In this study the investigators want to investigate to what extent the application of an artificial bone flape (space flap) influences the success of a decompressive craniectomy.

In all participants, a space flap is placed immediately after removal of the skull cap. In a second operation, after 1-3 months, an operation is performed, in which the stored own skull bone is re-inserted. The artificial bone cover is removed at this point.

The destruction of local brain parenchyma after cerebral infarction leads to local swelling within a few days. In the beginning the ischemic brain expand at the expense of the CSF and venous spaces. However, once these spaces are partially displaced further swelling invariably leads to increase of the intracranial pressure due to the limited space available inside the cranial vault. In cases of large infarctions this increase in intracranial pressure (ICP) may entail life threatening secondary injuries to the brain. The surgical removal of a large part of the skull (decompressive hemi-craniectomy) allows the ischemic brain to expand, therefore avoiding an increase of ICP and it's deleterious effects. After removal of a part of the skull the skin is closed again, and the skull flap is kept in sterile environment. Several months after decompression craniectomy patients undergo implantation of either their preserved bone flap or of a bone flap substitute (so-called patient specific implant, or PSI, mostly made out of Palacos®).

Decompressive hemi-craniectomy comes at a cost for the patient, despite its undisputed role as a life saving surgery after large cerebral infarction. During the first days after surgery the brain may use the space freed up by bone removal. In some cases the brain may prolapse even further out of the cranial vault, leading to brain herniation. Brain herniation are common and may lead to further damage due to axonal shearing injuries in the brain, and to hemorrhages and infarction at the craniotomy edges. The lack of the protective skull prior to re-implantation of the bone flap puts the brain at risk of injuries due to falls during rehabilitation and exposes the brain indirectly to atmospheric pressure. Various neurological deficits subsumed as the syndrome of the trephined have been described in these patients. The symptoms of the syndrome of the trephined have in common that they appear a few weeks after decompression and significantly improve after re-implantation of the patient's own bone. The symptoms range from orthostatic headache and dizziness to motor paresis, aphasia, cognitive decline and brainstem compression symptoms. The pathophysiology behind the syndrome of the trephined can be understood as an "open box" phenomenon. After removal of the bone the brain is separated from the atmospheric pressure only by the skin. The skin, however, does not hold against atmospheric pressure and sinks into the skull cavity (sinking skin flap) once the brain swelling diminishes. Physiologic dynamics of the cerebrospinal fluid are deranged, leading to hydrocephalus, subdural hygromas and parenchymal effusions. This assumption is enforced by pathophysiological observations of decreased cerebral blood flow in both hemispheres following decompression, and normalization thereof following re-implantation of the bone flap.

This pilot study aims at assessing feasibility of a change in surgical protocol. The rate of ICP control will be used to determine the sample size of a planned monocenter study.

Inclusion Criteria:

• Age between 18 and 65 years

• Decompressive hemi-craniectomy planed for*:

  • Impairment of consciousness or progressive reduction of consciousness and
  • Mass effect on brain imaging (oedema exceeding 50% of the MCA territory and midline shift), and
  • Exclusion of other causes of impaired consciousness (e.g. hypoperfusion, hypotension, cerebral reinfarction, epileptic seizures

• Informed consent from relatives

Exclusion Criteria:

• Bilateral, nonreactive, not drug-induced pupillary dilation, associated with coma*

• Simultaneous presence of all four of the following unfavorable prognostic factors: *

  • Age 50 years
  • Involvement of additional vascular territories
  • Unilateral pupillary dilation
  • GCS<8

• Severe comorbidity (severe heart failure or myocardial infarction, incurable neoplasia, etc. *

• Refusal by the patient of this treatment, as known from current interaction with the patient, from existing written documents or related by the patient's proxies. *

• Known pulmonary or cranial infection

• Any coagulopathy

• Rapid neurological decline prohibiting the extra time needed for space flab production (10min)

• Pregnancy