The patient came to the clinic 24-September-2008 after suffering severe head injury 11-July-2008 and was unconscious for more than 2 weeks. The patient underwent decompressive craniotomy in the left fronto-temporal region and the bone flap was preserved in the refrigerator.

Serial CT-scans were performed demonstrating the huge prolapse of the brain from the bone defect.

On examination: the patient had dense right sided plegia with hypalgesia of the right side of the body with spastic pattern. He could walk with aid with speech disturbances.

The father was advised not to undergo surgery for closing the bone defect since the brain still prolapsing with severe degree and there is no control of epilepsy, for what he was receiving Convulex 300 mg tid.

The patient was given medications to decrease the brain prolapse and to rescue the still surviving neural tissues in the massive gliotic left cerebral hemisphere.

The patient was seen 05-October-2008 with MRI of the brain demonstrating the above mentioned data.

The patient then came 07-July-2009 with slight improvement of the right plegia-paresis. The patient is left handed and the speech normalized. There is no prolapse of the brain and the bone defect is palpable with brain is lax transmitting the cardio-pulmonary pulsation.

The patient was admitted 10 days ago, but he had flue for what his operation was postponed.

The removed bone was requested from the other hospital and inspected and was autoclaved in 134 degrees for 15 min.

The old incision over the left fronto-temporal region was refreshed and the dura was separated from the the scalp. No CSF leak was noted. The left lateral ventricle was punctured to rule out the presence of cystic cavities with any brownish liquid collection. A clear CSF came out and the brain came more relax.  The bone graft was another time inspected and cleaned meticulously from debris  and it was fitting for the 90% of the posterior area of the defect. There were chips of his bones in the lower temporal region not fitting with construct, which were removed and there were inserted anterior to fixed bone graft, where there is still linear bony defect.  This act helped in 2 points: 1. The removed bony elements helped to achieve more fitting of the graft. 2. In case of postoperative complication, the only suspected triggering factor will be only the graft, which was preserved in another hospital.

Routine closure of the wound and smooth postoperative recovery.

In case that decompressive laminectomy was performed, it is better to wait until the brain becoming relax and not protruding through the bone defect. It needs at least 6-12 months depending at the severity of injury and the presence of other triggering factors and the epileptic activity.

The methods of bone preservation are deferent and in this case freezing the bone was performed. The shape and texture of the bone was acceptable for what it was used to cover the bone defect. To avoid possible contamination, it is preferable to autoclave the bone graft at 134 degrees for 15 min.

In skull X-rays the bone usually is translucent and becoming visible several months after surgery.

Surge of calcium could have place in the postoperative period, for what Ca level must be recorded for several days.