NEUROSURGICAL ANAESTHESIA
Applied cerebral
physiology
Pranoy Das
Astri Luoma
Abstract
This article reviews cerebral metabolism and blood flow, and the pres-
sure dynamics within the cranial cavity. The brain functions within the
confines of the cranial cavity and it is important to understand the dy-
namics of the parenchyma, cerebrospinal fluid and blood in relation to
intracranial pressure (ICP) and metabolic needs. It requires an uninter-
rupted supply of oxygen and glucose to maintain its basal energy re-
quirements and these are increased during periods of enhanced
activity. Cerebral blood flow (CBF) is therefore critical for normal cere-
bral function. Its control is dictated by local intrinsic metabolic needs
as well as extraneous factors such as arterial blood pressure, arterial
carbon dioxide and oxygen tension, temperature and neural factors;
all of which can be measured to guide therapy.
Keywords Cerebral autoregulation; cerebral blood flow; cerebral
metabolism; intracranial pressure
Royal College of Anaesthetists CPD Matrix: 1A01
The contents of the cranium are brain parenchyma (80%), blood
(9%), cerebrospinal fluid (CSF; 6%) and interstitial fluid (5%).
The brain’s primary function is the generation of neuronal action
potentials in response to stimuli. This function is mediated by
ionic movement against electrical gradients and the release of
neurotransmitters at synaptic junctions. The normal physiology
of the brain is energy intensive requiring large amounts of
adenosine triphosphate (ATP). Glucose is the primary metabolic
fuel and requires a sufficient supply of oxygen for the oxidative
process.
This article explores the pressure dynamics within the cra-
nium and the physiological mechanisms that maintain supply of
oxygen and glucose to the brain.
Monro-Kellie doctrine and intracranial pressure
After closure of the cranial sutures, the cranial cavity functions as
a rigid box with no room for expansion. The intracranial pressure
(ICP) is maintained between 7 and 12 mmHg in normal cir-
cumstances. The Monro-Kellie doctrine describes the pressuree
volume relationship within the cranial cavity. It states the sum
Pranoy Das MBBS MRCSEd is a Clinical Research Fellow at the
National Hospital for Neurology and Neurosurgery, London, UK.
Conflict of interest: none.
Astri Luoma MBChB FRCA FFICM is a Consultant Neuroanaesthetist at
the National Hospital for Neurology and Neurosurgery, London, UK.
Conflict of interest: none.
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Please cite this article as: Das P, Luoma A, Applied cerebral physiology, Anaesthesia and intensive care medicine, https://doi.org/10.1016/
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Learning objectives
After reading this article, you should understand the:
C importance of an uninterrupted supply of oxygen and glucose
for normal cerebral metabolism
C fundamentals of the regulation and measurement of cerebral
blood flow
C concept of intracranial pressure and how it affects cerebral
perfusion pressure
of the volumes of brain, CSF and intracranial blood is constant.
Since the intracranial volume is fixed, an increase in one of the
three intracranial components will result in a rise in ICP unless
compensated for by a reduction in volume of another compo-
nent. Initially, a rise in ICP is compensated for by CSF migration
into the spinal compartment accompanied by an increase in CSF
absorption and decrease in production, and a reduction in cere-
bral blood flow. As these compensatory mechanisms are over-
whelmed, intracranial compliance falls and ICP rises
dramatically with even a small increase in intracranial volume.
This could lead to brainstem compression if untreated, and
manifest as hypertension, bradycardia and irregular respiration
(Cushing’s reflex).
ICP is a dynamic pressure with fluctuations occurring with
arterial pulsation, position, respiration, coughing and straining. It
may be measured using an intracranial pressure bolt or external
ventricular drain (Figure 1).
Managing raised ICP
Surgically, raised ICP may be controlled by CSF diversion using
an external ventricular drain or by a decompressive craniectomy.
Medical measures for ICP control aim at reducing intracranial
blood volume or interstitial fluid volume. Reduction of intra-
cranial blood volume can be achieved by optimizing ventilation
to reduce arterial carbon dioxide tension (PaCO2) and improve
oxygenation, increasing venous drainage with a head-up posi-
tion, and providing adequate sedation and muscular relaxation to
reduce cerebral metabolic rate and intrathoracic pressure. Inter-
stitial fluid volume reduction can be achieved by fluid restriction
or by the administration of diuretics (e.g. mannitol and furose-
mide) or corticosteroids.
Cerebrospinal fluid (CSF)
CSF is an ultrafiltrate of plasma that circulates through the ce-
rebral ventricles and the central canal of the spinal cord. It is
formed (and reabsorbed) at the rate of 500 ml/day by energy
dependent perfusion-related processes in the choroid plexus and
the ependymal lining of the lateral ventricles. It flows via the
foramina of Monro to the third ventricle, and then to the fourth
ventricle through the aqueduct of Sylvius. CSF then flows into
