHON in Canada, and specifically Southwestern Ontario. The demographic and clinical data regarding LHON in this geographic location, as well as possible novel disease-causing mutations, provide important information to aid clinicians in recognizing cases of LHON that may otherwise be disregarded.

Half of Guillain–Barré syndrome (GBS) present elevated cerebrospinal fluid (CSF) protein levels within 1 week since symptom onset and 80% within 2 weeks. Our objective was to determine the clinical and prognostic implication of albuminocytological dissociation in early GBS.

An ambispective cohort study was conducted. Good outcome was considered if the patient was able to walk unaided (Guillain-Barré disability score [GDS] ≤ 2 points) at 3-month follow-up. Patients were classified into two groups: with and without albuminocytological dissociation; we compared clinical and paraclinic characteristics between the groups. We analyzed clinical and electrophysiological factors related to presenting early dissociation through a multivariate model.

We included 240 patients who fulfilled Asbury criteria for GBS. On further selection, only 94 patients fulfilled inclusion. Mean age was 45.94 ± 17.1 years and 67% were male. Median time from symptom onset to admission was 5 days (IQR 3–6). Regarding albuminocytological dissociation and electrophysiological variants, we found a significant difference: acute inflammatory demyelinating polyneuropathy (AIDP) [60.6% vs 26.2%, p = 0.002], acute motor axonal neuropathy (AMAN) [21.2% vs 49.1%, p = 0.009] and acute motor sensory axonal neuropathy (AMSAN) [12.1% vs 1.6%, p = 0.05]. We did not observe significant differences in recovery of independent walking in short term between both groups. The presence of conduction block in any variant (OR 3.21, 95% CI 1.12–9.16, p = 0.02) and absence of sural registration (OR 5.69, 95% CI 1.48–21.83, p = 0.011) were independent factors related to early dissociation.

Early dissociation (<7 days) is not associated with any particular clinical feature or unfavorable outcome. It is more common to see in AIDP rather than axonal variants.

Long latency reflexes (LLRs) are impaired in a wide array of clinical conditions. We aimed to illustrate the clinical applications and recent advances of LLR in various neurological disorders from a systematic review of published literature.

We reviewed the literature using appropriately chosen MeSH terms on the database platforms of MEDLINE, Web of Sciences, and Google Scholar for all the articles from 1st January 1975 to 2nd February 2021 using the search terms “long loop reflex”, “long latency reflex” and “C-reflex”. The included articles were analyzed and reported using synthesis without meta-analysis (SWiM) guidelines.

Based on our selection criteria, 40 articles were selected for the systematic review. The various diseases included parkinsonian syndromes (11 studies, 217 patients), Huntington’s disease (10 studies, 209 patients), myoclonus of varied etiologies (13 studies, 127 patients) including progressive myoclonic epilepsy (5 studies, 63 patients) and multiple sclerosis (6 studies, 200 patients). Patients with parkinsonian syndromes showed large amplitude LLR II response. Enlarged LLR II was also found in myoclonus of various etiologies. LLR II response was delayed or absent in Huntington’s disease. Delayed LLR II response was present in multiple sclerosis. Among the other diseases, LLR response varied according to the location of cerebellar lesions while the results were equivocal in patients with essential tremor.

Abnormal LLR is observed in many neurological disorders. However, larger systematic studies are required in many neurological disorders in order to establish its role in diagnosis and management.