Lazy eyelid, Lazy Eye; Crosseye

[AH]

springboarding from what others have posted:

CONTENTS:

€LAZY EYELID (Ptosis, etc)
€LAZY EYE (Amblyopia)
€WANDERING, CROSS-EYE, OR SQUINT (Strabismus)
€LAZY EYELID, PARALYSIS, PSEUDOPTOSIS, PTOSIS OF EYELID, HORNERS SYNDROME
==================================
Complete 2000:
RFW F:
EYES: Ptosis/droop/drooping: absin.188, acet-ac.139, achy.149, agar.,
alco.36, alum., am-br.8, anh.85, apis54, arg-n.54, arn.8, bar-c.54, bell.10,
benz-p., brom.139, caul.102, caust.54, chin-b.8, chlol.8, cina8, con.8,
crot-h.8, cur.8, dulc.28, euph.54, euphr., fago.25, 3Gels.5, ger.85,
gins.36, graph.102, haem.102, hell.139, helo.102, ign.8, kali-br.36,
kali-p.8, kalm.102, lat-m., led.8, mag-p.8, med.8, merc-i-f.8, morph.8,
naja85, nat-ar., nat-m.137, nit-ac.54, nux-m.8, nux-v.8, op.36, oreo.188,
phos.8, phys.8, plb.8, plumbg.102, rhus-t.8, rob.36, seneg.8, 2sep.8,
spig.8, squil.139, stann.8, stram.36, sulfon.102, sulph.8, syph.8, thuj.85,
upa.102, verat.28, viol-t.54, zinc.8

EYES: Paralysis [2] lid/eyelid: acon.5, agar., alum.5, alum-p., am-br.54,
apis5, arg-n.54, arn.5, ars.5, bapt.8, bar-c., bar-m.5, bell.5, bufo8,
cadm-s., cann-s., 3Caust.5, chin-b.54, chlol.54, cina54, cinnb., cocc.5,
coloc.5, con.54, crot-c., crot-h.54, cur.54, dig., dulc.5, euph.54, 3Gels.5,
gins., graph.5, guare.8, hydr-ac.8, ign.54, kali-p.5, kalm.5, lach.5,
led.54, lyc.5, lyss.8, mag-p.54, med.5, merc-i-f.8, merl.54, morph.36,
naja5, nat-ar., nat-c., nat-m.5, 3Nit-ac.5, nux-m.54, nux-v.8, op.5,
oxyu-s., phos.54, phys.54, phyt.5, 3Plb.5, puls.54, puls-n.36, rad-br.5,
3Rhus-t.5, sec.54, seneg.54, 2sep.5, 2spig.5, stann.54, stram.5, sulph.54,
syph.54, thuj.5, 2verat.5, verat-v.8, viol-t.54, vip.36, zinc.5, zinc-p.

Complete 2000
EYES; HORNER syndrome (1) : puls.
==================
PTOSIS

What makes people's eyes droop?

A muscle controls blinking. Drooping of the eyelid (medical term:
"ptosis") can be a consequence of either:

* Looseness of the Skin
* (This occurs with age.)
* Damage to the Nerves that Control the Levator Muscle
* Damage to the nerves can take place due to either:
* Injury or
* Disease
* Weakness or Severance of the Muscle Itself
* This can occur as a complication of an a condition that affects the
muscle directly or indirectly, for instance by
* Destroying its Nerves or by
* Compromising its Blood Supply
* Growth of a Tumor
* Ptosis in children (referred to as being "congenital") is present at
birth.
* In adults, the most common cause of ptosis is separation of the muscle
tendon from the eyelid.
Can ptosis be prevented?

Not if it is related to aging. It can be prevented to varying degrees
if it occurs as a repercussion of:

* Injury, including a complication of eye surgery
* Migraine
* Allergic Reaction
* Vitamin Deficiency (in particular of thiamine)
* Deficiency of vitamin B1 causes beriberi. Due to fortification of
foods, beriberi is hardly seen any longer in the United States.
* Eyelid surgery may or may not be warranted.
How is the surgery done?

Sometimes the surgeon is able to make a small tuck in the levator
muscle and the eyelid to raise the lid.

* In more severe cases, the muscle must be strengthened and reattached to
the eyelid in order to pull up.
How is ptosis treated?

Surgery is the usual treatment for ptosis.

*

Sometimes the ophthalmologist can make a small tuck in the lifting muscle
and eyelid to raise the lid.
* In more severe cases of ptosis the levator or lifting muscle must be
reattached to the eyelid and strengthened.
Will surgery take care of it?

