Unilateral medial longitudinal fasciculus lesion: internuclear ophthalmoplegia

A lesion to one MLF results in internuclear ophthalmoplegia If the oculomotor, trochlear, and abducent nerves and their nuclei are intact, but there is a unilateral MLF lesion, eye movements in all directions are possible. However, since the connections between the nuclei of these nerves are interrupted, horizontal ocular movements will not occur in a conjugate fashion. When there is a lesion of the right MLF, and the individual attempts to gaze to the right, the lesion is not apparent, since both eyes can move simultaneously to the right. However, when attempting to gaze to the left, the right eye cannot move inward (medially beyond the midline) but the left eye, which should move outward (laterally) in this lateral gaze, does since it is not affected. If you ask this same individual to look at a near object placed directly in front of him, which necessitates that both eyes adduct (converge), he is able to do so. This indicates that: (i) both oculomotor nerves (which innervate the medial recti) are intact; and (ii) the upper motoneurons arising from the motor cortex (which stimulate the motoneurons of the oculomotor nuclei) are also intact. Therefore, a unilateral lesion of the MLF becomes apparent only during conjugate horizontal eye movement, when gazing away from the side of the lesion.

“One-and-a-half”

A rare condition resulting from a lesion near the abducens nucleus, involving the ipsilateral abducens nucleus and decussating MLF fibers arising from the contralateral abducens nucleus. A rare condition referred to as “one-and-a-half” results following a lesion in the vicinity of the abducens nucleus, which involves the entire ipsilateral abducens nucleus as well as the decussating MLF fibers arising from the contralateral abducens nucleus. If a lesion is present in the vicinity of the left abducens nucleus the following things happen:

1 The GSE motoneurons, whose axons form the left abducent nerve innervating the left lateral rectus, are damaged. Therefore, the left lateral rectus muscle is paralyzed.

2 The internuclear neurons housed in the left abducens nucleus are also damaged. Their crossing fibers (coursing in the right MLF) do not, therefore, form excitatory synapses with the motoneurons of the contralateral oculomotor nucleus that innervate the right medial rectus muscle.

3 The crossing fibers of the internuclear neurons arising from the contralateral (right) abducens nucleus are also damaged; thus they do not form excitatory synapses with the motoneurons of the left oculomotor nucleus that innervate the left medial rectus.

Therefore, when attempting to gaze to the left, the left eye will not abduct and the right eye will not adduct during conjugate horizontal gaze to the left. When attempting to gaze to the right, the right eye responds normally, that is it is able to abduct, whereas the left eye will not be able to adduct during conjugate horizontal gaze to the right. It is important to note that the innervation to all the extraocular muscles of both eyes is intact, except one—the left lateral rectus. If you ask this individual to look at a near object placed directly in front of him, both eyes will converge, since both medial recti and their innervation (branches of the oculomotor nerve) are intact. Thus this type of lesion becomes apparent only during conjugate horizontal eye movement.

 

FACIAL NERVE (CN VII)

The facial nerve provides motor innervation to the muscles of facial expression The facial nerve (Fig. 15.12) provides branchiomotor innervation to the muscles of facial expression, the

platysma, the posterior belly of the digastric muscle, the stylohyoid muscle, and the stapedius muscle.

 

 

 

It also transmits taste sensation from the anterior two-thirds of the tongue, as well as parasympathetic (secretomotor) innervation to the lacrimal, submandibular, and sublingual glands. Additionally, it provides general sensation to the back of the ear, pinna, and external auditory meatus, as well as visceral sensation from the nasal cavity and the soft palate.

The facial nerve consists of two parts: the facial nerve proper and the nervus intermedius. The facial nerve proper is the motor root of the facial nerve consisting of the axons of SVE (branchiomotor) neurons whose cell bodies reside in the facial nucleus. This nucleus contains subnuclei, each supplying specific muscles or groups of muscles. The nervus intermedius is sometimes referred to as the “sensory root,” which is a misnomer since in addition to sensory fibers it also carries parasympathetic fibers. The nervus intermedius consists of the axons of the GVE (secretomotor) parasympathetic neurons, whose cell bodies reside in the superior salivatory nucleus. It also contains the central processes of first order, sensory pseudounipolar neurons whose cell bodies are housed in the geniculate (L., “bent like a knee”) ganglion, the only sensory ganglion of the facial nerve. Some of these pseudounipolar neurons transmit SVA (taste) sensation from the anterior two-thirds of the tongue, others convey GSA sensation from the area posterior to the ear, whereas others carry GVA sensation from the nasal cavity and soft palate.

Both nerve roots (motor root and nervus intermedius) emerge from the brainstem at the cerebellopontine angle. Near their exit from the brainstem, the two roots of the facial nerve accompany one another to the internal acoustic meatus of the petrous portion of the temporal bone and proceed to the facial canal where the nervus intermedius presents a swelling—the geniculate ganglion.

