Facial motor nucleus

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Facial motor nucleus
Gray788.png
Plan of the facial and intermediate nerves and their communication with other nerves. ("Nucleus of Facial N." labeled at upper left.)
Brain stem sagittal section.svg
Diagram of brain stem showing the nuclei of the cranial nerves
Details
Part of Medulla oblongata
Artery AICA
Vein Anterior medullary
Identifiers
Latin Nucleus nervi facialis
MeSH D065828
NeuroNames 586
NeuroLex ID birnlex_903
TA98 A14.1.05.412
TA2 5939
FMA 54572
Anatomical terms of neuroanatomy

The facial motor nucleus is a collection of neurons in the brainstem that belong to the facial nerve (cranial nerve VII). [1] These lower motor neurons innervate the muscles of facial expression and the stapedius. [2]

Contents

Structure

The nucleus is situated in the caudal portion of the ventrolateral pontine tegmentum. Its axons take an unusual course, traveling dorsally and looping around the abducens nucleus, then traveling ventrally to exit the ventral pons medial to the spinal trigeminal nucleus. These axons form the motor component of the facial nerve, with parasympathetic and sensory components forming the intermediate nerve.

The nucleus has a dorsal and ventral region, with neurons in the dorsal region innervating muscles of the upper face and neurons in the ventral region innervating muscles of the lower face.

Function

Because it innervates muscles derived from pharyngeal arches, the facial motor nucleus is considered part of the special visceral efferent (SVE) cell column, which also includes the trigeminal motor nucleus, nucleus ambiguus, and (arguably) the spinal accessory nucleus.

Cortical input

Like all lower motor neurons, cells of the facial motor nucleus receive cortical input from the primary motor cortex in the frontal lobe of the brain. Upper motor neurons of the cortex send axons that descend through the internal capsule and synapse on neurons in the facial motor nucleus. This pathway from the cortex to the brainstem is called the corticobulbar tract.

The neurons in the dorsal aspect of the facial motor nucleus receive inputs from both sides of the cortex, while those in the ventral aspect mainly receive contralateral inputs (i.e. from the opposite side of the cortex). The result is that both sides of the brain control the muscles of the upper face, while the right side of the brain controls the lower left side of the face, and the left side of the brain controls the lower right side of the face.

Clinical significance

As a result of the corticobulbar input to the facial motor nucleus, an upper motor neuron lesion to fibers innervating the facial motor nucleus results in central seven. The syndrome is characterized by spastic paralysis of the contralateral lower face. For example, a left corticobulbar lesion results in paralysis of the muscles that control the lower right quadrant of the face.

By contrast, a lower motor neuron lesion to the facial motor nucleus results in paralysis of facial muscles on the same side of the injury. If a cause, such as trauma or infection, cannot be identified (this situation is called idiopathic palsy) this condition is known as Bell's palsy. Otherwise it is described by its cause.

Mechanism of Facial Nerve Upper vs Lower Motor Neuron Lesions

Any lesion occurring within or affecting the corticobulbar tract is known as an upper motor neuron lesion. Any lesion affecting the individual branches (temporal, zygomatic, buccal, mandibular and cervical) is known as a lower motor neuron lesion.

Branches of the facial nerve leaving the facial motor nucleus (FMN) for the muscles do so via both left and right posterior (dorsal) and anterior (ventral) routes. In other words, this means lower motor neurons of the facial nerve can leave either from the left anterior, left posterior, right anterior or right posterior facial motor nucleus. The temporal branch travels out from the left and right posterior components. The inferior four branches do so via the left and right anterior components. The left and right branches supply their respective sides of the face (ipsilateral innervation). Accordingly, the posterior components receive motor input from both hemispheres of the cerebral cortex (bilaterally), whereas the anterior components receive strictly contralateral input. This means that the temporal branch of the facial nerve receives motor input from both hemispheres of the cerebral cortex whereas the zygomatic, buccal, mandibular and cervical branches receive information from only contralateral hemispheres.

