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DISTURBANCES OF CEREBROSPINAL FLUID
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venous system has been termed R0 and can be expressed in terms similar to Ohm s law (E IR); the voltage (E) re ects the difference in pressure between the CSF and the venous system (PCSF PV), which drives CSF into the dural sinuses, and the equivalent of electrical current, termed If, represents the ow rate of CSF In the steady state, this is equal to the rate of CSF production (03 mL/min) R0, the resistance to absorption, which under normal circumstances is approximately 25 understandably rises when there is a blockage in the CSF circulation The equation for CSF absorption can be expressed as PCSF PV If R0 When rearranged, therefore, PCSF PV If R0; since the product of If R0 is only 08 mmHg, it can be appreciated that the main contribution to CSF pressure as, for example, measured by spinal puncture is the venous pressure, PV Restated, CSF and ICP pressures, which are in equilibrium, are derived largely from transmitted vascular pressures and not from CSF out ow resistance In pathologic conditions such as bacterial meningitis and subarachnoid hemorrhage, R0 may rise to levels that impede CSF circulation and cause hydrocephalus
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DISTURBANCES OF CEREBROSPINAL FLUID PRESSURE, VOLUME, AND CIRCULATION Increased Intracranial Pressure
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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, speci cally, 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 ow/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 uctuations, 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 hy-
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