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What is Duane Syndrome?
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What is the cause of this
condition?
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Are there
variations in clinical presentation?
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Does the condition run in families? Any associated systemic conditions?
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How is this condition
managed?
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How do I get more information?
Duane syndrome
is a congenital eye movement disorder characterized by the following clinical
features: horizontal eye deviation on primary gaze, contralateral face turn,
limited abduction, lid fissure narrowing on adduction and lid fissure widening
on abduction.
Vision is almost
always normal unless there is an associated anisometropia and amblyopia. Gaze
towards the side of the unaffected eye and contralateral face turn are
compensatory head postures to allow binocular single vision.
The condition is
unilateral in most cases but bilateral cases occur in about 15-20%. It occurs
more commonly in females and the left eye is more commonly affected than the
right.
About 30-50% of
patients with Duane syndrome have associated congenital neurologic deficits that
localize to the brainstem such as crocodile tears, sensorineural hearing loss,
or structural defects involving ocular, skeletal, and neural structures.
It is caused by
a congenital absence of the sixth cranial nerve nucleus with misdirection of the
medial rectus nerve, innervating both the medial rectus and the lateral rectus
muscle. Since both the lateral rectus and medial rectus are innervated by the
nerve to the medial rectus, both muscles fire and contract simultaneously on
attempted adduction. This co-contraction of the muscles causes globe retraction
and lid fissure narrowing on attempted adduction.
There are three
clinical types based on the direction of the eye turn on primary gaze. Duane I
shows esotropia on primary gaze and has good adduction and poor abduction.
Duane II shows exotropia and has variable adduction and decreased to normal
abduction. Duane III shows variable horizontal deviation on primary gaze and
has poor adduction and abduction. All types show globe retraction on adduction
and lid fissure narrowing on adduction.
Duane syndrome
may be associated with Goldenhar syndrome and prenatal thalidomide exposure, a
known teratogen. However, the condition is most often isolated, sporadic, and
of unknown cause.
Familial
unilateral and bilateral cases occur, and is usually is transmitted in an
autosomal dominant pattern. The clinical presentation in familial cases
varies.
The basic
problem in Duane syndrome cannot be fixed by any means; however, any associated
strabismus, amblyopia, or refractive error must be treated and reviewed
appropriately.
The majority of
patients with Duane syndrome have few problems other than a head turn and do
not require surgery if mild. Parents should be reassured about this
compensatory position. Surgery is done to correct unacceptable head posture
associated with strabismus, relieve marked globe retraction, improve palpebral
fissure changes on eye movement, and improve severe upshoots or downshoots of
the affected eye. Although strabismus surgery is very effective for correcting
face turn and improving abduction, full abduction is rarely achieved.
References:
Jay WM, Hoyt
CS. Abnormal brainstem auditory-evoked potentials in Stilling-Turk Duane
retraction syndrome. AM J Ophthalmol 1980; 89: 814-8.
Miller NR, et
al. Unilateral Duane’s retraction syndrome (type 1). Arch Ophthalmol 1982;
100: 1468-1472.
Chung M, et
al. Clinical diversity of hereditary Duane’s retraction syndrome. Ophthalmology
2000; 107: 500-503.
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DUANE SYNDROME information compiled by
Dr. Barbara L. Roque
and initially uploaded on October 25, 2005.
Last updated on
September 20, 2007.
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