Facial paralysis
I. INTRODUCTION.The onset of nerve pathways responsible for facial motility starts at the level of
cerebral cortex and ends in the endplates of the muscles of facial expression. the
injuries at some point this path provoke facial paralysis, and, for a
etiologic and topographic correct diagnosis is essential to know the anatomy of the VII pair Cranial.
The route of the facial voluntary movement originates in the ascending or frontal gyri
pre rolandic and ascending parietal cerebral cortex. From these areas, the impulses
the corticobulbar beam traverses the nerve, internal capsule, and midbrain, to establish
synapse to the nucleus of the facial nerve at the pons. The dorsal aspect of the
core fibers emerge, after addressing in dorsomedial and higher sense, curve
surrounding the nucleus of the sixth nerve and head in ventrolateral and inferiorly oriented
towards the lower edge of the protrusion where the constituting emerge apparent origin
the motor root of the facial nerve. The fibers thereof to provide innervation
striated muscles derived from the second pharyngeal arch (Table 1).
The facial nerve is a mixed leaving the brain stem by the Groove bulboprotuberancial
through two divisions, one motor branch and the intermediary nerve Weisberg, the
which are joined at the innermost duct tube segment (this conduit presents
two angles that can divide it into three parts: first or rambling, second or
third or tympanic and mastoid; It is a tortuous bony canal that runs through the thickness
temporal bone and ending extracranially near the styloid process in the
stylomastoid hole). The origin of the facial nucleus is located deep in the
shell of the pontine. Its motor fibers follow a complicated path around the
VI core source of torque, contributing in part to form the teres eminence in the ground
ventricle LV. Among the centripetal fibers containing the facial nerve include the
taste sensory fibers, from the previous two third of the tongue,
incorporated into the facial nerve cord through the eardrum, and poor fiber contingent
the skin sensitivity of the ear canal. Cells fibers
skin sensitivity and taste are in the geniculate ganglion and its extensions
plants reach the solitary tract nucleus and spinal trigeminal nucleus,
respectively. The facial nerve also contains parasympathetic fibers to the glands
submandibular, sublingual and tear, following the intermediate nerve and Weisberg
greater superficial petrosal nerve and chords tympani.
The facial nerve from its origin, through the cerebellopontine angle and into the rock
the internal auditory canal (in this relates to the seventh pair, occupying a position
anterior regarding this) and covers a route with two bends. In the first
kink facial nerve geniculate ganglion, where the petrosal nerve originates stands
surface higher. In its downward path after the second kink, originates
a collateral branch to the stapedius, and then the rope tympani nerve.
Leaving the skull by stylomastoid hole through the parotid (between
inner and outer lobes), dividing by reaching the rear edge of the jaw into two
branches or temporary top and bottom or neck and facial. These will be subdivided to cause
various terminal branches that innervate the muscles of facial expression and the
platysma.
Peripheral facial nerve injuries occur paralysis of the facial muscles
a face side, accompanied by alterations of the tear and salivary secretion, and
taste sensitivity, depending on the course of the nerve injury. The next injury
in addition to the geniculate ganglion cause paralysis of motor function and taste
secretory. Injury geniculate ganglion and the junction of the nerve, with n.
chords tympani produce a similar picture, but without an involvement of tear secretion.
There hyperacusis, if the lesion is close to the emergence of collateral to muscle
stirrup. Lesions in the hole stylomastoid only cause paralysis of the muscles
facial.
Facial paralysis of central origin (supranuclear palsy) differs from paralysis
by the presence of peripheral symptoms of impairment of other CNS structures, the
front and preservation of orbicular of the eyelids, which have an innervation
bilateral, and by a remarkable discrepancy between the affectation of facial movements
volitional and emotional.
Irritant facial nerve injuries cause involuntary facial movements
various types. Clonic facial spasms can be observed in cases of tumors angle
basilar artery aneurysms. Spasm of unknown cause (Hemi facial spasm
idiopathic) can be very annoying and difficult to treat. They can originate from the
nerve compression or distortion in the posterior fossa by an aberrant artery or vein and,
severe cases, surgical nerve exploration is recommended in this area. without
But the injection of small doses of botulinum toxin can be effective. sclerosis
multiple and sometimes the trunk intraparenchymal tumors can cause
militia facial, a thin continuous or recurrent hamstring contraction of certain muscles
facials
