In contrast to the limited effect caused by changes in arterial BP, increased venous pressure exerts an almost immediate effect on CSF pressure by increasing the volume of blood in the cerebral veins, venules, and dural sinuses. If the jugular veins are compressed, there is a rise of ICP that is transmitted to the lumbar subarachnoid space (unless there is a spinal subarachnoid block). This was the basis of the now little used Queckenstedt test, mentioned in Chap. 2. In the case of a spinal block, pressure on the abdominal wall, which affects the spinal veins below the point of subarachnoid block, will still increase the lumbar CSF pressure. The valsalva maneuver, as well as coughing, sneezing, and straining, causes an increased intrathoracic pressure, which is transmitted to the jugular and then to the cerebral and spinal veins, and directly to the CSF compartment through the intervertebral foramina. The jugular venous valves prevent unimpeded transmission of thoracic pressure to the cranial veins but this threshold can be exceeded if central and jugular venous pressures become greatly elevated. Mediastinal tumors, by obstructing the superior vena cava, have the same effect.
The inhalation or retention of CO2 raises the blood PCO2 and correspondingly decreases the pH of the CSF. By a mechanism that is not fully understood, this acidification of the CSF acts as a potent cerebral vasodilator, causing an increase in cerebral blood flow and blood volume, thus leading to intracranial hypertension. Hyperventilation, which reduces PCO2, has the opposite effect; it increases the pH and cerebral vascular resistance and thereby decreases CSF pressure; this maneuver of lowering the arterial CO2 content by hyperventilation is used in the treatment of acutely raised ICP.
DISTURBANCES OF CEREBROSPINAL FLUID PRESSURE, VOLUME, AND CIRCULATION
The intact cranium and vertebral canal, together with the relatively inelastic dura, form a rigid container, such that an increase in the volume of any of its contents—brain, blood, or CSF—will elevate the ICP. Furthermore, an increase in any one of these components must be at the expense of the other two, a relationship that is known as the Monro-Kellie model. Small increments in brain volume do not immediately raise ICP because of the countervailing buffering effect of displacement of CSF from the cranial cavity into the spinal canal. To a lesser extent, there is deformation of the brain and stretching of the infoldings of the relatively unyielding dura, specifically, the falx cerebri between the hemispheres and the tentorium between the hemispheres and cerebellum. Once these compensating measures have been exhausted, a mass within one dural compartment leads to displacement, or “herniation” of brain tissue from that compartment into an adjacent one. Any further increment in brain volume necessarily reduces the volume of intracranial blood contained in the veins and dural sinuses. Also, the CSF is formed more slowly in circumstances of raised ICP. These accommodative volume-pressure relationships occur concurrently and are subsumed under the term intracranial elastance (the change in ICP for a given change in intracranial volume, or its inverse, compliance, the latter term used often in clinical work). As the volume of brain, blood, or CSF continue to increase, the accommodative mechanisms fail and ICP rises exponentially, as in an idealized elastance (compliance) curve. The shape of the normal curve begins a steep ascent at an ICP of approximately 25 mm Hg. After this point, small increments in intracranial volume result in marked elevations in ICP.