PMID- 18352834
OWN - NLM
STAT- MEDLINE
DCOM- 20080620
LR  - 20151119
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 25
IP  - 3
DP  - 2008 Mar
TI  - Traumatic axonal injury in the spinal cord evoked by traumatic brain injury.
PG  - 205-13
LID - 10.1089/neu.2007.0331 [doi]
AB  - Although it is well known that traumatic brain injury (TBI) evokes traumatic 
      axonal injury (TAI) within the brain, TBI-induced axonal damage in the spinal 
      cord (SC) has been less extensively investigated. Detection of such axonal injury 
      in the spinal cord would further the complexity of TBI while also challenging 
      some functional neurobehavioral endpoints frequently used to assess recovery in 
      various models of TBI. To assess TAI in the spinal cord associated with TBI, we 
      analyzed the craniocervical junction (CCJ), cervico-thoracic (CT), and 
      thoraco-lumber (ThL) spinal cord in a rodent model of impact acceleration of TBI 
      of varying severities. Rats were transcardially fixed with aldehydes at 2, 6, and 
      24 h post-injury (n = 36); each group included on sham-injured rodent. 
      Semi-serial vibratome sections were reacted with antibodies targeting TAI via 
      alteration in cytoskeletal integrity or impaired axonal transport. Consistent 
      with previous observations in this model, the CCJ contained numerous injured 
      axons. Immunoreactive, damaged axonal profiles were also detected as caudal, as 
      the ThL spinal cord displayed morphological characteristics entirely consistent 
      with those described in the brainstem and the CCJ. Quantitative analyses 
      demonstrated that the occurrence and extent of TAI is positively associated with 
      the impact/energy of injury and negatively with the distance from the brainstem. 
      These observations show that TBI can evoke TAI in regions remote from the injury 
      site, including the spinal cord itself. This finding is relevant to shaken baby 
      syndrome as well as during the analysis of data in functional recovery in various 
      models of TBI.
FAU - Czeiter, Endre
AU  - Czeiter E
AD  - Department of Neurosurgery, University of Pecs, Pecs, Hungary.
FAU - Pal, Jozsef
AU  - Pal J
FAU - Kovesdi, Erzsebet
AU  - Kovesdi E
FAU - Bukovics, Peter
AU  - Bukovics P
FAU - Luckl, Janos
AU  - Luckl J
FAU - Doczi, Tamas
AU  - Doczi T
FAU - Buki, Andras
AU  - Buki A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Biomarkers)
RN  - 0 (Cytoskeletal Proteins)
RN  - 0 (Nerve Tissue Proteins)
SB  - IM
MH  - Amyloid beta-Peptides/analysis/metabolism
MH  - Animals
MH  - Axons/*pathology
MH  - Biomarkers/analysis
MH  - Brain Injuries/complications/*physiopathology
MH  - Brain Stem/injuries/pathology/physiopathology
MH  - Cytoskeletal Proteins/analysis/metabolism
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Immunohistochemistry
MH  - Nerve Tissue Proteins/analysis/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Spinal Cord Injuries/etiology/*pathology/*physiopathology
MH  - Time Factors
MH  - Wallerian Degeneration/etiology/*pathology/*physiopathology
EDAT- 2008/03/21 09:00
MHDA- 2008/06/21 09:00
CRDT- 2008/03/21 09:00
PHST- 2008/03/21 09:00 [pubmed]
PHST- 2008/06/21 09:00 [medline]
PHST- 2008/03/21 09:00 [entrez]
AID - 10.1089/neu.2007.0331 [doi]
PST - ppublish
SO  - J Neurotrauma. 2008 Mar;25(3):205-13. doi: 10.1089/neu.2007.0331.