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Using data from the Alberta Health Care Insurance Plan, the prevalence of motor neurone disease (MND) was estimated for the Province of Alberta, Canada. Between January 1, 1994 and December 31, 1995, 208 cases of MND (125 males, 83 females) were identified from physician billing records giving a period prevalence of 7.38 (8.9 for males, 5.9 for females) per 100,000 population. On prevalence day, July 1, 1995, there were 171 cases (103 males, 68 females) of MND giving a point prevalence estimate of 6.07 (7.3 for males, 4.8 for females) per 100,000 population. Males were more likely to be diagnosed (OR = 1.52, 95% CI 1.1, 2.1) with MND and there was an increased risk of receiving a diagnosis with increasing age (chi 2trend = 281, p < 0.001). The mean age of the cases was 59.2 years (58.5 for males, 60.3 for females) and did not differ significantly between the sexes. Geographically, there was no statistically significant difference in the prevalence across regions of the Province. During the study period, 28% of the cases had died (30% of males, 25% of females). The prevalence of MND in Alberta, is among the highest reported in the literature and requires additional investigation to verify these estimates and identify possible causative factors.

An in vitro model of muscle damage was used to investigate the protective effect of mild hypothermia in muscle injury. Rat epitrochlearis muscles were dissected in their entirety and suspended in Krebs-Ringer solution and DNP, a mitochondrial uncoupler, was added. PGE2 and lactate release and the contractile response to stimulation were measured and compared to untreated controls. Experiments were done at 37, 35, 33 and 27 degrees C. At 37 degrees C, DNP stimulated muscle releases large amounts of PGE2 and lactate and is unable to contract. As the temperature is reduced, there is progressive preservation of contractile force, although high lactate levels at the lowest temperatures indicate that the metabolic stress is still present. In contrast, DNP stimulated PGE2 release is completely inhibited at or below 35 degrees C and may be related to a similar protective phenomenon seen in experimental ischemic neuronal death.