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CRANIAL NERVES V-VII

Cranial Nerve V: Trigeminal Nerve

large sensory root, which carries sensation from


the skin and mucosa of most of the head and face,
and a smaller motor root, which innervates most of
the chewing muscles (masseter, temporalis,
pterygoids, mylohyoid), and the tensor tympani
muscle of the middle ear.
The efferent fibers of the nerve (the minor portion)
originate in the motor nucleus of V in the pons
this cell group receives bilateral input from the
corticobulbar tracts and reflex connections from the
spinal tract of nerve V and controls the muscles
involved in chewing.
The sensory root (the main portion of the nerve)
arises from cells in the semilunar ganglion (also
known as the Gasserian, or trigeminal,
ganglion) in a pocket of dura (Meckel's cavity)
lateral to the cavernous sinus.
It passes posteriorly between the superior petrosal
sinus in the tentorium and the skull base and enters
the pons.
Fibers of the ophthalmic division enter the
cranial cavity through the superior orbital fissure.
Fibers of the maxillary division pass through the
foramen rotundum.
Sensory fibers of the mandibular division, joined
by the motor fibers involved in mastication, course
through the foramen ovale.
Trigeminal nerve fibers carrying light touch project
to the main (principal) trigeminal nucleus
After synapsing, this pathway passes from the
nerve's main sensory nucleus via crossed fibers in
the ventral trigeminothalamic tract and via
uncrossed fibers in the dorsal trigeminothalamic
tract to the ventral posteromedial (VPM) nuclei of
the thalamus and higher centers.
Pain and temperature fibers in the trigeminal nerve
enter the brain stem, turn caudally, and descend for
a short distance within the spinal tract of V.
These fibers then synapse with secondary neurons in
the spinal nucleus of V.
From there, the pathway passes to the thalamus via
the ventral trigeminothalamic tract.
Proprioceptive fibers in the trigeminal nerve project
to the mesencephalic trigeminal nucleus
(mesencephalic nucleus of V), where their cell
bodies are located. Collaterals project to the motor
nucleus of V.
The reflex connections pass to the cerebellum and
the motor nuclei of cranial nerves V, VII, and IX.
Corneal reflex

The afferent axons for the reflex(in which corneal


stimulation evokes a protective blink response) are
carried in the ophthalmic branch of nerve V and
synapse in the spinal tract and nucleus of V.
From there, impulses are relayed to the facial (VII)
nuclei, where motor neurons that project to the
orbicularis oculi muscles are activated. (The efferent
limb of the corneal reflex is thus carried by nerve
VII.)
The jaw jerk reflex

monosynaptic (stretch) reflex for the masseter


muscle.
Rapid stretch of the muscle (elicited gently with a
reflex hammer) evokes afferent impulses in Ia
sensory axons in the mandibular division of nerve V,
which send collaterals to the mesencephalic nucleus
of V, which sends excitatory projections to the motor
nucleus of V.
Both afferent and efferent limbs of the jaw jerk reflex
thus run in nerve V.
CLINICAL CORRELATIONS

Symptoms and signs of nerve V involvement include


loss of sensation of one or more sensory modalities
of the nerve
impaired hearing from paralysis of the tensor
tympani muscle
paralysis of the muscles of mastication, with
deviation of the mandible to the affected side
loss of reflexes (cornea, jaw jerk, sneeze)
trismus (lockjaw)
in some disorders, tonic spasm of the muscles of
mastication.
Because the spinal tract of V is located near the
lateral spinothalamic tract in the medulla and lower
pons, laterally placed lesions at these levels produce
a crossed picture of pain and temperature
insensibility on the ipsilateral face and on the
contralateral side of the body below the face.
This occurs, for example, in Wallenberg's
syndrome, in which there is damage to the lateral
medulla, usually because of occlusion of the
posterior inferior cerebellar artery.
Trigeminal neuralgia

characterized by attacks of severe pain in the


distribution of one or more branches of the
trigeminal nerve.
Although the cause is not always clear, it is known
that excruciating paroxysmal pain of short duration
can be caused by pressure from a small vessel on the
root entry zone of the nerve.
Trigeminal neuralgia is also seen in some patients
with multiple sclerosis.
Pain may follow even gentle stimulation of a trigger
zone, a point on the lip, face, or tongue that is
sensitive to cold or pressure. Involvement is usually
unilateral.
Cranial Nerve VII: Facial Nerve

