Branchial Motor

Overview

Figure 7-2. Branchial motor components of the facial nerve.

The largest component of the facial nerve.

Provides voluntary control of the muscles of facial expression (including buccinator, occipitalis and platysma muscles), as well as the posterior belly of the digastric, stylohyoid and stapedius muscles.

Note the branchial motor components of the facial nerve:

Origin and Central Course

Figure 7-3. Brainstem section: origin and central course of the branchial motor components of the facial nerve.

The branchial motor component originates from the motor nucleus of CN VII in the caudal pons.

Fibers leaving the motor nucleus of CN VII initially travel medially and dorsally to loop around the ipsilateral abducens nucleus (CN VI) producing a slight bulge in the floor of the fourth ventricle - the facial colliculus.

Fibers then course so as to exit the ventrolateral aspect of the brainstem at the caudal border of the pons in conjunction with the nervus intermedius components of CN VII.

Intracranial Course

Figure 7-4. Intracranial course- branchial motor components of the facial nerve. Facial nerve origin and inner ear anatomy.

Upon emerging from the ventrolateral aspect of the caudal border of the pons, all of the components of CN VII enter the internal auditory meatus along with the fibers of CN VIII (vestibulocochlear nerve).

The fibers of CN VII pass through the facial canal in the petrous portion of the temporal bone. The course of the fibers is along the roof of the vestibule of the inner ear, just posterior to the cochlea.

At the geniculate ganglion the various components of the facial nerve take different pathways.

Fibers of the branchial motor component pass through the geniculate ganglion without synapsing, turn 90 degrees posteriorly and laterally before curving inferiorly just medial to the middle ear to exit the skull through the stylomastoid foramen.

The nerve to the stapedius muscle is given off from the facial nerve in its course through the petrous portion of the temporal bone.

Lower Motor Neuron (LMN) Lesion

Figure 7-9. Lower Motor Neuron (LMN) Lesion. After Wilson-Pauwels, et al., 1988.

Results from damage to the motor nucleus of CN VII or its axons.

A LMN lesion results in the paralysis of all muscles of facial expression (including those of the forehead) ipsilateral to the lesion.

Voluntary Control of the Muscles of Facial Expression

Figure 7-7. Voluntary control of the muscles of facial expression. After Wilson-Pauwels, et al., 1988.

Signals for voluntary movement of the facial muscles originate in the motor cortex (in association with other cortical areas) and pass via the corticobulbar tract in the posterior limb of the internal capsule to the motor nuclei of CN VII.

Fibers pass to both the ipsilateral and contralateral motor nuclei of CN VII in the caudal pons:

The portion of the nucleus that innervates the muscles of the forehead receives corticobulbar fibers from both the contralateral and ipsilateral motor cortex.

The portion of the nucleus that innervates the lower muscles of facial expression receives corticobulbar fibers from only the contralateral motor cortex.

This is very important clinically as central (upper motor neuron) and peripheral (lower motor neuron) lesions will present differently.

Clinical Correlation- Bell's Palsy

Figure 7-10. Bell's Palsy: Lower Motor Neuron (LMN) Lesion. After Wilson-Pauwels, et al., 1988.

A LMN lesion of CN VII which occurs at or beyond the stylomastoid foramen is commonly referred to as a Bell's Palsy.

Characteristic indications of a LMN lesion or Bell's Palsy include the following, on the affected side:
  • Marked facial asymmetry

  • Atrophy of facial muscles

  • Eyebrow droop

  • Smoothing out of forehead and nasolabial folds

  • Drooping of the mouth corner

  • Uncontrolled tearing

  • Loss of efferent limb of conjunctival reflex (cannot close eye)

  • Lips cannot be held tightly together or pursed

  • Diificulty keeping food in mouth while chewing on the affected side

Clinical Correlation - LMN Lesions of Facial Nerve (VII)

A LMN lesion of CN VII in conjunction with deficits associated with CN VI (abducens nerve) indicate a lesion in the brainstem which affects both the motor nucleus of CN VII and the abducens nucleus.

A LMN lesion of CN VII in conjunction with deficits associated with CN VIII (vestibulocochlear nerve) are characteristic of a lesion in the region of the internal acoustic meatus.

An example of this type of lesion is an acoustic neuroma:

Clinical Correlation - Upper Motor Neuron (UMN) Lesion

Figure 7-11. Figure 7-11. Clinical correlation - Upper Motor Neuron (UMN) Lesion. After Wilson-Pauwels, et al., 1988.

Results from damage to neuronal cell bodies in the cortex or their axons that project via the corticobulbar tract through the posterior limb of the internal capsule to the motor nucleus of CN VII.

With an UMN lesion, voluntary control of only the lower muscles of facial expression on the side contralateral to the lesion will be lost.

Voluntary control of muscles of the forehead will be spared due to the bilateral innervation of the portion of the motor nucleus of CN VII that innervates the upper muscles of facial expression.

UMN lesions are usually the result of a stroke.

Characteristics of an UMN lesion of the facial nerve include:

  • Facial asymmetry

  • Atrophy of muscles of lower portion of the face on affected side*

  • No eyebrow droop*

  • Intact folds on forehead*

  • Intact conjunctival reflex (orbicularis oculi innervation is intact)

  • Smoothing of nasolabial folds on affected side

  • Lips cannot be held tightly together or pursed

  • Difficulty keeping food in mouth while chewing on affected side

 *Distinguishes UMN lesions from LMN lesions.