Pathophysiology

Resting intracranial pressure represents that equilibrium pressure at which cerebrospinal fluid (CSF) production and absorption are in balance and is associated with an equivalent equilibrium volume of CSF. CSF is actively secreted by the choroid plexus at about 0 35 ml/min and production remains constant provided cerebral perfusion pressure is adequate. CSF absorption is a passive process through the arachnoid granulations and increases with rising CSF pressure:

CSF pressure = Resistance to CSF outflow x CSF outflow rate + sagittal sinus pressure

According to the above formula (known as the Davson's equation), the mean intracranial pressure (ICP) explained solely by CSF circulation, is proportional to the resistance to CSF outflow, CSF production rate, and sagittal sinus pressure. Marmarou et al.s proposed a modification to this formula, stating that average ICP can be expressed by two components: CSF circulatory and vasogenic. Thus, the Davson formula can be rewritten as:

iv^i CSF circulation Vasogenic 1XCSF ^ formation T 1 SS

vasogenic where RCSF is the resistance to CSF outflow and Pss is the sagittal sinus pressure.

Tt is difficult to understand why, under steady conditions, a vascular bed which is anatomically separated from the CSF compartment may modify mean intracranial pressure. The hypothesis has been proposed recently6 that continuous pulsation of arterial blood is transformed by both non-linear components of CSF pressure-volume compensation (exponential pressure-volume curve) and regulation of CBF (autoregulation) to appear as the additional term "TCPvasogenic" to complete Davson's formula. Tts contribution to total tCp can be as large as 60% in pathological circumstances.

The "four-lump" concept describes most simply the causes of raised intracranial pressure: the mass, CSF accumulation, vascular congestion, and cerebral oedema (Box 7.2).7-9

Box 7.2 Mechanisms of raised intracranial pressure

A: Mass lesions

Haematoma, abscess, tumour

B: CSF accumulation

Hydrocephalus (obstructive and communicating), including contralateral ventricular dilatation from supratentorial brain shift C: Cerebral oedema

Increase in brain volume as a result of increased water content.

1. Vasogenic - vessel damage (tumour, abscess, contusion)

2. Cytotoxic - cell membrane pump failure (hypoxaemia, ischaemia, toxins)

3. Hydrostatic - high vascular transmural pressure (loss of autoregulation; post intracranial decompression)

4. Hypoosmolar - hyponatremia

5. Interstitial - high CSF pressure (hydrocephalus) D: Vascular (congestive) brain swelling

Increased cerebral blood volume Arterial vasodilatation (active, passive) Venous congestion/obstruction

The description of a patient with raised ICP as having cerebral congestion, vasogenic oedema, etc. can only be a working approximation, albeit useful, until our rather crude methods of assessment are refined. In adults the normal ICP under resting conditions is between 0 and 10 mmHg, with 15 mmHg being the upper limit of normal. Active treatment is normally instituted if ICP exceeds 25 mmHg for more than five minutes, although a treatment threshold of 15-20 mmHg has been suggested to improve outcome.10 In the very young, the upper limit of normal ICP is up to 5 mmHg.4,11 Small increases in mass may be compensated for by reduction in CSF volume and cerebral blood volume but, once such mechanisms are exhausted, ICP rises with increasing pulse pressure and with the appearance of spontaneous waves (plateau and B waves).12 There is an exponential relationship between increase in volume of an intracranial mass and the increase in ICP, at least within the clinically significant range. This relationship is also helpful in understanding the most specific fluctuating component of ICP: the pulse amplitude (Figure 7.1a). It is derived from pulsation of arterial blood pressure but the change of its shape can be considerable. Classically, the pulse waveform of ICP can be depicted using the pressure-volume curve with the pulsating changes in cerebral blood volume drawn along the x (volume) axis13 (Figure 7.1b). The curve has three major zones:14 in the initial range ICP changes proportionally to the change of intracerebral volume. This is a zone of good compensatory reserve. Then, ICP starts to increase exponentially when intracerebral volume expands further. This is a zone of poor compensatory reserve and can be seen in clinical practice most often whenever there is any difficulty in managing a cerebrospinal volume-evolving process (head injury, poor grade subarachnoid haemorrhage, acute hydrocephalus, etc.). Finally, at very high ICP, when a decrease in cerebral perfusion pressure is too deep to secure any further arterial dilatation (that is, vessels are maximally dilated), the pressure-volume curve bends to the right (Figure 7.1b). Entering this zone represents the transition of the cerebrovascular bed from the state of active dilatation to passive collapse. When the transmural pressure further decreases, the additional compensatory reserve is gained at the expense of reduction of arterial blood volume and derangement of the autoregulatory cerebrovascular response.

