Acute lower motor neurone facial paralysis is a common presentation in childhood. In most cases, an aetiological agent is not identified and the condition resolves spontaneously. A small number of cases are caused by a variety of underlying pathologies—some of which may have significant morbidity and mortality associated with them.

The facial nerve (VII) leaves the pons at the pontomedullary junction, enters the skull via the internal auditory meatus, and passes along the facial canal. The nerve passes in close proximity to the medial wall of the inner ear and the mastoid cavity. During its course through the petrous temporal bone, branches leave to supply the lacrimal glands, the stapedius muscle in the inner ear, sensation for auricular skin, the sublingual and submandibular salivary glands, and taste fibres to the anterior two thirds of the tongue. The facial nerve exits the skull via the stylomastoid foramen and terminal branches supply the muscles of facial expression.

Bilateral cortical innervation of the muscles of the upper face (orbicularis oculi and frontalis) means that complete facial paralysis is only seen with lower motor neurone lesions. The extent of additional impairment depends on the site of injury. Proximal lesions are associated with impaired lacrimation, hyperacusis, and loss of taste on the anterior two thirds of the tongue.

The pathophysiology of idiopathic facial nerve palsy is uncertain. The condition often occurs two to three weeks following a viral illness. Active viral invasion of the nerve or immune demyelination may be responsible for the underlying neuropathy. It is unclear as to whether physical swelling of the nerve plays a significant pathological role. A variety of specific pathologies can also produce an acute lower motor neurone facial paralysis. Table 1 lists some important examples. Acute facial paralysis may manifest itself as a presenting …