The facial nerve consists of the facial nerve


proper and the nervus intermedius
Both parts pass through the internal auditory
meatus, where the geniculate ganglion for the
taste component lies.
The facial nerve proper contains axons that arise in
the facial (VII) nucleus.
The nerve exits through the stylomastoid foramen; it
innervates the muscles of facial expression, the
platysma muscle, and the stapedius muscle in the
inner ear.
The nervus intermedius

sends parasympathetic preganglionic fibers to the


pterygopalatine ganglion to innervate the
lacrimal gland
via the chorda tympani nerve to innervate the
submandibular and sublingual salivary glands.
The visceral afferent component of the nervus
intermedius, with cell bodies in the geniculate
ganglion, carries taste sensation from the anterior
two-thirds of the tongue via the chorda tympani to
the solitary tract and nucleus.
The somatic afferent fibers from the skin of the
external ear are carried in the facial nerve to the brain
stem.
These fibers connect there to the trigeminal nuclei
and are, in fact, part of the trigeminal sensory system.
The superior salivatory nucleus receives cortical
impulses from the nucleus of the solitary tract
Visceral efferent axons run from the superior
salivatory nucleus via nerve VII to the
pterygopalatine and submandibular ganglia.
They synapse there with postganglionic
parasympathetic neurons that innervate the
submandibular and sublingual salivary glands.
The taste fibers run through the chorda tympani and
nervus intermedius to the solitary nucleus, which is
connected with the cerebral cortex through the
medial lemnisci and the VPM nucleus of the
thalamus and with the salivatory nucleus and motor
nucleus of VII by reflex neurons.
The facial nucleus receives crossed and uncrossed
fibers by way of the corticobulbar (corticonuclear)
tract
The facial muscles below the forehead receive
contralateral cortical innervation (crossed
corticobulbar fibers only).
Therefore, a lesion rostral to the facial nucleus—a
central facial lesion—results in paralysis of the
contralateral facial muscles except the frontalis and
orbicularis oculi muscles.
Clinical correlations

This can occur, for example, as a result of a stroke


which damages part of the motor cortex in one
cerebral hemisphere.
Because the frontalis and orbicularis oculi muscles
receive bilateral cortical innervation, they are not
paralyzed by lesions involving one motor cortex or its
corticobulbar pathways
The complete destruction of the facial nucleus itself
or its branchial efferent fibers (facial nerve proper)
paralyzes all ipsilateral face muscles; this is
equivalent to a peripheral facial lesion.
Peripheral facial paralysis (Bell's palsy)

can occur as an idiopathic condition, but it is seen as


a complication of diabetes and can occur as a result
of tumors, sarcoidosis, AIDS, and Lyme disease
When an attempt is made to close the eyelids, the
eyeball on the affected side may turn upward (Bell's
phenomenon
The symptoms and signs depend on the location of
the lesion.
A lesion in or outside the stylomastoid foramen
results in a flaccid paralysis (lower-motor-neuron
type) of all the muscles of facial expression in the
affected side
this can occur from a stab wound or from swelling of
the parotid gland (eg, as seen in mumps).
A lesion in the facial canal involving the chorda
tympani nerve results in reduced salivation and loss
of taste sensation from the ipsilateral anterior two-
thirds of the tongue.
A lesion higher up in the canal can paralyze the
stapedius muscle.
A lesion in the middle ear involves all components of
nerve VII
tumor in the internal auditory canal (e.g., a
schwannoma) can cause dysfunction of nerves VII
and VIII.

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