Volume and Pressure in the Craniospinal Axis* J.
DOUGLAS MILLER, M.D., PH.D. INTRODUCTION
Many disease processes which affect the brain-vascular, inflammatory, neoplastic, and traumatic-result eventually in intracranial hypertension. This happens because of the unique situation of the brain and its coverings within the rigid confines of the skull, in which a progressive increase of volume to the brain constituents-blood, CSF, and cerebral tissue-increases intracranial pressure. Problems relating to this pathological state, its diagnosis, management, and influence on outcome, encompass much of clinical neurosurgical practice. Appropriate to the importance of the subject, the relationship between changes of intracranial volume and pressure was one of the first areas of physiological investigation, and to enumerate those who have been involved in research into intracranial pressure is to encompass the history of neurosurgery. Although the factors governing directional changes in arterial and intracranial pressure have been known for many years, technological advances have made possible quantitative measurements of many of the variables related to intracranial pressure, both in man and in experimental animal models. Such investigations may be complex, but the questions asked are simple. What factors induce large increases in intracranial pressure? What harm does intracranial hypertension do? What is the best treatment, not only to lower intracranial pressure, but also to produce clinical improvement? Understanding of the relationship between volume and pressure in the craniospinal axis is fundamental to the solution of these questions and therefore forms the central part of this review. However, the phenomena of normal and raised intracranial pressure are delineated first. Finally, the mechanisms by which raised intracranial pressure may bring about neurological dysfunction are discussed. NORMAL INTRACRANIAL PRESSURE
It is perhaps more accurate to talk of "intracranial pressures" than a single pressure. Under normal conditions, however, any of a variety of methods used to measure intracranial pressure-a needle in the lumbar subarachnoid space, the cisterna magna, or the lateral ventricle, or transducers implanted in the supratentorial epidural or subdural space-,,'ill record the
* Supported by the
Secretary of State for Scotland's Fund for Medical Research. 76
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CHAPTER 7
77
FIG. 7.1. Schematic diagrams of craniospinal contents to contrast A (normal CSF pathways) with B (brain compression by supratentorial mass lesion). In B, note obliteration of the cranial subarachnoid space, reduction in size of the lateral ventricle on the side of the lesion, and examples of subfalcine, tentorial, and tonsillar herniation, with distortion and downward displacement of brain stem.
same pressure, providing the same reference point is used, because freely circulating CSF has a pressure-equalizing effect (8, 18, 68, 69, 128). In many of the circumstances in which intracranial pressure becomes raised, however, this condition no longer holds; obstruction of the CSF pathways occurs and valid recordings of intracranial pressure can be obtained only from recording sites rostral to the site of obstruction (53, 68, 69, 128) (Fig. 7.1 A and B). The .normal tracing of intracranial pressure displays both vascular and respiratory oscillations (104). The vascular "Taves are due to arterial pulsations in the larger vessels within the brain which produce an oscillation in the volume of the ventricular system, visible on fluoroscopy during ventriculography. Earlier views that the arterial pulsations in the CSF pressure wave were due to choroid plexus pulsation are not now generally held (2, 6, 7, 19, 61). The respiratory wave is synchronous with alterations in the central venous pressure, reflecting intrathoracic pressure. Normal intracranial pressure usually ranges between 0 and 10 mm. Hg (136 mm. H 20), with an upper limit of 15 mm. Hg (204 mm, H 20). Although
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CRANIOSPINAL VOLUME AND PRESSURE
CLINICAL NEUROSURGERY
INTRACRANIAL
PRESSURE
mmH20
mmHg
100
1360
90
1250
80 1000
70 60
750
50 ..
40
500
30 ..
20
250 136
10 0
FIG. 7.2. Nomogram comparing intracranial pressure measurements expressed in mm. Hg and mm. H 20. Points at 20 and 40 mm. Hg indicate arbitrary levels used to distinguish between "low," "medium," and "high" levels of intracranial pressure (42).
