Effects of Early Skull Repair With Titanium Mesh on Cerebral Blood Flow and Neurological Recovery: a Randomized Controlled Clinical Trial Based on CT Perfusion Evaluation

A skull defect is inevitable in patients with traumatic brain injury undergoing decompression treatment, which results in a loss of physiological and functional integrity of the brain that makes atmospheric pressure directly act on the brain tissue to induce environmental disorders in the brain. Moreover, with the changes in the body position, the contents of the brain often move in an unstable position, and with the extension of time, there may be compensatory ventricular enlargement and brain atrophy, eventually causing neurological dysfunction and cognitive disorders. Therefore, it is imperative to repair the skull defect.

There are many repair materials for skull defects, including autogenous bone, allogeneic bone, nonmetallic materials (plexiglass, bone cement, silicone rubber, etc.) and titanium mesh. The performance of different materials have their own advantages and disadvantages, and titanium alloy is an ideal repair material and has been widely used in clinical practice because of good biocompatibility and strength, no aging, low density, non-iron atoms, ability to be not magnetized in magnetic fields, and no influence on CT, MRI, EEG and X-ray examination.

The timing for repair of skull defect after traumatic brain injury is still controversial. Some scholars believe that if there is no hydrocephalus and intracranial infection after decompression with removal of bone flap, skull repair should be proceeded as soon as possible to isolate the scalp from the dura mater and recover the normal intracranial pressure by easing the negative effects of the scalp, such as cerebrovascular traction, compression and distortions. Most importantly, early skull repair is able to reduce a variety of secondary neurological deficits due to skull defects, increase brain surface blood flow, and thus reduce epileptic attack. Of course, some scholars recommend late-stage skull repair, and they believe hematoma absorption after decompressive surgery is a long process, and in some patients, hematoma will be completely absorbed in about 3 months or even longer, which may result in secondary brain edema. Moreover, surgical trauma exerts negative effect on the brain tissue recovery, which is not conducive to neurologic rehabilitation.

As there is no unified conclusion on the timing for the repair of skull defects, investigators conducted a multi-sample, double-blind, randomized, clinical trial, to collect craniocerebral injury patients undergoing decompression with removal of bone graft who were randomized into two groups to receive early skull repair in test group and late-stage skull repair in control group. CT perfusion technology was used to monitor the blood perfusion in the brain before and after skull repair and to compare the changes of blood perfusion in the brain tissue and neurological recovery in patients undergoing early or late-stage skull repair.