Ptosis can be corrected surgically when it occurs as a complication of
a birth defect ("congenital" ptosis). Surgery works well to lift the lid.
Treatment of the underlying cause may be able to resolve ptosis in the case
of:

* Horner's Syndrome (Horner's syndrome is characterized by inactivity of
a facial nerve that travels through the upper neck near the carotid artery.
Paralysis may be either temporary or permanent.)
* A Brain Tumor
* Head/Neck Cancer
Surgery is unlikely to be effective for ptosis due to:

* Myasthenia Gravis
* Diabetes
* Stroke
* For patients who are not candidates for surgery, or whose paralysis is
expected to be only temporary, an eyeglass frame designed to hold up the
eyelid with a wire can be worn.
What determines if surgery is necessary?

Ptosis should be evaluated by a physician. Be especially certain to
have sudden drooping of the eyelid(s) checked out. The eyelid may need to
be repaired when the condition is blocking vision.

* If it is noticed that the person is knitting his or her brows or
holding the chin up, ptosis may be the reason.
In most cases drooping of the eyelids is not an indication of a serious
problem. Nevertheless, besides its undesirable appearance, ptosis can be
problematic on account of interfering with eyesight.
* The eyelids may block vision and cause double vision.
* Lazy eye can develop if the ptosis is severe enough to produce optic
changes in the affected eye.
* Compensating by tilting the head back or raising the eyebrows can lead
to neck pain and eventually result in deformity.
* Another concern is that ptosis could obscure other eye abnormalities.
* In addition, decreased blinking motion reduces lubrication of the eyes.
* The examining physician will inquire as to whether:
* Drooping has been occurring in one eye or two?
* The eye(s) droop(s) all the time or just sometimes?
* Ptosis is getting any worse or not?
* An ophthalmologist will perform a slit-lamp examination.
* If symptoms suggest myasthenia gravis, a Tensilonï¿1Ž2 test may be
conducted.
* (Tensilonï¿1Ž2 is a drug that counteracts muscle fatigue.)
Which diseases make one eye droop, and which make both eyes do it?

Birth defects, normal aging, or a tumor can cause drooping of one or
both eyes.

Ptosis in just one eye would occur with:

* A Stye or other growth in the eye
* Injury
* Stroke
* Horner's Syndrome
Both eyes would be expected to be affected in the case of:

* Migraine
* Allergic Reaction
* Myasthenia Gravis
* Diabetes
* Beriberi
Source: American Academy of Ophthalmology
=============================================
HORNER'S SYNDROME

http://www.jeghers.com/annts/horner.htm

MATERIAL PRESENTED AT MEDICAL STAFF CONFERENCE, GEORGETOWN UNIVERSITY
HOSPITAL

Compiled December 1948

Harold Jeghers, M.D.

** Read First

* Read Next

*Fulton - Arch Surg. 18: 2025, 1929 (translation of Horner's original
article and historical data)

**Purves-Stewart - Textbook "Diagnosis of Nervous Diseases" 9th Edition
published by Williams & Wilkins pages 681-592 (Clinical description &
diagram of nerve supply)

*Cobb - Arch. Neurol. & Psychiat. 3: 636, 1920 (clinical)

*Wagener - Am. J. Ophth. 17: 209, 1934 (data proving enophthalmos is optical
illusion)

Harris - Brain 52: 484, 179 (skin changes)

Mutch - Edinburgh M. J. 43: 743, 1936 (studies an pupil)

Scarlett - Am. J. Ophth. 11: 961, 1928 (statistical study of frequency)

Calhoun - Am. J. Ophth. 2: 255, 1919 (H. syndrome as a cause of
heterochromia iridis)

Fulton, - Proc. Roy. Soc. Med. (Sect. Hist. Med.) 23: 24, 1929 (Hare's
description of syndrome)

Fisher - Permanent. Found. M. Bull. 3: 124, 1945 (due to hereditary multiple
exostoses)

* Hassin - JAMA 110:1440, 1938 (Langley-Sherrington protruding ear sign)

Wagener - Surg. Clin. N. Am. 11: 867, 1931 (studies on caliber of retinal
vessels)

**DeJong - Arch. Neurol. & Psychiat. 34: 734, 1935 (clinical discussion -
general)

Cogan - Arch. Ophth. 18: 739, 1937 (visual changes (tendency to myopia) in
H. Synd.)

Stead - Arch. Neurol. & Psychiat. 48:92, 1942 (central autonomic paralysis)

Horner's syndrome is the term used for the group of signs produced by
paralysis of the cervical sympathetics whether of peripheral or central
origin. At times known as the Claude Bernard - Horner's syndrome and also
incorrectly as the Hare's syndrome. As a general rule syndrome is
unilateral, therefore easier to detect and of localizing value.