it is simpler to measure intracranial pressure at the time of a spinal tap in mm, H 20 by using a simple manometer, the range of pressures encountered in neurosurgical practice and comparisons with arterial pressure favor the expression of intracranial pressure in mm. Hg (12) (Fig. 7.2). The intracranial pressure is not always low in normal persons, however, Some procedures, such as coughing, straining, or sneezing, can produce transient elevations of intracranial pressure to levels of 100 mm. Hg without apparent distress to the patient (63). These rises last only a few seconds, however, and the outstanding feature of a normal record of intracranial pressure measured over a period of hours is its lack of any sustained deviation of the pressure from the normal range. RAISED INTRACRANIAL PRESSURE
Because intracranial pressure is a continuous variable, an arbitrary decision must be made about the level at which pressure is deemed to be pathologically raised. In Glasgow, a sustained level in excess of 20 mm. Hg is regarded as abnormal (46). Others take 15 mm. Hg as the upper limit of normal (79, 137). Beyond this level, intracranial pressure may rise to more than 100 mm. Hg reaching an asymptote at the level of arterial blood pres-
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79
sure. Although intracranial pressure may be artificially increased well beyond the level of blood pressure in experimental preparations, this has seldom, if ever, been recorded clinically (most examples can be ascribed to calibration problems in the recording system). For practical purposes, therefore, arterial pressure should be regarded as the upper limit for intracranial pressure. As intracranial pressure rises, the amplitude of the arterial component of the pressure wave also increases (18, 145). When intracranial pressure is close to the level of arterial pressure, the pulse amplitude of the pressure wave is also close to that of the arterial pressure recording. The respiratory fluctuation, on the other hand, becomes less and less obvious as intracranial pressure rises. For this reason, it is recommended that mean intracranial pressure be calculated in the same way as mean arterial pressure, i.e., diastolic pressure plus one-third of the pulse pressure (12). If there is a marked sinusoidal respiratory component at low levels of intracranial pressure this derivation of mean pressure may be slightly inaccurate, but, at higher pressures, when estimates of the mean are of more importance, this derivation is preferable to the arithmetic mean of systolic and diastolic pressures. Rising intracranial pressure also becomes more passively related to changes in arterial pressure, emphasizing the need for simultaneous monitoring of arterial and intracranial pressure in patients with severe intracranial hypertension (63). In clinical practice, three basic forms of intracranial hypertension may be observed: sustained high pressure; a steady rise from normal levels to severe intracranial hypertension with intracranial pressure in excess of 50 rom. Hg; and episodic waves of increased intracranial pressure (46, 47, 66, 79, 82, 103, 115). Lundberg (79, 80), in his classical monograph on monitoring of intracranial pressure, described three pressure wave types, A, B, and C "Taves, but has more recently preferred descriptive titles. The most important is the plateau wave (formerly A wave). This consists of a sudden elevation of intracranial pressure to a level of more than 50 mm. Hg, sustained for periods between five and 20 minutes or sometimes longer, and followed by an equally rapid decrease in pressure. These waves, which may be accompanied by temporary neurological dysfunction, can recur at intervals of minutes or hours, and usually emerge from a background of moderately elevated intracranial pressure (20 to 40 mm. Hg). Most patients who have plateau "Taves also have papilledema. The other main forms of pressure wave are rhythmic variations in intracranial pressure: the B wave is a sharp peaked increase in pressure of 20 to 50 mm. Hg, which occurs once or twice per minute, and is related to changes in respiration, usually of the CheyneStokes type; the other rhythmic variation (formerly C wave) is less com-
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CRANIOSPINAL VOLUME AND PRESSURE
CLINICAL NEUROSURGERY
mon, runs at 4 to 8 .waves per minute, and corresponds to variations in arterial pressure of the Traube-Hering-Maycr type. Band C waves do not appear to have any clinical implications beyond those of the underlying respiratory or cardiovascular disorder, whereas plateau waves indicate a degree of intracranial pressure decompensation (63, 79). Other authors have described "pre-plateau" waves, in which the pressure rises from normal levels to 20 or 30 mm. Hg, but in the same abrupt "ray as true plateau "Taves (132, 136). The significance of these smaller changes in intracranial pressure is not known. Genesis of Raised Intracranial Pressure
Since the last century it has been accepted that the basis for raised intracranial pressure is that the cranial cavity is rigid with limited exits and contains incompressible substances, namely blood, CSF, and brain tissue which is largely water. The historical development of the modified MonroKellie doctrine has been fully described by Evans (20) and Langfitt (63). It has proved difficult to measure the exact proportions of the intracranial constituents, but, as an approximate guide, glial and neural tissue accounts for about 70 per cent of the contents, with CSF, cerebral blood, and extracellular fluid each accounting for about 10 per cent of the total volume. Two constituents may be expelled from the cranial cavity to accommodate an expanding mass lesion or an increase in the volume of any of the remaining constituents: CSF may be squeezed from the cranial subarachnoid space and ventricles into the spinal subarachnoid space, where extra capacity can be provided by expulsion of blood from the extradural vertebral venous plexus, and cerebral venous blood may be expelled into the jugular veins or into the scalp via emissary veins (76, 107). Increased intracranial pressure results from any addition to the volume of these intracranial constituents in excess of this compensatory capacity. The most usual extraneous sources of a volumetric increase are intracranial tumors (such as meningioma, pituitary adenoma, or metastases), hematomas (epidural, subdural, or intracerebral), and intracranial abscesses. Increased brain tissue volume occurs with primary cerebral tumors. The extent of the rise in intracranial pressure will depend upon the volume of the mass lesion, the rate at which it expands, the total volume of the intracranial cavity, and the relative volumes of blood and CSF available for displacement, together with the anatomical configuration of the tentorial hiatus. It is the combination of these factors which determines the intracranial volume-pressure status, to be described below (92). The definition of cerebral edema is an increase in brain tissue "Tater content (130, 131). The type of edema encountered in neurosurgical practice consists of an increase in extracellular water content and is mainly a phe-
