The recent guidelines on management of aneurysmal subarachnoid hemorrhage (aSAH) advise pharmacological thromboprophylaxis (PTP) after aneurysm obliteration. However, no study has addressed the safety of PTP in the aSAH population. Therefore, the aim of this study was to assess the safety of early PTP after aSAH.

Retrospective cohort of aSAH patients admitted between January 2012 and June 2013 in a single high-volume aSAH center. Traumatic SAH and perimesencephalic hemorrhage patients were excluded. Patients were grouped according to PTP timing: early PTP group (PTP within 24 hours of aneurysm treatment), and delayed PTP group (PTP started > 24 hours).

A total of 174 SAH patients (mean age 56.3±12.5 years) were admitted during the study period. Thirty-nine patients (22%) did not receive PTP, whereas 135 patients (78%) received PTP after aneurysm treatment or negative angiography. Among the patients who received PTP, 65 (48%) had an external ventricular drain. Twenty-eight patients (21%) received early PTP, and 107 (79%) received delayed PTP. No patient in the early treatment group and three patients in the delayed PTP group developed an intracerebral hemorrhagic complication. Two required neurosurgical intervention and one died. These three patients were on concomitant PTP and dual antiplatelet therapy.

The initiation of PTP within 24 hours may be safe after the treatment of a ruptured aneurysm or in angiogram-negative SAH patients with diffuse aneurysmal hemorrhage pattern. We suggest caution with concomitant use of PTP and dual antiplatelet agents, because it possibly increases the risk for intracerebral hemorrhage.

Few studies have assessed the performance of stroke prevention clinics. In particular, limited information exists on patient compliance, achievement of therapeutic targets, and related occurrence of vascular events.

We compared our clinical practice to recommendations from published guidelines in newly referred patients for transient ischemic attack (TIA) or ischemic stroke between 2008 and 2010. We monitored our cohort for at least 1 year and assessed for adequacy of vascular risk factor management, drug adherence, and occurrence of nonlethal vascular outcomes.

Of 408 patients, 57.8% had a stroke and 42.2% a TIA. The mean age was 68±13 years, and 52% male. Average follow-up was 15.8 months. During follow-up, 253 patients (70.3%) completely achieved their blood pressure target, 151 (45.5%) achieved their low-density lipoprotein (LDL) cholesterol target, and 407 (99.8%) were on antithrombotics. Eighty-nine patients (21.8%) attained optimal therapy status, defined as reaching targets for LDL cholesterol, blood pressure, and antithrombotic use. Adherence to drug therapy was associated with attainment of optimal therapy status (p=0.01). Diabetes was associated with lower probability of attaining optimal therapy status (odds ratio [OR], 0.36; 95% confidence interval [CI], 0.20-0.66) and blood pressure targets (OR, 0.09; 95% CI, 0.05-0.17). During follow-up, 52 (12.7%) patients had a nonlethal vascular event.

Our study shows good attainment of therapeutic goals associated with adherence to drug therapy. However, optimal therapy status and blood pressure targets were more difficult to attain in patients with diabetes; therefore, more intensive preventive efforts may be required for these individuals.

This retrospective study addresses for the first time the differences in clinical features and outcomes between those individuals with a cerebellar infarct who were correctly diagnosed on initial presentation compared to those who experienced delayed diagnosis.

A retrospective review was conducted of our stroke registry from 09/2003 to 02/2011. Forty seven patients had an isolated cerebellar infarction confirmed by MRI. Misdiagnosis was defined as the diagnosis given by the first physician.

Among 47 patients identified, 59.6% had delayed diagnosis. Five patients in the correct diagnosis group received intravenous tissue plasminogen activator, compared to none in the delayed diagnosis group. Complaints of weakness were protective from delayed diagnosis (OR 0.087, 95% CI 0.019-0.393, p=0.001).

Patients with an isolated cerebellar infarction need to be considered when patients present with acute non-specific symptoms. Critical components of the neurological examination are omitted which are imperative to diagnose cerebellar infarcts. A thorough neurological examination may increase clinical suspicion of an ischemic stroke.

Evaluate the incidence, neurologic morbidity, and mortality of patients with Terson syndrome.

Consecutive patients admitted to the Hamilton General Hospital from May 2012 to May 2013 with a diagnosis of spontaneous subarachnoid hemorrhage (SAH) were recruited. Funduscopic examinations were performed under pharmacological mydriasis. Outcome measures included: (1) the presence or absence of Terson syndrome; (2) The Glasgow Coma Scale (GCS), Hunt and Hess scale (H&H), and SAH Fisher score upon admission to the hospital; (3) the modified Rankin score upon discharge; and (4) and all-cause mortality.

