All-terrain vehicle (ATV) use is increasingly popular among people of all ages. Although ATV use is known to cause significant morbidity due to head and neck trauma, there is a lack of published data detailing ATV-related fatalities. We examined all ATV-related fatalities in Ontario from 1996 - 2005 to determine the epidemiology and risk factors as a guide for improved injury prevention strategies.

All ATV-related fatalities from 1996 - 2005 in Ontario were examined through Coroner's reports in the Office of the Chief Coroner of Ontario. Epidemiologic information and risk factors relating to the driver, environment, and vehicle were recorded.

There were 74 ATV-related fatalities from 1996 - 2005. There was only one fatality per year in 1996 and 1997 and a peak of 16 per year in 2004 and 2005. Head and neck injuries were the commonest causes of death. Males comprised 90.5% of the cases. The highest risk was from age 15 - 29, and 21% of fatalities occurred in children under 16. Northeastern Ontario had the highest fatality rate.

There was a major increase in the incidence of ATV-related fatalities in Ontario from 1996 - 2005 with the majority due to head trauma. Notable risk factors included alcohol use, riding at night, lack of helmet use, and excessive speed. We recommend the adoption of laws that focus on helmet requirements, a minimum driver age of 16, and certified training courses. Aggressive injury prevention efforts should be targeted toward males aged 15 - 29.

There is currently little information on the genetic epidemiology of Alzheimer disease (AD) among North American Aboriginal populations. No cases of familialAD (FAD) in these populations have been published to date.

Here, we describe a large North American Aboriginal kindred with early onset FAD (EOFAD) in which genetic testing was done.

A novel Presenilin 1 (PS1) gene mutation (L250F) has been identified. In contrast to the three previously reported families with PS1 codon 250 mutations, affected members of this kindred demonstrate neither myoclonus nor seizures. Furthermore, the identification of a PS1 mutation in a North American Aboriginal kindred presents several unique challenges with respect to knowledge transfer and continuity of care in a geographically remote and culturally distinct community.

Growing evidence shows that the deregulation of the circadian clock plays an important role in the development of malignant tumors, including gliomas. However, the molecular mechanisms of genes controlling circadian rhythm in glioma cells have not been explored.

Using reverse transcription polymerase chain reaction and immunohistochemistry techniques, we examined the expression of two important clock genes, Per1 and Per2, in 33 gliomas.

In this study, out of 33 gliomas, 28 were Per1-positive, and 23 were Per2-positive. The expression levels of Per1 and Per2 in glioma cells were significantly different from the surrounding non-glioma cells (P<0.01). The difference in the expression rate of Per1 and Per2 in high-grade (grade III and IV) and low-grade (grade 1 and II) gliomas was insignificant (P>0.05). While there was no difference in the intensity of immunoactivity for Per2 between high-grade gliomas and low-grade gliomas (r=-0.330, P=0.061), the expression level of Per1 in highgrade gliomas was significantly lower than that in low-grade gliomas(r=-0.433, P=0.012).

In this study, we found that the expression of Per1 and Per2 in glioma cells was much lower than in the surrounding non-glioma cells. Therefore, we suggest that disturbances in Per1 and Per2 expression may result in the disruption of the control of normal circadian rhythm, thus benefiting the survival of glioma cells. Differential expression of circadian clock genes in glioma and non-glioma cells may provide a molecular basis for the chemotherapy of gliomas.

Central nervous system (CNS) involvement is a common and less understood aspect of systemic lupus erythematosus (SLE). Microembolic signals (MES) have been reported in SLE. We conducted a prospective study to evaluate the frequency of MES among patients with CNS involvement and those without. The main aim of the study is to clarify the pathophysiology of the CNS involvement in SLE.

Sixty eight patients with a diagnosis of SLE (60 females, 8 males) participated in the study. Both middle cerebral arteries were monitored using transcranial Doppler for 60 min to detect MES. All cases underwent neurology and psychiatry assessments.

MES were detected in 7/68 patients (10.3%) with the mean number of 3.5 per hour. MES were significantly higher in patients with CNS involvement (6/24, 25%) than those without (1/44, 2.2%) (P=0.006). SLE disease activity index, duration of disease, plaque formation, intima-media thickness, and antiphospholipid antibodies were not associated with MES. MES were more frequent in patients receiving Aspirin and/or Warfarin (p=0.02).

MES may be a predictor for CNS involvement in SLE patients at risk for neuropsychiatric syndromes. Cerebral embolism may be implicated in the pathophysiology of neuropsychiatric SLE.

The aim of this study was to evaluate efficacy and tolerability of levetiracetam (LEV) in patients with different epilepsy syndromes.

We evaluated epileptic patients seen in the previous 18 months, including all patients with present or past exposure to LEV. Tolerability of LEV therapy was evaluated in all patients; efficacy was evaluated only in patients who had received LEV for at least six months. Two hundred and two patients were included in the study. Patients were considered responsive when showing a > 50% reduction in seizures frequency and non-responders when seizure frequency was unchanged, worsened or showed a reduction < 50%.

Thirty patients did not complete six months of LEV treatment and dropped out. 57.4% of the patients with uncontrolled seizures treated for at least six months were responders, with 27.7% seizure free. Adverse effects were observed in 46 patients (23%) and were responsible for early drop out in 26. Adverse effects occurred significantly more often in females than in males (30.6% vs 13.2%); moreover, nearly 30% of women with adverse effects complained of more than one adverse effect, while this was never observed in male patients.

Our study shows LEV as a well tolerated and effective treatment, both in monotherapy and as an add-on. Further investigations on larges samples are needed to investigate the issue of gender-related tolerability.

The course of multiple sclerosis may be slowed by use of the disease modifying drugs (DMDs): subcutaneous or intramuscular interferon beta-1a, interferon beta-1b, glatiramer acetate, and natalizumab. We set out to compare utilization of these drugs in the Canadian provinces from 2002-2007.

Using a retrospective cohort analysis, we reviewed population data from International Medical Statistics (IMS) Health between November 2001 and October 2007.

The total annual number of DMD prescriptions increased from 3.9, in 2002, to 5.1, in 2007, per 1,000 Canadians. The total annual cost of prescriptions rose from $187 million to $287 million. Of the four provinces responsible for the majority of prescriptions - Alberta, BC, Ontario, and Quebec - Quebec had the highest average annual prescription rate (7 per 1,000 population) and BC had the lowest rate (3.3 per 1,000 population). Subcutaneous interferon beta-1a was the most commonly used drug whereas glatiramer acetate showed the greatest growth in use from 2002 to 2007.

Disease modifying drugs prescription rates and costs increased by more than 30% between 2002 and 2007. There was wide variation in DMD prescription rates and relative drug preferences across the provinces.

The etiology of complex regional pain syndrome (CRPS) is unknown. Different environmental and genetic factors have been postulated to contribute to CRPS.

We reviewed the clinical data from a cohort of 69 patients with CRPS. Four families were identified with two or more members affected with CRPS yielding a total of nine patients. Six more patients reported the presence of pain symptoms in their family members, however; this could not be clinically confirmed.

The case histories of the nine individuals with ‘familial’ CRPS suggested a younger age at onset and more frequent history of migraine versus the non-familial patients. A pattern of inheritance could not be ascertained.

This data supports the hypothesis that CRPS can be familial and hence may have a genetic basis in some families. Larger studies will be needed to ascertain clearer patterns of inheritance and to determine whether the clinical features of ‘familial’ CRPS are the same as the sporadic form.