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81
nomenon affecting the white matter; this corresponds to vasogenic edema as described by Klatzo (56), attributed to leakage of water and solutes through defects in the "tight junctions" between adjacent endothelial cells in the capillary bed (9). The outward migration of water, and hence the severity of the edema and degree of intracranial hypertension, is increased by hypercapnia and arterial hypertension, and particularly by a combination of the two (17, 57, 58, 83, 119). Reduction in brain water content is the basis of treatment of raised intracranial pressure by hypertonic solutions and by corticosteroids. Hypertonic solutions depend for their action on intact brain barrier mechanisms across which an osmotic gradient can be developed, so that water tends to be preferentially removed from the brain (39, 62, 106, 144). The action of steroids on intracranial pressure is less well understood. Edema associated with focal and chronic lesions is more amenable to treatment than acute diffuse edema; CSF production is also reduced by glucocorticoid therapy (27,60,85, 143). An increase in the volume of the CSF compartment may cause raised intracranial pressure; this is synonymous with hydrocephalus, which may be the primary cause (the sources of obstructive and communicating hydrocephalus need not be enumerated here), or may develop as a secondary event, due to obstruction of the foramen magnum or tentorial hiatus during the expansion of a primary intracranial mass lesion (14). The most labile source of increase of intracranial pressure, and one which has great relevance for the clinical management of intracranial hypertension, is an increase in the cerebral blood volume (Table 7.1). This may be caused by an arterial vasodilatation, or by obstruction of the venous outflow from the intracranial cavity. The former mechanism is related to increases in cerebral blood flow, although these may be self-limiting due to the intracranial hypertension produced; the latter mechanism is related to reductions in cerebral blood flow, The most powerful vasodilating agent is carbon dioxide; any rise above TABLE 7.1 Factors Which Increase and Decrease Intracranial Pressure via Changes in Cerebral Blood Volume
Increase
Hypercapnia (any degree) Hypoxia (pA0 2 < 50 mm. Hg) REM sleep Volatile anesthetic agents Nitrous oxide
Decrease
Hypocapnia (any degree) Hyperoxia (pA0 2 1000-1500 mm. Hg) Hypothermia Barbiturates Neuroleptanalgesia
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CRANIOSPINAL VOLUME AND PRESSURE
SAP (mmHg)
SSP
(nmHg)
Left
VFP
(mmHg)
Right
VFP
ImmHg)
~l
;
;;.
~]---------_ , ~1__" " "," " -'·_",'JfC.'~" ~1---1IIlIlIllIIl"'-7. . . :>*i ,. 1000 mm. Hg) can both reduce intracranial pressure by causing cerebral vasoconstriction and a reduction in cerebral blood volume (81, 90, 97). Hypothermia also reduces intracranial pressure by a similar mechanism (66, 88, 122). The volatile anesthetic agents halothane, tricWoroethylene, and methoxyflurane cause cerebral vasodilatation and increase the intracranial pressure (24, 41, 87, 121). Nitrous oxide and the intravenous agent, ketamine, can
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CLINICAL NEUROSURGERY
82
83
also cause intracranial hypertension (36, 146). Conversely, neuroleptanalgesic agents and barbiturates, which reduce cerebral blood flow, produce a slight reduction of intracranial pressure (23, 93, 122, 129). Other drugs which increase intracranial pressure, such as morphine, pentazocine, and diazepam produce their effects through respiratory depression with production of hypercapnia (5, 54, 121, 129). Intracranial pressure commonly rises at night; pressure waves are more frequent then. This has been attributed to vasodilatation occurring particularly during periods of rapid eye movement sleep (37). Changes in arterial blood pressure may influence intracranial pressure by altering cerebral blood volume; this can occur when cerebrovascular autoregulation is severely impaired so that the blood vessels behave in a pressure-passive manner to changes in arterial pressure (31, 65, 67, 102). In some circumstances, increases in arterial pressure may cause an equivalent, passive rise in intracranial pressure with little change in cerebral blood flow; in this situation arterial distension must be balanced by capillary or venous obstruction (13, 84, 120). A change in cerebral blood volume is the likely common basis for all pressure waves. Band C waves can be directly linked to changes in respiration and blood pressure with secondary effects on the cerebral vasculature. The plateau or A waves are accompanied by angiographically observed vascular dilatation and by an increase in cerebral blood volume (116), although there is no increase in cerebral blood flow (16). In practice, several of the factors involved in the genesis of increased intracranial pressure may operate at the same time. For instance, patients with cerebral metastases from bronchial carcinoma often have severe cerebral edema, and may also develop hypercapnia and hypoxia, all of which will produce additive effects on intracranial pressure. These mechanisms determine the direction of change of intracranial pressure, but the factor which regulates the extent of the increase in pressure is the intracranial volume-pressure relationship of the patient at that particular time.
