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Facial Nerve (CN VII) and Nervus Intermedius
Facial Nerve (CN VII) and Nervus Intermedius
Facial Nerve (CN VII) and Nervus Intermedius
The voluntary responses of the facial
muscles arise from efferent discharge
from the motor face area of the
cerebral cortex. The motor face area is
situated on the precentral and
postcentral gyri.
Discharges from the facial motor area
are carried through fibers of the
corticobulbar tract to the internal
capsule, then through the upper
midbrain to the lower brainstem,
where they synapse in the pontine
facial nerve nucleus. The pontine
facial nerve nucleus is divided into an
upper and a lower half, bilaterally.
The corticobulbar tracts from the
upper face are double inervatted; the
tracts to the lower face cross only
once.
The deficits with unilateral
damage of the corticobulbar
fibers do not receive significant
cortical innervations and that
lower facial motor neurons
contralateral to the lesion,
which have functional loss, are
dependent on direct
contralateral cortical
innervation, with the
remaining ipsilateral cortical
projections. These findings may
explain why a focal lesion in
the facial area on 1 side of the
motor cortex in humans spares
eyelid closure and forehead
movement but results in
paralysis of the lower face.
The facial nerve has two components.
The larger component is motor and
innervates the muscles of facial
expression. It is accompanied by a
thinner nerve, the nervus intermedius,
which contains visceral and somatic
afferent fibers.
The nucleus of the motor component of
the facial nerve is located in the
pontine tegmentum . The root fibers of
this nucleus take a complicated course
Within the brainstem, they wind
around the abducens nucleus (forming
the so-called internal genu of the facial
nerve,). They then crosses the subarac-
hnoid space in the cerebellopontine
angle, and enters the internal acoustic
meatus together with the nervus
intermedius and the eighth cranial
nerve (the vestibulocochlear nerve).
Motor lesions involving the
distribution of the facial nerve.
The muscles of the forehead derive their
supranuclear innervation from both cerebral
hemispheres, but the remaining muscles of facial
expression are innervated only unilaterally, i.e.,
by the contralateral precentral cortex (If the
descending supranuclear pathways are
interrupted on one side only, e. g., by a cerebral
infarct, the resulting facial palsy spares the
forehead muscles. the patient can still raise his or
her eyebrows and close the eyes forcefully. This
type of facial palsy is called central facial palsy. In
a nuclear or peripheral lesion, however, all of the
muscles of facial expression on the side of the
lesion are weak. One can thus distinguish central
from nuclear or peripheral facial palsy by their
different clinical appearances
Idiopathic facial nerve palsy (Bell
palsy).
This most common disorder affecting the
facial nerve arises in about 25 per 100 000
individuals per year. Its cause is still
unknown. It is characterized by flaccid
paresis of all muscles of facial expression
(including the forehead muscles), as well as
other manifestations depending on the site
of the lesion. Differential diagnosis is
important in cases of acutely arising facial
palsy, as not all cases are idiopathic: 10 %
are due to herpes zoster oticus, 4 % to otitis
media, and 2 % to tumors of various types
(parotid tumors, neurinoma, and others.
A complete recovery occurs without
treatment in 60-80 % of all patients. The
administration of steroids (prednisolone, 1
mg/kg body weight daily for 5 days), if it is
begun within 10 days of the onset of facial
palsy, speeds recovery and leads to complete
recovery in over 90 % of cases, involuntary
lacrimation occurs when the patient eats.
Nervus Intermedius