The nucleus of the trochlear nerve is located in the caudal
mesencephalon beneath the cerebral aqueduct. It is immediately below
the nucleus of the oculomotor nerve (III) in the rostral mesencephalon.
The trochlear nucleus is unique in that its axons run dorsally and
cross the midline before emerging from the brainstem. Thus a lesion of
the trochlear nucleus affects the contralateral eye. Lesions of all
other cranial nuclei affect the ipsilateral side.
The trochlear nerve is unique among the cranial nerves in several
respects. It is the smallest nerve in terms of the number of axons it
contains. It has the greatest intracranial length. It is the only
cranial nerve that decussates (crosses to the other side) before
innervating its target. Finally, it is the only cranial nerve that
exits from the dorsal aspect of the brainstem.
The trochlear nerve emerges from the dorsal aspect of the brainstem at
the level of the caudal mesencephalon, just below the inferior
colliculus. It circles anteriorly around the brainstem and runs forward
toward the eye in the subarachnoid space. It passes between the
posterior cerebral artery and the superior cerebellar artery, and then
pierces the dura just under free margin of the tentorium cerebelli,
close to the crossing of the attached margin of the tentorium and
within millimeters of the posterior clinoid process.[3] It enters the
cavernous sinus, where it is joined by the other two extraocular nerves
(III and VI), the internal carotid artery, and portions of the
trigeminal nerve (V). Finally, it enters the orbit through the superior
orbital fissure and innervates the superior oblique muscle.
The superior oblique muscle ends in a tendon that passes through a
fibrous loop, the trochlea, located anteriorly on the medial aspect of
the orbit. Trochlea means "pulley" in Latin; the fourth nerve is
named after this structure.
Clinical syndromes
Injury to the trochlear nerve cause weakness of downward eye movement
with consequent vertical diplopia (double vision). The affected eye
drifts upward relative to the normal eye, due to the unopposed actions
of the remaining extraocular muscles. The patient sees two visual
fields (one from each eye), separated vertically. To compensate for
this, patients learn to tilt the head forward (tuck the chin in) in
order to bring the fields back together - to fuse the two images into
a single visual field. This accounts for the "dejected" appearance
of patients with "pathetic nerve" palsies.
As would be expected, the diplopia gets worse when the affected eye
looks toward the nose - the contribution of the superior oblique
muscle to downward gaze is greater in this position. Common activities
requiring this type of convergent gaze are reading the newspaper and
walking down stairs. Diplopia associated with these activities may be
the initial symptom of a fourth nerve palsy.
Trochlear nerve palsy also affects torsion (rotation of the eyeball in
the plane of the face). Torsion is a normal response to tilting the
head sideways. The eyes automatically rotate in an equal and opposite
direction, so that the orientation of the environment remains unchanged
- vertical things remain vertical.
Weakness of intorsion results in torsional diplopia, in which two
different visual fields, tilted with respect to each other, are seen at
the same time. To compensate for this, patients with trochlear nerve
palsies tilt their heads to the opposite side, in order to fuse the two
images into a single visual field.
The characteristic appearance of patients with fourth nerve palsies
(head tilted to one side, chin tucked in) suggests the diagnosis, but
other causes must be ruled out. For example, torticollis can produce a
similar appearance.
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Peripheral lesions
The most common cause of acute fourth nerve palsy is head trauma.[5]
Even relatively minor trauma can transiently stretch the fourth nerve
(by transiently displacing the brainstem relative to the posterior
clinoid process). Patients with minor damage to the fourth nerve will
complain of "blurry" vision. Patients with more extensive damage
will notice frank diplopia and rotational (torsional) disturbances of
the visual fields. The usual clinical course is complete recovery
within weeks to months.
The most common cause of chronic fourth nerve palsy is a congenital
defect, in which the development of the fourth nerve (or its nucleus)
is abnormal or incomplete. Congenital defects may be noticed in
childhood, but minor defects may not become evident until adult life,
when compensatory mechanisms begin to fail. Congenital fourth nerve
palsies are amenable to surgical treatment.
Isolated injury to the fourth nerve can be caused by any process that
stretches or compresses the nerve. A generalized increase in
intracranial pressure - hydrocephalus, pseudotumor cerebri,
hemorrhage, edema - will affect the fourth nerve, but the abducens
nerve (VI) is usually affected first (producing horizontal diplopia,
not vertical diplopia). Infections (meningitis, herpes zoster),
demyelination (multiple sclerosis), diabetic neuropathy and cavernous
sinus disease can affect the fourth nerve, as can orbital tumors and
Tolosa-Hunt syndrome. In general, these diseases affect other cranial
nerves as well. Isolated damage to the fourth nerve is uncommon in
these settings.
Central lesions
Central damage to the trochlear nucleus affects the contralateral eye.
The nuclei of all other cranial nerves affect ipsilateral structures.
The trochlear nucleus and its axons within the brainstem can be damaged
by infarctions, hemorrhage, arteriovenous malformations, tumors and
demyelination. Collateral damage to other structures will usually
dominate the clinical picture.
The vestibulocochlear nerve (also known as the auditory or acoustic
nerve) is the eighth of twelve cranial nerves, and is responsible for
transmitting sound and equilibrium (balance) information from the inner
ear to the brain.
The vestibulocochlear nerve is the nerve along which the sensory cells
(the hair cells) of the inner ear transmit information to the brain. It
consists of the cochlear nerve, carrying information about hearing, and
the vestibular nerve, carrying information about balance. It emerges
from the medulla oblongata and enters the inner skull via the internal
acoustic meatus (or internal auditory meatus) in the temporal bone,
along with the facial nerve.
Functions:
The eighth cranial nerve has two prime roles. It is needed to convey
information of vestibular sensation - that is, the position and
movement of the head. Secondly, it is used for hearing.
Innervations:
The nerve splits into two large divisions - the cochlear nerve and the
vestibular nerve. Broadly speaking, the cochlear nerve innervates the
cochlea, while the vestibular nerve goes to the vestibular apparatus.
Physiology:
How hearing information is coded on the nerve has long been a matter of
scientific debate between two competing theories, a place theory and a
rate theory.
Name:
Some older texts call the nerve the acoustic or auditory nerve, but
these terms have fallen out of widespread use because they fail to
recognize the nerve's role in the vestibular system. Vestibulocochlear
nerve is therefore preferred by most.