In the 19th century, many neurologists thought that supratentorial lesions caused stupor or coma by impairing function of the cortical mantle, although the mechanism was not understood. Cushing proposed that the increase in ICP caused impairment 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 supratentorial 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, Meyer29 pointed out the importance of temporal lobe herniation into the tentorial gap in patients with brain tumors; Kernohan and Woltman30 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 opposite 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 important than the absolute value or direction of the movement.
Structural Causes of Stupor and Coma 111 proximity of the oculomotor nerve to the
posterior
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 herniation of the medial temporal lobe and aneurysm of the posterior communicating artery.
98
Structural Causes of Stupor and Coma 113
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. TheCIBA Collection of Medical Illustrations. CIBA Pharmaceuticals, New Jersey, 1983, p. 46. By permission of CIBA Pharmaceuticals.)
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 surfaceofthemidbrainjustcaudaltotheinferior 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 intothe
superiorcerebellarpedunclesand the surrounding parabrachial nuclei.38,39 The trochlearnervesmayalsobeinjuredinthisway.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 compressits 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.