B. HERNIATION EFFECTS OF SPACE-OCCUPYING LESIONS (SOL)

1. Displacement Effects of Rapidly Expanding SOL Include:

a. Cingulate gyrus herniation under the falx cerebri

The cingulate gyrus above the corpus callosum has herniated toward the right side of the image.


b. Midline shift (lateral displacement)

c. Uncal herniation - herniation of the medial temporal lobe (uncus) across the tentorium cerebelli

The circle indicates uncal herniation


d. Cerebellar tonsil herniation through the foramen magnum

The cerebellar tonsils has been pushed downward to compress the medulla, expected to cause respuratory arrest.


e. Downward displacement of the diencephalon and brainstem


2. Consequences of Uncal (Temporal Lobe) Herniation

a.Compression of cranial nerve III. The ipsilateral third nerve, as it passes between the posterior cerebral and superior cerebellar arteries, is initially flattened and may show hemorrhage. The first clinical sign is ipsilateral pupil dilation, since the parasympathetic fibers are located on the outside of the nerve and are inactivated first by compression. Complete third nerve paralysis may also occur. As the herniation progresses, the contralateral oculomotor nerve may be compressed, producing bilateral pupil dilation.

b.Compression of midbrain cerebral peduncles. Most often the ipsilateral cerebral peduncle is compressed, resulting in contralateral hemiparesis or hemiplegia. In addition the cerebral peduncle on the side opposite the space-occupying lesion may be compressed against, or indented by, the free edge of the tentorium cerebelli. This results in ipsilateral hemiparesis or hemiplegia (if it occurs alone) or quadriplegia (if both peduncles are compressed)

c.Compression of the posterior cerebral artery. Obstruction of the posterior cerebral artery or its branches, due to compression of the artery against the free edge of the tentorium, produces hemorrhagic infarction on the medial and inferior aspects of the ipsilateral occipital lobe (occasionally the infarction is bilateral). Hemorrhagic infarction occurs because the compression may be reduced after damage to arterial walls and blood then enters the infarcted area. The lesion is often confined to the distribution of the calcarine branches of the posterior cerebral artery. Clinically, cortical blindness is a common result.

d.Brainstem compression. The patient becomes comatose and may develop bradycardia secondary to increasing brainstem compression. Decerebrate posturing in response to noxious stimuli and hyperventilation may be seen. Secondary brainstem hemorrhages (Duret hemorrhages) may occur, probably because of compression and stretching of blood vessels, especially veins. Brainstem decompensation will gradually progress caudally. As the lower pons and upper medulla are involved, regular, shallow respirations appear and the extremities become flaccid. Finally, as the damage in the medulla causes slow irregular respirations, an irregular pulse and falling blood pressure, death may occur due to respiratory arrest.



This section of pons shows duret hemorrhages after herniation due to intracerebral hemorrhage.


3. Consequences of Central Herniation (Rostrocaudal deterioration)

a. General comments. Rostrocaudal deterioration (or rostrocaudal decompensation) is the progressive decline in neurological status due to lesions progressively more caudal as a result of a supratentorial space occupying mass and downward displacement of the brainstem. Lesions lying medially or in the frontal pole may not compress the diencephalon and midbrain laterally, but rather result in rostrocaudal dysfunction of the brainstem with bilateral progression of impairment. As in uncal herniation, secondary or Duret hemorrhages may occur in the midbrain and pons as the brainstem is displaced.

b. Clinical Signs.

i. Changes in consciousness begin with decreasing alertness, progressing to drowsiness, stupor and coma.

ii. Respiratory changes which occur with lesions in various sites are:

 

 Site of lesion

 Respiratory pattern

 Diencephalon  Cheyne-Stokes respiration
 Midbrain  Central neurogenic hyperventilation
 Pons  Apneustic respiration
Medulla

 Ataxic respiration


iii. Decorticate rigidity, characterized by leg extension and arm flexion, results from wide-spread lesions in the cerebral cortex. Decerebrate rigidity, characterized by extension of both arms and legs, follows lesions disconnecting the cerebral hemispheres from the brainstem e.g. lesions in the upper midbrain commonly produce decerebrate rigidity.

iv. Pupillary changes in a comatose patient can be used to evaluate the general location of lesions. Examples of abnormalities include:

Small reactive: Compression of the diencephalon impairs sympathetic fibers which originate there; impairment of sympathetic mediation of pupil dilation leads to small pupils. Unilateral Dilated, fixed: Compression of one oculomotor nerve (III nerve) by the uncus impairs the parasympathetic fibers travelling along the periphery of the III nerve; inactivation of these parasympathetic fibers leads to dilation of the ipsilateral pupil and loss of the light reflex in that pupil. Bilateral Midposition, fixed: Compression of both III nerves or compression of the midbrain results in bilateral impairment of both parasympathetic and sympathetic fibers travelling to the pupil; thus the pupils are midposition (medium size) and fixed (no light reflex in either pupil).

4. Consequences of cerebellar tonsil herniation

Displacement of the cerebellar tonsils through the foramen magnum compresses the medullary respiratory centers, leading to death.

5. Consequences of lateral displacement of brain

Changing levels of consciousness have been correlated with lateral displacement of diencephalon.

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