What brain territory is associated with facial paresis?

From the Guidelines

The brain territory associated with facial paresis is the pons, specifically the facial nuclei located within it 1.

Key Points

• The facial nerve (CN VII) is a complex cranial nerve that contains branchial motor, visceral motor, general sensory, and special sensory functions 1, 2.
• The intraparenchymal fascicular or attached segment of the facial nerve courses superiorly along the surface of the pons, and its pathology can result in peripheral, nuclear, or infranuclear facial nerve paralysis 1.
• Facial nerve palsy can present with facial droop, pain around the jaw or ear, hyperacusis, tinnitus, reduced taste, and decreased lacrimation or salivation 1, 3.
• The most common cause of acute peripheral facial nerve palsy is Bell's palsy, which is attributed to inflammation of the facial nerve and can be treated with steroids 3, 4.
• Some key characteristics of Bell's palsy include:
  • Acute unilateral facial nerve paresis or paralysis with onset in less than 72 hours 3
  • Without identifiable cause 3, 5
  • May cause significant temporary oral incompetence and an inability to close the eyelid, leading to potential eye injury 4 ### Clinical Considerations
• Clinicians should assess patients with acute onset unilateral facial paresis or paralysis using history and physical examination to exclude identifiable causes of facial paresis or paralysis 5.
• Treatment options for Bell's palsy are designed to improve facial function and facilitate recovery, and may include corticosteroids and antiviral medications 3, 4.

From the Research

Brain Territory Associated with Facial Paresis

The brain territory associated with facial paresis can be identified through various studies, including:

• A case report of a pontine infarct resulting in Millard-Gubler syndrome, which involves the facial nerve, abducens nerve, and pyramidal tracts, typically resulting in ipsilateral facial weakness and contralateral hemiparesis 6.
• A study on dysarthria-facial paresis and rostral pontine ischemic stroke, which suggests that brainstem lesions above the level of the pontine facial nucleus may present with central facial paresis contralateral to the lesion 7.
• A report on the localization of emotional and volitional facial paresis, which found that lesions involving the frontal lobe white matter, striatocapsular territory, anterolateral thalamus and insula, posterior thalamus and operculum, and mesial temporal lobe and insula can result in emotional facial paresis, while lesions involving the motor cortex and pyramidal tract can result in volitional facial paresis 8.
• A case report of pure ipsilateral central facial palsy and contralateral hemiparesis secondary to ventro-medial medullary stroke, which suggests that ventromedial medullary infarcts can result in contralateral facial and limb weakness 9.
• A study on pure monoparesis, which found that the lesion for a facial deficit was most frequently located subcortically, such as in the internal capsule 10.

Key Findings

Key findings from these studies include:

• Facial paresis can result from lesions in various brain territories, including the brainstem, frontal lobe, and subcortical structures.
• The location and type of lesion can affect the presentation of facial paresis, with some lesions resulting in ipsilateral or contralateral weakness.
• Facial paresis can occur in combination with other neurological deficits, such as dysarthria, hemiparesis, and monoparesis.