Forty-six patients were included and 10 had Terson syndrome (21%). The median H&H, GCS, and Fisher scores were 4, 6.5, and 4.0 for patients with Terson syndrome vs. 2, 14, and 3 for patients without Terson syndrome (p=0.0032, 0.0052, and 0.031), respectively. The median Rankin score was 6 for patients with Terson syndrome vs. 3.5 for patients without Terson syndrome (p=0.0019). The odds of all-cause mortality with Terson syndrome vs. no Terson syndrome was 12: 1 (95% confidence interval 2.33-61.7), p =0.003. Only four of the 10 patients with Terson syndrome survived.

Based on this study, approximately one-fifth of patients admitted to the hospital with a spontaneous SAH could have Terson syndrome. Patients with Terson syndrome have significantly worse GCS and H&H scores upon admission to the hospital, lower modified Rankin scores upon discharge, and greater mortality. Thus, Terson syndrome is not rare among patients with SAH and carries a worse prognosis.

Whether an association exists between cerebral microbleeds (CMBs) and functional recovery after ischemic stroke is unclear. We aimed to evaluate the association between CMBs and functional outcome after acute ischemic stroke.

Consecutive patients with acute stroke were enrolled, and all patients were stratified into good and poor functional outcome groups at discharge and 6 months after ischemic stroke by using a modified Rankin Scale score. Cardiovascular risk factors, CMBs, and white matter hyperintensities were compared between these two outcome groups. Logistic regression analysis was used to estimate the risk of poor functional outcomes.

A total of 225 patients were enrolled, 121 of whom were classified as having a good functional outcome at discharge and 142 as having a good 6-month functional outcome. The presence of CMBs was associated with a poor functional outcome at discharge [CMBs (+) patients in poor vs. good functional group; 48.1% vs. 30.6%; p=0.007] and 6 months [53.0% vs. 30.3%; p=0.001]. After adjustment for confounding factors, only the presence of infratentorial CMBs was associated with a poor functional outcome at discharge and 6 months. The poor functional outcome group had more CMBs than the good outcome group at 6 months.

Infratentorial cerebral microbleeds were significantly associated with worse functional outcomes not only in the early phase of ischemic stroke but also in the chronic phase. These findings suggest that the presence of infratentorial CMBs can predict poor functional outcome after acute ischemic stroke.

Neurosurgery may involve significant blood loss and frequently requires allogeneic red blood cell (RBC) transfusion. Preoperative recombinant erythropoietin (EPO) may be used to improve erythroid status and recovery, and used either alone or in combination with preoperative autologous donation (PAD) it may reduce exposure to allogeneic RBC. We wished to study the use of EPO with and without PAD and the risk of RBC transfusion in neurosurgery.

Using a retrospective case-control design, 57 patients who received EPO preoperatively were matched 2:1 for age, sex, year of surgery, and International Classification of Diseases code most responsible for surgery (three were excluded because of stringent matching criteria, leaving 54 cases and 108 comparison subjects). Thirty-two cases participated in PAD. Medical and anesthetic records as well as laboratory investigations were reviewed and extracted.

Allogeneic RBC exposure was identical for EPO cases and comparison subjects (18.5%). Concomitant PAD and EPO did not reduce allogeneic RBC exposure (21.9%), and resulted in a greater number of RBC units transfused. Last recorded hemoglobin levels suggested that autologous RBCs were not more liberally used. Patients who engaged in PAD and EPO suffered from iatrogenic anemia. A significant proportion (58.6%) of the autologous RBCs was ultimately not used and discarded.

Further research is needed to determine the efficacy of EPO in neurological surgery. PAD does not appear to reduce the risk of allogeneic RBC transfusion, despite concomitant EPO. Indeed, PAD resulted in iatrogenic anemia and increased transfusion requirements. The cost-effectiveness of blood conservation efforts in neurosurgery deserves additional research.

Le développement au cours des deniers années des interventions neurochirurgicales sous anesthésie locale, en particulier dans le champ neuro-oncologique, rend possible la question d’une éventuelle révocation per opératoire du consentement du patient à la procédure chirurgicale.

Les auteurs décrivent la révocation de son consentement par un patient au cours de l’exérèse chirurgicale d’un gliome de bas grade fronto-temporo-insulaire droit.

Les aspects spécifiques aux conditions de révocation du consentement dans le contexte particulier de la chirurgie sous anesthésie locale sont discutés. La possibilité d’un pacte d’Ulysse est proposée et discutée.