Intracranial Volume-Pressure Relationships During progressive expansion of an intracranial mass lesion there is little increase in intracranial pressure at first because an equivalent volume of CSF and venous blood can be expelled from the cranial cavity to accommodate the mass (63). This mechanism has been known since the last century, but it forms the basis of the intracranial volume-pressure relationship. If the additional volume is plotted against intracranial pressure, the resultant is not a straight line but an exponential curve rising little at first, but steepening progressively as intracranial compensation is exhausted. This curvilinear relationship has been shown in experimental animals subjected
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CRANIOSPINAL VOLUME AND PRESSURE
CLINICAL NEUROSURGERY
to inflation of intracranial balloons at a steady rate (67), in children with hydrocephalus (125), and more recently in patients with raised intracraniaJ pressure from a variety of causes including tumor, head injury, cerebrovascular disease, and hydrocephalus (94, 96). The critical factor is the increase in pressure that results from a given increase in intracranial volume (Fig. 7.4). In effect this is a measure of the gradient of the volume-pressure curve at any point; the expression dPjdV is the inverse of compliance and can be termed elastance (75). The elastance value of the intracranial contents determines the amount of increase in intracranial pressure which will result from any of the stimuli described in the last section. A good illustration of this is seen by comparing the action of the volatile anesthetic agents on intracranial pressure in patients with normal CSF pathways and those with intracranial space-occupying lesions. These agents, which cause cerebral vasodilatation, produce only a small increase in intracranial pressure in patients with normal CSF pathways, but produce large increases up to 50 mm. Hg in patients with intracranial tumors, even when the resting intracranial pressure is not increased (24,41, 121). Hypercapnia in the presence of an intracranial mass will have a similarly augmented effect (Fig. 7.5). Another example of this phenomenon is the plateau wave, which occurs characteristically in patients" ith mildly elevated intracranial ICP
mmHg 70 60
dP2> dP1
50
dP2
40 30 20 10
UNITS OF VOLUME FIG. 7.4. Theoretical intracranial volume-pressure curve. As additional volume increases and intracranial pressure (ICP) rises, uniform increments of volume (dV) cause larger and larger rises of intracranial pressure (dP). Intracranial elastance (dP jdV) thus increases in parallel with the intracranial pressure during progressive addition to the volume of the intracranial con tents.
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84
85
SAP (mmHg)
SSP
(mnHg)
Left
VFP
(mmHgJ
FIG. 7.5. Effect of carbon dioxide on baboon with intracranial space-occupying lesion. Ventricular fluid pressure (VFP) and anterior sagittal sinus pressure (SSP) rise steeply with inhalation of 3 per cent CO 2 , followed rapidly by systemic arterial pressure (SAP) in a vasopressor response. Contrast this striking response with Figure 7.3.
pressure, many of whom have brain tumors and most of "hom have papilledema (79). In both of these situations spatial compensation is practically exhausted, intracranial elastance is increasing, and the small additional volume produced by slight cerebrovascular dilatation is sufficient to cause an enormous rise in intracranial pressure. A similar mechanism may explain sudden neurological deterioration in patients with head injuries and other intracranial pathological processes. Clearly, a measurement of brain elastance ,~\ ould be of value since measurement of intracranial pressure alone can detect intracranial hypertension only as it occurs, but cannot forecast its occurrence; changes in elastance may precede large rises in intracranial pressure. This 'wish for further in-
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CRANIOSPINAL VOLUME AND PRESSURE
CLINICAL NEUROSURGERY
formation has led to our investigations of the volume-pressure response as an index of intracranial elastance. The V olume-Pressure Response In patients in whom intracranial pressure monitoring is being conducted by means of an intraventricular catheter connected to an externally placed transducer, it is sometimes necessary to flush the system with small volumes of saline in order to clear the catheter (79). In doing this, we were struck by the varying changes in intracranial pressure that could result from these small alterations in CSF volume, and it was felt worthwhile to perform small volumetric changes in a better regulated manner. After a period of trial and error, a volumetric change in patients of 1 ml. in one second was used and the resultant immediate change in intracranial pressure (properly, ventricular fluid pressure) was termed the volume-pressure response. It is expressed in mm. Hgjml. and is therefore an index of intracranial elastance (94). As resting intracranial pressure rises, the volume-pressure response is increased in parallel, although this relationship is less clear in patients with considerably enlarged ventricles (99) (Fig. 7.6). The volume-pressure response is also related to the amount of brain shift seen in patients with head injuries and brain tumors, and is reduced following surgical decompression 10 9
