This issue has never come up in the CICM exam, perhaps because it is the least serious form of traumatic brain injury. However, it comes up in discussion. Specifically, it is important to be able to use this word correctly, knowing precisely what it means, and being able to descend smoothly into academic gibberish (commotio cerebri, etc.) if asked to elaborate.

The majority of the information gathered below comes from the massively authoritative Consensus statement on Concussion in Sport (The 4th International Conference on Concussion in Sport held in Zurich, November 2012). Exploration of this document requires some genuine interest in mild head injury. If one were much less interested, one would be well served by the concise treatment offered to this topic by the LITFL Clinical Case on Minor Head Injury.

In brief:

A more interesting and ICU-worthy question is "why do head-injured patients become unconscious?" Quite apart from parenchymal damage, which should cause focal deficits only, there are some mechanisms at work here which disrupt consciousness on a grand global scale. These mechanisms (or the limitations of our understanding thereof) are discussed in a nice 2010 review article by Blyth and Bazarian. This article, in turn, references an older article by Nigel Shaw, which is also available as full-text.

In short, the affected region must be either both cerebral hemispheres or the brainstem reticular activating system. Four major theories exist, none of which are perfect, but among which the convulsive theory is the most satisfying, as it is supported by the strongest evidence.

The Reticular Hypothesis

• Supposedly, shear or rotational forces acting on the brainstem somehow disturb the polysynaptic pathways of the reticular activating system, and result in a global "inactivation" of consciousness.
• However:
  • This does not explain post-traumatic amnesia.
  • EEG does not demonstrate depression of the reticular activating system.

The Pontine-Cholinergic Hypothesis

• Reticular activating system dysfunction is thought to occur as a consequence of trauma-induced activation of the inhibitory cholinergic system of the dorsal pontine tegmentum.
• Certainly, unconsciousness of the household cat can be achieved by the injection of cholinergic drugs into the dorsal pontine tegmentum.
• Also, elevated acetylcholine is found in the CSF of patients after TBI.
• However:
  • Exactly how this is triggered by head trauma is unclear.

The Centripetal Hypothesis

• Supposedly, sudden rotational forces cause shearing strains and stresses that result in functional decoupling of nerve fibers.
• Thus, the greater the rotational forces, the greater the injury, and the more profound the neurodeficit. That would explain the association of milt head trauma with mild deficits and amnesia rather than coma.
• However:
  • This theory requires high energy injuries to generate coma, and they frequently do not.
  • To reverse the logic, patients who lose consciousness should have more structural brain damage, and they frequently do not.

The Convulsive Hypothesis

• Post-ictal patients have a decreased level of consciousness.
• EEG findings of concussed animals demonstrate initial transient epileptiform activity.
• Ergo, symptoms associated with concussion are due to direct injury to neurons resulting in hyperexcitability and widespread membrane depolarization followed by neuronal exhaustion.
• This neuronal exhaustion may account for the amnesia and "foggy thinking" of the post-concussive syndrome.
• Shaw (2002) viewed this to be the most plausible theory for the neurophysiological mechanisms of concussion 
• However:
  • Structural abnormalities are observed in the brains of concussed patients, but not in the brains of post-ictal patients.