the central canal of the spinal cord and the subarachnoid spaces
through the median foramen of Magendie and lateral foramina of
Luschka. CSF is ultimately absorbed by the subarachnoid villi
into the cerebral venous sinuses. If the rate of CSF formation
exceeds that of absorption, hydrocephalus ensues.
1 Ó 2019 Published by Elsevier Ltd.
 NEUROSURGICAL ANAESTHESIA
Intracranial pressure–volume curve
30
'P2
ICP (mmHg)
20
'P1 'V2
'V1
10
0 Although the brain constitutes only 2% of the total body
Intracranial volume
(arbitrary units)
ICP, intracranial pressure; P, pressure; V, volume.
Figure 1
Blood–brain barrier
The blood–brain barrier (BBB) exists between the bloodstream
and the central nervous system (CNS). It is a semi-permeable
membrane consisting of three layers: the vascular endothelium
with its basement membrane, the astrocyte foot processes and
pericytes. The endothelial cells have very few pinocytic vesicles
and are sealed by tight junctions with no anatomical gaps. This
provides a high electrical resistance barrier. The BBB explains the
difference in constitution of the CSF and plasma. CSF has a very
low protein content when compared to plasma (0.2 versus 60 g/
L). Increased levels of protein in CSF would indicate a disruption
to the BBB. Concentrations of potassium, calcium, glucose, urea
and lymphocytes are lower in CSF.
The passage of substances across the BBB is directly propor-
tional to their lipid solubility but is inversely proportional to
molecular weight, ionic charge and degree of plasma-protein
binding. It is facilitated by active transport mechanisms that
require energy. Lipophilic substances (carbon dioxide, oxygen,
volatile anaesthetic agents) pass freely, unlike large-molecular-
weight molecules (e.g. proteins) and highly charged moieties
(e.g. sodium ions). Proteins and drugs (e.g. penicillin) cannot
cross the barrier unless it is inflamed (e.g. in meningitis). The
integrity of the barrier can be examined by the intravenous in-
jection of radioactive isotopes bound to protein; scanning tech-
niques can then be used to determine whether the radioactive
label is escaping from cerebral vessels. Ruptured aneurysms and
increased permeability at tumour sites may be detected using
such techniques.
Water moves freely across the BBB via astrocytes expressing
aquaporin-4 (AQP4). This depends on osmotic gradients. Sudden
changes in plasma osmolality secondary to changes in electrolyte
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or glucose concentrations can therefore lead to potentially
problematic fluid shifts in the brain. This emphasizes the
importance of correcting sodium and glucose abnormalities
slowly. Changing osmotic gradients may also be used to reduce
ICP via fluid shifts (e.g. using hypertonic saline). The BBB is
disrupted by a number of processes such as hypertension, stroke,
trauma, status epilepticus, hypercarbia, hypoxia, and especially
inflammation (chemical, infective or autoimmune). When
disruption occurs, fluid movement becomes largely dependent
on hydrostatic gradients.
Cerebral blood flow
Blood flow to the brain is primarily by the paired internal ca-
rotid arteries anteriorly and the paired vertebral arteries poste-
riorly. About 70% of cerebral blood flow (CBF) is supplied by
the internal carotid arteries. The anterior and posterior circu-
lations anastomose at the base of the brain to form the Circle of
Willis. There are numerous anatomical variations in the Circle
of Willis with an incomplete anastomosis in around 50%
individuals.
mass, it receives 15% of the cardiac output (750 ml/min in
adults). Resting CBF is approximately 50 ml/100 g/min. The flow
is not evenly distributed. Grey matter, which is metabolically
more active, receives approximately 90 ml/100 g/min and in
these regions the rate of oxygen consumption, termed the cere-
bral metabolic rate for oxygen (CMRO2), is about 3 ml/100 g/
min. White matter receives about 20 ml/100 g/min and its
CMRO2 is approximately 1 ml/100 g/min. The level of CBF is
critical. Complete interruption of CBF produces loss of con-
sciousness within seconds as does a reduction of CBF to
approximately 20 ml/100 g/min. Neuronal conversion to anaer-
obic metabolism occurs below 18 ml/100 g/min and the elec-
troencephalogram becomes flat. Brain cell death (infarction)
takes place at about 3 h with flows of 10 ml/100 g/min and after
30 minutes at flows of 5 ml/100 g/min (Table 1).
Cerebral perfusion pressure (CPP)
The perfusion pressure (i.e. the arteriovenous pressure gradient)
in the brain is more complex than that of other organs because it
is confined within an incompressible vault. It is dependent on the
pressure difference between the mean arterial pressure (MAP) or
Normal cerebral physiological values
CBF 750 ml/min or 15% of cardiac output
CBF (global) 50 ml/100 g/min
Grey matter 90 ml/100 g/min
White matter 20 ml/100 g/min
CMRO2 (grey matter) 3 ml/100 g/min
CMRO2 (white matter) 1 ml/100 g/min
CMRGI (global) 30 mg/100 g/min or 25% of total body
consumption
CBF, cerebral blood flow; CMRO2, cerebral metabolic rate for oxygen; CMRGl,
cerebral metabolic rate for glucose.
Table 1
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 NEUROSURGICAL ANAESTHESIA

