C h a p t e r 3 7
Disorders of Brain Function
919
rupture, allowing the escape of intracellular contents into
the surrounding extracellular fluid. This leads to damage
of neighboring cells. Major changes in cerebral function,
such as stupor and coma, occur with cytotoxic edema. The
edema associated with ischemia may be severe enough to
produce cerebral infarction with necrosis of brain tissue.
Increased Intracranial Pressure,
Herniation, and Hydrocephalus
Intracranial pressure is, literally, the pressure inside the
cranium. Its increase can cause herniations or hydro-
cephalus. Neurons can be injured when excessive pres-
sure is exerted upon brain tissue, whether that pressure
builds up gradually, such as from increasing CSF levels,
or occurs suddenly, as from trauma.
The cranial cavity contains blood (approximately
10%), brain tissue (approximately 80%), and CSF
(approximately 10%) in the rigid confines of a nonex-
pandable skull.
7,8
Each of these three intracranial volumes
contributes to the intracranial pressure, which normally
is maintained within a range of 0 to 15 mm Hg when
measured in the lateral ventricles. Increased intracranial
pressure (ICP) is a common pathway for brain injury
from different types of insults and agents.
The volumes of each of three intracranial compo-
nents can vary slightly without causing marked changes
in ICP. This is because small increases in the volume of
one component can be compensated for by a decrease in
the volume of one or both of the other two components.
This association is called the
Monro-Kellie hypothe-
sis.
4,7,8
Reciprocal compensation occurs among the three
intracranial compartments. Of the three intracranial
compartments, the CSF and blood volume are best able
to compensate for changes in ICP, with the tissue vol-
ume being relatively restricted in its ability to change.
Initial increases in ICP are buffered by a translocation
of CSF to the spinal subarachnoid space and increased
reabsorption of CSF. The compensatory ability of the
blood compartment is limited by the small amount of
blood that is in the cerebral circulation, most of which
is contained in the low-pressure venous system. As the
volume-buffering capacity of this compartment becomes
exhausted, venous pressure increases, and cerebral blood
volume and ICP rise. Also, cerebral blood flow is highly
controlled by autoregulatory mechanisms, which affect
its compensatory capacity. For example, conditions such
as ischemia and an elevated partial pressure of carbon
dioxide (PCO
2
) in the blood produce a compensatory
vasodilation of the cerebral blood vessels. A decrease
in PCO
2
has the opposite effect. For this reason, hyper-
ventilation, which results in a decrease in PCO
2
levels, is
sometimes used in the treatment of ICP.
The impact of increases in blood, brain tissue, or CSF
volumes on ICP varies among individuals and depends
on the amount of increase, effectiveness of compensa-
tory mechanisms, and compliance or “distensibility”
of brain tissue.
7
An increase in intracranial volume will
have little or no effect on ICP as long as the compli-
ance is high. Factors that influence compliance include
the amount of volume increase, the time frame for
accommodation, and the size of the intracranial com-
partments. For example, small volume increments over
long periods of time can be better accommodated than
a comparable increase introduced over a short period
of time.
The cerebral perfusion pressure (CPP), which rep-
resents the difference between the mean arterial blood
pressure (MABP) and the ICP (CPP = MABP − ICP), is
the pressure perfusing the brain.
7,8
CPP (normally 70
to 100 mm Hg) is determined by the pressure gradient
between the internal carotid artery and the subarach-
noid veins. The MABP and ICP are monitored fre-
quently in persons with brain conditions that increase
ICP and impair brain perfusion. When the pressure in
the cranial cavity approaches or exceeds the MABP,
tissue perfusion becomes inadequate, cellular hypoxia
results, and neuronal death may occur. The highly spe-
cialized cortical neurons are the most sensitive to oxy-
gen deficit; a decrease in the level of consciousness is one
of the earliest and most reliable signs of increased ICP.
Continued cellular hypoxia leads to general neurologic
deterioration, with the level of consciousness deteriorat-
ing from alertness to confusion, lethargy, obtundation,
stupor, and coma.
Brain Herniation
The brain is protected by the nonexpandable skull and
two supporting septa, the falx cerebri and the tentorium
cerebelli, which divide the intracranial cavity into com-
partments that normally protect against excessive move-
ment (Fig. 37-3A).
1,4,7
The
falx cerebri
is a sickle-shaped
septum that divides the supratentorial space into right
and left hemispheres. The
tentorium cerebelli
(so named
because it is shaped like a tent) is a double fold of dura
mater that forms a sloping partition between the cerebrum
and cerebellum. In the center of the tentorium is a large
semicircular opening called the
incisura
or
tentorial notch
(Fig. 37-3B). The brain stem, blood vessels
(
anterior cere-
bral, internal carotid, posterior communicating, and pos-
terior and superior cerebellar arteries), and oculomotor
nerve (cranial nerve [CN] III) pass through the inciscura.
Brain herniation represents a displacement of brain
tissue under the falx cerebri or through the tentorial
notch of the tentorium cerebelli. It occurs when an ele-
vated ICP in one brain compartment causes displace-
ment of the cerebral tissue toward an area of lower
pressure. The different types of herniation syndromes
are based on the area of the brain that has herniated
and the structure under which it has been pushed. They
commonly are divided into two broad categories,
supra-
tentorial
and
infratentorial
, based on whether they are
located above or below the tentorium.
Supratentorial Herniation.
Progressive supratento-
rial lesions develop sequential signs and symptoms of
ocular, motor, and respiratory function. This pattern
follows the predictable continuum of rostal-to-caudal
(head to tail) failure that proceeds from the diencepha-
lon to the midbrain (ocular), followed by pons (motor),
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