Substance P Immunoreactivity Increases Following Human Traumatic Brain Injury
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. Wheth
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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
R. Vink (*), P.C. Blumbergs Discipline of Pathology, School of Medical Sciences, University of Adelaide, Adelaide, SA 5005, Australia and Hanson Institute Center for Neurological Diseases, Institute of Medical and Veterinary Sciences, Adelaide, SA 5000, Australia e-mail: [email protected] A.C. Zacest Disciplines of Pathology, University of Adelaide, South Australia 5005, Australia J. Manavis Hanson Institute Centre for Neurological Diseases, Institute of Medical and Veterinary Sciences, Adelaide, SA 5000, Australia G.T. Sarvestani Division of Haematology, Institute of Medical and Veterinary Sciences, Adelaide, SA 5000, Australia
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
Introduction A number of studies have now demonstrated that much of the mortality and morbidity in survivors following traumatic brain injury (TBI) is associated with the development of a secondary injury cascade that occurs between hours and days after the insult (23). While a number of factors have been identified as participating in this secondary injury, it has been recognised that edema formation is a critical determinant of outcome after TBI. Our recent experimental studies have shown that neurogenic inflammation may play an important role in edema formation following CNS insults (9,21,26). Neurogenic inflammation is a neurally elicited reaction that has typical characteristics of an inflammatory reaction including vasodilation, protei
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