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In neurosurgical practice different viewpoints have been expressed about the value of decompressive craniectomy as a last resource to control untreatable ICP elevations [2]. In an experimental model of cold induced brain injury we examined the effects of an appropriately tailored cranio-dural opening on whole brain perfusion and on local fluid dynamics. An edematous lesion induced by cold injury produces a critical mass effect and compromises the volume buffering capacity of the intracranial system. This produces an increase in the cerebrovascular resistance (CVR) thereby generating a vicious circle which can enhance edema formation. It is supposed that cranio-dural removal, opening the intracranial system to the atmosphere and reducing ICP, could facilitate the cerebral venous outflow from the skull, thereby decreasing the CVR and disrupting the vicious circle linking primary and secondary pathological events.

Head injury represents the cause of injury deaths in 50–70% of cases and is the main cause of death in the group under 20 years of age. Brain sequelae are often so severe as to hinder a satisfactory social reintegration. Prevention and control of the extension of the secondary cerebral lesions are important. Ischaemia has been recognized as the common final pathway in post-traumatic brain damage and seems to be mainly due to acute intracranial hypertension and decreased cerebral perfusion pressure (CPP) [3].

It is generally accepted that myogenic, metabolic and neurogenic regulation mechanisms exist for the cerebral blood flow (CBF). Recently, a hydraulic control acting at the predural level has been suggested by Chopp et al. [2] These mechanisms, however, do not take into consideration the problem represented by the peculiar feature of the brain (an incompressible organ) within the skull and dura mater (a rigid box and a stiff envelope), perfused by a pulsatile blood flow through a vascular tree with elastic walls. On the basis of this consideration we think that the progressive CBF reduction up to cerebral circulatory arrest following severe intracranial hypertension is probably due to an unbalance between cerebral blood volume variations during each cardiac cycle and the compensatory systems, primarily the venous vascular bed.

Benign intracranial hypertension (BIH), otherwise called “pseudotumour cerebri”, is a pathological condition characterized by the presence of chronic or intermittent signs of raised intracranial pressure (ICP), such as headache, papilledema, and spontaneous cerebrospinal fluid (CSF) leakage, without any evidence of an intracranial space occupying mass lesion or CSF protein concentration increase. This condition is frequently observed in female patients suffering from endocrine disorders (obesity, hypertrichosis, irregular menses, and sometimes galactorrhea) and is often associated with a typical radiological feature depicting an intrasellar arachnoidal herniation (the so-called “empty sella”) (Anile and Maira 1986).Some authors have suggested that an impairment in CSF absorptive capacity due, probably, to an increase in the venous outflow resistance resulting from an obstacle at postcerebral level in the dural sinuses, could be the most important pathogenetical factor in BIH (Junck 1986). In spite of this assumption, however, patients diagnosed as affected by this syndrome show, at neuroradiological examinations, normal, or even small ventricles (Hansen et al. 1987).

Since the introduction of the CT scan, a clinical picture, mainly observed in female patients and represented by signs of intracranial hypertension (headache, visual disturbances with or without papilledema) and endocrinological disorders (obesity, hypertrichosis, irregular menses, sometimes galactorrhea), has been found, often associated with radiological findings of subarachnoid herniation into the pituitary fossa. Such an association, when noticed in subjects who have not received previous surgical and/or radiotherapeutic procedures on the sellar region, is defined as “primary empty sella syndrome” (PESS) (4).

Brain tamponade (BT) represents a condition of cerebral blood flow (CBF) arrest due to a progressive or often sudden increase in intracranial pressure (ICP) up to values close to the corresponding systemic arterial pressure values. This situation, peculiar to an anatomical configuration characterized by the presence of an incompressible organ within a rigid envelope, as the brain substance within the skull, can induce as its final step a diffuse or compartmental brain ischemia. Considering the scarce metabolic autonomy of the CNS, this could produce irreversible damages. Implicated in this process are the direct relationships between cerebral blood volume changes and vascular impedances. To investigate the hemodynamic mechanisms underlying BT we have carried out an experimental study in the rabbit because its cerebral blood supply is analogous to the human (Meyer et al. 1986).

Many pathogenetic factors have been reported to be involved in the genesis and development of so-called normal pressure hydrocephalus (NPH). Among these, the most current are a defect in CSF absorptive capacity (Borgesen 1984) and an increase in the intraventricular CSF pulse amplitude (Di Rocco et al. 1976). However no recent paper has clarified the relationships between the disturbances in CSF and ICP dynamics, often observed in this pathology, with the severity of the clinical picture and/or the brain damage demonstrated by the ventricular enlargement.