CRANIAL
NERVE VI PALSY
Signs and
Symptoms
The patient will
present with horizontal uncrossed diplopia, which worsens at distance and in
either right or left gaze. The patient will have an abduction deficit in the
involved eye and either an esophoric or esotropic position, which is
non-comitant. The onset is typically sudden. If the palsy is isolated, there
will be neither visual acuity nor visual field loss. There may be some degree
of head pain. The patient typically is older and has a concurrent history of
hypertension and/or diabetes. The fundus is typically normal, except when the
patient manifests a bilateral cranial nerve VI palsy, where there typically
will also be papilledema.
Pathophysiology
Cranial nerve VI
arises in the pons, in close association with the facial nerve and paramedian
pontine reticular formation (PPRF). Due to this arrangement, damage to the
sixth nerve within the brain stem will produce a sixth nerve palsy as well as a
facial nerve palsy or an internuclear ophthalmoplegia. Associated findings may
also include leg paralysis with sixth nerve palsy (Raymond's syndrome), or leg
paralysis, facial paralysis and sixth nerve palsy (Millard-Gubler syndrome).
These additional findings identify the location of damage as the pons, where
ischemic infarct, tumor and demyelinization are the common causes.
The sixth nerve
travels through the subarachnoid space where it ascends the clivus and enters
the cavernous sinus. Within the subarachnoid space, the sixth nerve may be
stretched against the clivus as the brain stem herniates through the foramen
magnum due to increased intracranial pressure. This will give a bilateral sixth
nerve palsy (which is often intermittent) and papilledema. As the sixth nerve
passes over the petrous apex of the temporal bone, damage here can result in a
sixth nerve palsy, facial pain and hearing loss. This occurs due to
inflammation of the temporal bone (Gradenigo's syndrome) or nasopharyngeal
carcinoma.
Within the
cavernous sinus, the sixth nerve is joined by the oculosympathetic nerves, and
cranial nerves III, IV and V-1. Damage here will yield a sixth nerve palsy and
Horner's syndrome, as well as a concurrent CN III and IV palsy. The etiology
may be aneurysm, meningioma, pituitary adenoma, inflammation, or fistula. The
sixth nerve is also vulnerable to ischaemic infarct from diabetes and
hypertension; this remains a prime cause of isolated sixth nerve palsy.
Management
A sixth nerve
palsy combined with any of the above mentioned neurological signs indicates a
need for MRI of the appropriate area. In children, sixth nerve palsy often
occurs from a presumed viral cause and has an excellent prognosis. However, if
the palsy does not recover, or worsens over several weeks, the child should be
examined for a pontine glioma. In the adult under 50 years, obtain MRI studies
of the brain. Adult sover 50 with an isolated sixth nerve palsy require a
workup for ischaemic vascular diseases such as diabetes and hypertension. If
the patient is over the age of 65 years, order an erythrocyte sedimentation
rate (ESR) to rule out giant cell arteritis.
If no etiology is
discovered on MRI or hematology studies, monitor the patient monthly for
several months until resolution (or until other signs develop which would
indicate an etiology). The vast majority of CN VI palsies due to ischemic
vasculopathy (or idiopathic etiology) will resolve without treatment in three
to six months. Fresnel prism correction or unilateral occlusion will
temporarily alleviate the diplopia.
Clinical
Pearls
The etiology of
isolated CN VI palsy in adults is undetermined in 25 percent of cases, despite
full diagnostic evaluation. These palsies, and those due to diabetes or
hypertension, resolve in three to six months without treatment. A diagnostic
workup should include intracranial MRI, CBC with differential, fasting blood
glucose, ESR, blood pressure measurement, Lyme titer and syphilis serology. If
these tests are negative, monitor the patient for resolution. Clinical
worsening over time indicates the need for more thorough or repeat
investigation. Myasthenia gravis may mimic a sixth nerve palsy and should
always be considered in the differential diagnosis, especially if the palsy
takes on a variable course with exacerbations and remissions. Always consider
the possibility of myasthenia gravis in cases of non-restrictive, pupil sparing
CN III, IV and VI nerve palsy as well as unilateral and bilateral internuclear
ophthalmoplegia.
Other reports
in this section
á Anterior Ischemic Optic Neuropathy
á Optic Disc Edema & Papilledema
á Cranial Nerve III Palsy
á Cranial Nerve IV Palsy
á Cranial Nerve VI Palsy
á Cranial Nerve VII (Facial Nerve) Palsy
á Horner's Syndrome
á Internuclear Ophthalmoplegia
á Optic Nerve Head Hypoplasia
á Optic Pit
á Tonic Pupil
á The Many Faces of the Optic Nerve Head (Pictorial)