The motor vehicle collision injury syndrome.
OBJECTIVE
The objective of this study was to examine the central nervous system changes that may occur after acceleration/deceleration injuries in motor vehicle accidents.


BACKGROUND
Occupants of motor vehicles involved in a collision often develop a disabling syndrome consisting of head, neck, and back pain; impaired short-term memory and concentration; fatigue and a loss of stamina; poor balance; and a change in personality. Injury victims experience a loss of motivation, emotional lability, and a decrease in libido. The major features of this injury syndrome are subjective, and there usually are few objective findings on physical examination. The pathogenesis of this syndrome is poorly understood, but it is hypothesized that the collision impact produces an inertial strain injury to the anterior regions of the brain which depresses the functions of the frontotemporal lobes, at the same time, sensitizing somatosensory neural afferent systems. Damage to the orbital surfaces of the frontotemporal lobes, in particular, impairs the gating mechanisms that normally limit sensory input to the brain and further promotes central sensitization. The psychiatric disorders that emerge in the wake of these injuries are likely grounded in these pathologic events.


METHODS
The current literature on the biomechanics of head injury and the associated brain imaging findings in minor head injury are reviewed. A summary of some of the biochemical sequelae of strain injury to the brain is also provided, with an emphasis on the changes in energy metabolism and excitatory amino acid release.


CONCLUSIONS
Early intervention to arrest the injury-induced metabolic cascade, and treatment with agents that activate cerebral metabolism may mitigate the symptoms of this injury syndrome.
Mamelak
M
M
Department of Psychiatry, University of Toronto, and Baycrest Centre for Geriatric Care, Ontario, Canada.
D000063:Accidents, Traffic; D000818:Animals; D001696:Biomechanical Phenomena; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D001930:Brain Injuries / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D006259:Craniocerebral Trauma / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D004195:Disease Models, Animal; D004734:Energy Metabolism; D005625:Frontal Lobe / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D001523:Mental Disorders / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D019838:Neck Injuries / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D013313:Stress Disorders, Post-Traumatic / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D013577:Syndrome; D014055:Tomography, Emission-Computed; D015899:Tomography, Emission-Computed, Single-Photon; D014947:Wounds and Injuries / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology