In Canada and the USA, ice hockey is a cause of traumatic brain injury. Post-concussive symptoms are the most important feature of the diagnosis of concussion in sports and it is recommended that athletes not return to play while still symptomatic. Lack of knowledge of concussions could therefore be one of the main detriments to concussion prevention in hockey. The purpose of this research is to describe what minor league hockey players, coaches, parents and trainers know about concussion and its management.

A questionnaire to assess concussion knowledge and return to play guidelines was developed and administered to players at different competitive levels (n = 267), coaches, trainers and parents (total adults n = 142) from the Greater Toronto Area.

Although a majority of adults and players could identify mechanisms responsible for concussion, about one-quarter of adults and about a quarter to a half of children could not recall any symptoms or recalled only one symptom of a concussion. A significant number of players and some adults did not know what a concussion was or how it occurred. Almost half of the players and a fifth of the adults incorrectly stated that concussion was treated with medication or physical therapy. Nearly one quarter of all players did not know if an athlete experiencing symptoms of concussion should continue playing.

This study demonstrated that a significant number of people held misconceptions about concussion in hockey which could lead to serious health consequences and creates a need for better preventive and educational strategies.

Although electromyography (EMG), electroencephalography (EEG) and evoked potential (EP) studies are common investigation tools for patients with neurologic illnesses, no formal data on the manpower supply in Canada exists. Because of the importance of these on training requirements and future planning, the purpose of this study was to establish a comprehensive profile of the human resources situation in clinical neurophysiological services across Canada.

A questionnaire was sent to all clinical neurophysiologists in Canada. To capture the maximal number of respondents, a total of three rounds of mail out were done. In addition, to obtain accurate demographic data on supporting technologists, a separate survey was also carried out by the Association of Electrophysiological Technologists of Canada.

Of the 450 clinical neurophysiologists identified and surveyed, the provincial response rate was 59±14% (mean±SD). Of these, the vast majority practiced in urban centres. There was substantial regional disparity in different provinces. While the wait time for most EEG and EP laboratories was less than six weeks, the wait time for EMG was substantially longer. With the age of the largest number of practitioners in their sixth decade, projected retirement over the next 15 years was 58%. The demographic distribution of the supporting technologists showed a similar trend.

In addition to considerable regional disparity and urban/rural divide, a large percentage of clinical neurophysiologists and supporting technologists planned to retire within the coming decade. To ensure secure and high standard services to Canadians, solutions to fill this void are urgently needed.

Clinical judgment, the ability to make appropriate decisions in uncertain situations, is central to neurological practice, but objective measures of clinical judgment in neurology trainees are lacking. The Script Concordance Test (SCT), based on script theory from cognitive psychology, uses authentic clinical scenarios to compare a trainee’s judgment skills with those of experts. The SCT has been validated in several medical disciplines, but has not been investigated in neurology.

We developed an Internet-based neurology SCT (NSCT) comprising 24 clinical scenarios with three to four questions each. The scenarios were designed to reflect the uncertainty of real-life clinical encounters in adult neurology. The questions explored aspects of the scenario in which several responses might be acceptable; trainees were asked to judge which response they considered to be best. Forty-one PGY1-PGY5 neurology residents and eight medical students from three North American neurology programs (McGill, Calgary, and Mayo Clinic) completed the NSCT. The responses of trainees to each question were compared with the aggregate responses of an expert panel of 16 attending neurologists.

The NSCT demonstrated good reliability (Cronbach alpha = 0.79). Neurology residents scored higher than medical students and lower than attending neurologists, supporting the test’s construct validity. Furthermore, NSCT scores discriminated between senior (PGY3-5) and junior residents (PGY1-2).

Our NSCT is a practical and reliable instrument, and our findings support its construct validity for assessing judgment in neurology trainees. The NSCT has potentially widespread applications as an evaluation tool, both in neurology training and for licensing examinations.

Carotid angioplasty and stenting is an accepted alternative treatment for severe restenosis following carotid endarterectomy. Balloons may not be required to effectively treat these lesions, given their altered histopathology compared to primary atherosclerotic plaque and tendency to be less calcified. Primary stenting using self-expanding stents alone may, therefore, be a safe and effective treatment for restenosis post-carotid endarterectomy.

We review our experience in the treatment of 12 patients with symptomatic severe restenosis following carotid endarterectomy with primary stent placement alone.

Self-expanding stent placement alone reduced the mean internal carotid artery stenosis from 85% to 29%. Average peak systolic velocity determined at the time of ultrasonography decreased from 480 cm/s at initial presentation to 154 cm/s post-stent deployment and further decreased to 104 cm/s at one year follow-up. The stented arteries remained widely patent with no evidence of restenosis. A single peri-procedural ipsilateral transient ischemic event occurred. There were no cerebral or cardiac ischemic events recorded at one year of follow-up.

In this series, primary stent placement without use of angioplasty balloons was a safe and effective treatment for symptomatic restenosis following carotid endarterectomy.

Osteomalacia is an uncommon cause of muscle weakness. Our objectives were to describe features of myopathy associated with Vitamin D deficiency and examine the contributing factors leading to osteomalacic myopathy in our region.

Patients identified retrospectively for the six year period ending in December 2006 with the diagnosis of osteomalacia and/or Vitamin D deficiency associated proximal muscle weakness were included. They were followed in three major centers in western Saudi Arabia. Clinical, biochemical, radiological, and electrophysiological findings were collected before and after Vitamin D treatment by chart review.

