Abstract
Diffuse axonal injury (DAI) leads to disconnection of various brain regions, a condition which translates into much of the morbidity seen with head injury [1–3, 7, 8]. Following spinal cord injury (Table 2), damage to major white matter tracts disrupts sensory and motor circuits. Moderate hypothermia has recently been reported to reduce axonal injury after experimental traumatic brain injury (TBI) [4,5]. Marion and White [5] first reported that posttraumatic hypothermia delayed up to 24 min after cortical impact injury significantly decreased the frequency of immunoreactive damaged axons. Using an impact acceleration rat model, Koizumi and Povlishock [4] reported that postinjury hypothermia delayed for 1h (32°C/1h) reduced beta-amyloid precursor protein (beta-APP) damaged axons at 24h compared to non-treated controls. Reduced axonal swelling and abnormal beta-APP immunoreactivity was also reported with hypoth ermia treatment after severe spinal cord compression [10].
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© 2004 Springer Japan
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Hayashi, N., Dietrich, D.W. (2004). Traumatic Axonal Injury. In: Brain Hypothermia Treatment. Springer, Tokyo. https://doi.org/10.1007/978-4-431-53953-7_6
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DOI: https://doi.org/10.1007/978-4-431-53953-7_6
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