Objectives: To ascertain the levels of trauma from an acceleration-decelera
tion event which would expose a person to brain trauma, and to suggest clin
ical guidelines to the evaluation of injury outcomes which would indicate s
ignificant brain trauma was a potential sequelae.
Methods: The brain-injury literature that related to clinical, psychologica
l, biomechanical, and imaging studies was reviewed and compared for correla
tion to injury outcomes.
Results: The severity of cranio-cervical tissue damage is clearly correlate
d to the degree of acceleration-deceleration trauma exposure. The size of a
brain lesion is in a direct correlation to the duration and depth of uncon
sciousness, and the duration of post-traumatic amnesia. The acceleration-de
celeration mechanism of injury would expose the prefrontal, frontal, or tem
poral cortex to diffuse axonal injury. These brain regions are crucial for
complex attentional functioning. Indicators of trauma severity [loss of con
sciousness] are correlated to both clinical [cognitive impairment] and neur
o-imaging findings [PET]. Presumed head-neck trauma that leads to an uncons
cious period of less than 10 minutes, or an amnesia period that spans less
than four hours [a minor concussion] is not likely to cause any lasting bra
in damage or dysfunctional mental sequelae based on brain trauma. If these
relationships cannot be established, factors other than brain damage [pain,
adverse effect of medication, alcohol, psychological-personality problems,
other agendas] should be considered the basis of complaints following cran
io-cervical acceleration-deceleration trauma.
Conclusions: Minor trauma exposure without a significant unconscious period
, including amnesia, is very unlikely to have caused diffuse axonal injury,
nor brain trauma.