Forty seven female patients aged 13-46 years (mean 23.5, SD 4.5) were included. All were veiled and covered heavily when outside the house for social and cultural reasons. Only eight (17%) had adequate varied diet with daily milk ingestion. All patients presented with progressive proximal muscle weakness lasting 6-24 months (mean 14) prior to our evaluation. The weakness was severe in six (13%) patients leading to wheel chair bound states. Associated musculoskeletal pain involving the back, hips, or lower limbs was common (66%). Osteomalcia was the referral diagnosis in only 11 patients and the remaining 36 (77%) patients were misdiagnosed. All patients had metabolic and radiological profiles suggestive of osteomalacia. Remarkable recovery was documented in all patients following oral cholecalciferol and calcium supplementation.

Vitamin D deficiency is an important treatable cause of osteomalacic myopathy in Saudi Arabia. The diagnosis is frequently delayed or missed. Screening for Vitamin D deficiency in patients with acquired myopathy is needed to identify this treatable disorder.

The purpose of this study was to develop and validate a self-administered questionnaire to measure the health-related quality of life (QOL) of patients with brain cancer. We wanted to assess both core and disease-specific concerns in a single, easy-to-use instrument, thus promoting concision and clinical utility. The questionnaire departs from its predecessors in that it was designed for- and validated among French speaking Canadians.

A focus group of health professionals was used to develop items for the questionnaire, which was later validated with 105 patients suffering from brain cancer. The underlying structure of the questionnaire was investigated using principal component analysis and confirmed using a principal factor analysis.

The final version of the questionnaire contains 30 items. Seven multi-item scales, tapping into distinct dimensions of QOL, were uncovered (i.e., functional well-being, symptom severity/fear of death, social support/acceptance of disease, autonomy in personal care, digestive symptomatology, neurocognitive function, and pain). Assessment of reliability revealed elevated internal consistency for each of the seven scales (Cronbach coefficient alpha ≥≥.65), whereas known-groups validity (anchor-based approach) revealed that the different dimensions uniquely discriminated between patients with different functional levels (Karnofsky Performance Scores) and clinical status (exposure to neurosurgery, radiotherapy, and use of chemotherapy and anticonvulsants).

Our QOL questionnaire, the Sherbrooke Neuro-Oncology Assessment Scale, or SNAS, taps into both core and disease-specific issues relevant to neuro-oncology patients. It has good validity and reliability, and clearly reflects the multidimensional nature of QOL. Depending on the research focus, it may be used in clinical trials to track the impact of disease and/or treatment on satisfaction, functional status, and general well-being.

Sema4D/CD100 is a type of class 4 semaphorin, exhibiting crucial rôles in growth cone guidance in developing neurons. Sema4D is widely expressed throughout the central nervous system in embryonic mouse brain, and is selectively localized to oligodendrocytes and myelin in the postnatal brain. However, direct evidence of the actual involvement of Sema4D in the neuronal network development crucial for neurobehavioral performance is still lacking. The present study therefore examined whether Sema4D deficiency leads to abnormal behavioral development.

Both wild-type and Sema4D-deficient mice were subjected to behavioral analyses including open-field, adhesive tape removal, rotarod tests and a water maze task.

Open-field tests revealed increased locomotor activity in Sema4D-deficient mice with less percentage of time spent in the center of the field. In both the adhesive tape removal and rotarod tests, which examine motor coordination and balance, Sema4D-deficient mice showed significantly superior performance, suggesting facilitated motor behavior. Both Sema4D-deficient and wild-type mice successfully learnt the water maze task, locating a hidden escape platform, and also showed precise memory for the platform position in probe tests. However, the swimming speed of Sema4D-deficient mice was significantly faster than that of wild-type mice, providing further evidence of their accelerated motor behavior.

Our mouse behavioral analyses revealed enhanced motor activity in Sema4D-deficient mice, suggesting the crucial involvement of Sema4D in the neurodevelopmental processes of the central structures mediating motor behavior in mice.

To examine the ultrastructural effects of maternal deprivation during developmental periods of limbi-chypothalamo-pituitary-adrenal system on hippocampal dendritic structures in adult rats.

The experiments were carried out with male and female wistar rats in our department. The rats were mated and, after birth, the pups were divided into four groups. The first group (control group) pups remained undisturbed with their dam until postweaning day 22. Maternal deprived groups were separated from their dams for 24 hours at postnatal day 4, 9 and 18. The subjects were provided with food and water ad libitum until 3-months-of-age. At the third month, the rats were transcardially perfused, samples were taken from CA1 and CA3 regions of the hippocampus. Tissues were prepared for electron microscopy.

When the data were analyzed, there were no differences between male and female rats in both ultrastructure and semiquantitative analysis of axodendritic synapses. The ultrastructure of Group 1 was seen as normal while in the second Group some neurons nuclear envelope made deep invagination into the nucleus. Additionally, axodendritic synapses were found normal. In Group 3, micrographs and axodendritic synapses were showed normal structure. However, in Group 4 in some neurons invaginations were seen similar to Group 2. Axodendritic synapses were found to be normal.

These experiments establish that MD in rats produces slight ultrastructural changes and decreases the number of synapses in CA1 and CA3 subregions of the hippocampus.