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the cingulate gyrus (see falcine herniation, page 100).

The tentorium cerebelli (Figure 3–3) separates the cerebral hemispheres (supratentorial compartment) from the brainstem and cerebellum (infratentorial compartment/posterior fossa). The tentorium is less flexible than the falx, because its fibrous dural lamina is stretched across the surface of the middle fossa and is tethered in position for about three-quarters of its extent (see Figure 3–3). It attaches anteriorly at the petrous ridges and posterior clinoid processes and laterally to the occipital bone along the lateral sinus. Extending posteriorly into the center of the tentorium from the posterior clinoid processes is a large semioval opening, the incisura or tentorial notch, whose diameter is usually between 25 and 40 mm mediolaterally and 50 to 70 mm rostrocaudally.34 The tentorium cerebelli also plays a key role in the pathophysiology of supratentorial mass lesions, as when the tissue volume of the supratentorial compartments exceeds that compartment’s capacity, there is no alternative but for tissue to herniate through the tentorial opening (see uncal herniation, page 100).

Tissue shifts in any direction can damage structures occupying the tentorial opening. The midbrain, with its exiting oculomotor nerves,

traverses the opening from the posterior fossa to attach to the diencephalon. The superior portion of the cerebellar vermis is typically applied closely to the surface of the midbrain and occupies the posterior portion of the tentorial opening. The quadrigeminal cistern, above the tectal plate of the midbrain, and the peduncular and interpeduncular cisterns along the base of the midbrain provide flexibility; there may be considerable tissue shift before symptoms are produced if a mass lesion expands slowly (Figure 3–2).

The basilar artery lies along the ventral surface of the midbrain. As it nears the tentorial opening, it gives off superior cerebellar arteries bilaterally, then branches into the posterior cerebral arteries (Figure 3–4). The posterior cerebral arteries give off a range of thalamoperforating branches that supply the posterior thalamus and pretectal area, followed by the posterior communicating arteries.35 Each posterior cerebral artery then wraps around the lateral surface of the upper midbrain and reaches the ventral surface of the hippocampal gyrus, where it gives off a posterior choroidal artery.36 The posterior choroidal artery anastomoses with the anterior choroidal artery, a branch of the internal carotid artery that runs between the dentate gyrus and the free lateral edge of the tentorium. The

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 compression causes cortical blindness (see Patient 3–1).

The oculomotor nerves leave the ventral surface 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 proximity of the oculomotor nerve to the posterior

communicating artery (Figure 3–4) and the medial temporal lobe (Figure 3–5). Compression of the oculomotor nerve by either of these structures results in early injury to the pupillodilator fibers that run along its dorsal surface37; 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 hemorrhage into the superior cerebellar peduncles and the surrounding parabrachial nuclei.38,39 The trochlearnervesmay alsobe injured inthisway.40

Figure 3–5. Relationship of the oculomotor nerve to the medial temporal lobe. Note that the course of the oculomotor 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 Neuroanatomy of Man. WB Saunders, Philadelphia, 1975, p. 929. By permission of Elsevier B.V.)

The abducens nerves emerge from the ventral surface of the pons and run along the ventral surface of the midbrain to enter the cavernous sinus as well. Abducens paralysis is often a nonspecific sign of increased41 or decreased42 (e.g., after a lumbar puncture or CSF leak) ICP. However, the abducens nerves are rarely damaged by supratentorial or infratentorial mass lesions 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 supratentorial mass lesion inevitably results in herniation through the tentorial opening, continued downward displacement either from an expanding supratentorial or infratentorial mass lesion ultimately causes herniation of the cerebellum and the brainstem through the foramen magnum.43 Here the medulla, the cerebellar tonsils, and the vertebral arteries are

juxtaposed. Usually, a small portion of the cerebellar tonsils protrudes into the aperture (and may even be grooved by the posterior 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 transtentorial herniation, rostrocaudal brainstem deterioration, tonsillar herniation, and upward brainstem herniation. The first five patterns are caused by supratentorial mass lesions, whereas tonsillar herniation and upward brainstem herniation 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 hemisphere that swells and further increases the compression. Eventually, the ischemia may advance to frank infarction, which increases the cerebral mass effect further.44