the driving pressure (measured at brain level) and ICP or the

pressure that needs to be overcome to supply adequate blood to Effect of PaCO2 on cerebral blood flow
the brain. This pressure difference is known as the CPP. A
normal CPP is 70e80 mmHg; the threshold for critical ischaemia 100
is 30e40 mmHg. As can be seen from the equation below, even
at normal levels of MAP, an elevated ICP of more than 20 mmHg
will compromise CPP and therefore reduce cerebral blood flow.

CBF (ml/100 g/minute)

This emphasizes the importance of maintaining an adequate
MAP in circumstances such as head injury to ensure adequate
perfusion.
50
Cerebral perfusion pressure ðCPPÞ ¼ Mean arterial pressure ðMAPÞ
 Intracranial pressure ðICPÞ

Control of cerebral blood flow 20

Various mechanisms exist to maintain an adequate basal supply

of blood and therefore substrate to meet the energy demands of
0
the brain. Physiological variables, such as arterial carbon dioxide
0 3 8
and oxygen levels, influence CBF and local regulatory mecha-
PaCO2 (kPA)
nisms direct blood flow to regions of the brain that are particu-
larly active (i.e. blood flow is coupled to local metabolic needs) CBF, cerebral blood flow; PaCO 2 , arterial carbon dioxide tension.
(Box 1).
Figure 2
Arterial carbon dioxide tension (PaCO2)
Carbon dioxide is a potent vasodilator of cerebral blood vessels.
oxygen content). This effect explains the modest increase in CBF
As PaCO2 rises, there is a linear increase in CBF between 3.5 kPa
(an increase of 10%) when breathing 100% oxygen.
(26 mmHg) and 8 kPa (60 mmHg) (Figure 2).
Above 8 kPa cerebral vessels are maximally dilated and no Autoregulation
further increase in vessel diameter is possible; conversely, at a Autoregulation is the maintenance of a constant CBF despite
PaCO2 of 3 kPa cerebral vessels are maximally constricted. The variations in CPP. Under normal conditions when both ICP and
effect of hypocarbia on cerebral vasculature is achieved by an cerebral venous pressure are low, systemic arterial perfusion
increase in brain hydrogen ion (Hþ) concentration and takes
place in minutes, reflecting the time taken for the conversion of
CO2 to HCO3 and Hþ in the perivascular space. The vaso-
constricting effect of a low PaCO2 is progressively attenuated by a
Effect of PaO2 on cerebral blood flow
fall in the brain’s bicarbonate level, which normalizes pH. The
100
opposite is true for prolonged hypercarbia.