ICPd 70o [mmHg]D52.5D

17-5D Go

ABPD 15Go [mmHg]o 12Go 90o 60o 30o--Go

4o 6o 8o

ICPo 25o [mmHg]o

ABPo 150o [mmHg]o 120o 9Go 60o 30o 0o

4o 6o 8o

4o 6o 8o

12-5o

"Critical' ICP

Derangedn cerebrovasculars reactivity

Derangedn cerebrovasculars reactivity

"Critical' ICP

Pulsatile cerebral bloodn volume

Figure 7.1 (a) Examples of ICP pulse waves. Peak-to-peak amplitude increases with increasing mean ICP (upper panel). Three distinctive "peaks" can be sometimes recorded (lower panel). (b) In a simple model, pulse amplitude of ICP (expressed along the y-axis on the right side of the panel) results from pulsatile changes in cerebral blood volume (expressed along the x-axis) transformed by the pressure-volume curve. This curve has three zones: a flat zone, expressing good compensatory reserve, an exponential zone, depicting poor compensatory reserve, and a flat zone again, seen at very high ICP (above the "critical" ICP) depicting derangement of normal cerebrovascular responses. The pulse amplitude of ICP is low and does not depend on mean ICP in the first zone. The pulse amplitude increases linearly with mean ICP in the zone of poor compensatory reserve. In the third zone, the pulse amplitude starts to decrease with rising ICP.

CO I

Pulsatile cerebral bloodn volume

Figure 7.1 (a) Examples of ICP pulse waves. Peak-to-peak amplitude increases with increasing mean ICP (upper panel). Three distinctive "peaks" can be sometimes recorded (lower panel). (b) In a simple model, pulse amplitude of ICP (expressed along the y-axis on the right side of the panel) results from pulsatile changes in cerebral blood volume (expressed along the x-axis) transformed by the pressure-volume curve. This curve has three zones: a flat zone, expressing good compensatory reserve, an exponential zone, depicting poor compensatory reserve, and a flat zone again, seen at very high ICP (above the "critical" ICP) depicting derangement of normal cerebrovascular responses. The pulse amplitude of ICP is low and does not depend on mean ICP in the first zone. The pulse amplitude increases linearly with mean ICP in the zone of poor compensatory reserve. In the third zone, the pulse amplitude starts to decrease with rising ICP.

Adapted from Miller et al.2 and Bingham et a/.21; based on data from Lofgren et al.14 and Avezaat et al.30

Pulse amplitude of ICP does not change with ICP in the first zone, then grows linearly with ICP in the second zone. In the third zone it starts to decrease with a further increase in ICP (Figure 7.2).

When monitored continuously, mean ICP presents a number of stereotypic patterns (Figure 7.3). The first eight

Figure 7.2 Relationship between mean intracranial pressure and amplitude of the intracranial pressure waveform in two patients. In the lower trace, there is an upper breakpoint in this relationship when cerebral perfusion pressure (mean arterial pressure - intracranial pressure) is less than 30 mmHg

panels (a-h) are representative for acute cases, such as head injury. Long term monitoring in other, non-acute cases, such as chronic hydrocephalus, produces specific but usually different patterns (Figure 7.3i,j):

1. Low and stable ICP (below 20 mmHg) - this pattern is specific for uncomplicated patients following head injury or during the first hours after trauma before ICP increases further (Figure 7.3a).