Les interventions chirurgicales en condition éveillée créent un contexte particulier en ce qu’une révocation du consentement per opératoire devient possible. Dans ces conditions, l’information préopératoire pourrait aussi aborder avec le malade la question de la conduite à tenir au cas où il serait amené à solliciter un retrait de consentement lors de son réveil per opératoire.

Cognitive impairments are common in Parkinson’s disease (PD). Despite its clinical importance, the development of dementia is still difficult to predict. In this study, we investigated the possible associations between non-motor symptoms and the risk of developing dementia within a 2-year observation period in PD.

A total of 80 patients with PD participated in this study. Nonmotor symptoms (the Nonmotor Symptoms Questionnaire), PD status (Unified Parkinson’s Disease Rating Scale), depression (Geriatric d Depression Scale or Montgomery-Asberg Depression Scale), stereopsis and severity of nonmotor symptoms (Non-motor symptoms scale) were assessed. Global cognitive function (Mini-Mental State Examination) were evaluated at baseline and 2 years later.

Presence of depression, vivid dreaming, REM sleep behavior disorders, hyposmia, abnormal stereopsis, non-smoking and postural instability/ gait disturbance phenotype were associated with a significantly more rapid decline of Mini-Mental State Examination. Logistic regression analyses demonstrated that depression (odds ratio=13.895), abnormal stereopsis (odds ratio=10.729), vivid dreaming (odds ratio=4.16), REM sleep behavior disorders (odds ratio=5.353) and hyposmia (odds ratio=4.911) were significant independent predictors of dementia risk within 2 years. Postural instability/ gait disturbance phenotype and age >62 years were also independent predictors of dementia risk (odd ratio=38.333, odds ratio=10.625).

We suggest that depression, vivid dreaming, REM sleep behavior disorders, hyposmia and abnormal stereopsis are closely associated with cognitive decline, and that presence of these nonmotor symptoms predict the subsequent development of Parkinson’s disease dementia.

The primary objective was to evaluate the effects of pregabalin relative to placebo in patients with chronic unilateral cervicogenic headache.

To assess the change from baseline in the frequency of cervicogenic headache days per 28-day period between placebo and treatment group. To assess the change from baseline in the intensity of headache, and health outcome measures.

This was a double-blind, randomized, placebo-controlled, parallel-group study, evaluating the efficacy and safety of pregabalin in patients with cervicogenic headache.

The study consisted of two phases. A baseline of -28 days and a double-blind placebo-controlled phase: with an escalation and maintenance phase, during which patients remained at their highest dose until the end of the study, at Day 86.

Forty one patients were randomized, predominantly females, with a mean age of 52 years old. At screening, both groups had, on average, 26 headache-days per month. By the final phase of the study, the number of headache days dropped to 16 per month for the pregabalin group while remaining stable for the placebo group (p=0.037). No serious adverse events were reported during the study.

In this study, primary objectives were achieved with a statistically significant change of ten days in frequency of headache days; with minor side effects that were well tolerated.

To study stimulation-related facial electromyographic (FEMG) activity in intensive care unit (ICU) patients, develop an algorithm for quantifying the FEMG activity, and to optimize the algorithm for monitoring the sedation state of ICU patients.

First, the characteristics of FEMG response patterns related to vocal stimulation of 17 ICU patients were studied. Second, we collected continuous FEMG data from 30 ICU patients. Based on these data, we developed the Responsiveness Index (RI) algorithm that quantifies FEMG responses. Third, we compared the RI values with clinical sedation level assessments and adjusted algorithm parameters for best performance.

In patients who produced a clinically observed response to the vocal stimulus, the poststimulus FEMG power was 0.33 µV higher than the prestimulus power. In nonresponding patients, there was no difference. The sensitivity and specificity of the developed RI for detecting deep sedation in the subgroup with low probability of encephalopathy were 0.90 and 0.79, respectively.

Consistent FEMG patterns were found related to standard stimulation of ICU patients. A simple and robust algorithm was developed and good correlation with clinical sedation scores achieved in the development data.

Iterative reconstruction has been reported to reduce radiation dose in CT, while preserving and even improving image quality. The purpose of this study was to evaluate the effects of sinogram-affirmed iterative reconstruction (SAFIRE) on radiation dose reduction and image quality for noncontrast adult head CT and to compare SAFIRE with conventional filtered back-projection (FBP) reconstruction.

Institutional review board approval was obtained for this retrospective analysis of head CT scans reconstructed with SAFIRE and/or FBP for 107 patients. Radiation dose parameters were recorded from scanner-generated CT dose reports. Signal-to-noise and contrast-to-noise ratios (SNR, CNR) were calculated from gray and white matter (GM, WM) attenuation measurements. Image noise, artifacts, GM-WM differentiation, small structure visibility, and sharpness were graded by two readers. Statistical analysis included the independent-samples t test for quantitative data, the related samples Wilcoxon signed-rank test for qualitative data, the coefficient of repeatability for intraobserver variation, and κ statistics for interobserver agreement.

