Traumatic brain injury resulting from an
explosive blast is one of the most serious
wounds suffered by warfighters, yet the effects of
explosive blast overpressure directly impacting the head are poorly understood. We developed a rodent model of direct cranial
blast injury (dcBI), in which a blast overpressure could be delivered exclusively to the head, precluding indirect
brain injury via thoracic transmission of the blast wave. We constructed and validated a Cranium Only
Blast Injury Apparatus (COBIA) to deliver blast overpressures generated by detonating .22 caliber cartridges of
smokeless powder. Blast waveforms generated by COBIA replicated those recorded within armored vehicles penetrated by munitions. Lethal dcBI (LD(50) ∼ 515 kPa) was associated with: (1) apparent brainstem failure, characterized by immediate opisthotonus and
apnea leading to
cardiac arrest that could not be overcome by
cardiopulmonary resuscitation; (2) widespread
subarachnoid hemorrhages without
cortical contusions or intracerebral or intraventricular
hemorrhages; and (3) no pulmonary abnormalities. Sub-lethal dcBI was associated with: (1)
apnea lasting up to 15 sec, with transient abnormalities in oxygen saturation; (2) very few delayed deaths; (3)
subarachnoid hemorrhages, especially in the path of the blast wave; (4) abnormal immunolabeling for
IgG, cleaved
caspase-3, and β-
amyloid precursor
protein (β-APP), and staining for
Fluoro-Jade C, all in deep brain regions away from the
subarachnoid hemorrhages, but in the path of the blast wave; and (5) abnormalities on the accelerating Rotarod that persisted for the 1 week period of observation. We conclude that exposure of the head alone to severe
explosive blast predisposes to significant neurological dysfunction.