Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/61937
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Type: Journal article
Title: Substance P immunoreactivity increases following human traumatic brain injury
Author: Zacest, A.
Vink, R.
Manavis, J.
Sarvestani, G.
Blumbergs, P.
Citation: Acta Neurochirurgica. Supplementum, 2010; 106:211-216
Publisher: Springer-Verlag Wien
Issue Date: 2010
ISSN: 0065-1419
Statement of
Responsibility: 
Andrew C. Zacest, Robert Vink, Jim Manavis, Ghafar T. Sarvestani, and Peter C. Blumbergs
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
Rights: © Springer-Verlag/Wien 2010
RMID: 0020100120
DOI: 10.1007/978-3-211-98811-4_39
Appears in Collections:Pathology publications

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