Lateral displacement of the diencephalon occurs when an expanding mass lesion, such as a basal ganglionic hemorrhage, pushes the diencephalon laterally (Figure 3–2B). This process may be monitored by displacement of the calcified pineal gland, whose position with respect to the midline is easily seen on plain CT scanning.45 This lateral displacement is roughly correlated with the degree of impairment of consciousness: 0 to 3 mm is associated with alertness, 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 cerebral hemisphere forces the medial edge of the temporal lobe to herniate medially and downward over the free tentorial edge into the tentorial notch (Figure 3–2). In contrast to central

herniation, in which the first signs are mainly those of diencephalic dysfunction, in uncal herniation 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 oculomotor nerve. There is usually also evidence of some impairment of ocular motility by this stage, but it may be less apparent to the examiner as the patient may not be sufficiently awake either to complain about it or to follow commands 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 completely awake. However, examining oculocephalic 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, distortion of the adjacent diencephalon, or perhaps 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 unilateral fixed and dilated pupil and normal level of consciousness, the examiner must look for another cause of pupillodilation. Pupillary dilation 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 compression of the cerebral peduncle by the uncus. The paresis may be contralateral to the herniation (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 enlarged 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 distribution.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 results in bilateral visual field infarction and cortical blindness (see Patient 3–1, Figure 3–6).51

Patient 3–1

A 30-year-old woman in the seventh month of pregnancy 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 hospital, 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 oligodendroglioma was removed, and she rapidly recovered consciousness. Upon awakening she complained 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 gradually 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 between 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 diencephalon in the lateral direction.31 The diencephalon is mainly supplied by small penetrating endarteries that arise directly from the

Figure 3–6. Bilateral occipital infarction in Patient 3–1. Hemorrhage into a large frontal lobe tumor caused transtentorial herniation, compressing both posterior cerebral arteries. The patient underwent emergency craniotomy to remove the tumor, but when she recovered from surgery she was cortically blind.

vessels of the circle of Willis. Hence, even small degrees of displacement may stretch and compress important feeding vessels and reduce blood flow. In addition to accounting for the pathogenesis of coma (due to impairment of the ascending arousal system at the diencephalic level), the ischemia causes local swelling and eventually infarction, which causes further edema, thus contributing to gradually progressive displacement of the diencephalon. In severe cases, the pituitary stalk may even become partially avulsed, causing diabetes insipidus, and the diencephalon may buckle against the midbrain. The earliest and most subtle signs of impending central herniation tend to begin with compression of the diencephalon.

Less commonly, the midbrain may be forced downward through the tentorial opening by a mass lesion impinging upon it from the dorsal surface. Pressure from this direction produces the characteristic dorsal midbrain or Parinaud’s syndrome (loss of upgaze and convergence, retractory nystagmus; see below).

Rostrocaudal deterioration of the brainstem may occur when the distortion of the brainstem

compromises its vascular supply. Downward displacement of the midbrain or pons stretches the medial perforating branches of the basilar artery, which itself is tethered to the circle of Willis and cannot shift downward (Figure 3–4). Paramedian ischemia may contribute to loss of consciousness, and postmortem injection of the basilar artery demonstrates that the paramedian arteries are at risk of necrosis and extravasation. The characteristic slit-like hemorrhages seen in the area of brainstem displacement postmortem are called Duret hemorrhages53 (Figure 3–7). Such hemorrhages can be replicated experimentally in animals.54 It is also possible for the venous drainage of the brainstem to be compromised by compression of the great vein of Galen, which runs along the midline on the dorsal surface of the midbrain. However, in postmortem series, venous infarction is a rare contributor to brainstem injury.55

