Abducens Nerve and Facial Nerve Palsy in the Setting
of an Extracranial Mass and Vascular Disease
Abstract: Cranial neuropathies are a common neurological
presentation with a multitude of potential etiologies. This case
report details a patient who presented to the clinic with a left sixth
cranial and a right seventh cranial neuropathy. Further follow
up and analysis revealed significant microvascular disease to be
the likely main etiology. The purpose of this report is to further
correlate vascular disease with atypical neurological presentations.
Our discussion on common cranial nerve etiologies seeks to guide
clinicians when deciding clinical diagnostic and treatment options.
Background: The 6th cranial (abducens nerve) nerve originates
from the dorsal pontine just below the fourth ventricle. Its primary
function is to innervate the lateral rectus, which functions to
laterally rotate the eye. The abducens nerve has the longest course
of any of the cranial nerves as it originates from the pons, enters the
cavernous sinus, travels near the internal carotid artery, and then
proceeds through the superior orbital fissure to reach the lateral
rectus muscles. The abducens nerve’s extended course makes it
extremely vulnerable to any interrupting process and this allows
the nerve to act as a tripwire for many brainstem pathologies.
Unsurprisingly, abducens 6th nerve palsy is the most common
acquired oculomotor palsy. Abducens nerve palsy presents as
horizontal diplopia that worsens with horizontal gaze toward the
affected lateral rectus muscle. Common etiologies of abducens
palsy in adults include vascular disease, inflammation, tumors, and
trauma. Diagnosis can be suspected with physical examination of
extra-ocular movements with confirmation preferably done by MRI
as it provides greater detail in relation to the orbits, cavernous sinus,
posterior fossa, and cranial nerves . Idiopathic and ischemic cases
usually resolve in 2 months. The 7th (facial) nerve originates from
the ventrolateral pontine tegmentum, and it courses through the
facial canal in the temporal bone and exits through the stylomastoid
foramen . It terminates in the posterior edge of the parotid gland.
The facial neve differs from the abducens nerve in that it carries
both sensory and motor fibers. The facial nervates the muscle of
facial expression and the stapedius muscle. Its sensory component
consists of innervation to the external auditory meatus, tympanic
membrane, and the pinna of the ear. As opposed to abducens
nerve palsy, most facial nerve palsies are idiopathic or an autoimmune
sequala of herpes simplex or herpes zoster infection .
Diagnosis is usually made via clinical examination with CT or MRI if
other neurological symptoms present. In both abducens and facial
palsy, ESR should be ordered if vasculitis is suspected. Treatment
of idiopathic cases of facial nerve palsy consists of corticosteroids and valacyclovir if herpes simplex is suspected. Prognosis of facial
neve palsy depends on the extent of nerve damage. If there is some
remaining nerve function, full recovery is expected within a few
Objective: The purpose of our case report is to inform readers
of the clinical presentation of a concurrent abducens and facial
nerve palsy. Discussion of the patient’s extra-cranial mass and
vascular disease was given to guide clinicians in identifying a main
contributing etiology in cases of cranial neuropathies.
I present a case of a 59-year-old female patient who presented
to a primary care clinic in August 2021 after she woke up from a
nap with sudden onset horizontal binocular diplopia that worsened
on far vision. She also reported a severe left side headache that
worsened with loud noises. Gait instability was also noted. Physical
exam revealed significant right eye esotropia and left eye CN 6
palsy which did not cross the midline on lateral gaze. Signs of right
cranial nerve 7 palsy were seen with right side facial drop and
ptosis apparent on inspection. Cranial nerves two and three were
deemed to be intact as both pupils reacted equally to light and
accommodation. She denied any history of trauma. At this initial
visit, the etiology was suspected to be a viral auto-immune sequala
and a steroid dose pack was prescribed. Her medical history is
significant for hypertension, dyslipidemia, diabetes mellitus,
and hypothyroidism. She has a 60-pack year smoking history.
CTA in August 2021 was negative for any large vessel occlusion
or hemorrhage. MRI was negative for any significant occlusion
but revealed an extra-cranial mass, which measured 1cm and
impacting the right trigeminal nerve. Subsequent follow up visits in
August 2021 revealed no improve after corticosteroid therapy with
persistent 6 and 7th nerve palsy, worsening alternating esotropia
and further balance issues. No surgical intervention was made and
a repeat MRI in 6 months was planned. At that time, the focus of
treatment was to improve glycemic control, more tightly control
lipids levels, and advise smoking cessation. Nearly three months to
the date of onset, the patient awoke with restored lateral gaze and
absent diplopia. Her facial palsy improved in subsequent weeks.
Even in the presence of a facial palsy mass, vascular risk factors
for patients with abducens nerve palsy must be evaluated. In adults,
vascular disease constitutes a majority of abducens nerve palsy as
shown by a retrospective chart review in 2014 . Major risk factors
for cranial atherosclerosis include diabetes mellitus, hypertension,
metabolic syndrome, smoking, and a sedentary lifestyle . The
right extra-cranial mass was considered a possible etiology of both
cranial neuropathies but was subsequently ruled out based on
imaging and patient presentation. The patient’s right cranial nerve
7 palsy improved making the compression from a growing mass
an unrealistic etiology. In relation to the left abducens nerve palsy,
its contralateral location and sudden improvement highlighted the
vascular nature of her etiology. A clearly defined etiology for facial
palsies proves difficult to find. 70% of unilateral facial palsies are
idiopathic with trauma, infection, and neoplasia as the remaining
most common causes. In idiopathic cases, a viral prodrome period
occurs before the onset of palsy .
The patient denied any preceding symptoms making a viral
cause less likely but not impossible cause. The facial nerve has a
robust vascular supply due to its thick epineurium; this vascular
dependency proposes an ischemic connection to facial nerve palsy
. Although the facial nerve vascular supply has many anastomoses,
this system can be compromised by diabetes mellitus, which is
present in this case, especially at certain points along its tract that
do have as proficient collateral perfusion as in the stylomastoid
and petrosal branches . Concurrent abducens and facial nerve
palsies are a very uncommon finding. A 51-patient prospective
study on bell’s palsy found that the most common concurrent
cranial nerve palsies involved the trigeminal, glossopharyngeal,
and hypoglossal nerves . At this time, it is difficult to predict the
long-term outcome for the patient presented in this case report but
the prognosis for isolated abducens nerve palsy is encouraging.
A 213-patient review found that 78.5% experience spontaneous
recovery of their symptoms, with 36.6% by 8 weeks .
Patients that present with cranial neuropathies require a
comprehensive vascular assessment in addition to the evaluation of
neoplasms, trauma, and infectious causes. In the setting of a facial
palsy, the etiology should not be immediately assumed to be of
viral or auto-immune origin especially in diabetes mellitus, which
predisposes the facial nerve to microvascular infarct. Multiple
concurrent cranial neuropathies further stress the need for the
evaluation of vascular risk factors.
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