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Detailed physical examination, imaging, and other tests can reduce the possibility of misdiagnosis; accurately locating the site of nerve injury and objectively assessing the grading of facial nerve palsy can be used to evaluate prognosis, guide clinical treatment, and achieve good clinical efficacy.
When patients present with facial asymmetry such as mouth and eye deviation, relevant examinations must be performed to differentiate between peripheral and central facial nerve palsy in order to avoid misdiagnosis and missing the optimal treatment window; clarifying the localization diagnosis of nerve injury, assessing prognosis, and guiding clinical treatment to improve clinical efficacy.
Peripheral facial nerve palsy refers to a lower motor neuron facial weakness caused by diseases outside the central nervous system, involving the peripheral facial nerve, without evidence of auditory or more widespread neurological diseases, known as Bell palsy, i.e., peripheral facial nerve palsy.
This article will discuss peripheral facial nerve palsy from aspects including the composition of facial nerve fibers, localization, and differential diagnosis of facial nerve palsy, for reference by colleagues.
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Composition of Facial Nerve Fibers
Figure 1 Branches and distribution of the facial nerve
The facial nerve is a mixed cranial nerve, primarily composed of motor fibers responsible for facial expression muscles, with secondary components being the intermediate nerve containing somatic and visceral afferent fibers as well as visceral efferent fibers. It receives sensory impulses from the tympanic membrane, inner ear, external ear, and skin of the external auditory canal; it is responsible for taste and secretion of glands (lacrimal gland, salivary glands), as shown in Figure 1.
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Motor Fibers
They arise from the facial motor nucleus located in the ventrolateral part of the lower pontine tegmentum. The fibers pass dorsomedially, circumvent the abducens nucleus, then descend anteroinferiorly, exiting the brainstem near the lower edge of the pons, adjacent to the vestibulocochlear nerve.
Afterward, they course parallel with the vestibulocochlear nerve through the internal auditory canal. At the bottom of the internal auditory canal, the facial nerve separates from the vestibulocochlear nerve, then descends through the facial canal. At the bend of the facial canal, it passes the geniculate ganglion branch, giving off the stapedius nerve and chorda tympani nerve along the way, finally exiting the skull via the stylomastoid foramen, passing through the parotid gland and innervating all facial muscles except the muscles of mastication and levator palpebrae superioris, as well as the platysma, stapedius, and auricular muscles.
Neurons controlling the upper facial muscles (frontalis, corrugator supercilii, orbicularis oculi) within the pons are bilaterally controlled by the corticobulbar tract, while neurons innervating the lower facial muscles (zygomaticus, buccinator, orbicularis oris, platysma, etc.) receive contralateral corticobulbar tract innervation.
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Sensory Fibers
(1) Gustatory fibers: These are the main sensory fibers responsible for taste sensation in the anterior two-thirds of the tongue. Starting from taste buds in the anterior two-thirds of the tongue, the fibers travel via the lingual nerve (a branch of the mandibular division of the trigeminal nerve), enter the chorda tympani nerve, continue through the facial nerve trunk to the geniculate ganglion (first-order neurons). The central processes form the intermediate nerve of the facial nerve, entering the brainstem laterally to the motor root and terminating in the solitary nucleus (second-order neurons).
Fibers from the solitary nucleus cross to the contralateral side, ascend medially within the medial lemniscus, terminate in the ventral posteromedial nucleus of the thalamus (third-order neurons), then project to the lower part of the postcentral gyrus.
(2) General sensory fibers: The geniculate ganglion contains a small number of sensory neurons, receiving sensory impulses from the tympanic membrane, inner ear, and skin of the external auditory canal. Lesions in these fibers can cause ear pain.
Parasympathetic fibers supply the lacrimal gland, submandibular gland, and sublingual gland secretions. Parasympathetic fibers of the facial nerve originate from the superior salivatory nucleus in the pons, travel via the intermediate nerve → chorda tympani → lingual nerve to the submandibular ganglion. Postganglionic fibers innervate the sublingual and submandibular glands for secretion. Fibers controlling lacrimal gland secretion pass via the intermediate nerve through the greater superficial petrosal nerve to the pterygopalatine ganglion. Postganglionic fibers innervate the lacrimal gland secretion.
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Manifestations of Facial Nerve Injury and Localization Diagnosis
Let’s first look at the clinical differences between central and peripheral facial nerve palsy:
Figure 2 Localization differences between central and peripheral facial nerve palsy
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Central Facial Nerve Palsy
Caused by upper motor neuron lesions in the lower part of the precentral gyrus or corticobulbar tract on one side.
Clinically, only contralateral lower facial muscles are paralyzed, i.e., nasolabial fold becomes shallow, corner of the mouth slightly droops, while upper facial muscles (frontalis, orbicularis oculi) are spared. Commonly seen in cerebrovascular diseases.
