Central facial palsy colloquially referred to as central seven is a symptom or finding characterized by paralysis or paresis of the lower half of one side of the face. It usually results from damage to upper motor neurons of the facial nerve. The facial motor nucleus has dorsal and ventral divisions that contain lower motor neurons supplying the muscles of the upper and lower face, respectively.
Facial palsy has an annual incidence of approximately 20 perIt has a favorable prognosis in most cases, but as many as 8, people in the United States each year are left with a permanent, potentially disfiguring facial weakness. The facial nerve is the 7th cranial nerve and has both sensory and motor components.
Facial nerve palsy includes both paralysis and weakness of the seventh cranial nerve. Ocular signs and symptoms of facial nerve palsy include inability to close the eye, dry eye syndrome, as well as eye redness, tearing, burning, and foreign body sensation. Conservative management of ophthalmic complications of facial nerve palsy include instilling artificial tears, applying lubricating ointment, and taping the eyelids closed, while surgery is reserved for refractory cases with limited potential for recovery. Overall, the prognosis of facial nerve palsy depends on the cause of the palsy, and ophthalmologists have an important role in managing the symptoms and limiting the sequelae of this condition.
Facial nerve 7th cranial nerve palsy is often idiopathic formerly called Bell palsy. Idiopathic facial nerve palsy is sudden, unilateral peripheral facial nerve palsy. Symptoms of facial nerve palsy are hemifacial paresis of the upper and lower face.
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Click on image for details. A case of emotional facial palsy with ipsilateral anterior inferior cerebellar artery territory infarction. Open access journal indexed with Index Medicus.
Facial nerve palsy is a neurological condition in which function of the facial nerve cranial nerve VII is partially or completely lost. It is often idiopathic but in some cases, specific causes such as trauma, infections, or metabolic disorders can be identified. Two major types are distinguished: central facial palsy lesion occurs between cortex and nuclei in the brainstem and peripheral facial palsy lesion occurs between nuclei in the brainstem and peripheral organs. Central facial palsy manifests with impairment of the lower contralateral mimic musculature.
Clinical pictures of medial medullary syndrome are variable, depending upon the extent of the lesion. Facial palsy has rarely been observed even in medullary infarction. However, central-type facial palsy is usually found contralaterally to the infarct area at the level of the rostral medulla. In the present report, we discuss the pathogenesis of the neurological manifestations in a year-old man with hypertension.