Citation

MacFarlane MP, Glenn TC. Brain Inj. 2015; 29(2): 139-153.

Affiliation

UCLA Cerebral Blood Flow Laboratory , Los Angeles, CA , USA and.

Copyright

(Copyright © 2015, Informa - Taylor and Francis Group)

DOI

10.3109/02699052.2014.965208

PMID

25587743

Abstract

Primary objective: The aim of this literature review was to systematically describe the sequential metabolic changes that occur following concussive injury, as well as identify and characterize the major concepts associated with the neurochemical cascade. Research design: Narrative literature review.

CONCLUSIONS: Concussive injury initiates a complex cascade of pathophysiological changes that include hyper-acute ionic flux, indiscriminant excitatory neurotransmitter release, acute hyperglycolysis and sub-acute metabolic depression. Additionally, these metabolic changes can subsequently lead to impaired neurotransmission, alternate fuel usage and modifications in synaptic plasticity and protein expression. The combination of these metabolic alterations has been proposed to cause the transient and prolonged neurological deficits that typically characterize concussion. Consequently, understanding the implications of the neurochemical cascade may lead to treatment and return-to-play guidelines that can minimize the chronic effects of concussive injury.

Language: en