CLINICAL DESCRIPTION

(A) FEATURES

MIOSIS: Appears at once after sympathectomy or block. Difference in size of
pupils evident in daylight and accentuated in dim light since pupil does not
dilate in dark. Yet pupil contracts briskly to light and convergence since
third cranial nerve (thru ciliary ganglion) still controls spheicter
pupillae. Homatropine but not cocaine dilates Horner pupil. Cilio-spinal
pupil reflex lost.

NARROWING PALPEBRAL FISSURE: Due to combination of drooping of the upper lid
and raising of the lower lid (at times with convex up appearance). Lid
droops due to paralysis of non-striated part of levator palpebrae. Since
voluntary portion of levator is controlled by 3rd nerve, ptosed lid can be
voluntarily raised. Hence ptosis of Horner's syndrome is a pseudo-ptosis.

ENOPHTALMOS: This is usually due to at optical illusion produced by the
narrowed palpebral fissure. Evidence favors idea that muscle of Muller
although important in animals is vestigal in man and does not contribute to
either enophthalmos by paralysis or exophthalmas by stimulation.
Occasionally atrophy of orbit contens and hypotony of globe produce some
degree of enophthalmos

(B) LESS CONSTANT FEATURES

ANHIDROSIS: (lack of sweating) on ipsilateral side.

FLUSHING: on ipsilateral side.

DILITATION OF ARTERIOLES and occasionally venules on affected side, best
seen in retina. HYPOTONY OF GLOBE (softer eye ball

LANGLEY-SHERRINGTON EAR PHENOMENON ear on affected side protrudes more from
side of head. Tendency for Horner's eye to be more myopic than good side.
Occasionally associated Klumpke type of paralysis.

HEMIATROPHY OF FACE especially if Horner's syndrome was present early in
life.

HETEROCHROMIA IRIDIS as rule only in children, iris lighter since normal
pigmentation fails to develop or is patchy. Rarely noted in lesion in adult

HORNER'S SYNDROME MAY OCCUR WITH INJURY OR LESIONS OF:

1. Cervical sympathetic chain

2. Anterior roots of D1 or D2.

3. White Rami communicantes from D1 or D2.

4. Ciliospinal center located in lower part of cervical cord and uppermost
part of thoracic cord (i.e. in springomyelia)

5. Sympathetic fibers (bulbospinal fibers) as they pass from hypothalmic
center to ciliospinal center in the lower cervical cord. (i.e. lesion in
medulla or upper cervical cord).

6. Lesions along ophthalmic division of 5th nerve (since post ganglionic
sympathetic fibers pass behind carotid sheath in neck up to the Gasserian
ganglion, and then to orbit along the ophthalmic division of 5th nerve.

Syndrome of irritation or stimulation of the cervical sympathetic
(occasionally known as the Pourfour duPetit Syndrome)

Signs exact opposite of the Horner's Syndrome namely dilitation of pupil,
widening of palpebral aperature (Dalyrumple's Sign), optical illusion of
exophthalmos, infrequency of involuntary blinking (Stellwag's Sign), (Von
Graefe's Sign) delayed descend of upper lid on looking down, and tendency to
moist pale skin over the ipsilateral side of face. To some degree, a drop of
cocaine in the eye simulates the above. This syndrome is rarely seen in
clinical practice since lesions which irritate or stimulate soon paralyze.
(See section by Purves-Stewart under Horner's Syndrome for detailed
description. Also article by Fulton.

TOURNAY'S SIGN

With extreme lateral abduction of an eye the pupil of this eye manifests a
dilation. This unilateral dilation occurs after an interval of a few seconds
and persists during maintenance of lateral fixation and is usually the seat
of hippus at the sametime. Said to be present in every case of Horner's
Syndrome.

Rournay Arch. d'ophth (French) 44: 574, 1927

KLYMPKE SYNDROME

(Klympke Dejerine Syndrome)