Tonsillar herniation occurs in cases in which the pressure gradient across the foramen magnum impacts the cerebellar tonsils against the foramen magnum, closing off the fourth ventricular outflow and compressing the medulla (Figures 3–7 and 3–8). This may occur quite suddenly, as in cases of subarachnoid hemorrhage, when a large pressure wave drives the cerebellar tonsils against the foramen magnum, compressing the caudal medulla. The patient suddenly stops breathing, and blood pressure rapidly increases as the vascular reflex pathways in the lower brainstem attempt to perfuse the lower medulla against the intense local pressure. A similar syndrome is sometimes seen when lumbar puncture is performed on a patient whose intracranial mass lesion has exhausted the intracranial compliance.56 In patients with sustained tonsillar herniation, the cerebellar tonsils are typically found to be necrotic due to their impaction against the unyielding edge of the foramen magnum. This problem is discussed further below.

Upward brainstem herniation may also occur through the tentorial notch in the presence of a rapidly expanding posterior fossa lesion.3 The superior surface of the cerebellar vermis and the midbrain are pushed upward, compressing the dorsal mesencephalon as well as the adjacent blood vessels and the cerebral aqueduct (Figure 3–8).

The dorsal midbrain compression results in impairment of vertical eye movements as well as consciousness. The pineal gland is typically

displaced upward on CT scan.57 The compression of the cerebral aqueduct can cause acute hydrocephalus, and the superior cerebellar artery may be trapped against the tentorial edge, resulting in infarction and edema of the superior cerebellum and increasing the upward pressure.

tion (i.e., no ptosis or ocular motor signs). Once the herniation advances to the point where the function of the brainstem is compromised, signs of brainstem deterioration may proceed rapidly, and the patient may slip from full consciousness to deep coma over a matter of minutes (Figure 3–9).

Clinical Findings in Uncal

Herniation Syndrome

EARLY THIRD NERVE STAGE

The proximity of the dorsal surface of the oculomotor nerve to the medial edge of the temporal lobe (Figure 3–5) means that the earliest and most subtle sign of uncal herniation is often an increase in the diameter of the ipsilateral pupil. The pupil may respond sluggishly to light, and typically it dilates progressively as the herniation continues. Early on, there may be no other impairment of oculomotor func-

Patient 3–2

A 22-year-old woman was admitted to the emergency room with the complaint of erratic behavior ‘‘since her boyfriend had hit her on the head with a gun.’’ She was awake but behaved erratically in the emergency room, and was sent for CT scanning while a neurology consult was called. The neurologist found the patient in the x-ray department and the technician noted that she had initially been uncooperative, but for the previous 10 minutes she had lain still while the study was completed.

Immediate examination on the radiology table showed that breathing was slow and regular and she was unresponsive except to deep pain, with localizing movements of the right but not the left extremities. The right pupil was 8 mm and unreactive to light, and there was no adduction, elevation, or depression of the right eye on oculoce-

phalic testing. Muscle tone was increased on the left compared to the right, and the left plantar response was extensor.

She was immediately treated with hyperventilation and mannitol and awakened. The radiologist reported that there were fragments of metal embedded in the skull over the right frontal lobe.

The patient confirmed that the boyfriend had actually tried to shoot her, but that the bullet had struck her skull with only a glancing blow where it apparently had fragmented. The right frontal lobe was contused and swollen and downward pressure had caused transtentorial herniation of the uncus. Following right frontal lobectomy to decompress her brain, she improved and was discharged.

LATE THIRD NERVE STAGE

As the foregoing case illustrates, the signs of the late third nerve stage are due to more complete impairment of the oculomotor nerve as well as compression of the midbrain. Pupillary dilation becomes complete and the pupil no longer reacts to light. Adduction, elevation, and depression of the affected eye are lost, and there is