8 7
VPR mmHg
6
y=0·16x-0·08 r = O·84 P
DOUGLAS MILLER, M.D., PH.D. INTRODUCTION
Many disease processes which affect the brain-vascular, inflammatory, neoplastic, and traumatic-result eventually in intracranial hypertension. This happens because of the unique situation of the brain and its coverings within the rigid confines of the skull, in which a progressive increase of volume to the brain constituents-blood, CSF, and cerebral tissue-increases intracranial pressure. Problems relating to this pathological state, its diagnosis, management, and influence on outcome, encompass much of clinical neurosurgical practice. Appropriate to the importance of the subject, the relationship between changes of intracranial volume and pressure was one of the first areas of physiological investigation, and to enumerate those who have been involved in research into intracranial pressure is to encompass the history of neurosurgery. Although the factors governing directional changes in arterial and intracranial pressure have been known for many years, technological advances have made possible quantitative measurements of many of the variables related to intracranial pressure, both in man and in experimental animal models. Such investigations may be complex, but the questions asked are simple. What factors induce large increases in intracranial pressure? What harm does intracranial hypertension do? What is the best treatment, not only to lower intracranial pressure, but also to produce clinical improvement? Understanding of the relationship between volume and pressure in the craniospinal axis is fundamental to the solution of these questions and therefore forms the central part of this review. However, the phenomena of normal and raised intracranial pressure are delineated first. Finally, the mechanisms by which raised intracranial pressure may bring about neurological dysfunction are discussed. NORMAL INTRACRANIAL PRESSURE
It is perhaps more accurate to talk of "intracranial pressures" than a single pressure. Under normal conditions, however, any of a variety of methods used to measure intracranial pressure-a needle in the lumbar subarachnoid space, the cisterna magna, or the lateral ventricle, or transducers implanted in the supratentorial epidural or subdural space-,,'ill record the
* Supported by the
Secretary of State for Scotland's Fund for Medical Research. 76
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CHAPTER 7
77
FIG. 7.1. Schematic diagrams of craniospinal contents to contrast A (normal CSF pathways) with B (brain compression by supratentorial mass lesion). In B, note obliteration of the cranial subarachnoid space, reduction in size of the lateral ventricle on the side of the lesion, and examples of subfalcine, tentorial, and tonsillar herniation, with distortion and downward displacement of brain stem.
same pressure, providing the same reference point is used, because freely circulating CSF has a pressure-equalizing effect (8, 18, 68, 69, 128). In many of the circumstances in which intracranial pressure becomes raised, however, this condition no longer holds; obstruction of the CSF pathways occurs and valid recordings of intracranial pressure can be obtained only from recording sites rostral to the site of obstruction (53, 68, 69, 128) (Fig. 7.1 A and B). The .normal tracing of intracranial pressure displays both vascular and respiratory oscillations (104). The vascular "Taves are due to arterial pulsations in the larger vessels within the brain which produce an oscillation in the volume of the ventricular system, visible on fluoroscopy during ventriculography. Earlier views that the arterial pulsations in the CSF pressure wave were due to choroid plexus pulsation are not now generally held (2, 6, 7, 19, 61). The respiratory wave is synchronous with alterations in the central venous pressure, reflecting intrathoracic pressure. Normal intracranial pressure usually ranges between 0 and 10 mm. Hg (136 mm. H 20), with an upper limit of 15 mm. Hg (204 mm, H 20). Although
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CRANIOSPINAL VOLUME AND PRESSURE
CLINICAL NEUROSURGERY
INTRACRANIAL
PRESSURE
mmH20
mmHg
100
1360
90
1250
80 1000
70 60
750
50 ..
40
500
30 ..
20
250 136
10 0
FIG. 7.2. Nomogram comparing intracranial pressure measurements expressed in mm. Hg and mm. H 20. Points at 20 and 40 mm. Hg indicate arbitrary levels used to distinguish between "low," "medium," and "high" levels of intracranial pressure (42).
