A large proximal branch of the AICA,

the internal auditory artery, supplies the CN VIII complex in the subarachnoid space and
follows it into the internal auditory canal. Along the course of the BA (basiller artery), small perforators
arise directly to supply portions of the pons and midbrain. The median perforators of
the BA supply the medial longitudinal fasciculus, the paramedian pontine formation, and
the medially located nuclei of CN s III, IV, and VI. Interruption of these branches ( which
occurs commonly with vertebrobasilar atherosclerotic disease or emboli to these endarteries)
often produces variable ophthalmoplegia, internuclear ophthalmoplegia, and skew
deviation. Pontine branches of the BA also supply the proximal portions of the cranial
nerves (particularly CN V) as they exit the brainstem.

The lateral rectus muscle is supplied

directly through ipsilateral CN VI. The contralateral medial rectus muscle is stimulated
by interneurons that cross in the pons and ascend in the contralateral MLF. Therefore, pathology
affecting the right MLF will result in a right internuclear ophthalmoplegia- a right
(ipsilateral) adduction deficit with attempted left gaze-often accompanied by abducting
nystagmus of the left (contralateral) eye and a skew deviation (see Chapter 8).

Pursuit movements made into a blind hemifield

are often poor or absent. Smooth pursuit deficits are usually present in both horizontal
and vertical planes, although the vertical plane may be involved selectively in patients
who have bilateral internuclear ophthalmoplegia or PSP.

In the context of eye movement control, an "internuclear" lesion is one that disrupts the
medial longitudinal fasciculus (MLF), a bundle of fibers that connects the sixth nerve nucleus
on one side of the pons to the medial rectus sub nucleus ( of the third nerve) on the contralateral side of the
mid brain ( see Chtpter 1, Fig 1- 28). This type oflesion produces
an internuclear ophthalmoplegia (INO).

Third nerve palsy in younger patients

Children may experience transient ophthalmoplegia after a viral infection or vaccination.
If an immediate workup is deferred, follow-up should be scheduled to monitor recovery.
Although aneurysms are rare in children, a pupil-involving third nerve palsy necessitates
a workup to exclude an aneurysm or other structural etiology. Ophthalmoplegic migraine,
with onset in childhood, can cause pain and third nerve dysfunction, but the 2 conditions
are not coincident. MRI results may demonstrate reversible thickening and enhancement
at the root exit zone of the third nerve. Curiously, the ophthalmoplegia develops days after
the onset of head pain. Third nerve schwannoma may mimic the fluctuating nature of this
condition; however, cranial nerve enhancement will persist after resolution of the third
nerve palsy. Therefore, follow-up MRI is indicated.
Friedman DI. The ophthalmoplegic migraines: a proposed classification. Cephalalgia. 2010;
30(6):646-647. Epub 2010 Feb 22.
Schumacher-Feero LA, Yoo SW, Solari FM, Biglan AW. Third cranial nerve palsy in children.
Am J Ophthalmol. 1999;128(2):216-221.

Orbital Myositis
Idiopathic inflammation of I or more extraocular muscles typically produces ophthalmoplegia
and pain, often with conjunctiva! hyperemia, chemosis, and sometimes proptosis.
The pain may be quite intense and is accentuated by eye movements. If the inflammation
is confined to the posterior orbit, the eye may appear to be white and quiet. Results of CT
or MRI typically show enlargement of 1 or more of the extraocular muscles with tendon
involvement, and the inflammation often extends into the orbital fat. Orbital myositisrelated
pain usually responds within 24 hours to systemic corticosteroid therapy, whereas
diplopia may take longer to resolve. Orbital myositis is usually an isolated phenomenon
but may be part of a systemic disease such as Wegener granulomatosis (ie, granulomatosis
with polyangiitis), systemic lupus erythematosus, or sarcoidosis (see also Chapter 14 and
BCSC Section 7, Orbit, Eyelids, and Lacrimal System).