Arterial oxygen tension (PaO2) and oxygen content

CBF is directly responsive to changes in oxygen delivery and
CBF (ml/100 g/minute)

remains unaltered until a threshold PaO2 of 6.8 kPa (50 mmHg) is

reached. Below this threshold CBF dramatically rises (Figure 3).
This corresponds to the steep part of the oxyhaemoglobin
dissociation curve (i.e. CBF is responsive not to PaO2 but to 50

Factors influencing cerebral blood flow

C Local neuronal activity 20

C Autoregulation
C Raised intracranial pressure
C Arterial carbon dioxide tension (PaCO2)
0
C Arterial oxygen tension (PaO2)
0 6.6
C Haematocrit
PaO2 (kPA)
C Temperature
C Autonomic nervous system regulation CBF, cerebral metabolism blood flow; PaO2, arterial oxygen tension.

Box 1 Figure 3

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 NEUROSURGICAL ANAESTHESIA
pressure (i.e. MAP) is the primary determinant of CPP. Between
a MAP of 50 mmHg and 150 mmHg the mean CBF remains
constant at 50 ml/100 g/min. However, autoregulation has its
physiological limits, above and below which CBF is directly
related to perfusion pressure (see Figure 4).
Autoregulation is achieved by alterations in cerebrovascular
resistance (CVR) (occurring over 10e60 s) caused by myogenic
reflexes to transmural tension in the resistance vessels; as CPP
increases from 50 to 150 mmHg, cerebral arterioles constrict and
therefore restrict increases in CBF. Autoregulation may be
modified by sympathetic nervous system activity. Chronic hy-
pertension or sympathetic stimulation shifts the autoregulatory
curve to the right, whereas sympathetic blockade or cervical
sympathectomy shifts the curve to the left. Symptoms of
ischaemia occur only when the MAP falls below 60% of the
lower autoregulatory limit. Above the upper autoregulatory limit,
mechanisms such as forced cerebral arteriolar dilatation, reversal
of hydrostatic gradients and cerebral oedema result in increases
of cerebral blood volume and ICP. Autoregulation is disrupted in
the presence of intracranial pathology, hypoxaemia, hypercarbia,
fixed vascular obstructions (e.g. carotid atheroma), and volatile
anaesthetic agents.
Cerebral metabolism
The brain requires more energy than any other organ in the
body. Glucose is the main energy source. Cerebral metabolic rate
for glucose (CMRGl) is about 30 mg/100 g/min, approximately
25% of the body’s total glucose consumption. The majority of
this energy is used to maintain ion gradients across neuronal
membranes via the Naþ/Kþ-ATPase ion pumps. Glucose crosses
the bloodebrain barrier via the GLUT 1 transporter and then
Autoregulation
Vessel
diameter
CVR
CBF (ml/100 g/minute)
CBF
50
CBV
0 relaxation and the application of positive end-expiratory pressure
0 50 100 150
CPP (mmHg)
CBF, cerebral blood flow; CBV, cerebral blood volume; CPP, cerebral
perfusion pressure; CVR, cerebrovascular resistance.
Figure 4
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enters cells via the appropriate glucose transporter (i.e. GLUT 1
to astrocytes, GLUT 3 to neurons and GLUT 5 to microglial cells).
Under normal aerobic conditions, glucose contributes to
tricarboxylic acid (TCA) cycle and oxidative phosphorylation to
provide ATP for energy. The remainder is converted to amino
acids, proteins and lipids. Under hypoxic conditions the glucose
receptors are upregulated. Glucose is anaerobically metabolized
by glycolysis to form lactate, which is converted to pyruvate in
neurons and can then be used in the TCA cycle. Lactate can be
actively removed across the bloodebrain barrier via a mono-
carboxylate transporter. During fasting the brain utilizes ketone
bodies (exported from the liver) which are broken down to acetyl
coenzyme A (acetyl-CoA). This is oxidized via the TCA cycle to
yield energy. Gluconeogenesis can also occur in such conditions.
If CBF ceases, glycogen reserves can be exhausted within 2 min.
Hypoglycaemia results in cerebral cellular dysfunction, mani-
festing as anxiety and confusion, convulsions and eventually
coma.
Flow metabolism coupling and local chemical
regulators
Local neuronal activity causes an increase in CMRO2 and CMRGl,
and is accompanied by an increased regional CBF to match