it is simpler to measure intracranial pressure at the time of a spinal tap in mm, H 20 by using a simple manometer, the range of pressures encountered in neurosurgical practice and comparisons with arterial pressure favor the expression of intracranial pressure in mm. Hg (12) (Fig. 7.2). The intracranial pressure is not always low in normal persons, however, Some procedures, such as coughing, straining, or sneezing, can produce transient elevations of intracranial pressure to levels of 100 mm. Hg without apparent distress to the patient (63). These rises last only a few seconds, however, and the outstanding feature of a normal record of intracranial pressure measured over a period of hours is its lack of any sustained deviation of the pressure from the normal range. RAISED INTRACRANIAL PRESSURE
Because intracranial pressure is a continuous variable, an arbitrary decision must be made about the level at which pressure is deemed to be pathologically raised. In Glasgow, a sustained level in excess of 20 mm. Hg is regarded as abnormal (46). Others take 15 mm. Hg as the upper limit of normal (79, 137). Beyond this level, intracranial pressure may rise to more than 100 mm. Hg reaching an asymptote at the level of arterial blood pres-
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78
79
sure. Although intracranial pressure may be artificially increased well beyond the level of blood pressure in experimental preparations, this has seldom, if ever, been recorded clinically (most examples can be ascribed to calibration problems in the recording system). For practical purposes, therefore, arterial pressure should be regarded as the upper limit for intracranial pressure. As intracranial pressure rises, the amplitude of the arterial component of the pressure wave also increases (18, 145). When intracranial pressure is close to the level of arterial pressure, the pulse amplitude of the pressure wave is also close to that of the arterial pressure recording. The respiratory fluctuation, on the other hand, becomes less and less obvious as intracranial pressure rises. For this reason, it is recommended that mean intracranial pressure be calculated in the same way as mean arterial pressure, i.e., diastolic pressure plus one-third of the pulse pressure (12). If there is a marked sinusoidal respiratory component at low levels of intracranial pressure this derivation of mean pressure may be slightly inaccurate, but, at higher pressures, when estimates of the mean are of more importance, this derivation is preferable to the arithmetic mean of systolic and diastolic pressures. Rising intracranial pressure also becomes more passively related to changes in arterial pressure, emphasizing the need for simultaneous monitoring of arterial and intracranial pressure in patients with severe intracranial hypertension (63). In clinical practice, three basic forms of intracranial hypertension may be observed: sustained high pressure; a steady rise from normal levels to severe intracranial hypertension with intracranial pressure in excess of 50 rom. Hg; and episodic waves of increased intracranial pressure (46, 47, 66, 79, 82, 103, 115). Lundberg (79, 80), in his classical monograph on monitoring of intracranial pressure, described three pressure wave types, A, B, and C "Taves, but has more recently preferred descriptive titles. The most important is the plateau wave (formerly A wave). This consists of a sudden elevation of intracranial pressure to a level of more than 50 mm. Hg, sustained for periods between five and 20 minutes or sometimes longer, and followed by an equally rapid decrease in pressure. These waves, which may be accompanied by temporary neurological dysfunction, can recur at intervals of minutes or hours, and usually emerge from a background of moderately elevated intracranial pressure (20 to 40 mm. Hg). Most patients who have plateau "Taves also have papilledema. The other main forms of pressure wave are rhythmic variations in intracranial pressure: the B wave is a sharp peaked increase in pressure of 20 to 50 mm. Hg, which occurs once or twice per minute, and is related to changes in respiration, usually of the CheyneStokes type; the other rhythmic variation (formerly C wave) is less com-
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CRANIOSPINAL VOLUME AND PRESSURE
CLINICAL NEUROSURGERY
mon, runs at 4 to 8 .waves per minute, and corresponds to variations in arterial pressure of the Traube-Hering-Maycr type. Band C waves do not appear to have any clinical implications beyond those of the underlying respiratory or cardiovascular disorder, whereas plateau waves indicate a degree of intracranial pressure decompensation (63, 79). Other authors have described "pre-plateau" waves, in which the pressure rises from normal levels to 20 or 30 mm. Hg, but in the same abrupt "ray as true plateau "Taves (132, 136). The significance of these smaller changes in intracranial pressure is not known. Genesis of Raised Intracranial Pressure
Since the last century it has been accepted that the basis for raised intracranial pressure is that the cranial cavity is rigid with limited exits and contains incompressible substances, namely blood, CSF, and brain tissue which is largely water. The historical development of the modified MonroKellie doctrine has been fully described by Evans (20) and Langfitt (63). It has proved difficult to measure the exact proportions of the intracranial constituents, but, as an approximate guide, glial and neural tissue accounts for about 70 per cent of the contents, with CSF, cerebral blood, and extracellular fluid each accounting for about 10 per cent of the total volume. Two constituents may be expelled from the cranial cavity to accommodate an expanding mass lesion or an increase in the volume of any of the remaining constituents: CSF may be squeezed from the cranial subarachnoid space and ventricles into the spinal subarachnoid space, where extra capacity can be provided by expulsion of blood from the extradural vertebral venous plexus, and cerebral venous blood may be expelled into the jugular veins or into the scalp via emissary veins (76, 107). Increased intracranial pressure results from any addition to the volume of these intracranial constituents in excess of this compensatory capacity. The most usual extraneous sources of a volumetric increase are intracranial tumors (such as meningioma, pituitary adenoma, or metastases), hematomas (epidural, subdural, or intracerebral), and intracranial abscesses. Increased brain tissue volume occurs with primary cerebral tumors. The extent of the rise in intracranial pressure will depend upon the volume of the mass lesion, the rate at which it expands, the total volume of the intracranial cavity, and the relative volumes of blood and CSF available for displacement, together with the anatomical configuration of the tentorial hiatus. It is the combination of these factors which determines the intracranial volume-pressure status, to be described below (92). The definition of cerebral edema is an increase in brain tissue "Tater content (130, 131). The type of edema encountered in neurosurgical practice consists of an increase in extracellular water content and is mainly a phe-
