Compliance is the ability to distend and increase volume
It is the reciprocal of “elastance”, hence elastance is a measure of the tendency of a hollow organ to recoil toward its original dimensions upon removal of a distending or compressing force.
Aside from the change in compliance with mean pressure, there are other potential sources of compliance change in the body which need to be considered, the most important being vascular compliance (e.g., hardening of the arteries with arteriosclerosis), which can affect pulsatility even in the absence of mean pressure changes. Thus, pulsatility can increase in a disease process involving either increased mean tissue pressure, or decreased tissue compliance. Examples of diseases exhibiting increased pulsatility abound: 1) age-related macular degeneration, in which intraocular pulsatility increases with disease severity 1).
The brain is enclosed in a rigid container, and any transfer of pulsatility from the arterial walls into the surrounding tissue is felt almost instantaneously everywhere throughout the cranium. This leads to the observation that intraparenchymal and CSF pressure waveforms tend to be similar and independent of location. This is sometimes over generalized to suggest that pressures are everywhere equal intracranially, but this obviously does not apply to the very important arterial and venous compartments. Secondly, this leads to the interesting and potentially important phenomenon of measurable flow pulsatility in the microvasculature 2) and in the venous system. In the brain, the substitute for tissue compliance, which dissipates arterial pulsations in non-cranial tissues, is the overall intracranial compliance. This compliance, is comprised of four main components: actual brain tissue compliance (which is small), arterial compliance, venous compliance (veins have highly compliant walls) and compliance of the spinal thecal sac (which communicates with the brain via the cerebrospinal fluid spaces). Traditionally, intracranial compliance is assumed to decrease primarily with increased ICP, due to the exponential pressure-volume relationship 3).
Decreased compliance with elevated ICP leads to increased pressure pulsatility. However, an additional factor which must be considered is the transfer of pulsations out of the cranium through either venous or CSF outflow pathways; while usually not considered as a factor which affects intracranial compliance, this is another way in which pulsatility is modified in the brain. Thus, intracranial pulsatility can also be affected by restriction of these flow pathways (which can manifest itself as a change in either pressure or flow pulsatility), such as with venous hypertension or a blockage in the outflow CSF pathways at the craniocervical junction (e.g., in Chiari malformation or Dandy-Walker variant) 4).