2. High and stable ICP (above 20 mmHg) - the most common picture following head injury (Figure 7.3b).

3. Vasogenic waves — B waves (Figure 7.3c), plateau waves (Figure 7.3d), or waves related to changes in arterial pressure and hyperaemic events (Figure 7.3e-g).

4. Refractory intracranial hypertension (Figure 7.3h) which usually leads to the death of the patient unless radical measures are taken (for example, surgical decompression).

5. Overnight recording of ICP in patients suffering from hydrocephalus with cyclically increased activity of B waves (Figure 7.3i) and benign intracranial hypertension (Figure 7.3j).

Spontaneous waves of intracranial pressure are usually associated with cerebrovascular dilatation. Cerebral blood volume increases during plateau waves (intracranial pressure > 50 mmHg for more than five minutes) and may be the result in some cases of inappropriate autoregulatory vasodilatation, described by Rosner and Becker15 as the so-called vasodilatatory cascade. An increase in cerebral blood volume causes an increase in ICP, a decrease in cerebral perfusion pressure, leading to vasodilatation, and a further increase in cerebral blood volume, etc., until the system reaches the state of maximal vasodilatation. Plateau waves are observed in patients with preserved cerebral autoregulation but reduced pressure volume compensatory reserve. Very high increases in ICP when associated with a reduction in cerebral perfusion pressure may dramatically decrease cerebral blood flow (Figure 7.4, p 200).16

Transcranial Doppler examinations reveal that middle cerebral artery flow velocity increases at the same rate as B waves (05-2/min) of intracranial pressure (Figure 7.5, p 201).17 Gradients of intracranial pressure may develop when herniation occurs - transtentorial, subfalcine, and foramen magnum. Blockage to the free flow of CSF between intracranial compartments leads to a much greater and more rapid rise in intracranial pressure in the compartment harbouring the primary pathology and hence to the final common sequence of transtentorial and foramen magnum coning. When intracranial pressure equals arterial blood pressure, angiographic pseudoocclusion occurs and reverberation, systolic spikes, or no flow may be seen on transcranial Doppler sonography (Figure 7.6, p 201). Patients will often satisfy the formal clinical criteria for

ABP 120

100 80 60

20 30

Time [min]

ICPn 30 [mmHg]

ABPn 120 [mmHg] 105

Time [min]

ABP 120 [mmHg] 90

ICP 50

ABP 120 [mmHg] 106

64 50

CPP 100 [mmHg] 86 72

ICP 50

ABP 120 [mmHg] 106

64 50

CPP 100 [mmHg] 86 72

20 30

Time [min]

ICP 50

10 0

ABP 120 [mmHg] 106 92 78

64 50 100 86 72 58 44 30

CPP [mmHg]

20 30

Time [min]

10 15

Time [min]

ABP [mmHg]

44 30 150

120 90 60 30 0 120

ICPn 120

ABPD

ICPn 120

Time [hours]

40 45

Time [hours]

Time [hours]

AMPn [mmHg]

Time [hours]

Time [hours]

Figure 7.3 Typical recordings of intracranial pressure.

(b) Increased and stable ICP after head injury.

(d) Plateau wave after head injury.

(e-g) Waves of ICP different from plateau commonly recorded after head injury:

(e) increases in ICP due to rapid increases in arterial blood pressure;

(f) changes in ICP caused by constriction/dilatation of vascular bed, due to variation in arterial pressure;

(g) longer increase in ICP associated with an increase in blood flow (monitored using TCD- FV).

(h) Intracranial hypertension - refractory (after head injury).

(i) Overnight recording in normal pressure hydrocephalus. Baseline pressure is specifically low with increased vasogenic dynamics observed as periods of increasing pulse amplitude (AMP) and magnitude of B waves.

