The pressure in any capillary in the body is close to 15 mm Hg; any peripheral increase leads to major disruption in the local exchanges.

It is also the case for the cranial cavity: the local homeostasy does not allow for any increase in pressure. In the case of intracranial hypertension (IH), the CRL (cephalo-rachidian liquid) pressure exceeds 15 mm Hg leading to the well known pathology. These differences in pressure are much too slight to be perceptible by hand.

A "cranial mobility" would not increase the pressure enough to make it perceptible at the level of the skull. Furthermore, the surplus in pressure within the cranial tissue would evenly spread out at the CRL level which would not lead to a double positioning of the skull (flexion / extension), but to a "swelling / deflating" of it.

We also suggest the study of Jean-Claude HERNIOU's text about the Primary Respiratory Mechanism which does not leave much room for the theory of an internal drive to the cranial dynamics.


The source of the cranial mobility we perceive can not be internal!

Cranial joint motility has the same origin as the motility of other joints in the body and the same effect: lymph and joints drainage. It follows that the balance between those fluids as well as the quality of cranial motility amplitude is of major importance for the local homeostasy.