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Physiologic Considerations
The intact cranium and vertebral canal, together with the relatively inelastic dura,
form a rigid container, such that an increase of any of its contents—brain, blood,
or CSF—will elevate the ICP. Furthermore, an increase in volume of any one of
these three components must be at the expense of the other two, a relationship that
is known as the Monro-Kellie doctrine. Small increments in brain volume do not
immediately raise the ICP because the 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 limited 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,― 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 compliance (the change in ICP for a
given change in intracranial volume). As the brain, blood, or CSF volumes
continue to increase, the accommodative mechanisms fail and ICP rises
exponentially, as in the idealized compliance curve. The normal compliance curve
begins its steep ascent at an ICP of approximately 25 mmHg. After this point,
small increases in intracranial volume result in marked elevations in ICP.
The numerical difference between ICP and mean blood pressure within the
cerebral vessels is termed cerebral perfusion pressure (CPP). Besides the
aforementioned brain tissue shifts, which are discussed more fully in relation to
their clinical signs in Chap. 17, elevation in ICP that approaches the level of mean
systemic blood pressure eventually causes a widespread reduction in cerebral
blood flow/perfusion. In its most severe form, this global ischemia produces brain
death. Lesser degrees of raised ICP and reduced cerebral circulation cause
correspondingly less severe, but still extensive, cerebral infarction of a type quite
similar to what arises after cardiac arrest. In all circumstances, not only the
severity but also the duration of reduction of CPP are the main determinant of the
degree of cerebral damage.
Lundberg is credited with recording and analyzing intraventricular pressures
over long periods of time in patients with brain tumors. He found ICP to be
subject to periodic spontaneous fluctuations, of which he described three types
of pressure waves designated as A, B, and C. Only the A waves have proved to
be separable from arterial and respiratory pulsations and of clinical
consequence. They consist of rhythmic rises of ICP, up to 50 mmHg, occurring
every 15 to 30 min and lasting about 1 min, or of smaller but more protracted
elevations. These plateau waves, as they have come to be known, coincide with
an increase in intracranial blood volume, presumably as a result of a temporary
failure of cerebrovascular autoregulation. Rosner and Becker have observed that
plateau waves are sometimes preceded by a brief period of mild systemic
hypotension. In their view, this slight hypotension induces cerebral vasodilation
in order to maintain normal blood flow. Upon recovery of the blood pressure,
the response in cerebrovascular tone is delayed, thereby allowing intracranial
blood volume to accumulate in the dilated vascular bed and raising ICP. In
support of this explanation is the observation that a brief period of induced
elevation of blood pressure paradoxically restores the normal cerebrovascular
tone and leads to an abrupt cessation of a plateau wave.
It has been demonstrated that the high mortality and morbidity of acute cerebral
mass lesions is in large part related to uncontrolled elevation in ICP. In a normal
adult reclining with the head and trunk elevated to 45 degrees, the ICP is in the
range of 2 to 5 mmHg. Levels up to 15 mmHg are not in themselves hazardous; in
fact, adequate cerebral perfusion can be maintained at an ICP of 40 mmHg
provided blood pressure (BP) remains normal. A higher ICP or a lower BP may
combine to reduce cerebral perfusion pressure and cause diffuse ischemic damage,
as discussed further on.
Causes of Raised ICP
In clinical practice, one of several general mechanisms causing elevated ICP can
be identified: