A 63-year-old man was referred to the stroke unit after waking with an isolated right-sided lower motor neurone facial palsy. MR brain imaging was reported as normal. He was diagnosed with Bell’s palsy and discharged home with a short course of oral prednisolone.

Three weeks later, he was readmitted with additional left-sided facial weakness, double vision, mild bilateral leg weakness and associated distal numbness. Neurological examination showed weakness of right eye abduction, bilateral lower motor neurone facial nerve palsies and mild generalised lower limb weakness with reduced or absent reflexes. Upper limb motor function and reflexes were normal. Peripheral sensory testing showed a high sock distribution of reduced pinprick sensation with additional involvement in the distribution of the right ulnar nerve. Other than abdominal bloating, systemic examination was normal.

He had a history of late-onset hypogonadotropic hypogonadism with low serum testosterone concentration, diagnosed 7 years previously (MR brain imaging at the time was normal) and hypothyroidism. He was taking replacement therapy for both.

Unilateral facial nerve palsy is common with an incidence of around 25 per 100 000.1 The most common cause is Bell’s palsy (idiopathic facial paralysis), accounting for around 65% of cases. This has a typical presentation of acute, unilateral lower motor neurone facial palsy, often associated with mild postauricular pain and sometimes with other features of facial nerve dysfunction, such as altered taste and hyperacusis, that should improve within 4 weeks. This has been termed ‘Bell’s palsy syndrome’.2 Features outwith this typical presentation should raise concern and lead to consideration of ­alternative diagnoses. In particular, simultaneous bilateral facial nerve palsy, as in this case, is rare, occurring in less than 1% of cases of facial weakness, and should always prompt a search for …