NEWBORN WITH FACIAL PALSY

• 10 days old child reports with asymmetry of face
• normal delivery
• no prolonged labour
• no cpd
• Facial nerve palsy in the neonate may follow birth injuryor rarely may result from agenesis of the facial nervenucleus. he latter condition occasionally is hereditary,but usually is sporadic.Etiology. Traumatic facial nerve palsy most often followscompression of the peripheral portion of the nerve, eithernear the stylomastoid foramen through which it emerges,or where the nerve traverses the ramus of the mandible.
• The neonate is vulnerable to these injuries because ofthe superficial course of the extracranial facial nerves. Thenerve may be compressed by forceps, especially when thefetal head has been grasped obliquely. The condition alsooccurs after spontaneous deliveries in which prolonged pressure was applied by the maternal sacral promontory.Less requently injury is sustained in utero, often in associationwith a mandibular deformity, by the persistent position of the etal foot against the superior ramus of the mandible. An extremely rare cause is the pressure of a uterine tumor on the nerve.
• This condition may occur rarely with simultaneous ipsilateral brachial plexus palsy, most likely secondary tocompressive forces during delivery.22 Contributing factors include prolonged second stage of labor and midforceps delivery.
• Traumatic facial nerve palsy may follow a contralateral injury to the CNS such as a temporal bone fracture, or hemorrhage, tissue destruction, or both to structures within the posterior fossa. This CNS injury is less frequent than peripheral nerve injury.
• Clinical Manifestations. Paralysis is usually apparent on the first or second day but may be present at birth. It us edema occurs over the area of nerve trauma. The type and distribution of paralysis are different in central facial paralysis compared with peripheral paralysis.
• Central paralysis is a spastic paralysis limited to the lower half or two thirds of the contralateral side of theface. The paralyzed side is smooth and full and often appears swollen. The nasolabial fold is obliterated, and the corner of the mouth droops. When the infant cries, the mouth is drawn to the normal side, the wrinkles are deeper on the normal side, and movement of the forehead and eyelid is unaffected. Usually other manifestations of intracranial injury appear, most often a sixth cranial nerve palsy.
• Peripheral paralysis is flaccid and, when complete,involves the entire side of the face. When the infant is at rest, the only sign may be a persistently open eyelid on the affected side, caused by paralysis of the orbicular muscle of the eye. With crying, the findings are the same as in a central facial nerve injury, with the addition of a smooth forehead on the involved side. Because the tongue is not involved, feeding is not affected.
• A small branch of the nerve may be injured, with involvement of only one group of facial muscles. Paralysis is then limited to the forehead, eyelid, or mouth. Peripheral paralysis caused by nerve injury distal to the geniculate ganglion may be accompanied by a hematotympanum on the same side.

Differential Diagnosis.

• Central and peripheral facial nerve palsies must be distinguished from nuclear agenesis (Möbius syndrome). The latter frequently results in bilateral facial nerve palsy; the face is expressionless and immobile, suggesting muscle fibrosis. Other cranial nerve palsies and deformities of the ear, palate, tongue, mandible, and other bones may be associated with Möbius syndrome.
• Congenital absence or hypoplasia of the depressor muscle of the angle of the mouth also may simulate congenital facial palsy and has been associated with an increased incidence of other congenital anomalies.

Prognosis.

• Most facial palsies resolve spontaneously within several days; total recovery may require several weeks or months. Electrodiagnostic testing is beneficial in predicting recovery; repeatedly normal nerve excitability indicates a good prognosis, but decreased or absent excitability early in the course suggests a poor outlook. The subsequent appearance of muscle fibrillation potentials indicates nerve degeneration. The prognosis in surgically treated infants worsens with increasing age at treatment