Chapter

Brain Edema XIV

Volume 106 of the series Acta Neurochirurgica Supplementum pp 211-216

Date:

Substance P Immunoreactivity Increases Following Human Traumatic Brain Injury

  • Andrew C. ZacestAffiliated withDisciplines of Pathology, University of Adelaide
  • , Robert VinkAffiliated withDiscipline of Pathology, School of Medical Sciences, University of AdelaideHanson Institute Centre for Neurological Diseases, Institute of Medical and Veterinary Sciences Email author 
  • , Jim ManavisAffiliated withHanson Institute Centre for Neurological Diseases, Institute of Medical and Veterinary Sciences
  • , Ghafar T. SarvestaniAffiliated withDivision of Haematology, Institute of Medical and Veterinary Sciences
  • , Peter C. BlumbergsAffiliated withDiscipline of Pathology, School of Medical Sciences, University of AdelaideHanson Institute Centre for Neurological Diseases, Institute of Medical and Veterinary Sciences

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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

Neurotrauma edema brain swelling neurogenic inflammation tachykinin substance P