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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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for large-bore venous access usually requires the insertion of a double-lumen subclavian or internal jugular catheters and this may be the main source of complications (pneumothorax, infection, hemorrhage) In some patients, treatment can be instituted, and sometimes the entire course completed, through the antecubital veins During and after the procedure, hypotension, hypoprothrombinemia with bleeding (eg, epistaxis), and cardiac arrhythmias may occur Some units prefer to measure the level of brinogen, which is greatly reduced by exchanges before the next exchange so as a gauge to the risk of potential hemorrhage Reactions to the citrate that is used to prevent blood from clotting in the plasma exchange machine are common but can be obviated by the cautious addition of calcium to the intravenous return line Hepatitis and AIDS are not risks if plasma is replaced with albumin and saline rather than with pooled plasma As effective as plasma exchange is, IVIG (04 g/kg per day for 5 consecutive days) is both easier to administer and probably safer because there is no need for large intravenous access The results of the original trial conducted by van der Meche and col leagues have been corroborated in an international study led by Hughes, in which we participated The latter study compared plasma exchange to IVIG and also evaluated their serial use There was a tenuous trend toward a better outcome in patients who received plasma exchange, and results were perhaps slightly better in a group who were treated with plasma exchange followed immediately by 5 days of immune globulin infusions; in both instances, however, the differences failed to attain statistical signi cance and the three modes of treatment were said to be equivalent Renal failure, proteinuria, and aseptic meningitis manifested most often by severe headache are rare complications of IVIG The only serious reactions we have encountered were in a very few patients who congenitally lacked IgA and in whom pooled gamma globulin caused anaphylaxis We have also encountered a few cases of marked in ammatory local venous thrombosis in the region of the infusion site After the use of either plasma exchange or IVIG, 5 to 10 percent of patients who initially improve will have a relapse that becomes apparent several days or up to 3 weeks after completion of treatment If there was a good response to the initial therapy, the same treatment may be repeated or the alternative treatment may be tried; either can be successful A few such patients relapse repeatedly and have a course indicative of chronic in ammatory demyelinating polyneuropathy (see further on) In a few such patients under our care the disease stabilized after several months in response to the administration of corticosteroids, with very gradual tapering of the dose over several months, or in combination with repeated courses of IVIG or plasma exchanges It should be pointed out that the clinical improvement that follows the administration of IVIG or PE usually cannot be readily discerned in an individual patient, ie, it is apparent only by comparing treated and untreated large groups For this reason it is not possible to judge that a patient who fails to improve or who worsens through the period of treatment has indeed derived no bene t from therapy The question nevertheless arises regarding further plasma exchanges or continued infusion of immune globulin in cases of continued worsening or lack of improvement Further complicating the matter are the limited expectations for early improvement in cases of axonal GBS Our advice has been to repeat either of the two treatments if a patient is clearly declining, particularly if there is evidence of mainly demyelinating disease on the EMG, and if.

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