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MOTOR NUCLEUS OF CRANIAL NERVE VII (MOTOR VII)

Before turning to the motor VII, you should note that the pons consists of two zones, a dorsal portion called the tegmentum of the pons and a ventral zone called the basilar pons. The tegmentum contains cranial nerve nuclei and ascending pathways such as the medial lemniscus, lateral lemniscus, ALS (spinothalamic tract), STT (solitariothalamic tract) and TTT (trigeminothalamic tract). The basilar region contains the pontine grey nuclei and massive groups of descending fibers, including the corticospinal, corticobulbar, and corticopontine tracts.

The motor nucleus VII contains motor neurons (branchiomotor) that innervate the muscles of facial expression including the orbicularis oculi (CLOSES eyelid), the stapedius, the stylohyoid and the posterior belly of the digastric. Neurons comprising motor VII possess axons that pursue a rather circuitous route in order to exit the brain stem. Initially they pass dorsally and medially to loop over the abducens nucleus. The fibers then course ventrally and laterally to exit the brain stem. The bump in the floor of the fourth ventricle caused by the motor fibers of C.N. VII looping over the abducens nucleus is called the FACIAL COLLICULUS.





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A unilateral lesion interrupting the axons of C.N. VII results in the following: On the ipsilateral side, the forehead is immobile, the corner of the mouth sags, the nasolabial folds of the face are flattened, facial lines are lost, and saliva may drip from the corner of the mouth. The patient is unable to whistle or puff the cheek because the buccinator muscle is paralyzed. When the patient is smiling, the normal muscles draw the contralateral corner of the mouth up while the paralyzed corner continues to sag. Corneal sensitivity remains (C.N. V), but the patient is unable to blink or close the eyelid (CN VII). To protect the cornea from drying, therapeutic closure of the eyelids or other measures are taken (patient wears an eye mask, or lids are closed with sutures). Because of the paralysis of the stapedius muscle, which normally dampens the amplitude of the vibrations of the ear ossicles, the patient will experience sounds as uncomfortably loud. THIS IS CALLED HYPERACUSIS. REMEMBER, THERE WILL BE ATROPHY OF ALL OF THE ABOVE MUSCLES (i.e. Lower Motor Neuron).

You will recall that the cortex sends axons to cranial nerve motor nuclei. These are called CORTICOBULBAR fibers (remember those to the hypoglossal and nucleus ambiguus?). A unilateral lesion of the corticobulbar fibers to motor VII, for example in the motor cortex, results in weakness of the muscles of expression of the face BELOW THE EYE ON THE SIDE CONTRALATERAL TO THE LESION. The frontalis muscle (wrinkles forehead) and the orbicularis oculi muscle (closes eyelid) are unaffected. The accepted explanation states that BILATERAL (crossed and uncrossed) corticobulbar projections from the cerebral cortex influence the lower motor neurons (within Motor VII) innervating the frontalis muscle and orbicularis oculi, while only crossed corticobulbar projections influence the lower motor neurons innervating the muscles of the LOWER face. Think about it like this, the lower part of Motor VII is like the hypoglossal nucleus (crossed corticobulbars), while the upper part is like nucleus ambiguus (bilateral corticobulbars).

A lesion in the face representation of area 4 (motor cortex) will mean that those motor neurons in the contralateral region (ventral) of motor VII that innervate the lower facial muscles are completely deprived of cortical input. In contrast, the lower motor neurons in that part of motor VII that innervate the upper facial muscles still have cortical input from the ipsilateral motor cortex. Such muscles, therefore, contract when the patient wants to voluntarily contract them. REMEMBER, THERE IS NO MUSCLE ATROPHY FOLLOWING A LESION OF THE CORTICOBULBAR FIBERS.

You should now think about the resulting neurological deficits following a lesion of the LEFT motor cortex that interrupts all CORTICOSPINAL fibers and CORTICOBULBAR fibers to motor VII, nucleus ambiguus and the hypoglossal nucleus. There will be a RIGHT hemiplegia, the tongue will deviate to the RIGHT upon protrusion, and the lower facial muscles on the RIGHT will be weak. Any problems with swallowing? Will the uvula deviate when you say ahhh? THINK! THIS IS VERY IMPORTANT.





AN INTERESTING CLINICAL OBSERVATION

It is known that following a stroke muscles of facial expression of the lower face on the opposite side are weak and the patient cannot voluntarily move these muscles. However, reflex smiling (at a joke) did result in movement of these muscles. This suggests that there are different pathways involved in moving these muscles during voluntary and reflex movements.



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