glucose and oxygen use with delivery. The parallel change in CBF
with CMRO2 and CMRGl is known as flow-metabolism coupling.
There is evidence to suggest that CBF may be modulated by
changes in glucose consumption rather than oxygen consump-
tion under hypoxic conditions. Vasoconstriction occurs by the
action of free calcium ions, thromboxane (a product of arach-
idonic acid/endoperoxidase metabolism) and endothelin
(secreted by endothelial cells by endothelin-converting enzyme
acting on endothelin A receptors in vascular smooth muscle).
Some calcium-channel blockers blunt hypoxic vasodilation and
prevent adenosine release. Potent vasodilators include peri-
vascular potassium (released in high concentrations during sei-
zures, hypoxia, and electrical stimulation), adenosine (an ATP
metabolite produced in response to arterial hypotension and
hypoxia), as well as prostaglandins (e.g. PGE2 and prostacyclin
(PGI2)), lactate, acetylcholine, serotonin, substance P and nitric
oxide.
Other factors affecting cerebral blood flow and
intracranial pressure
CBV (ml/100 g)
Raised cerebral venous pressure
4.0 An elevated cerebral venous pressure reduces cerebral venous
drainage, expands cerebral blood volume, disrupts capillary
Starling’s forces leading to cerebral oedema, raises intracranial
pressure and therefore reduces CBF. It may be caused by
obstruction of venous drainage by neck compression from neck
collars or tracheal tube ties, from head-down positioning (e.g.
during central line insertion) or from increased intrathoracic
pressure (e.g. from coughing, straining, incomplete muscle
during positive pressure ventilation).
Haematocrit
Haematocrit is the main determinant of blood viscosity and of
oxygen content (and therefore oxygen delivery). CBF changes
inversely with whole blood viscosity. Within the normal range of
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 NEUROSURGICAL ANAESTHESIA
haematocrit, this has a minimal effect on CBF. However, in
certain situations when CBF is pathologically decreased (e.g.
cerebral vasospasm following subarachnoid haemorrhage), a
decrease in haematocrit by haemodilution may improve CBF.
Temperature
Hypothermia (body temperature of less than 35 C) reduces
CMRO2 and CMRGl, and as a result of flow-metabolism
coupling, CBF decreases. The converse is true for hyperther-
mia up to a body temperature of 42 C, above which neuronal
damage occurs with a corresponding reduction in oxygen up-
take. For every 1 C change in body temperature CBF changes by
5%. At 18 C, the cerebral metabolic rate is so low that safe
circulatory arrest (e.g. during cardiac surgery) is possible
without causing ischaemic cerebral damage. This effect forms
the basis of clinical trials of hypothermia in head injury and
cerebrovascular surgery.
Autonomic nervous system regulation
Cerebrovascular vessels have a rich innervation. Large intracra-
nial and pial vessels have a nerve supply originating from
autonomic and sensory ganglia. These contain many vasoactive
transmitters, which seem to have a role in the regulation of CBF.
Although the exact function of the various neurons is difficult to
define, it seems that parasympathetic stimulation produces ce-
rebral vasodilation and sympathetic stimulation produces vaso-
constriction. Similarly, smaller intracerebral arterioles have rich
innervation with many neurotransmitters.
The cerebral physiology described forms the basis of man-
agement of patients undergoing intracranial neurosurgery and on
neurocritical care. In both situations, maintenance of normal
intracranial physiology and the prevention of brain injury are
key. For example, to prevent secondary injury after traumatic
brain injury careful maintenance of MAP, oxygenation and
control of PaCO2 are required. ICP, cerebral blood flow and ce-
rebral oxygenation and metabolic status may be measured for
diagnosis and to optimize therapy and develop individualized
treatment plans for patients. For example, in cerebral vasospasm
following aneurysmal subarachnoid haemorrhage, brain tissue
oxygenation may be measured and used to guide therapy
(oxygenation and blood pressure management) and as a prog-
nostic indicator. Similarly, ICP monitoring and brain tissue