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Peripheral Facial Nerve Palsy
Caused by lower motor neuron lesions affecting the facial nerve nucleus or peripheral nerves below the nucleus.
Clinically, ipsilateral upper and lower facial muscles are paralyzed, i.e., forehead wrinkles shallow or disappear, inability to frown, widened palpebral fissure, incomplete eyelid closure.
When forcibly closing eyes, the eyeball turns upward and outward, exposing the white sclera, known as the Bell phenomenon.
The nasolabial fold on the affected side becomes shallow, mouth corner droops, there is cheek puffing and air leakage, inability to whistle, and food accumulates between the cheeks and gums during eating.
Peripheral facial nerve palsy lesions within and outside the facial canal present differently clinically and can be further localized based on accompanying symptoms and signs (see Figure 2).
So, how to localize facial nerve injury precisely?
Extracranial lesion localization from proximal to distal (as shown in Figure 3):
① Lesions above the geniculate ganglion: If the greater petrosal nerve is involved, lacrimal secretion is impaired, causing dry eyes and conjunctivitis.
② Geniculate ganglion: Manifested as taste disturbance + hyperacusis, mastoid pain, often accompanied by decreased sensation or pain in the external auditory canal and herpes, constituting Hunt syndrome caused by herpes virus infection.
③ Lesions from within the stylomastoid foramen to the entire facial canal:
(a) Above the stapedius nerve branch: taste disturbance + hyperacusis.
(b) Above the chorda tympani branch: may have sensory disturbance of the anterior two-thirds of the tongue, accompanied by reduced salivary secretion.
(c) Below the chorda tympani branch: typical peripheral facial nerve palsy symptoms, without taste, hearing, or lacrimal secretion abnormalities.
④ Lesions of the facial nerve trunk within and beyond the stylomastoid foramen (the mastoid portion where the facial nerve exits the canal): Typical peripheral facial nerve palsy symptoms but no other symptoms (no taste, hearing, or lacrimal secretion abnormalities).
Figure 3 Diagram of various stages of the facial nerve
Generally, the lower the site of facial nerve injury, the better the therapeutic effect.
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Grading Criteria for Peripheral Facial Nerve Palsy
The severity of facial nerve palsy relates to prognosis; usually, patients with mild palsy recover faster, while those with severe palsy recover more slowly. The House-Brackmann grading system is commonly used clinically to assess the prognosis of facial nerve palsy recovery, as shown below (Table 1).
Table 1 Grading criteria for peripheral facial nerve palsy
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Differences Between Central and Peripheral Facial Nerve Palsy
Summarized in two tables
Table 2 Key points for differential diagnosis of central and peripheral facial nerve palsy
Table 3 Key points for differential diagnosis of central and peripheral facial nerve palsy
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Four Points to Aid Accurate Diagnosis
For patients with peripheral facial nerve palsy, we need to:
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Exclude peripheral facial nerve palsy caused by other secondary reasons.
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Inquire in detail about the onset speed of clinical symptoms, clarify the initial symptom and sequence of onset of facial nerve palsy.
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Examination should pay special attention to signs related to brainstem lesions such as dizziness, diplopia, ataxia, pyramidal signs, hearing loss, decreased facial or limb sensation; check for otologic diseases, such as herpes, infection, trauma, ulcers, or space-occupying lesions in the external auditory canal, parotid gland, head and face, or cheek skin; pay attention to presence of headache, fever, vomiting.
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Pay attention to medical history such as diabetes, stroke, trauma, connective tissue disease, facial or skull base tumors, and any history of special infections or exposure.
Summary:
Accurate localization and differential diagnosis are prerequisites for good therapeutic outcomes. Detailed physical examination, imaging, and other tests can reduce misdiagnosis; precisely locating the nerve injury site and objectively grading facial nerve palsy can be used to assess prognosis, guide clinical treatment, and achieve good clinical efficacy.
References:
[1] Zhou Xueying, Dong Yan, Wang Lili. Current Research Status of Bell Palsy [J]. Chinese Medical Innovation, 2022, 19(10).
[2] James AO, C Matthew Stewart, Kofi Boahene. Facial Nerve Paralysis [J]. Med Clin North Am, 2018, 102(6):1135-1143.
[3] Luis Lassaletta, José Manuel M, Xabier Altuna, et al. Facial paralysis: Clinical practice guideline of the Spanish Society of Otolaryngology [J]. Acta Otorrinolaringol Esp. 2020;71(2):99-118.
[4] Han Juchan, Wen Shirong, Pan Yujun. Current Research Status of Idiopathic Facial Nerve Palsy [J]. Journal of Stroke and Nervous Diseases, 2021, 38(09).
Originally published on: MedSci Neurology Channel
Author: Wang Lulu