Q J Med 2015; 108:145–146

doi:10.1093/qjmed/hcs110 Advance Access Publication 13 June 2012

Case report

Facial nerve palsy in the setting of malignant hypertension:

a link not to be missed
M. TOMEK1, A. NANDOSKAR2, N. CHAPMAN3 and C. GABRIEL2

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From the 1Department of Medicine, Charing Cross Hospital, 2Department of Neurology,
3
Department of Clinical Pharmacology, St Mary’s Hospital, Imperial College Healthcare NHS Trust,
London, UK

Address correspondence to Michal Tomek, Department of Medicine, Charing Cross Hospital, Fulham Palace
Road, London W6 8RF, UK. email: michal.tomek@cantab.net

Case history changes in the cerebral hemispheres and diffuse

A 38-year-old truck driver presented to our depart-
ment with 1-week history of blurred vision and
recent worsening of frontal headaches, which had
been present for 6 months. He had no significant
past medical history but could not recall if his
blood pressure had ever been measured. His older
sister had been diagnosed with malignant hyperten-
sion 4 years ago. He smoked 20 cigarettes per day.
On examination, he was alert and orientated with
a blood pressure of 242/150 mmHg. Visual acuity
was decreased to 6/36 bilaterally and fundoscopy
revealed bilateral papilloedema with exudates and
haemorrhages. Neurological and systemic examin-
ation was otherwise unremarkable.
Initial tests demonstrated renal impairment (cre-
atinine 142 mmol/l), blood and protein in the urine
and electrocardiographic evidence of left ventricular
hypertrophy. A computerised tomogram (CT) of the
brain was normal. A diagnosis of malignant hyper-
tension was made and the patient’s blood pressure
was lowered gradually with a combination of oral
modified-release nifedipine, bisoprolol and
bendroflumethiazide.
Two days after admission the patient developed
acute-onset left-sided facial weakness. Examination
revealed a lower motor neuron facial palsy and im-
paired taste in the anterior left tongue but no other
abnormalities. Magnetic resonance imaging (MRI)
demonstrated bilateral ischaemic white matter
small vessel disease, without a brainstem lesion
that would explain the facial palsy. Although it
was felt that the facial weakness was most likely
related to the severe hypertension, he was treated
empirically with a short course of prednisolone and
aciclovir for possible Bell’s palsy.
Further investigations excluded the presence of a
vasculitic or primary renal disorder or other second-
ary causes of hypertension such as hyperaldosteron-
ism, renal artery stenosis or phaeochromocytoma.
He was discharged home once his blood pressure
was under control. At follow up, mild renal impair-
ment had persisted but his blood pressure remained
well controlled. His facial weakness resolved com-
pletely over several months.
Discussion
The commonest cause of acute unilateral facial
weakness is Bell’s palsy (accounting for 60–75%
of cases),1 which has traditionally been regarded as
idiopathic. Although a viral aetiology has been sug-
gested, a recent meta-analysis found little benefit of
antiviral therapy in Bell’s palsy.2 An association with
hypertension has also been observed, suggesting a
possible vascular mechanism.3 Interestingly, the ma-
jority of previously reported cases of this association
have occurred in children.4–8 Here we present a
case of facial nerve palsy developing in an adult

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146 M. Tomek et al.
patient in the setting of malignant hypertension. The
onset of the paralysis appeared to coincide with the
rise in blood pressure, with gradual resolution fol-
lowing blood pressure control.
The link between hypertension and facial nerve
palsy was first suggested in 1869 by Moxon, who
described a patient with facial weakness in the set-
ting of renal disease (and presumed hypertension,
although this predated indirect measurement of
blood pressure and so can only be inferred).9
Since then, a number of reports of the association
have been published; however, only a handful of
these occurred in adults,9–11 and only one such
case has been reported since the early 1980’s.11 A
case series from 1967 reported the presence of facial
palsy in 6 of 55 (11%) children with severe hyper-
tension;4 an earlier report from the same institution
had suggested an incidence as high as 20%.5 In an-
other series of 45 children with severe hypertension,
all had developed some neurological manifestation
(principally seizures) but only 2 (4%) had facial
palsy.6 In contrast, a study of 190 adult patients re-
ported presence of isolated facial nerve palsy in
5 (2.6%) subjects, while overall neurological mani-
festations were present in 79 (42%) patients.10
Although the pathogenic mechanisms underlying
hypertension-induced facial paralysis remain un-
clear, the cause has been hypothesized to lie in
the widespread arteriolar injury characteristic of
malignant hypertension. Specifically, the facial
nerve is thought to be particularly vulnerable to
hypertension-induced injury (due to haemorrhage,
oedema or focal ischaemia) in the enclosed space
of the facial canal.6 This is supported by autopsy
findings of facial canal haematoma in two previ-
ously published cases,5,9 suggesting nerve compres-
sion due to haemorrhage and thrombus formation.
Similar pressure effects may also occur due to thick-
ened vessel walls or the formation of peri-neural
oedema, such as has been postulated to occur in
pre-eclampsia-induced Bell’s palsy.12
In conclusion, we report a case of an adult patient
with facial paralysis associated with malignant
hypertension. While knowledge of this link has
existed for over a century, it is no longer well
recognized, particularly in the adult population.
As a result, in two cases reported in the more
recent literature, there was a delay in identification
of the underlying severe hypertension.7,8 Given that
facial nerve palsy can be the initial (and only) pre-
senting feature of malignant hypertension,13 we urge
clinicians to maintain a high index of suspicion, if
only so that patients presenting with ‘idiopathic
Bell’s palsy’ have their blood pressure recorded
and so avoid the potentially disastrous conse-
quences of a delayed diagnosis of malignant
hypertension.
Conflict of interest: None declared.
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