Study Design: A 6 year retrospective study was conducted. Objectives: The populations at risk for spinal cord injury (SCI) in the northwestern Kentucky (KY) and southern Indiana (IN) regions were identi®ed following examination of the causes and factors associated with SCI. Setting: The database included patients primarily from the surrounding KY and IN counties admitted to the University of Louisville (U of L) Hospital. Method: Speci®cation of SCI patient demographics, injury causes and related factors was achieved utilizing the hospital's trauma institute database and an extensive review of patient medical records. Results: An adjusted average incidence rate of 27.1 cases per million per year was obtained for this region. A high rate of SCI was found for the youngest age group, 14 ± 24 year olds, and for African Americans. A high frequency of injuries was also observed for adults between the ages of 25 ± 39 years. Motor vehicle accidents (MVA) were the leading cause of SCI. Contributing factors included alcohol and widespread non-use of vehicle safety precautions. Conclusions: In addition to the high proportion of youth at risk for SCI, a higher proportion of older adults with SCI was observed for this region compared to other studies. Because the primary source of transportation in this area is the use of private vehicles, rather than public transportation, greater eort is warranted in emphasizing the potential risks of combining driving with alcohol consumption and non-use of seatbelts. Spinal Cord (2001) 39, 274 ± 278

There is evidence that posttraumatic ischemia is important in the pathogenesis of acute spinal cord injury (SCI). In the present study spinal cord blood flow (SCBF), measured by the hydrogen clearance technique, and motor and somatosensory evoked potentials (MEP and SSEP) were recorded to evaluate whether the administration of nimodipine and dextran 40, alone or in combination, could increase posttraumatic SCBF and improve axonal function in the cord after acute SCI. Thirty rats received a 53-gm clip compression injury on the cord at T-1 and were then randomly and blindly allocated to one of six treatment groups (five rats in each). Each group was given an intravenous infusion of one of the following over 1 hour, commencing 1 hour after SCI: placebo and saline; placebo and dextran 40; nimodipine 0.02 mg/kg and saline; nimodipine 0.02 mg/kg and dextran 40; nimodipine 0.05 mg/kg and saline; and nimodipine 0.05 mg/kg and dextran 40. The preinjury physiological parameters, including the SCBF at T-1 (mean +/- standard error of the mean: 56.84 +/- 4.51 ml/100 gm/min), were not significantly different (p greater than 0.05) among the treatment groups. Following SCI, there was a significant decrease in the SCBF at T-1 (24.55 +/- 2.99 ml/100 gm/min; p less than 0.0001) as well as significant changes in the MEP recorded from the spinal cord (MEP-C) (p less than 0.0001), the MEP recorded from the sciatic nerve (MEP-N) (p less than 0.0001), and the SSEP (p less than 0.002). Only the combination of nimodipine 0.02 mg/kg and dextran 40 increased the SCBF at T-1 (43.69 +/- 6.09 ml/100 gm/min; p less than 0.003) and improved the MEP-C (p less than 0.0001), MEP-N (p less than 0.04), and SSEP (p less than 0.002) following SCI. With this combination, the changes in SCBF were significantly related to improvement in axonal function in the motor tracts (p less than 0.0001) and somatosensory tracts (p less than 0.0001) of the cord. This study provides quantitative evidence that an increase in posttraumatic SCBF can significantly improve the function of injured spinal cord axons, and strongly implicates posttraumatic ischemia in the pathogenesis of acute SCI.

The human auditory steady state evoked potentials were recorded during all-night sleep in 10 subjects. The effects of stimulus rate and intensity on these potentials were measured using on-line Fourier analysis. The amplitude of the response was greatest at stimulus rates of 30 to 50/sec. Although the response amplitude was lower during sleep, the rate at which the amplitude was greatest did not change between sleep and wakefulness. As the intensity was increased above threshold, the amplitude of the response increased linearly. The responses recorded during wakefulness showed a larger amplitude change with increasing intensity than during sleep. The estimated thresholds for the responses, however, did not differ significantly between wakefulness and sleep.