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We evaluated by in situ nick end labeling the presence of apoptotic glial cells in the spinal cord of rats which have sustained a moderate and severe compression injury at the level of T8-9, resulting in a severe but reversible paraparesis and irreversible paraplegia, respectively. In a previous investigation we found apoptotic glial cells (oligodendrocytes) in the immediate vicinity of the primary lesion (T7 and T10). The present study was designed to evaluate the extent of such cells in the spinal cord even at long distances away from the primary injury. Rats sustaining a moderate and severe compression injury and surviving 4 and 9 days showed a significant increase in the number of apoptotic glial cells at the T1, T5, T7, T12 and L2 levels. At the T10 level the elevation was significant only after day 9. There was no significant increase in the number of these cells at 4 h and 1 day after moderate and severe compression. In general, the apoptotic cells were most often seen in segments adjacent to the compression. They were randomly located in the ventral, lateral and dorsal tracts but were rarely present in the gray matter of the cord. In conclusion, compression trauma to rat spinal cord induces signs of apoptosis in glial cells, presumably oligodendrocytes of the long tracts. This newly discovered type of secondary injury is widely distributed in the damaged spinal cord and occurs even at long distances remote from the initial compression injury. Apoptotic cell death of oligodendrocytes will induce myelin degeneration and cause additional disturbances of axonal function. This cell damage may be a target for future therapy since it occurs after a delay and chemical compounds are now available by which apoptotic cell death can be modified.

The purpose of this study was to develop a spinal cord injury model in the mouse. Various degrees of extradural compression were used to induce mild, moderate or severe compression injuries. Furthermore, a locomotor rating scale was developed by which the functional outcome of the spinal cord injury could be assessed. The introduction of such a model will be useful for further studies on the pathogenesis and treatment strategies of spinal cord injury. To assess hindlimb motor function, a 10-point scale was used. Initially, the animals were allowed to move freely in an open field and were rated 0-5, 0 being no movement and 5 being almost normal. Animals scoring a 5 were then assessed using steel bars with decreasing widths from 2 cm to 5 mm. For each bar successfully crossed over, they gained additional points. Before injury the hindlimb motor function score (MFS) in all the animals was 10. In mice with mild compression, MFS was decreased slightly on day 1 and recovered to 9 +/- 0.6 on day 14. For mice with moderate compression, the MFS decreased to 4.6 +/- 0.4 on day 1 after injury and gradually improved to 8.1 +/- 0.6 on day 14. Severe injury resulted in paraplegia of the hindlimbs day 1 after injury with a score of 0.6 +/- 0.2. By day 14 after injury, these animals gradually recovered to 3.9 +/- 0.1, could bear the weight on the hindlimbs and walk with a severe deficit. There was a 3%, 9% and 19% decrease in the total cross-sectional area of the spinal cord 14 days after mild, moderate and severe injury, respectively. Microtubule-associated protein immunostaining revealed that the gray matter decreased to 61 +/- 7% in moderately injured animals, while severe compression resulted in a complete loss of gray matter. White matter decreased to 86 +/- 6% in moderately injured animals and 29 +/- 11% in severely injured animals. This study shows that the mouse can be used to achieve reproducible spinal cord compression injuries of various degrees of severity. The force of the impact correlates well with the neurological and light microscopic outcome. The motor function test presented in this paper and the computerized quantification of tissue damage can be used to evaluate the efficacy of different treatment strategies.

Study design: In order to study the role of gender in recovery, we induced a thoracic compression spinal cord injury (SCI) separately in 2-month-old male and female C57Bl/6 mice. Objectives: We intended to assess effects of gender on recovery of hindlimb motor function and to correlate these with histomorphologic profiles of injured spinal cord tissue. Methods: Locomotor function was evaluated by three means: a modified locomotor scoring system for rodents, beam walking and computerized activity meter. Histology was analyzed by comparison of hematoxylin and eosin-stained perfused specimens. Results: Locomotor scores were 2.270.9 on day 1 in male mice, while, in contrast, they were significantly higher, 7.371.7, in females (Po0.02). On day 14 Basso, Beattie and Bresnahan scores were 9.572.2 in male mice and 16.072.2 in females (Po0.03). Terminal histology showed that the spinal cord architecture was relatively better preserved in female mice and that the extent of necrosis and infiltration of inflammatory cells was less compared to males. Setting: Neurobiology Research Laboratory of University of Kansas Medical School in US Department of Veterans Affairs Medical Center, Kansas City, Missouri. Conclusion: We found that the severity of the initial injury as well as the ultimate recovery of motor function after SCI is significantly influenced by gender, being remarkably better in females. The mechanism(s) of neuroprotection in females, although not yet elucidated, may be associated with the effects of estrogen on pathophysiological processes (blood flow, leukocyte migration inhibition, antioxidant properties, and inhibition of apoptosis).

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Study design: It is well known that changes of the body temperature as well as trauma in¯uence the blood¯ow in the brain and spinal cord. However, there is still a lack of knowledge concerning the levels of blood¯ow changes, especially during hypothermia. Objectives: This investigation was carried out to examine the e ects of systemic hypothermia and trauma on spinal cord blood¯ow (SCBF). Methods: Twenty-four rats were randomized either to thoracic laminectomy only (Th VII ± IX) or to 35 g spinal cord compression trauma. The animals were further randomized to either constant normothermia (388C) or to a systemic cooling procedure, ie reduction of the esophageal temperature from 38 to 308C. SCBF was recorded 5 mm caudal to the injury zone using Laser-Doppler¯owmetry which allows a non-invasive continuous recording of local changes in the blood¯ow. The autoregulation ability was tested at the end of the experiments by inducing a 30 ± 50 mmHg blood-pressure fall, using blood-withdrawal from the carotid artery. Results: The mean SCBF decreased 2.8% and 3.5% per centigrade reduction of esophageal temperature in the animals sustained to hypothermia with and without trauma, respectively. This could be compared to a decrease of 0.2%/min when only trauma was applied. No signi®cant di erences were seen between the groups concerning auto regulatory ability. Conclusions: Our results indicate that the core temperature has a high impact on the SCBF independent of previous trauma recorded by Laser-Doppler¯owmetry. This in¯uence exceeds the response mediated by moderate compression trauma alone. Sponsorship: The study was supported by grants from the Laerdal foundation. Spinal Cord (2001) 39, 74 ± 84

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