Facial Nerve Palsy in the Newborn

Facial nerve palsy in the newborn is unilateral or bilateral weakness of the muscles of facial expression from a lesion of the facial nerve or its nucleus. Most cases are traumatic and follow compression of the nerve by forceps blades or the maternal sacral promontory during delivery.

It is reported in about 1 in 1000 births, though estimates vary widely. Traumatic palsy usually resolves spontaneously within days to weeks, while developmental palsy is permanent.

Developmental causes include Moebius syndrome (with abducens palsy), hemifacial microsomia, CHARGE syndrome, congenital absence of the facial nerve nucleus and cardiofacial syndrome.

Pathophysiology.

The extratemporal part of the facial nerve in the newborn is superficial and unprotected because the mastoid process is not developed, so pressure from forceps or the pelvis damages it. The injury is usually neurapraxia and recovers.

Temporal bone fracture or haemotympanum can cause injury within the temporal bone. Developmental disease results from nuclear agenesis or brainstem malformation.

• Asymmetric face when crying: the mouth is pulled to the normal side, with loss of the nasolabial fold and flattening of the forehead on the affected side.
• Eye on the affected side cannot close (lagophthalmos), and a lower motor neuron lesion also weakens the forehead.
• Feeding difficulty with milk leakage from the weak side of the mouth.
• Face is symmetrical at rest in mild cases. Associated bruising, forceps marks or haemotympanum.

Red flags.

• Bilateral palsy, lateral gaze palsy or other cranial nerve involvement (Moebius syndrome).
• Dysmorphic features, ear anomalies, heart defect or deafness suggesting a syndrome.
• No improvement within 4 to 6 weeks, or later progressive weakness.

• Clinical examination at rest and when crying. Examine the ear for haemotympanum and look for forceps marks.
• Hearing screen, and examination for associated anomalies. Eye examination for exposure.
• Electroneurography or EMG at 1 to 3 weeks of life if recovery is delayed, and CT temporal bone if a fracture is suspected or there is no recovery.
• Genetic testing and echocardiography when syndromic features are present.

Differential diagnosis. Congenital hypoplasia of the depressor anguli oris (asymmetric crying face with normal forehead and eye closure), Moebius syndrome, hemifacial microsomia, CHARGE syndrome and intracranial lesions.

• Eye protection for incomplete closure: preservative free lubricating drops (hypromellose 0.3%) 1 drop every 2 to 4 hours while awake and paraffin based eye ointment at night, with taping of the lid if closure is poor. Ophthalmology review for corneal exposure.
• Feeding support, with a nipple that helps seal the lips, and speech and swallowing review in persistent cases.
• Reassure that most traumatic palsies recover within weeks to 3 months. Review every 2 weeks at first.
• Refer to ENT if there is no improvement by 4 to 6 weeks, or earlier if there is haemotympanum, bilateral palsy or a suspected syndrome. Surgical options (nerve decompression, grafting, or later reanimation) are considered in persistent cases.

Monitoring. Facial movement, eye closure, corneal health, feeding and hearing.

Referral and escalation. Refer urgently to ophthalmology for corneal exposure, and to ENT and genetics for syndromic or non-recovering palsy.