The Many Faces
of
Diabetic Eye Disease: Eye Muscle Dysfunction
Paul Chous, M.A., O.D.
Doctor of Optometry
Type 1 diabetic since 1968
Diabetes
is a frequent cause of double vision, poor dark adaptation,
and reduced ability to change visual focus from one distance
to another. Each of these phenomena is attributable, in part
or whole, to efferent diabetic cranial neuropathy; that is,
motor neurons responsible for coordinated, binocular movement,
physiologic (autonomic) pupil dilation and constriction, and
accommodation by the ciliary muscle and crystalline lens, are
adversely affected by chronic hyperglycemia (for a discussion
of afferent, or sensory, neuropathy affecting the diabetic eye,
see the previous sections on glaucoma and keratopathy.)
If you are going to be at the
AADE Conference in Salt Lake City then stop by and meet Dr.
Chous on Thursday or Friday
For a person with “straight
eyes” and normal sensory binocular vision, precise alignment
of both eyes is required to maintain clear, single vision (fusion),
and any deviation results in double vision (diplopia). The coordinated
movements of both eyes are controlled by six pairs of extraocular
muscles; these are innervated by three pairs of cranial nerves
(CN III, CN IV, and CN VI). Microangiopathy affecting these
cranial nerves causes ischemia and focal demyelinization, and
can result in either partial (paresis) or total (paralysis)
loss of muscle function and some degree of diplopia (provided
there are no abnormal sensory adaptations like suppression of
the deviating eye); loss of any extraocular muscle function
is denoted by the less specific term, palsy. Symptoms are acute
in onset, and may include pain. Let us consider various manifestations
of diabetes related eye muscle dysfunction (please note: the
complexity of the following discussion is not intended to overwhelm,
but to enhance non-ophthalmic practitioners’ appreciation
for the complexity of eye muscle control and symptomatology
of their diabetic patients.) It is important to know that recovery
of voluntary motor function is the rule in 1- 6 months (most
within 90 days).
The oculomotor nerve (CN III)
has divisions controlling: eyelid elevation (levator palpebrae
muscle); adduction of the eyeball (inward toward the nose) via
the medial rectus and secondary actions of the superior and
inferior recti muscles; supraduction of the eyeball (upward)
via the superior rectus and inferior oblique muscles; abduction
of the eyeball (outward toward the ear) via secondary action
of the inferior oblique muscle; cyclotorsion of the eyeball
via the inferior oblique muscle and secondary actions of the
superior and inferior recti; parasympathetic pupillary function
(constriction of the iris sphincter muscle) and lens accommodation
(via the ciliary muscle).
CN III has a lot of jobs, and
cranial neuropathy affecting it has a profound impact upon vision
(the lid becomes ptotic, the pupil is fixed and dilated, accommodation
is lost, and the affected eye wanders down and out – vertical,
horizontal and torsional diplopia result if the lid is held
open.) Diabetes is a leading cause of IIIrd Nerve palsy, and
characteristically spares the pupil (80% of cases). Aberrant
regeneration of affected nerve fibers is common. Neuro-imaging
is obligatory if the pupil is not spared or if other neurologic
abnormalities are present (e.g. multiple cranial neuropathies).
The trochlear nerve (CN IV) controls
the superior oblique muscle, which is responsible for turning
the eye downward (infraduction), particularly when the eye is
turned inward (adduction), for secondarily turning the eye outward
(abduction), and for incyclotorsion (torsional movement of the
12 o:clock reference point in, toward the nose). Diabetes is
a common cause of neuropathy affecting CN IV, which results
in diplopia with vertical, horizontal, and torsional components;
patients typically compensate by tipping the head toward the
shoulder that is opposite the affected side. Many cases are
traumatic or idiopathic.
The abducens nerve (CN VI) innervates
the lateral rectus muscle, which controls abduction of the eyeball
(outward toward the ear). The affected eye is unable to turn
outward past the midline. The most common etiologies are trauma,
diabetes, and hypertension. Other serious causes include intracranial
masses and multiple sclerosis. Neuro-imaging is obligatory in
children or those with multiple neuro-ophthalmic signs or symptoms.
Patients typically turn their head toward the affected side
in order to minimize horizontal diplopia.
Though less disconcerting to
patients than frank diplopia, the effects of diabetes on pupil
size and dynamics, and on the eyes’ focusing mechanism
(accommodation) are both bothersome and much more common. Autonomic
neuropathy of sympathetic innervation to the iris leads to sluggish
pupil responses and reduced capacity for pupillary dilation,
the combination of which impairs the patient’s adaptation
in the transition from brighter to dimmer lighting. As proliferative
diabetic retinopathy and pan-retinal laser photocoagulation
(PRP) used to treat it also impair vision in dim light, these
patients often experience great difficulty in this environment.
In contradistinction, diabetics often have reduced accommodative
amplitude (“near focusing ability”) relative to
their age due to neuropathy of parasympathetic fibers serving
the ciliary muscle, as well as premature hardening of the flexible
crystalline lens. PRP may exacerbate loss of accommodation by
injuring parasympathetic fibers carried within the short posterior
ciliary nerves en route to the iris and ciliary body.
Although cranial neuropathies
causing double vision are not an infrequent symptom of diabetes,
the mere presence of one (or more) of these neuropathies in
a diabetic patient does not exclude other causes. Only thorough
evaluation by a knowledgeable, experienced examiner can establish
a definitive cause, and complex cases are well-served by referral
to a neurophthalmic subspecialist. Fortunately, diplopia related
to diabetes typically is caused by dysfunction of only one nerve
at a time (and on one side), and resolves without intervention;
in the interim, alternately patching the eyes both eliminates
double vision and prevents secondary contractures of antagonist
muscles (or any possibility of occlusion amblyopia in children).
Pupillary dysfunction is not readily amenable to treatment,
but deficiencies of accommodation are easily treated with reading
glasses or bifocal lenses. Diabetic patients, in particular,
can reduce their chances of cranial neuropathy and eye muscle
dysfunction through optimal glycemic, blood pressure, and blood
lipid control.
Next time, we’ll consider
some “clinical pearls” for helping your patients
avoid, or at least minimize, the eye complications of diabetes.
Dr. Paul Chous received his undergraduate
education at Brown University and the University of California
at Irvine, where he was elected to Phi Beta Kappa in 1985. He
received his Masters Degree in 1986 and his Doctorate of Optometry
in 1991, both with highest honors from the University of California
at Berkeley. Dr. Chous was selected as the Outstanding Graduating
Optometrist in 1991. He has practiced in Renton, Kent, Auburn
and Tacoma, Washington for the last 12 years, emphasizing diabetic
eye disease and diabetes education. Dr. Chous has been a Type
1 diabetic since 1968. He lives in Maple Valley, Washington
with his wife and son.
About the Author
Dr.
Paul Chous is the recent author of a critically acclaimed book
for patients and health care providers on diabetes and the eye,
Diabetic Eye Disease: Lessons From A Diabetic Eye Doctor –
How To Avoid Blindness and Get Great Eye Care (Fairwood Press).
He may be reached via his web site at
http://www.diabeticeyes.com.
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