The abducens nerves emerge from the ven-
tral surface of the pons and run along the ven-
tral surface of the midbrain to enter the cavern-
ous sinus as well. Abducens paralysis is often a
nonspecific sign of increased
41
or decreased
42
(e.g., after a lumbar puncture or CSF leak) ICP.
However, the abducens nerves are rarely dam-
aged by supratentorial or infratentorial mass le-
sions unless they invade the cavernous sinus or
displace the entire brainstem downward.
The foramen magnum, at the lower end of
the posterior fossa, is the only means by which
brain tissue may exit from the skull. Hence,
just as progressive enlargement of a supraten-
torial mass lesion inevitably results in hernia-
tion through the tentorial opening, continued
downward displacement either from an ex-
panding supratentorial or infratentorial mass
lesion ultimately causes herniation of the cere-
bellum and the brainstem through the fora-
men magnum.
43
Here the medulla, the cere-
bellar tonsils, and the vertebral arteries are
juxtaposed. Usually, a small portion of
the cerebellar tonsils protrudes into the aper-
ture (and may even be grooved by the poste-
rior lip of the foramen magnum). However,
when the cerebellar tonsils are compressed
against the foramen magnum during tonsillar
herniation, compression of the tissue may
compromise its blood supply, causing tissue
infarction and further swelling.
Patterns of Brain Shifts That
Contribute to Coma
There are seven major patterns of brain shift:
falcine herniation, lateral displacement of the
diencephalon, uncal herniation, central trans-
tentorial herniation, rostrocaudal brainstem de-
terioration, tonsillar herniation, and upward
brainstem herniation. The first five patterns are
caused by supratentorial mass lesions, whereas
tonsillar herniation and upward brainstem her-
niation usually result from infratentorial mass
lesions, as described below.
Falcine herniation occurs when an expanding
lesion presses the cerebral hemisphere medially
against the falx (Figure 3–2A). The cingulate
gyrus and the pericallosal and callosomarginal
arteries are compressed against the falx and may
be displaced under it. The compression of the
pericallosal and callosomarginal arteries causes
ischemia in the medial wall of the cerebral hemi-
sphere that swells and further increases the com-
pression. Eventually, the ischemia may advance
to frank infarction, which increases the cerebral
mass effect further.
44
Lateral displacement of the diencephalon oc-
curs when an expanding mass lesion, such as
a basal ganglionic hemorrhage, pushes the di-
encephalon laterally (Figure 3–2B). This pro-
cess may be monitored by displacement of the
calcified pineal gland, whose position with re-
spect to the midline is easily seen on plain CT
scanning.
45
This lateral displacement is roughly
correlated with the degree of impairment of con-
sciousness: 0 to 3 mm is associated with alert-
ness, 3 to 5 mm with drowsiness, 6 to 8 mm with
stupor, and 9 to 13 mm with coma.
1
Uncal herniation occurs when an expanding
mass lesion usually located laterally in one ce-
rebral hemisphere forces the medial edge of the
temporal lobe to herniate medially and down-
ward over the free tentorial edge into the ten-
torial notch (Figure 3–2). In contrast to central
Figure 3–5. Relationship of the oculomotor nerve to the
medial temporal lobe. Note that the course of the oculo-
motor nerve takes it along the medial aspect of the temporal
lobe where uncal herniation can compress its dorsal surface.
(From Williams, PL, and Warwick, R. Functional Neuroan-
atomy of Man. WB Saunders, Philadelphia, 1975, p. 929.
By permission of Elsevier B.V.)
100
Plum and Posner’s Diagnosis of Stupor and Coma
herniation, in which the first signs are mainly
those of diencephalic dysfunction, in uncal her-
niation the most prominent signs are due to
pressure of the herniating temporal lobe on the
structures that occupy the tentorial notch.
