Substance P Immunoreactivity Increases Following Human Traumatic Brain Injury (original) (raw)

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.

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Acknowledgment

Supported, in part, by the Motor Accident Comm-ission of SA.

Author information

Authors and Affiliations

  1. Discipline of Pathology, School of Medical Sciences, University of Adelaide, Adelaide, SA, 5005, Australia
    Robert Vink & Peter C. Blumbergs
  2. Hanson Institute Centre for Neurological Diseases, Institute of Medical and Veterinary Sciences, Adelaide, SA, 5000, Australia
    Robert Vink, Jim Manavis & Peter C. Blumbergs
  3. Disciplines of Pathology, University of Adelaide, Adelaide, South Australia, 5005, Australia
    Andrew C. Zacest
  4. Division of Haematology, Institute of Medical and Veterinary Sciences, Adelaide, SA, 5000, Australia
    Ghafar T. Sarvestani

Authors

  1. Andrew C. Zacest
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  2. Robert Vink
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  3. Jim Manavis
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  4. Ghafar T. Sarvestani
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  5. Peter C. Blumbergs
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Corresponding author

Correspondence toRobert Vink .

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Editors and Affiliations

  1. Medical Research Center, PAN Warszawa, Ceglowska St. 80, Warszawa, 01-809, Poland
    Zbigniew Czernicki
  2. Klinikum Großhadern, Universitätsklinikum München, Marchioninistr. 15, München, 81377, Germany
    Alexander Baethmann
  3. Dept. Neurosurgery, Musashino Red Cross Hospital, Kyonan-cho 1-26-1, Musashino City, Tokyo, 180, Japan
    Umeo Ito
  4. School of Medicine, Nihon University, Oyaguchikami-machi 30-1 , Tokyo, 173-8610, Japan
    Yoichi Katayama
  5. Dept. Neuropathology, Medical Research Institute, Yushima 1-5-45, Tokyo, 113-8510, Japan
    Toshihiko Kuroiwa
  6. Dept. Neurosurgery, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne, NE46BE, United Kingdom
    David Mendelow

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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. https://doi.org/10.1007/978-3-211-98811-4\_39

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