Facial nerve malformation
Damage to the facial nerve may occur with or without petrous bone malformation. (Figure 183.1) Facial nerve damage is often associated with deafness and abnormal ears.

A	B

Figure 183.1.— Lower motor neuron facial weakness. [A] Asymmetrical facial grimacing. [B] Brain CT demonstrating an abnormal left petrous bone.

Facial nerve damage with or without radiological evidence of petrous bone malformation occurs in CHARGE association (Figure 183.2). CHARGE stands for coloboma, heart disease, atresia choanae, retarded growth and retarded development, genital hypolasia, and ear anomalies. In a large series, facial palsy occurred in 38% of patients with CHARGE association.

A	B

Figure 183.2.— CHARGE association. [A] Asymmetrical facial grimacing and cleft palate. [B] Ear abnormality.

Facial nerve damage due to parotid gland tumor
Tumors of the parotid gland may involve the facial nerve (Figure 183.3). Signs of infection or hemangioma of the parotid gland may be present (Figure 183.3)

A	B	C

Figure 183.3— Facial asymmetry due to parotid gland hemangioma. The asymmetry is present [A] while crying but [B] not during quiet awake. [C] The parotid hemangioma creates a bluish mass behind the ear.

Diagnosis of facial nerve lesion

Regarless of the etiology, the diagnosis of a facial nerve lesion may be confirmed by electrodiagnostic studies. Nerve conduction studies determine threshhold, latency, and amplitude of the compound muscle potential in the normal and the affected side. Electromyography shows fibrillations and positive sharp waves 12 to 14 days after the injury. An EMG abnormality in the first 48 hours of life implies that the injury occurred before delivery. Computed tomography of the petrous bone may be used to evaluate the osseous facial nerve canal and the middle ear.
The temporal evolution of peripheral facial nerve deficit depends on whether the damage is transient, permanent, or progressive. Transient deficits improve starting with the forehead and periocular muscle.Permanent deficits remain unchanged. Deterioration implies a progressive etiology (parotid gland tumor or a complication).
A facial nerve lesion is distinguished from an intrapontine facial lesion by the absence of signs of involvement of the central sympathetic tract, cranial nerve VI, and upper motor neuron limb weakness. Treatment is dictated by the etiology. At an older age, nerve grafting and muscle transplantation may be performed in selected cases. Tumors may require surgery. Congenital petrous bone abnormalities do not have specific treatment. Traumatic cases usually do not require treatment.