gms | German Medical Science

If, how, and when decompression craniotomy should be used for the treatment of increased intracranial pressure after traumatic brain injury is a widely discussed clinical subject. Despite the large number of clinical studies addressing this issue, experimental evidence for the beneficial or detrimental role of decompression craniotomy after traumatic brain injury are scarce. We have therefore investigated the influence of a decompression craniotomy on intracranial pressure, contusion volume, brain edema and functional outcome in a model of traumatic brain injury in mice.

Male C57/Bl6 mice were anaesthetized with a combination of Meditomidine, Fentanyl and Dormicor (i.p.), intubated, and ventilated. In groups with short surgery of less than 15 minutes, animals were anaesthetized with 1% Halothane, 30% oxygen and 69% nitrous oxide. Animals were craniotomized above the right parietal cortex and subjected to controlled cortical impact injury. In control animals the craniotomy was closed immediately after trauma, while in treated animals the craniotomy was left open or closed and reopend after a delay of 1, 3, or 8 hrs. The intracranial pressure was measured with a micro-ICP probe 2 mm rostral to the craniotomy. Contusion volumes were assessed on Nissl stained cryo-sections. Brain edema was determined by measuring brain water content.

In control mice intracranial pressure (ICP) increased continuously after traumatic brain injury (TBI) to a maximum of 23.7 ± 3.1 mmHg 6 h after CCI (p<0.001), while in craniotomized animals no ICP increase was observed. Twenty-four hours after trauma, the time point of maximal lesion expansion, contusion volume in craniotomized animals was reduced by 40% as compared to controls (18.3 ± 2.0 vs. 30.2 ± 3.5 mm³, p<0.04). Also the extension of brain edema could be reduced by 52% due to a decompression craniotomy 24 h after CCI (78.7% ± 0.3%, vs. 79.4% ± 0.5%, p<0.05). Even a delay of the craniotomy of 1 or 3 h after trauma could completely prevent a secondary growth of necroses 24 h after CCI referring to a control group that was craniotomized immediately after trauma (20.86 ± 2.23 mm³ and 21.35 ± 3.27 mm³ vs. 19.99 ± 4.05 mm³, n=7). Furthermore craniotomized mice showed significantly improved motor function in beam walking task (p<0.04) and faster recovery in body weight (p<0.02).

Our results demonstrate that craniotomy blunts the post-traumatic ICP increase, significantly reduces both contusion volume and brain edema and improves functional outcome after experimental TBI. Craniotomy may therefore be a useful therapeutic option after TBI in man, provided it is applied early enough.