Downloaded from https://academic.oup.com/neurosurgery/article-abstract/22/CN_suppl_1/76/4099471 by University of Otago user on 13 October 2019
80
81
nomenon affecting the white matter; this corresponds to vasogenic edema as described by Klatzo (56), attributed to leakage of water and solutes through defects in the "tight junctions" between adjacent endothelial cells in the capillary bed (9). The outward migration of water, and hence the severity of the edema and degree of intracranial hypertension, is increased by hypercapnia and arterial hypertension, and particularly by a combination of the two (17, 57, 58, 83, 119). Reduction in brain water content is the basis of treatment of raised intracranial pressure by hypertonic solutions and by corticosteroids. Hypertonic solutions depend for their action on intact brain barrier mechanisms across which an osmotic gradient can be developed, so that water tends to be preferentially removed from the brain (39, 62, 106, 144). The action of steroids on intracranial pressure is less well understood. Edema associated with focal and chronic lesions is more amenable to treatment than acute diffuse edema; CSF production is also reduced by glucocorticoid therapy (27,60,85, 143). An increase in the volume of the CSF compartment may cause raised intracranial pressure; this is synonymous with hydrocephalus, which may be the primary cause (the sources of obstructive and communicating hydrocephalus need not be enumerated here), or may develop as a secondary event, due to obstruction of the foramen magnum or tentorial hiatus during the expansion of a primary intracranial mass lesion (14). The most labile source of increase of intracranial pressure, and one which has great relevance for the clinical management of intracranial hypertension, is an increase in the cerebral blood volume (Table 7.1). This may be caused by an arterial vasodilatation, or by obstruction of the venous outflow from the intracranial cavity. The former mechanism is related to increases in cerebral blood flow, although these may be self-limiting due to the intracranial hypertension produced; the latter mechanism is related to reductions in cerebral blood flow, The most powerful vasodilating agent is carbon dioxide; any rise above TABLE 7.1 Factors Which Increase and Decrease Intracranial Pressure via Changes in Cerebral Blood Volume
Increase
Hypercapnia (any degree) Hypoxia (pA0 2 < 50 mm. Hg) REM sleep Volatile anesthetic agents Nitrous oxide
Decrease
Hypocapnia (any degree) Hyperoxia (pA0 2 1000-1500 mm. Hg) Hypothermia Barbiturates Neuroleptanalgesia
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CRANIOSPINAL VOLUME AND PRESSURE
SAP (mmHg)
SSP
(nmHg)
Left
VFP
(mmHg)
Right
VFP
ImmHg)
~l
;
;;.
~]---------_ , ~1__" " "," " -'·_",'JfC.'~" ~1---1IIlIlIllIIl"'-7. . . :>*i ,. 1000 mm. Hg) can both reduce intracranial pressure by causing cerebral vasoconstriction and a reduction in cerebral blood volume (81, 90, 97). Hypothermia also reduces intracranial pressure by a similar mechanism (66, 88, 122). The volatile anesthetic agents halothane, tricWoroethylene, and methoxyflurane cause cerebral vasodilatation and increase the intracranial pressure (24, 41, 87, 121). Nitrous oxide and the intravenous agent, ketamine, can
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CLINICAL NEUROSURGERY
82
83
also cause intracranial hypertension (36, 146). Conversely, neuroleptanalgesic agents and barbiturates, which reduce cerebral blood flow, produce a slight reduction of intracranial pressure (23, 93, 122, 129). Other drugs which increase intracranial pressure, such as morphine, pentazocine, and diazepam produce their effects through respiratory depression with production of hypercapnia (5, 54, 121, 129). Intracranial pressure commonly rises at night; pressure waves are more frequent then. This has been attributed to vasodilatation occurring particularly during periods of rapid eye movement sleep (37). Changes in arterial blood pressure may influence intracranial pressure by altering cerebral blood volume; this can occur when cerebrovascular autoregulation is severely impaired so that the blood vessels behave in a pressure-passive manner to changes in arterial pressure (31, 65, 67, 102). In some circumstances, increases in arterial pressure may cause an equivalent, passive rise in intracranial pressure with little change in cerebral blood flow; in this situation arterial distension must be balanced by capillary or venous obstruction (13, 84, 120). A change in cerebral blood volume is the likely common basis for all pressure waves. Band C waves can be directly linked to changes in respiration and blood pressure with secondary effects on the cerebral vasculature. The plateau or A waves are accompanied by angiographically observed vascular dilatation and by an increase in cerebral blood volume (116), although there is no increase in cerebral blood flow (16). In practice, several of the factors involved in the genesis of increased intracranial pressure may operate at the same time. For instance, patients with cerebral metastases from bronchial carcinoma often have severe cerebral edema, and may also develop hypercapnia and hypoxia, all of which will produce additive effects on intracranial pressure. These mechanisms determine the direction of change of intracranial pressure, but the factor which regulates the extent of the increase in pressure is the intracranial volume-pressure relationship of the patient at that particular time.
