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ANISOCORIA |
Anisocoria is defined as a
difference in pupil size between the two eyes. Anisocoria is associated with a
variety of neurologic conditions, some benign and other serious. |
Pupil Physiology
Pupil size is controlled by two sets of antagonist muscles:
• the pupillary
sphincter (parasympathetic)
and
• the pupillary dilator
muscles (sympathetic)
Under normal conditions, the pupils remain equal at all levels of light. |
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The parasympathetic pathway (figure
above) originates in the Edinger-Westphal
nucleus in the dorsal mid brain and exits to run with
cranial nerve III (oculomotor nerve) through
the cavernous sinus to the
ciliary ganglion. From the cililary ganglion,
postganglionic fibers then travel to the pupilloconstrictor muscle of the iris.
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The sympathetic pathway (figure
above) originates in the hypothalamus
to run down in the brainstem laterally to reach at spinal column at
C8-T2. Fibers then run with the ventral roots
to the paravertebral sympathetic chain.
These fibers then pass through the stellate ganglion near the apex of the lung
to run to the superior cervical ganglion.
The postganglionic fibers then travel in the sheath of the
internal
carotid artery to innervate the pupillary dilator muscle. In
addition, sympathetic fibers supply innervation to smooth muscles of the upper
and lower eyelids. Lastly, sympathetic fibers also travel with the external
carotid artery to supply blood vessels and sweat glands of the face. Thus,
a complete Horner's syndrome (at or proximal to the
internal carotid artery) will result in ptosis, miosis and anhydrosis. |
Common Causes of Anisocoria
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Physiologic anisocoria
Mild anisocoria (typically 1 mm or less) is common
in the general population. As long as there are no other accompanying signs and
symptoms (e.g., diplopia, pain, ptosis), this represents a benign, normal
anatomic variant. |
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Horner's Syndrome
Horner's syndrome results from disruption of the
sympathetic fibers anywhere between the hypothalamus and the eye. Thus, Horner's
syndrome can be seen in primary brainstem pathology; lesions of the superior
cervical ganglia and disorders of the carotid artery. Common causes include
Wallenberg's syndrome
(i.e., infarction of the lateral medulla), cervical cord disease (e.g., syrinx),
apical lung disease (e.g., pancoast tumor), carotid
artery dissection, and cavernous sinus disease (i.e., infection or
neoplastic invasion). |
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As noted above, a full Horner's syndrome will
produce miosis, anhydrosis and ptosis. As the primary problem in Horner's
syndrome is a failure of pupillary dilatation, the anisocoria will be more
marked in the dark than the light. |
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Above:
Horner's syndrome is the left eye. (A) In the light; (B) In the dark; and (C) In
the dark after a brief lapse of time. Note the difference in the anisocoria
between light and dark. Often a subtle sign of a mild Horner's will be a
dilatation lag when going from light to dark. |
Pharmacologic
testing with eye drops can be very helpful in localizing the site of
the lesion in a patient with Horner's syndrome. Cocaine
(a norepinephrine reuptake blocker) eye drops will fail to dilate the affected
side, and can confirm the presence of a Horner's syndrome.
Hydroxyamphetamine
drops are used to stimulate norepinephrine release from the postganglionic
sympathetic neuron (i.e., the neuron at the superior sympathetic ganglia that
then runs to the eye). If the site of the lesion is the postganglionic neuron,
dilation will not occur with the use of hydroxyamphetamine, where a lesion in
the brainstem or between the cord and the superior cervical ganglion will dilate
normally. |
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Third Nerve Palsy
A cranial nerve III palsy results in a dilated,
poorly reactive pupil. As the pupil is unable to constrict to light, the
anisocoria is more apparent in the light than dark. As the third nerve also
innervates several extraocular muscles, a third nerve palsy often results in an
accompanying ptosis and diplopia (the latter from weakness of the medial rectus,
inferior rectus, inferior oblique, and superior rectus muscles).
The most important causes of a third nerve palsy
are external compression of an aneursym (typically one arising from the
posterior communicating artery) and uncal
herniation where the medial temporal lobe compresses the adjacent third
nerve. Of course, third nerve palsies may occur in other conditions, including
diabetes, vasculitis, and infiltrating disorders (e.g., neoplasm, sarcoid, etc.) |
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Pharmacologic
Atropine and many other drugs have anticholingeric
side effects. Inadvertent or unintentional exposure to these agents may result
in a dilated, fixed pupil. This can often occur in medical personnel, especially
nurses who dispense medications. In contrast to a third nerve palsy, the
remainder of the examination is normal (i.e., no ptosis or extrocular muscle
weakness). Proving inadvertent pharmacologic administration can be performed by
instilling 1% pilocarpine eye drops. In pharmocologic paralysis, no constriction
will occur, where in a third nerve palsy, the pupil will quickly constrict. |
• Local Damage to the Iris
Mechanical damage to the iris may result in
anisocoria. This is most often seen after cataract surgery, but can also occur
with trauma, and some inflammatory disorders (e.g., uveitis). |
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