0) Overnight monitoring in benign intracranial hypertension. Baseline pressure is elevated with moderate dynamics and gradually increasing magnitude of B waves

Figure 7.4 Rare occurrence of very deep plateau wave, when blood flow velocity (FVx) decreased by more than 60% of baseline. Notice the decrease in heart rate (HR) and hyperaemic increase in flow velocity after the ICP wave subsided. From Obrist et a/.20

brain stem death, for which transcranial Doppler examination is not a substitute.18,19 When ICP rises uncontrollably, it is often called "refractory intracranial hypertension". Mean ICP may increase to well above 80 mmHg, probably due to rapid brain swelling over a period of a few hours. Pulse amplitude of ICP is commonly secondarily reduced with activation of a Cushing response and a gradual rise of mean arterial pressure. The moment of brain stem herniation is commonly marked by a rapid decrease in mean arterial pressure, a rise in a heart rate, and a terminal decrease in cerebral perfusion pressure to negative values (Figure 7.7).

Cerebral perfusion pressure (CPP) is commonly defined as mean arterial blood pressure minus mean intracranial

ABP [mmHg]

ABP [mmHg]

Figure 7.5 B waves of intracranial pressure in a head-injured patient and their relationship to similar variations in middle cerebral artery flow velocity compared with fluctuations in arterial blood pressure (ABP)
Figure 7.6 Reversal of middle cerebral artery flow velocity (FV) in a patient who fulfils the criteria for brain stem death

pressure. Mean intracranial pressure closely approximates to mean cerebral venous pressure. The lower limit of CPP which will permit autoregulation, when intracranial pressure is raised, is about 40 mmHg. There is a paradox, however: the level of cerebral perfusion pressure below which outcome after severe head injury and associated parameters deteriorate is of the order of 60-65 mmHg (mean arterial pressure < 80 mmHg;

Figure 7.7 Example of two-day monitoring of a patient who died in the course of refractory intracranial hypertension on day 2. This was marked by a final decrease in CPP below 30 mmHg and an increase in heart rate (HR)

ICP >20 mmHg). Conventionally any elevation of ICP requires treatment if CPP is below 60 mmHg in adults for over five minutes. This paradox may partly reflect the "split brain" problem: autoregulation of cerebral blood flow to changes in CPP and the response to changes in arterial carbon dioxide tension (Paco2) may be impaired focally, leaving intact reactivity in other areas of the brain. If vasospasm is present, an even higher perfusion pressure may be required to provide adequate levels of cerebral blood flow.

Total cerebral blood flow may be increased or decreased in areas with absent reactivity. Hyperaemia is non-nutritional "luxury perfusion" where cerebral blood flow is in excess of the brain's metabolic requirements20 and accompanied by early filling of veins on angiography and "red veins" at operation. Cerebral vasodilators such as carbon dioxide will dilate "normal" arterioles, increase intracranial pressure, and may run the risk of reducing flow to damaged areas of brain (intracerebral "steal"). Inverse "steal" is one reason for the treatment of raised intracranial pressure by hyperventilation: an acute reduction of Paco2 vasoconstricts normal cerebral arterioles, thereby directing blood to focally abnormal areas.

Normally, cerebral blood flow is coupled to cerebral oxidative metabolism via multiple mechanisms involving local concentrations of hydrogen ions, potassium, and adenosine, for example. Status epilepticus leads to gross cerebral vasodilatation and intracranial hypertension as a result of greatly increased cerebral metabolism and local release of endogenous vasodilator agents. Depression of cerebral energy metabolism by anaesthesia and hypothermia may reduce cerebral blood flow and intracranial pressure where there is a large area of the brain with reasonable electrical activity21 and where normal flow-metabolism coupling mechanisms are intact as indicated by a reasonable cerebral blood flow carbon dioxide reactivity.22 There is a complex interaction between the properties of the CSF and the cerebral circulations that may be modelled (Figure 7.8).23-25 The relative contributions of abnormalities of CSF absorption and cerebral blood volume may be approximated by calculating the proportion of CSF pressure attributable to CSF outflow resistance and venous pressure from Davson's equation. Phenomena such as the interaction of autoregulation to changing CPP with Paco2 may be quantified.26

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