The facial nerve gives rise to three of its branches in the facial canal: the greater petrosal nerve, the nerve to the stapedius muscle (which innervates the stapedius muscle in the middle ear), and the chorda tympani nerve. The facial nerve exits the facial canal via the stylomastoid foramen and courses to the parotid bed where its main trunk gives rise to numerous muscular branches, which radiate from within the substance of the gland to innervate their respective muscles (muscles of facial expression, platysma, posterior belly of the digastric, and stylohyoid muscles).

The superior salivatory nucleus contains GVE preganglionic parasympathetic nerve cell bodies (Figs 15.12, 15.13) whose axons leave the brainstem via the nervus intermedius.

These preganglionic fibers are distributed by the greater petrosal and chorda tympani nerves. The fibers in the greater petrosal nerve subsequently join the nerve of the pterygoid canal to enter the pterygopalatine fossa where they terminate and synapse in the pterygopalatine ganglion, one of the two parasympathetic ganglia of the facial nerve. Postganglionic parasympathetic fibers from this ganglion are distributed to the lacrimal gland and the glands of the nasal and oral cavity to provide them with secretomotor innervation. The chorda tympani nerve joins the lingual nerve, a branch of the mandibular division of the trigeminal nerve. The chorda tympani carries preganglionic parasympathetic fibers to the submandibular ganglion (the second parasympathetic ganglion of the facial nerve), where the fibers synapse with its postganglionic parasympathetic neurons. The postganglionic parasympathetic fibers from this ganglion course to the submandibular and sublingual glands providing them with secretomotor innervation. The geniculate ganglion houses the cell bodies of the SVA neurons, which are responsible for transmission of taste sensation from the anterior two-thirds of the tongue (Fig. 15.14). The peripheral processes of these neurons run in the chorda tympani, and reach the tongue via the lingual nerve of the mandibular division of the trigeminal nerve. The central processes of the SVA neurons enter the brainstem via the nervus intermedius to join the ipsilateral solitary tract and terminate in the solitary nucleus.

Other pseudounipolar neurons of the geniculate ganglion mediate GVA sensation. Their peripheral processes run in the greater petrosal nerve and terminate in the nasal cavity and the soft palate. Their central processes course in the nervus intermedius, join the ipsilateral solitary tract, and terminate in the solitary nucleus.

Still other pseudounipolar neurons of the geniculate ganglion are responsible for pain, temperature, and touch sensation from the pinna and the external auditory meatus (GSA fibers). The peripheral processes of these neurons terminate in the pinna and the external auditory meatus. Their central processes course in the nervus intermedius and join the spinal tract of the trigeminal, and terminate to synapse in the spinal nucleus of the trigeminal.

CLINICAL CONSIDERATIONS

A lesion to the facial nerve within the facial canal or near its exit from the stylomastoid foramen causes Bell’s palsy A unilateral lesion of the facial nerve near its root or in the facial canal prior to giving off any of its branches (thus damaging all of its fibers), results in the following conditions ipsilateral to the lesion: damage to the SVE (branchiomotor fibers), results in a flaccid paralysis or paresis (impairment) of the muscles of facial expression, the platysma, stylohyoid, and posterior belly of the digastric muscles with subsequent muscle atrophy. The stapedius muscle will also be paralyzed and the individual will experience hyperacusis (an acute sense of hearing). Usually the stapedius muscle dampens vibrations of the ossicles, but when it is paralyzed, vibrations from the tympanic membrane are transmitted to the ossicles and subsequently to the inner ear receptors for hearing. Furthermore, damage of the SVA fibers relaying taste results in a loss of taste from the anterior two-thirds of the tongue. Damage of the GVE parasympathetic fibers causes decreased salivary secretion from the submandibular and sublingual glands. Since both parotid glands (innervated by a different cranial nerve) and the contralateral sublingual and submandibular glands remain functional, it is difficult to determine from salivary action alone whether there is an interruption of the parasympathetic innervation to the psilateral submandibular and sublingual glands. In addition, the efferent limb of the corneal blink reflex will be damaged. Bell’s palsy may be idiopathic, or result following trauma or viral infection of the facial nerve within the facial canal or near its exit from the stylomastoid foramen. This condition is characterized by a paresis or paralysis of the muscles of facial expression ipsilateral to the lesion. Bell’s phenomenon is exhibited by individuals with a Bell’s palsy. As the individual attempts to close the eyes, he eye on the affected side deviates up and out. A unilateral lesion of the facial nerve proximal to the geniculate ganglion causes loss of tear formation by the ipsilateral lacrimal gland. A condition referred to as “ crocodile tear syndrome ” (lacrimation while eating) may result as follows. As the preganglionic parasympathetic (“salivation”) fibers originating from the superior salivatory nucleus are regenerating, they may be unsuccessful at finding their way to their intended destination, the submandibular ganglion, and instead take a wrong route to terminate in the pterygopalatine ganglion. The fibers then establish inappropriate synaptic contacts with postganglionic (“lacrimation”) neurons whose fibers project to the lacrimal gland.