The key sign associated with uncal herniation
is an ipsilateral fixed and dilated pupil due to
compression of the dorsal surface of the ocu-
lomotor nerve. There is usually also evidence
of some impairment of ocular motility by this
stage, but it may be less apparent to the exam-
iner as the patient may not be sufficiently awake
either to complain about it or to follow com-
mands on examination (i.e., to look to the side
or up or down), and some degree of exophoria is
present in most people when they are not com-
pletely awake. However, examining oculocepha-
lic responses by rotating the head usually will
disclose eye movement problems associated
with third nerve compression.
A second key feature of uncal herniation
that is sufficient to cause pupillary dilation is
impaired level of consciousness. This may be
due to the distortion of the ascending arousal
systems as they pass through the midbrain, dis-
tortion of the adjacent diencephalon, or per-
haps stretching of blood vessels perfusing the
midbrain, thus causing parenchymal ischemia.
Nevertheless, the impairment of arousal is so
prominent a sign that in a patient with a uni-
lateral fixed and dilated pupil and normal level
of consciousness, the examiner must look for
another cause of pupillodilation. Pupillary di-
lation from uncal herniation with a preserved
level of consciousness is rare enough to be the
subject of case reports.
46
Hemiparesis may also occur due to com-
pression of the cerebral peduncle by the uncus.
The paresis may be contralateral to the herni-
ation (if the advancing uncus impinges upon the
adjacent cerebral peduncle) or ipsilateral (if the
uncus pushes the midbrain so that the opposite
cerebral peduncle is compressed against the
incisural edge of Kernohan’s notch,
47
but see
48
). Hence, the side of paresis is not helpful in
localizing the lesion, but the side of the en-
larged pupil accurately identifies the side of the
herniation over 90% of the time.
49
An additional problem in many patients with
uncal herniation is compression of the posterior
cerebral artery in the tentorial notch, which may
give rise to infarction in the territory of its dis-
tribution.
50
Often this is overlooked at the time
of the herniation, when the impairment of con-
sciousness may make it impossible to test visual
fields, but emerges as a concern after the crisis is
past when the patient is unable to see on the
side of space opposite the herniation. Bilateral
compression of the posterior cerebral arteries re-
sults in bilateral visual field infarction and corti-
cal blindness (see Patient 3–1, Figure 3–6).
51
Patient 3–1
A 30-year-old woman in the seventh month of preg-
nancy began to develop right frontal headaches.
The headaches became more severe, and toward
the end of the eighth month she sought medical
assistance. An MRI revealed a large right frontal
mass. Her physicians planned to admit her to hos-
pital, perform an elective cesarean section, and
then operate on the tumor. She was admitted to
the hospital the day before the surgery. During the
night she complained of a more severe headache
and rapidly became lethargic and then stuporous.
An emergency CT scan disclosed hemorrhage into
the tumor and transtentorial herniation, and at
craniotomy a right frontal hemorrhagic oligoden-
droglioma was removed, and she rapidly recov-
ered consciousness. Upon awakening she com-
plained that she was unable to see. Examination
revealed complete loss of vision including ability
to appreciate light but with retained pupillary light
reflexes. Repeat MRI scan showed an evolving
infarct involving the occipital lobes bilaterally (see
Figure 3–6). Over the following week she gradu-
ally regained some central vision, after which it
became clear that she had severe prosopagnosia
(difficulty recognizing faces).
52
Many months after
recovery of vision she was able to get around and
read, but she was unable to recognize her own
face in the mirror and could only distinguish be-
tween her husband and her brother by the fact that
her brother was taller.
Central transtentorial herniation is due to
pressure from an expanding mass lesion on the
diencephalon. If the mass effect is medially
located, the displacement may be primarily
downward, in turn pressing downward on the
midbrain, although the mass may also have a
substantial lateral component shifting the dien-
cephalon in the lateral direction.
31
The dien-
cephalon is mainly supplied by small penetrat-
ing endarteries that arise directly from the
Structural Causes of Stupor and Coma
101