1. ≈ 75% will exhibit an traumatic intracranial hematoma
a) may be present on initial evaluation and can then worsen
b) may develop in a delayed fashion
delayed epidural hematoma (EDH)
delayed subdural hematoma (SDH)
delayed traumatic contusions
Posttraumatic diffuse cerebral edema
Hypoxia: etiologies include pneumothorax, MI, CHF…
Hypoglycemia: including insulin reaction
Drug or alcohol withdrawal
Carotid artery dissection (or rarely, vertebral)
Cerebral embolism: including fat embolism syndrome
Harris et al, suggest a link between head injury and Parkinson's disease and indicates further scrutiny of workplace incurred head injuries is warranted 1).
Olfactory loss due to head trauma is a frequent finding. It is attributed to the tearing or severing of the olfactory fibers at the cribriform plate. In contrast, posttraumatic gustatory loss is observed and reported rarely and the underlying mechanism is less understood. Rahban et al. present a case of a concomitant post-traumatic anosmia and ageusia. Imaging showed a considerable frontobasal brain damage and it is speculated that the gustatory impairment is due to a central injury of the secondary taste cortex. Based on this observation, Rahban et al.we believe that this clinical presentation might be much more frequent than previously reported 4).
Autonomic impairment after acute traumatic brain injury has been associated independently with both increased morbidity and mortality. Links between autonomic impairment and increased intracranial pressure or impaired cerebral autoregulation have been described as well. However, relationships between autonomic impairment, intracranial pressure, impaired cerebral autoregulation, and outcome remain poorly explored.