Now, because the anterior FMN receives only contralateral cortical input whereas the posterior receives that which is bilateral, a corticobulbar lesion (UMN lesion) occurring in the left hemisphere would eliminate motor input to the right anterior FMN component, thus removing signaling to the inferior four facial nerve branches, thereby paralyzing the right mid- and lower-face. The posterior component, however, although now only receiving input from the right hemisphere, is still able to allow the temporal branch to sufficiently innervate the entire forehead. This means that the forehead will not be paralyzed.

The same mechanism applies for an upper motor neuron lesion in the right hemisphere. The left anterior FMN component no longer receives cortical motor input due to its strict contralateral innervation, whereas the posterior component is still sufficiently supplied by the left hemisphere. The result is paralysis of the left mid- and lower-face with an unaffected forehead.

On the other hand, a lower motor neuron lesion is a bit different.

A lesion on either the left or right side would affect both the anterior and posterior routes on that side because of their close physical proximity to one another. So, a lesion on the left side would inhibit muscle innervation from both the left posterior and anterior routes, thus paralyzing the whole left side of the face (Bell’s palsy). With this type of lesion, the bilateral and contralateral inputs of the posterior and anterior routes, respectively, become irrelevant because the lesion is below the level of the medulla and the facial motor nucleus. Whereas at a level above the medulla a lesion occurring in one hemisphere would mean that the other hemisphere could still sufficiently innervate the posterior facial motor nucleus, a lesion affecting a lower motor neuron would eliminate innervation altogether because the nerves no longer have a means to receive compensatory contralateral input at a downstream decussation.

Thus, the main distinction between an UMN and LMN lesion is that in the former, there is hemiplegia of the contralateral mid- and lower-face, whereas in the latter, there is complete hemiplegia of the ipsilateral face.

Additional images

Related Research Articles

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The facial nerve, also known as the seventh cranial nerve, cranial nerve VII, or simply CN VII, is a cranial nerve that emerges from the pons of the brainstem, controls the muscles of facial expression, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue. The nerve typically travels from the pons through the facial canal in the temporal bone and exits the skull at the stylomastoid foramen. It arises from the brainstem from an area posterior to the cranial nerve VI and anterior to cranial nerve VIII.

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Central facial palsy is a symptom or finding characterized by paralysis or paresis of the lower half of one side of the face. It usually results from damage to upper motor neurons of the facial nerve.

<span class="mw-page-title-main">Ventral cochlear nucleus</span>

In the ventral cochlear nucleus (VCN), auditory nerve fibers enter the brain via the nerve root in the VCN. The ventral cochlear nucleus is divided into the anterior ventral (anteroventral) cochlear nucleus (AVCN) and the posterior ventral (posteroventral) cochlear nucleus (PVCN). In the VCN, auditory nerve fibers bifurcate, the ascending branch innervates the AVCN and the descending branch innervates the PVCN and then continue to the dorsal cochlear nucleus. The orderly innervation by auditory nerve fibers gives the AVCN a tonotopic organization along the dorsoventral axis. Fibers that carry information from the apex of the cochlea that are tuned to low frequencies contact neurons in the ventral part of the AVCN; those that carry information from the base of the cochlea that are tuned to high frequencies contact neurons in the dorsal part of the AVCN. Several populations of neurons populate the AVCN. Bushy cells receive input from auditory nerve fibers through particularly large endings called end bulbs of Held. They contact stellate cells through more conventional boutons.

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References

  1. Sherwood, Chet C. (2 October 2005). "Comparative anatomy of the facial motor nucleus in mammals, with an analysis of neuron numbers in primates". The Anatomical Record Part A: Discoveries in Molecular, Cellular, and Evolutionary Biology. 287A (1): 1067–1079. doi:10.1002/ar.a.20259. ISSN   1552-4884. PMID   16200649. S2CID   17331516.
  2. Rouiller, Eric M.; Capt, Mauricette; Dolivo, Michel; De Ribaupierre, Francois (1989-01-02). "Neuronal organization of the stapedius reflex pathways in the rat: a retrograde HRP and viral transneuronal tracing study". Brain Research. 476 (1): 21–28. doi:10.1016/0006-8993(89)91532-1. ISSN   0006-8993. PMID   2464420. S2CID   19371444.