Recently developed rodent models of acute subdural hematoma have shown
an associated large area of infarction underlying the clot. Excitotox
ic processes have been postulated to play an important role in the ext
ensive cell death seen with these models. However, whether increased p
ressure, vasoactive effects, or toxicity of the blood itself is respon
sible for initiating or sustaining these processes remains unclear. To
study the effect of blood itself, an opaque layer of autologous clot
was placed on the widely exposed parietal cortex of 15 Long-Evans rats
and left in place for 72 h. In control animals the cortical surface w
as exposed but no blood was placed and contact with blood products was
carefully limited. These animals were compared to a group in whom blo
od was injected into the closed subdural space. Histologic analysis sh
owed that the majority of the cortex in both control and experimental
animals in the open cranial model group appeared normal. Scattered sma
ll, discrete hemorrhagic lesions on the cortical surface of both contr
ol and experimental animals were seen, which had the appearance of foc
al mechanical trauma or vessel avulsion. There was no significant diff
erence in average volume of lesions between experimental and control a
nimals (9.1 versus 9.7 mm(3), p = 0.85). No areas of infarction or sel
ective neuronal loss were seen. In comparison, animals in which blood
was injected into the subdural space had significantly larger lesions
underlying clot, averaging 133.6 mm(3) in volume (p < 0.0003). Blood i
n prolonged contact with the cortical surface in the absence of increa
sed pressure, ischemia, or other insult is insufficient to cause under
lying infarction like that seen when a similar volume of blood is inje
cted into the closed subdural space.