Mean effective dose was significantly reduced with SAFIRE from 2.0 to 1.7 mSv (p<0.0001). SAFIRE also significantly improved GM SNR, WM SNR, and GM-WM CNR (p<0.0001). Significant reductions in image noise and posterior fossa artifact as well as improvements in GM-WM differentiation, small structure visibility, and sharpness were noted with SAFIRE (P<0.005).

SAFIRE for noncontrast adult head CT reduces patient radiation dose by 15% for the settings employed at our institution, while significantly improving multiple quantitative and qualitative measures of image quality.

Multiple sulfatase deficiency (MSD) is a rare autosomal recessive inborn error of lysosomal metabolism. The clinical phenotypic spectrum encompasses overlapping features of variable severity and is suggestive of individual single sulfatase deficiencies (i.e., metachromatic leukodystrophy, mucopolysaccharidosis, and X-linked ichthyosis).

We describe a 3-year-old male with severe hypotonia, developmental regression and progressive neurodegeneration, coarse facial features, nystagmus (from ocular albinism), and dysmyelinating motor sensory neuropathy. Ethics approval was obtained from the Western University Ontario.

Extensive investigative work-up identified deficiencies of multiple sulfatases: heparan sulfate sulfamidase: 6.5 nmoles/mg/protein/17 hour (reference 25.0-75.0), iduronate-2-sulfate sulfatase: 9 nmol/mg/protein/4 hour (reference 31-110), and arylsulfatase A: 3.8 nmoles/hr/mg protein (reference 22-50). The identification of compound heterozygous pathogenic mutations in the SUMF1 gene c.836 C>T (p.A279V) and c.1045C>T (p.R349W) confirmed the diagnosis of MSD.

The complex clinical manifestations of MSD and the unrelated coexistence of ocular albinism as in our case can delay diagnosis. Genetic counselling should be provided to all affected families.

Eosinophils may affect each stage of tumour development. Many studies have suggested that tumour-associated tissue eosinophilia (TATE) is associated with favourable prognosis in some malignant tumours. However, only a few studies exist on TATE in central nervous system (CNS) tumours. Our recent study exhibited eosinophils in atypical teratoid/rhabdoid tumours (AT/RTs), pediatric malignant CNS tumours with divergent differentiation. This study examines eosinophils in pilocytic astrocytomas (PAs).

The study included 44 consecutive cases of patients with PAs and no concurrent CNS inflammatory disease.

We found eosinophils in 19 (43%) of 44 PAs (patient age range, 0.5-72 years). Eosinophils were intratumoural and clearly distinguishable. The density of eosinophils was rare to focally scattered. PAs containing eosinophils were located throughout the CNS. Furthermore, eosinophilic infiltration was identified in 18 (62%) of 29 pediatric (age range, 0.5-18 years) PAs but only 1 (7%) of 15 (p<0.001, significantly less) adult (age range, 20-72 years) PAs. Eosinophilic infiltration showed no significant differences between PAs with and without MRI cystic formation, surgical procedures, or PAs with and without leptomeningeal infiltration. In comparison, eosinophils were absent in 10 pediatric (age range, 0.5-15 years) ependymomas (or anaplastic ependymomas).

These results suggest that eosinophils are common in pediatric PAs but rare in adult PAs. This difference is probably related to the developing immune system and different tumour-specific antigens in children. TATE may play a functional role in the development of pediatric PAs, as well as some other pediatric CNS tumours such as AT/RTs.

Statins have recently been reported to cause a rare autoimmune inflammatory and/or necrotic myopathy that begins or persists after drug cessation.

We report on 26 patients seen at a neuromuscular centre between 2005 and 2011 who demonstrated muscle weakness/myalgias and creatine kinase elevations during or after statin treatment with continuation of signs and symptoms despite statin withdrawal.

All patients were treated with immunosuppressive therapy with good response; all improved biochemically and 86% improved clinically. Sixty-five percent of patients who attempted to taper off immunosuppressive therapy relapsed. We report on a novel finding whereby five of the seven patients who underwent multiple biopsies throughout their disease demonstrated a transformation of their histological diagnosis, with four progressing from having myofibre necrosis with minimal or no inflammation to a diagnosis of polymyositis.

This study offers preliminary evidence that statin-associated necrotizing myopathy and statin-associated polymyositis may not be separate entities but are part of the same pathophysiological spectrum. Both entities respond well to immunosuppression.