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    • Supranuclear (upper motor neuron) pathways

    • Facial nucleus and fascicles (lower motor neuron)

    • Subarachnoid space

    • Temporal bone and peripheral course


    • Facial motor function

    • Taste

    • Tear function

    • Hearing


    • Bell palsy

    • Herpes zoster oticus

    • Other infectious diseases

    • Acute inflammatory demyelinating polyradiculopathy

    • Trauma

    • Other causes


    • Risk factors

    • Management


    • Blepharospasm

    • Hemifacial spasm

    • Facial myokymia

    • Benign eyelid myokymia





The facial nerve is the seventh cranial nerve (CN VII). CN VII is of major importance to ophthalmologists for at least two reasons. First, the facial motor pathways are in close anatomic proximity to the ocular motor pathways; therefore, the evaluation of facial motor function may offer important clues in the diagnosis and localization of lesions that cause ocular motility disorders. Second, CN VII controls eye closure (orbicularis oculi). Weakness of eye closure can lead to exposure keratopathy and visual loss.





Corticobulbar Pathway

Volitional (voluntary) facial movements originate in the precentral gyrus of the frontal lobe cortex. Fibers descend within the corticobulbar tract through the internal capsule and cerebral peduncles to synapse in the facial motor nuclei located in the pons. Cortical fibers controlling the lower face decussate to innervate the contralateral facial nucleus. Fibers innervating the upper face (forehead muscles and orbicularis oculi) originate from both the ipsilateral and contralateral facial nuclei (Figure 12–1). Thus, a unilateral hemispheric lesion that affects the supranuclear pathway (upper motor neuron) produces a contralateral lower facial paresis; voluntary eye closure and forehead movement are relatively spared because the upper face can be controlled by either hemisphere.

Figure 12–1.
Corticobulbar (supranuclear) facial pathway.

Observe that the upper face has bilateral supranuclear input. Thus, a left supranuclear lesion (1) produces a right facial palsy that spares the upper face. However, a left facial nerve lesion (2) would likely affect both the upper and lower left face. (Modified, with permission, from Sibony PA, Evinger C: Anatomy and physiology of normal and abnormal eyelid position and movement. In Miller NR, Newman NJ, editors. Walsh and Hoyt's clinical neuro-ophthalmology, ed 5. Vol 1, Baltimore, 1998, Lippincott, Williams & Wilkins.)

Graphic Jump Location

Other neurological signs and symptoms frequently accompany a facial palsy from upper motor neuron disease. The portion of the precentral motor gyrus that serves the hand and fingers lies immediately superior to the facial motor area, and motor control for the tongue lies adjacent inferiorly (see Figure 12–1). Therefore, hemispheric lesions in this area may produce contralateral weakness of the lower face, hand, and tongue, as well as other hemispheric signs.

Limbic (Extrapyramidal) Pathway

Patients with upper motor neuron disease involving the corticobulbar ...

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