The neuroprotective effects of Riluzole, a compound with several mechanisms of action including the inhibition of sodium channel activity and glutamate release, were evaluated in a rat model of parasagittal fluid-percussion (FP) brain injury. Male Sprague-Dawley rats (350-400 g, n β«Ψβ¬ 17) were anest
Loss of hypocretin (orexin) neurons with traumatic brain injury
β Scribed by Christian R. Baumann; Claudio L. Bassetti; Philipp O. Valko; Johannes Haybaeck; Morten Keller; Erika Clark; Reto Stocker; Markus Tolnay; Thomas E. Scammell
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 430 KB
- Volume
- 66
- Category
- Article
- ISSN
- 0364-5134
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β¦ Synopsis
Abstract
Chronic, daytime sleepiness is a major, disabling symptom for many patients with traumatic brain injury (TBI), but thus far, its etiology is not well understood. Extensive loss of the hypothalamic neurons that produce the wakeβpromoting neuropeptide hypocretin (orexin) causes the severe sleepiness of narcolepsy, and partial loss of these cells may contribute to the sleepiness of Parkinson disease and other disorders. We have found that the number of hypocretin neurons is significantly reduced in patients with severe TBI. This observation highlights the often overlooked hypothalamic injury in TBI and provides new insights into the causes of chronic sleepiness in patients with TBI. Ann Neurol 2009;66:555β559
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The factor structure of the WISC-R was examined in a sample of 108 children with traumatic brain injury. Principal factor analysis of 1 1 WISC-R subtests yielded three factors, which were subjected to varimax rotation. The rotated factor pattern suggested the existence of a Verbal Comprehension fact