Facial nerve paralysis in hypertension: Answers

Answers

• 1. For approximately half of patients, the cause of facial nerve paralysis is idiopathic, which is termed ‘Bell’s palsy’. Diagnosis depends on exclusion of other causes such as congenital, infectious, malignancy, metabolic, traumatic or cardiovascular.

• 2. The role for the use of corticosteroids in acute phase of facial nerve palsy is the potent anti-inflammatory action, to reduce the oedema of the facial nerve and minimising nerve damage [1].

• 3. This patient was not started on corticosteroids to prevent exacerbating his hypertension.

Discussion

Peripheral facial nerve palsy is the most common functional disturbance of a cranial nerve [2]. The underlying etiology is still poorly understood and the majority of cases are idiopathic. Symptoms are hemifacial paresis of the upper and lower face. The incidence is higher in adults and relatively low in children [2].

There is a well-known association between facial nerve palsy and severe systemic hypertension [3]. The facial nerve is vulnerable to hypertension injury due to the enclosed space of the facial canal—this can be in the form of haemorrhage, oedema or focal ischaemia [4].

This was first suggested over 150 years ago by Moxon, who described a patient with kidney disease developing a lower motor neuron palsy [5]. There have since been a number of reports of this association, with most described in children and adolescents. Despite this, a recent systematic review on peripheral facial nerve paralysis in severe hypertension found that this is often not promptly recognised in the paediatric population [3]. The study reviewed 26 cases from 1990 to 2011, of which 23 were children. The time between the first facial symptoms and diagnosis of arterial hypertension was a median of 45 days (range, 0 days–2 years). This is likely because blood pressure is not as frequently performed in the initial assessment of a child, compared with adults. One study in the UK found that only 9% of children attending emergency departments had their blood pressure measured [6]. A timely diagnosis of hypertension in the case of peripheral facial nerve palsy is crucial, as with prompt antihypertensive treatment, the prognosis is excellent. While A&E departments are not aimed at carrying out primary prevention, these simple measurements can prevent disease and improve outcomes.

In idiopathic cases, the use of oral corticosteroids is recommended and preferably within 3 days from the onset of symptoms [7]. This further highlights the need for blood pressure measurement, as inappropriate administration of steroid therapy for suspected Bell’s palsy would worsen hypertension. Hypertension for those under 16 years is defined as blood pressure greater than the 95th percentile [8]. Our patient was greater than the 99th centile for his blood pressure. After initial treatment and stabilization of the patient, further evaluation is required to identify the underlying etiology. Hypertension may be a sign of underlying cardiac, endocrine or most frequently renovascular disease. However, elevated blood pressure in children may also represent an early onset of essential hypertension [9].

An interesting point to this case was the fact this was the second presentation with facial palsy. The patient had presented 3 years ago to his local hospital with unilateral facial nerve palsy, which resolved after 3 days. There was no documentation of blood pressure taken, and the patient and parents could not recall him ever having his blood pressure measured before.

Our patient responded well to antihypertensive therapy and appropriate investigations were performed to rule out the possible differential diagnoses. Given that hypertension can often be overlooked, we urge that all paediatric patients should have blood pressure measurements when presenting with facial palsy.