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Figure 2–7 shows an overview of the arterial system supplying the brain. The major arteries
are the vertebral and internal carotid arteries. The two posterior and single anterior
communicating arteries form the circle of Willis, which equalises blood pressures in the
brain’s anterior and posterior regions, and protects the brain from damage should one of the
arteries become occluded. However, there is little communication between smaller arteries
on the brain’s surface. Hence occlusion of these arteries usually results in localised tissue
damage.
Cerebral haemodynamics
The cardiac output is about 5 l/min of blood for a resting adult. Blood flow to the brain is
about 14% of this, or 700 ml/min. For any part of the body, the blood flow can be calcu-
lated using the simple formula
Resistance
Pressure
= flow Blood (2.1)
Pressure in the arteries is generated by the heart which pumps blood from its left ventricle
into the aorta. (Since pressure was historically measured with a mercury manometer, the
units are commonly expressed in terms of [mm Hg], although the official SI unit is the
Pascal [Pa].) Resistance arises from friction, and is proportional to the following expression
4
Diameter) (Vessel
Length Vessel
Viscosity Resistance × ∝ (2.2)
Hence blood flow is slowest in the small vessels of the capillary bed, thus allowing time for
the exchange of nutrients and oxygen to surrounding tissue by diffusion through the
capillary walls.
Approximately 75% of total blood volume is ‘stored’ in the veins which, because of
their high capacity, act as reservoirs. Their walls distend and contract in response to the
amount of blood available in the circulation. However, the function of cerebral veins,
formed from sinuses in the dura mater, is somewhat different from other veins of the body,
as they are non-collapsible.
Autoregulation
[Panerai 1998] describes autoregulation of blood flow in the cerebral vascular bed as the
mechanism by which cerebral blood flow (CBF) tends to remain relatively constant despite
changes in cerebral perfusion pressure (CPP). With a constant metabolic demand, changes
in CPP or arterial blood pressure that would increase or reduce CBF, are compensated by
adjusting the vascular resistance. This maintains a constant O2 supply and constant CBF.
Therefore cerebral autoregulation allows the blood supply to the brain to match its
metabolic demand and also to protect cerebral vessels against excessive flow due to arterial
hypertension. Cerebral blood flow is autoregulated much better than in almost any other
organ. Even for arterial pressure variations between 50 and 150 mm Hg, CBF only changes
by a few percent. This can be accomplished because the arterial vessels are typically able to
change their diameter about 4-fold, corresponding to a 256-fold change in blood flow. Only
when the brain is very active is there an exception to the close matching of blood flow to
metabolism, which can rise by up to 30-50% in the affected areas. It is an aim of PET,
functional MRI, near infrared spectroscopy (NIRS), and, possibly, near infrared imaging, to
detect or image such localised changes in cortical activity and associated blood flow.
Structure and pathologies of the neonatal brain
Having introduced some basics of the anatomy and physiology of the adult brain, this
section focuses on the specific differences in the neonate, as well as common neonatal
pathologies which have motivated the construction of an instrument capable of imaging
cerebral oxygenation, blood volume and, possibly, myelination.
The embryonic brain and spinal cord develop from the neural tube, which is formed by
the fourth week of pregnancy. The brain grows immensely in both size and complexity
during pregnancy and even soon after birth. Because a membranous skull restricts expan-
sion, the forebrain is bent towards the brain stem, and the cerebral hemispheres almost
completely envelop the diencephalon and midbrain. Moreover, the spatial restrictions cause
the cerebral hemispheres to increase their surface area by becoming highly convoluted such
that about two thirds of its surface are hidden in its folds. The skull bones of the foetus and
neonate are soft and the sutures are not yet fused. Hence the skull is very flexible and
deforms under light pressure. Brain development of the foetus, neonate and infant are more
thoroughly reviewed by [Herschkowitz 1988].
Compared to the adult, neonates have a smaller head size (ca. 6-12 cm in diameter),
thinner surface tissue, skull and CSF layers, lower scattering coefficients of grey and white
matter (due to lesser myelination in the case of white matter), as well as a comparatively
small mismatch between the two (see also Table 4–1). These anatomical features are all
favourable to NIR imaging. The neonatal skull, because it is less mineralised, may also have
a lower scattering coefficient, but there is no data at present. All these factors greatly
benefit penetration of light deep into the white matter and enable measurements to be made
across the head, which is essential for tomographic imaging.
Arterial and venous haemoglobin saturation values for the foetus in utero are relatively
low at 56 % and 18% [Rooth 1963], respectively, compared to about 97% and 67% for
adults. This is because there is a gradient in oxygen concentration across the placenta which
ensures diffusion of sufficient amounts of oxygen from maternal blood into the foetal
bloodstream. A higher oxygen affinity of neonatal haemoglobin (dissociation curve shifted
to the ‘left’, c.f. Figure 4–3) compensates for this. Over a period of about 6 months after
delivery the neonatal haemoglobin is gradually substituted by the adult haemoglobin, which
has a lower oxygen affinity.
The autoregulation mechanism of the (adult) brain was discussed in the previous sec-
tion. However, in the newborn infant, and particularly in the very preterm infant, there is no
consensus on whether, or to what extent, autoregulation in the brain occurs. It is also not
clear what effect ischaemia has on cerebral blood flow and the evolution of haemorrhage.
Neurodevelopmental disorders in some preterm infants are due to either hypoxic-
ischaemic damage to the periventricular white matter, or to intraventricular haemorrhage
and its consequences. The period of highest risk is between 26 and 32 weeks of gestation.
In preterm infants the majority of haemorrhages occur into the ventricles and the surround-
ing white matter, the periventricular region. Hypoxic-ischaemic damage is caused by
cerebral underperfusion, often combined with a global oxygen deficiency due to an
impaired lung function. It also affects the periventricular white matter, which is thought to
be a result of the following two effects:
• Increased vulnerability due to high metabolic demands at this phase of the brain
development.
• The area is at a ‘watershed’ of perfusion from the territories of the posterior and middle
cerebral arteries (c.f. Figure 2–7).
Enduring neurodevelopmental disorders can lead to diminished neurological function in
later life, and in particular spasticity, since motor fibres run through this region of the white
matter. Given the potential of the premature infant’s developing brain to repair some
damage, spasticity is often restricted to stiff limbs and/or subtle learning disabilities.
Cerebral damage in the mature infant is most commonly a result of perinatal (‘birth’)
asphyxia, leading initially to cerebral oedema (resulting in compressed ventricles and
flattening of the convolutions of the brain), and later to tissue necrosis (tissue death) and
apoptosis (cell suicide). The subcortical white matter, basal ganglia, cerebellum and
brainstem are the areas predominantly affected, frequently leading to learning disabilities or
global developmental delay and cerebral palsy.
Sample neonatal brain images, including that of a patient with hypoxic-ischaemia
(Figure 3–4), can be found in chapter 3, which describes various conventional imaging
modalities. A comprehensive review of common neurologic disorders is given by [Hill
1996].