oxygenation may be used in the management of traumatic brain
injury.
Monitoring of cerebral blood flow and function
(see article on Principles of intraoperative neurophysiological
monitoring and anaesthetic considerations on pp 00e00 of this
issue)
A variety of monitoring techniques are used singularly or
together to assess and monitor cerebral physiology in patients
who cannot be clinically assessed due to intracranial pathology
such as traumatic brain injury or intracranial haemorrhage.
Measurement of cerebral blood flow
A number of techniques for the measurement of CBF have
emerged since the pioneering method of Kety and Schmidt in
1945. Many techniques now allow measurement of regional
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blood flow, giving useful information about changes in blood
flow in diseased parts of the brain.
Kety-Schmidt technique: The Fick principle states that the blood
flow through an organ can be measured by determining the
amount of an inert substance (Q) removed from the bloodstream
by the organ per unit time, and dividing that value by the dif-
ference between the concentration of the substance in arterial
blood [A] and the concentration in the venous blood [V] from the
organ.
CBF ¼ Q = ð½A  ½vÞ
Kety and Schmidt used nitrous oxide (N2O) as the inert sub-
stance. Patients breathed 15% N2O for 10 minutes while serial
samples were taken from a peripheral artery and the jugular
venous bulb and analysed for N2O content until equilibrium
was reached. The total value of N2O taken up was determined
by calculating the N2O content of jugular venous blood at
equilibrium. This technique has a number of disadvantages:
the N2O assay is time consuming and tedious and, when low
CBF exists, the technique underestimates CBF. Most impor-
tantly, it gives a value for global CBF but not regional CBF. A
variation of the Kety-Schmidt technique substitutes heat for
the inert substance allowing a thermodilution principle to
assess CBF.
Xenon-133 wash-out: Regional cortical blood flow can be
measured by monitoring the decay of inhaled radioactive isotope
xenon-133 by positioning scintillation counters over the head.
The slope of the wash-out curve of the radioactive tracer is
proportional to the CBF under the detector. The technique pro-
vides a two-dimensional analysis of regional CBF but primarily
evaluates cortical blood flow. Three-dimensional resolution can
be achieved using CT reconstruction in a technique called single-
photon emission CT (SPECT).
Other imaging techniques: Since metabolism is so tightly
coupled to blood flow, the uptake of 2-deoxyglucose can be used
to estimate regional blood flow. If 2-deoxyglucose is labelled with
a positron emitter (e.g. oxygen-15, fluorine-18, carbon-11), its
uptake can be followed using positron emission tomography
(PET) scanning and CBF can be estimated.
Functional MRI (fMRI) can produce brain function maps,
where changes in brain neuronal activity are reflected in changes
in regional CBF. Tomographic images can also be produced
without the use of external contrast agents by a technique called
blood oxygen-level-dependent (BOLD) fMRI. Regional neuronal
activation, especially in the cerebral cortex, triggers an influx of
oxygenated haemoglobin that decreases the regional deoxy
haemoglobin levels, causing an increased MRI signal intensity.
Transcranial Doppler ultrasonography (TCD) involves the
application of a low-frequency (2 MHz) pulse range-gated ul-
trasound beam to the thin-boned trans-temporal window,
allowing assessment of the middle and anterior cerebral arteries.
Flow velocities within these vessels can be determined using the
Doppler effect. If the angle of the ultrasound beam and the
5 Ó 2019 Published by Elsevier Ltd.
 NEUROSURGICAL ANAESTHESIA
diameter of the vessel remain constant, relative changes in flow
velocity correlate closely with changes in CBF.
Monitoring of cerebral oxygenation
Jugular bulb oximetry: The jugular bulb is a dilatation of the
internal jugular vein just below the base of the skull and may be
catheterized using the Seldinger technique. Blood may be
sampled for oxygen tension and saturation, giving an indication
