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
- 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
- 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
- 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
Site of lesion
|| Cheyne-Stokes respiration|
|| Central neurogenic hyperventilation|
|| Apneustic 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.