Journal of neurotrauma
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Journal of neurotrauma · Feb 2003
Post-acute alterations in the axonal cytoskeleton after traumatic axonal injury.
All previous analyses of axonal responses to traumatic axonal injury (TAI) have described the ultrastructure of changes in the cytoskeleton and axolemma within 6 h of injury. In the present study we tested the hypothesis that there are, in addition, ultrastructural pathological changes up to 1 week after injury. TAI was induced in the adult guinea pig optic nerve of nine animals. ⋯ Quantitative analysis of the number or proportion of axons within 0.5-micro m-wide bins showed an increase in the number of axons with a diameter of less than 0.5 micro m at 4 h, 24 h, and 7 d, the presence of lucent axons at 24 h and 7 d and that the highest number of injured axons occurred about half way along the length of the nerve. A spectrum of pathological changes occurred in injured fibers-pathology of mitochondria; dissociation of myelin lamellae but little damage to the axon; loss of linear register of the axonal cytoskeleton; differential responses between microtubules (MT) and neurofilaments (NF) in different sizes of axon; two different sites of compaction of NF; loss of both NF (with an increase in their spacing) and MT (with a reduction in their spacing); replacement of the axoplasm by a flocculent precipitate; and an increased length of the nodal gap. These provide the first ultrastructural evidence for Wallerian degeneration of nerve fibers in an animal model of TAI.
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Journal of neurotrauma · Jan 2003
Noninvasive cerebrovascular autoregulation assessment in traumatic brain injury: validation and utility.
A moving correlation index (Mx-CPP) of cerebral perfusion pressure (CPP) and mean middle cerebral artery blood flow velocity (CBFV) allows continuous monitoring of dynamic cerebral autoregulation (CA) in patients with severe traumatic brain injury (TBI). In this study we validated Mx-CPP for TBI, examined its prognostic relevance, and assessed its relationship with arterial blood pressure (ABP), CPP, intracranial pressure (ICP), and CBFV. We tested whether using ABP instead of CPP for Mx calculation (Mx-ABP) produces similar results. ⋯ This index is also valid if ABP is used instead of CPP, which eliminates the need for invasive ICP measurements for CA assessment. An unfavorable outcome is associated with early CA failure. Further studies using the Mx-ABP will reveal whether CA improves along with patients' clinical improvement.
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Journal of neurotrauma · Dec 2002
Comparative StudyNeutralizing intraspinal nerve growth factor with a trkA-IgG fusion protein blocks the development of autonomic dysreflexia in a clip-compression model of spinal cord injury.
Increased intraspinal nerve growth factor (NGF) after spinal cord injury (SCI) is detrimental to the autonomic nervous system. Autonomic dysreflexia is a debilitating condition characterized by episodic hypertension, intense headache, and sweating. Experimentally, it is associated with aberrant primary afferent sprouting in the dorsal horn that is nerve growth factor (NGF)-dependent. ⋯ Likewise, the MAP response to cutaneous stimulation was also reduced in rats treated with trkA-IgG (20 +/- 1 vs. 29 +/- 2). In contrast, trkA-IgG treatment had no effect on heart rate responses during colon distension or cutaneous stimulation. These results indicate that treatment with trkA-IgG to block NGF suppresses the development of autonomic dysreflexia after a clinically relevant spinal cord injury.
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Journal of neurotrauma · Dec 2002
Comparative StudyTemporal and spatial profile of phosphorylated mitogen-activated protein kinase pathways after lateral fluid percussion injury in the cortex of the rat brain.
Mitogen-activated protein kinases (MAPK) play a crucial role in signal transduction that regulates gene expression through transcriptional factor activity. The purpose of this study was to investigate the temporal expression and topographic distribution of the activated MAPK pathways including extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), and p38 MAPK following traumatic brain injury (TBI) in the cortex of the rat brain. Adult male Sprague-Dawley rats (300-400 g) were subjected to lateral fluid percussion injury of moderate severity (3.5-4.0 atm) using the Dragonfly device model (no. ⋯ The immunoreactivity for p-ERK was confirmed up until 30 min after TBI in the superficial neuronal layers. Double immunostaining using a glial-specific marker demonstrated that p-ERK was prominent in astrocytes 6 h after TBI. The current results suggest that the ERK and JNK pathways, but not the p38 MAPK pathways are involved in signal transduction in the cortex following TBI.
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Journal of neurotrauma · Dec 2002
Comparative StudyAlcohol consumption in traumatic brain injury: attenuation of TBI-induced hyperthermia and neurocognitive deficits.
Clinical and animal studies indicate that hyperthermia during or after traumatic brain injury (TBI) is associated with poor outcome. Alcohol intoxication, a complicating risk factor in many cases of head injury, has been found to both worsen or attenuate posttraumatic neural damage and outcome. The purpose of the present study was to determine whether chronic ethanol consumption would affect TBI-induced hyperthermia and deficits in spatial learning. ⋯ When tested at 3-4 weeks after TBI, E-E rats required significantly fewer trials than E-P rats to reach criterion in the Morris water maze. In sum, continuous consumption of ethanol before and after TBI attenuated TBI-induced hyperthermia and deficits in spatial learning. Whereas the results suggest that this ethanol regimen may be neuroprotective, a causal relationship between the two outcomes remains to be determined.