of CBF (lower values reflecting greater uptake by the brain and
therefore less blood flow, assuming O2 consumption remains
constant). The major disadvantage of this technique is that only
global CBF can be estimated and not regional changes. In addi-
tion, if CBF and oxygen consumption both decrease (e.g. in se-
vere brain injury), jugular venous saturation may be unchanged.
Intracerebral microdialysis: This technique involves the inser-
tion of a fine catheter, containing a dialysis membrane perfused
with Ringer’s solution, into brain parenchyma. It enables mole-
cules involved in cerebral metabolic pathways to be directly
monitored and this can provide information on the adequacy of
cerebral oxygenation and blood flow. Metabolites such as
glucose, pyruvate, lactate, glutamate and glycerol or drugs (e.g.
phenytoin) diffuse into the solution of the probe from the inter-
stitial fluid (extracellular space) across the membrane and are
analysed. The lactate:pyruvate ratio reflects regional cerebral
oxygen availability, and has been used clinically in the treatment
of head injury and subarachnoid haemorrhage. A rise in the ratio
suggests that anaerobic metabolism due to insufficient regional
cerebral blood flow is occurring (secondary to hypoxia); treat-
ment may then be taken to correct this impaired physiology.
Cerebral oxygen partial pressure: Sensors can be inserted into
the brain parenchyma to measure the partial pressure of oxygen
in the extracellular fluid of the brain (pBRO2); this reflects the
availability of oxygen for oxidative metabolism. Values obtained
generally reflect the balance between oxygen delivery and con-
sumption. Correct siting of the probe is essential to measure focal
pBRO2. The per haematoma site in TBI is ideal but is technically
challenging and increases the risk of further injury. In routine
practise, the non-dominant frontal lobe is the chosen site for
probe insertion. This technique is also used in research to
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optimize the treatment of subarachnoid haemorrhage and trau-
matic brain injury.
Near infra red spectroscopy: This monitoring technique is based
on the principle that light with wavelengths in the near infra red
region (650e900 nm) transmits through biological tissues. It is
increasingly being used to image biological events in the cerebral
cortex. Photons produced by a laser photodiode are directed into
the skull, and while many are reflected and dispersed, some are
transmitted. Certain coloured compounds within the tissues
(chromophores), especially oxyhaemoglobin, deoxyhaemoglobin
and oxidized cytochrome oxidase, have characteristic absorption
spectra. The emergent light intensity is detected and a computer
converts the changes in light intensity into changes in chromo-
phore concentration. Clinical applications of this technique
include monitoring of cerebral oxygenation, CBF and volume.
Measuring intracranial pressure
The commonly used methods of monitoring ICP are ventricular
catheters (EVD) and intracranial pressure bolts. An EVD mea-
sures global ICP and also therapeutically diverts CSF. These
require high levels of training for insertion, and have the risk of
infection and brain injury. Microtransducer systems or paren-
chymal catheters measure focal ICP. It is important to consider
the location of the catheter when assessing the measured ICP.A
FURTHER READING
Barrett KE, Barman SM, Boitano S, Brooks H. Ganong’s review of
medical, physiology. 26th edn. New York: McGraw Hill Medical,
2016.
Edvinsson L, Krause DN, eds. Cerebral blood flow and metabolism.
Philadelphia: Lippincott, Williams and Wilkins, 2002.
Lawther Bradley K, Kumar Sajith, Krovvidi Hari. Bloodebrain barrier.
Cont Educ Anaesth Crit Care Pain August 2011; Volume 11:
128e32. https://doi.org/10.1093/bjaceaccp/mkr018.
Smith Martin. Multimodality neuromonitoring in adult traumatic brain
injury: a narrative review. Anesthesiology 2018; 128: 401e15.
https://doi.org/10.1016/j.anclin.2016.04.005.
Tosh W, Patteril M. Cerebral oximetry. BJA Education December 2016;
Volume 16: 417e21. https://doi.org/10.1093/bjaed/mkw024.
6 Ó 2019 Published by Elsevier Ltd.