Intracranial Volume-Pressure Relationships During progressive expansion of an intracranial mass lesion there is little increase in intracranial pressure at first because an equivalent volume of CSF and venous blood can be expelled from the cranial cavity to accommodate the mass (63). This mechanism has been known since the last century, but it forms the basis of the intracranial volume-pressure relationship. If the additional volume is plotted against intracranial pressure, the resultant is not a straight line but an exponential curve rising little at first, but steepening progressively as intracranial compensation is exhausted. This curvilinear relationship has been shown in experimental animals subjected
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CRANIOSPINAL VOLUME AND PRESSURE
CLINICAL NEUROSURGERY
to inflation of intracranial balloons at a steady rate (67), in children with hydrocephalus (125), and more recently in patients with raised intracraniaJ pressure from a variety of causes including tumor, head injury, cerebrovascular disease, and hydrocephalus (94, 96). The critical factor is the increase in pressure that results from a given increase in intracranial volume (Fig. 7.4). In effect this is a measure of the gradient of the volume-pressure curve at any point; the expression dPjdV is the inverse of compliance and can be termed elastance (75). The elastance value of the intracranial contents determines the amount of increase in intracranial pressure which will result from any of the stimuli described in the last section. A good illustration of this is seen by comparing the action of the volatile anesthetic agents on intracranial pressure in patients with normal CSF pathways and those with intracranial space-occupying lesions. These agents, which cause cerebral vasodilatation, produce only a small increase in intracranial pressure in patients with normal CSF pathways, but produce large increases up to 50 mm. Hg in patients with intracranial tumors, even when the resting intracranial pressure is not increased (24,41, 121). Hypercapnia in the presence of an intracranial mass will have a similarly augmented effect (Fig. 7.5). Another example of this phenomenon is the plateau wave, which occurs characteristically in patients" ith mildly elevated intracranial ICP
mmHg 70 60
dP2> dP1
50
dP2
40 30 20 10
UNITS OF VOLUME FIG. 7.4. Theoretical intracranial volume-pressure curve. As additional volume increases and intracranial pressure (ICP) rises, uniform increments of volume (dV) cause larger and larger rises of intracranial pressure (dP). Intracranial elastance (dP jdV) thus increases in parallel with the intracranial pressure during progressive addition to the volume of the intracranial con tents.
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84
85
SAP (mmHg)
SSP
(mnHg)
Left
VFP
(mmHgJ
FIG. 7.5. Effect of carbon dioxide on baboon with intracranial space-occupying lesion. Ventricular fluid pressure (VFP) and anterior sagittal sinus pressure (SSP) rise steeply with inhalation of 3 per cent CO 2 , followed rapidly by systemic arterial pressure (SAP) in a vasopressor response. Contrast this striking response with Figure 7.3.
pressure, many of whom have brain tumors and most of "hom have papilledema (79). In both of these situations spatial compensation is practically exhausted, intracranial elastance is increasing, and the small additional volume produced by slight cerebrovascular dilatation is sufficient to cause an enormous rise in intracranial pressure. A similar mechanism may explain sudden neurological deterioration in patients with head injuries and other intracranial pathological processes. Clearly, a measurement of brain elastance ,~\ ould be of value since measurement of intracranial pressure alone can detect intracranial hypertension only as it occurs, but cannot forecast its occurrence; changes in elastance may precede large rises in intracranial pressure. This 'wish for further in-
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CRANIOSPINAL VOLUME AND PRESSURE
CLINICAL NEUROSURGERY
formation has led to our investigations of the volume-pressure response as an index of intracranial elastance. The V olume-Pressure Response In patients in whom intracranial pressure monitoring is being conducted by means of an intraventricular catheter connected to an externally placed transducer, it is sometimes necessary to flush the system with small volumes of saline in order to clear the catheter (79). In doing this, we were struck by the varying changes in intracranial pressure that could result from these small alterations in CSF volume, and it was felt worthwhile to perform small volumetric changes in a better regulated manner. After a period of trial and error, a volumetric change in patients of 1 ml. in one second was used and the resultant immediate change in intracranial pressure (properly, ventricular fluid pressure) was termed the volume-pressure response. It is expressed in mm. Hgjml. and is therefore an index of intracranial elastance (94). As resting intracranial pressure rises, the volume-pressure response is increased in parallel, although this relationship is less clear in patients with considerably enlarged ventricles (99) (Fig. 7.6). The volume-pressure response is also related to the amount of brain shift seen in patients with head injuries and brain tumors, and is reduced following surgical decompression 10 9
8 7
VPR mmHg
6
y=0·16x-0·08 r = O·84 P
