Brain Edema XIV pp 211-216

Substance P Immunoreactivity Increases Following Human Traumatic Brain Injury

  • Andrew C. Zacest
  • Robert Vink
  • Jim Manavis
  • Ghafar T. Sarvestani
  • Peter C. Blumbergs
Conference paper

DOI: 10.1007/978-3-211-98811-4_39

Volume 106 of the book series Acta Neurochirurgica Supplementum (NEUROCHIRURGICA)
Cite this paper as:
Zacest A.C., Vink R., Manavis J., Sarvestani G.T., Blumbergs P.C. (2010) Substance P Immunoreactivity Increases Following Human Traumatic Brain Injury. In: Czernicki Z., Baethmann A., Ito U., Katayama Y., Kuroiwa T., Mendelow D. (eds) Brain Edema XIV. Acta Neurochirurgica Supplementum, vol 106. Springer, Vienna

Abstract

Recent experimental evidence suggests that neuropeptides, and in particular substance P (SP), are released following traumatic brain injury (TBI) and may play a significant role in the aetiology of cerebral edema and increased intracranial pressure. Whether SP may play a similar role in clinical TBI remains unknown and was investigated in the current study. Archival post-mortem material was selected from patients who had sustained TBI, had died and had undergone post-mortem and detailed neuropathological examination (n = 13). A second cohort of patients who had died, but who showed no neuropathological abnormality (n = 10), served as case controls. Changes in SP immunoreactivity were examined in the cerebral cortex directly beneath the subdural haematoma in 7 TBI cases and in proximity to contusions in the other 6 cases. Increased SP perivascular immunoreactivity was observed after TBI in 10/13 cases, cortical neurones in 12/13 and astrocytes in 10/13 cases. Perivascular axonal injury was observed by amyloid precursor protein (APP) immunoreactivity in 6/13 TBI cases. Co-localization of SP and APP in a small subset of perivascular fibres suggests perivascular axonal injury could be a mechanism of release of this neuropeptide. The abundance of SP fibres around the human cerebral microvasculature, particularly post capillary venules, together with the changes observed following TBI in perivascular axons, cortical neurones and astrocytes suggest a potentially important role for substance P in neurogenic inflammation following human TBI.

Keywords

Neurotraumaedemabrain swellingneurogenic inflammationtachykininsubstance P

Copyright information

© Springer-Verlag/Wien 2010

Authors and Affiliations

  • Andrew C. Zacest
    • 3
  • Robert Vink
    • 1
    • 2
  • Jim Manavis
    • 2
  • Ghafar T. Sarvestani
    • 4
  • Peter C. Blumbergs
    • 1
    • 2
  1. 1.Discipline of Pathology, School of Medical SciencesUniversity of AdelaideAdelaideAustralia
  2. 2.Hanson Institute Centre for Neurological Diseases, Institute of Medical and Veterinary SciencesAdelaideAustralia
  3. 3.Disciplines of PathologyUniversity of AdelaideAdelaideAustralia
  4. 4.Division of HaematologyInstitute of Medical and Veterinary SciencesAdelaideAustralia