posterior cerebral artery then runs caudally
along the medial surface of the occipital lobe to
supply the visual cortex. Either one or both
posterior cerebral arteries are vulnerable to
compression when tissue herniates through the
tentorium. Unilateral compression causes a
homonymous hemianopsia; bilateral compres-
sion causes cortical blindness (see Patient 3–1).
The oculomotor nerves leave the ventral sur-
face of the midbrain between the superior
cerebellar arteries and the diverging posterior
cerebral arteries (Figure 3–3). The oculomotor
nerves cross the posterior cerebral artery and
run along the posterior communicating artery
to penetrate through the dural edge at the
petroclinoid ligament and enter the cavernous
sinus. Along this course, the oculomotor nerves
run along the medial edge of the temporal lobe
(Figure 3–5). The uncus, which represents the
bulging medial surface of the amygdala within
the medial temporal lobe, usually sits over the
tentorial opening, and its medial surface may
even be grooved by the tentorium.
A key relationship in the pathophysiology of
supratentorial mass lesions is the close prox-
imity of the oculomotor nerve to the posterior
Box 3–1 Historical View of the Pathophysiology
of Brain Herniation
In the 19th century, many neurologists thought that supratentorial lesions caused
stupor or coma by impairing function of the cortical mantle, although the mecha-
nism was not understood. Cushing proposed that the increase in ICP caused im-
pairment of blood flow, especially to the medulla.
27
He was able to show that
translation of pressure waves from the supratentorial compartments to the lower
brainstem may occur in experimental animals. Similarly, in young children, a supra-
tentorial pressure wave may compress the medulla, causing an increase in blood
pressure and fall in heart rate (the Cushing reflex). Such responses are rare in
adults, who almost always show symptoms of more rostral brainstem failure before
developing symptoms of lower brainstem dysfunction.
The role of temporal lobe herniation through the tentorial notch was appreciated
by MacEwen in the 1880s, who froze and then serially cut sections through the
heads of patients who died from temporal lobe abscesses.
28
His careful descriptions
demonstrated that the displaced medial surface of the temporal uncus compressed
the oculomotor nerve, causing a dilated pupil. In the 1920s, Meyer
29
pointed out the
importance of temporal lobe herniation into the tentorial gap in patients with brain
tumors; Kernohan and Woltman
30
demonstrated the lateral compression of the
brainstem produced by this process. They noted that lateral shift of the midbrain
compressed the cerebral peduncle on the side opposite the tumor against the oppo-
site tentorial edge, resulting in ipsilateral hemiparesis. In the following decade, the
major features of the syndrome of temporal lobe herniation were clarified, and the
role of the tentorial pressure cone was widely appreciated as a cause of symptoms in
patients with coma.
More recently, the role of lateral displacement of the diencephalon and upper
brainstem versus downward displacement of the same structures in causing coma
has received considerable attention.
31,32
Careful studies of the displacement of
midline structures, such as the pineal gland, in patients with coma due to forebrain
mass lesions demonstrate that the symptoms are due to distortion of the structures
at the mesodiencephalic junction, with the rate of displacement being more im-
portant than the absolute value or direction of the movement.
Structural Causes of Stupor and Coma
97
Figure 3–3. The intracranial compartments are separated by tough dural leaflets. (A) The falx cerebri separates the two
cerebral hemispheres into separate compartments. Excess mass in one compartment can lead to herniation of the cingulate
gyrus under the falx. (From Williams, PL, and Warwick, R. Functional Neuroanatomy of Man. WB Saunders, Philadelphia,
1975, p. 986. By permission of Elsevier B.V.) (B) The midbrain occupies most of the tentorial opening, which separates the
supratentorial from the infratentorial (posterior fossa) space. Note the vulnerability of the oculomotor nerve to both her-
niation of the medial temporal lobe and aneurysm of the posterior communicating artery.
98
communicating artery (Figure 3–4) and the me-
dial temporal lobe (Figure 3–5). Compression
of the oculomotor nerve by either of these struc-
tures results in early injury to the pupillodilator
fibers that run along its dorsal surface
37
; hence,
a unilateral dilated pupil frequently heralds a
neurologic catastrophe.
The other ocular motor nerves are generally
not involved in early transtentorial herniation.
The trochlear nerves emerge from the dorsal
surface of the midbrain just caudal to the inferior
colliculi. These slender fiber bundles wrap
around the lateral surface of the midbrain and
follow the third nerve through the petroclinoid
ligament into the cavernous sinus. Because the
free edge of the tentorium sits over the posterior
edge of the inferior colliculi, severe trauma that
displaces the brainstem back into the unyielding
edge of the tentorium may result in hemor-
rhage into the superior cerebellar peduncles and
the surrounding parabrachial nuclei.
38,39
The
trochlear nerves may also be injured in this way.
40
Figure 3–4. The basilar artery is tethered at the top to the posterior cerebral arteries, and at its lower end to the vertebral
arteries. As a result, either upward or downward herniation of the brainstem puts at stretch the paramedian feeding vessels
that leave the basilar at a right angle and supply the paramedian midbrain and pons. The posterior cerebral arteries can be
compressed by the medial temporal lobes when they herniate through the tentorial notch. (From Netter, FH. The CIBA Col-
lection of Medical Illustrations. CIBA Pharmaceuticals, New Jersey, 1983, p. 46. By permission of CIBA Pharmaceuticals.)
Structural Causes of Stupor and Coma
99