Paralysis of small muscles of the hand and the flexors of the hand with some
minor degree of ulnar sensory changes. Horner's and Klumpke's Syndrome may
occur simultaneously by a lesion affecting the anterior roots (C8, D1, D2)
proximal to the point of departure of the white rami communicantes. A lesion
distal to where the white rami communicantes are given off produces an
uncomplicated Klumpke's paralysis.
============================================
Horner's Syndrome
An interruption of the oculo-sympathetic pathway leading to sympathetic
inactivity
= Horner's syndrome (HS)
Clinical Triad of (Click HERE to see picture):
1. Miosis
2. Ptosis
3. Anhidrosis
Anatomy:
Sympathetic pathway extends from hypothalamus via lateral brainstem and
cervical cord, with first-order neuron synapsing in ciliospinal center (of
Budge) at level of C8-T2, in interomediolateral cell columns
- exits out of T1 nerve root in thoracic sympathetic trunk, over apex of
lung and near subclavian artery, passing through stellate ganglion
- synapses in superior cervical ganglion (near bifurcation of common carotid
artery)
- sudomotor and vasoconstrictor fibres to face travel then with external
carotid artery
- fibres to pupillary dilators and eyelid retractor muscles travel with
internal carotid artery to long ciliary nerve and nasociliary nerve (3rd
order neuron, post-ganglionic)
- divide from ICA and travel transiently with abducens nerve within
cavernous sinus, then with V1 branch of trigeminal nerve
Etiology and Localization of HS:
1. First-order neuron (brainstem and spinal cord) 50-60%
- Stroke (commonly Wallenberg's lateral medullary infarction)
- Neoplasm
- Demyelinating disease
- Syringomyelia
- Transverse myelitis
2. Second-order neuron (pre-ganglionic) 20-30%
- thoracic or neck tumor esp Pancoast's tumor at apex of lung, breast
malignancy
- "Rowland-Payne" syndrome with HS + paresis of phrenic, vagus, and
recurrent laryngeal nerve (elevation of hemidiaphragm, hoarse voice)
- neck trauma and disc protrusion at C8-T1
- compression from cervical ribs, lower plexus avulsions (eg obstetric),
aortic aneurysms, thyroid malignancy, lymphadenopathy
- iatrogenic from thyroidectomy, radical neck exploration / surgery, carotid
angiography (in days of direct carotid puncture !), vascular catheters,
chest tubes, pacemaker insertion
3. Third-order neuron (post-ganglionic) 20%
NB: will not see facial anhidrosis in this localization
- some similar causes to #2
- vascular headaches (as in autonomic cephalgias, cluster headache)
- cavernous sinus / superior orbital fissure lesion (eg. tumor, aneurysm)
- carotid-cavernous fistula ... usually associated ophthalmoplegia, facial
pain
- internal carotid artery dissection (with headache, represents Raeder's
paratrigeminal neuralgia)
- nasopharyngeal carcinoma (or tumors at jugular foramen)
- complicated otitis media
- trauma with basal skull fracture
Congenital HS usually due to early brachial plexus injury (at birth),
post-viral or with some early tumors
- may see straight hair on side of HS in patients with naturally curly hair
!!
Differential Diagnosis:
Anisocoria:
- physiologic anisocoria (up to 0.5-1 mm in 20% of population)
- pharmacologic (eyedrops)
- if greater in light then parasympathetic defect such as CN III palsy,
Adie's pupil, iris trauma or scopolamine / atropine effects
Ptosis:
- myasthenia gravis
- CN III palsy (with dilated pupil, may be unreactive, +/- ophthalmoplegia)
- levator dehiscence
Coincidental occurrence of physiological anisocoria and age-related ptosis
can mimic closely a Horner's syndrome, but dilatation lag and other subtle
features will be absent
History:
- notice pupillary asymmetry (affected side smaller, esp in dark)
- drooping of the eyelid (usually mild)
- when first noticed?
- does the ptosis fluctuate (suggesting neuromuscular dysfunction, not HS)
- is there any double vision (absent in isolated HS; suggests either another
cause or associated damage to brainstem / cranial nerve structures by lesion
causing HS)
- noticed any change in sweating on affected side of face (implies lesion
proximal to carotid bifurcation in post-ganglionic neuron, or pre-ganglionic
lesion)
- was the eye ever red (seen in acute stages of HS)?
- any associated brainstem features such as dysarthria, dysphagia, ataxia,
vertigo, facial weakness, sensory abnormality (on face or in limbs)?
- any neck symptoms including neck pain (eg carotid dissection), masses
palpated?
- pulmonary symptoms such as cough, hemoptysis, dyspnea or pain (suggestive
of apical lung tumor)
- ipsilateral arm symptoms including pain, numbness / paresthesias,
weakness, wasting suggesting involvement of brachial plexus
- headache (if ipsilateral and facial pain consider carotid dissection; if
occipital consider vertebral artery dissection with brainstem infarct)
- any Hx of prior neurological events (such as strokes or demyelinating
episodes)
Examination:
Confirmation of Horner's syndrome (Click HERE to see picture):
1. Miosis
- affected pupil smaller, more apparent in dark or dim illumination than in
light (where it may be inapparent); also stimulate sympathetics with sudden
noise (accentuating anisocoria)
- anisocoria usually mild (0.5 - 1 mm) with paresis of iris dilators
- pupil reacts normally to light and accommodation
- dilation lag found when darken room (affected pupil dilates more slowly)
- may see paradoxical pupillary dilatation on affected side in states of
adrenergic hyperactivity (eg emotional excitement or stress) due to
denervation supersensitivity to circulating catecholamines
- look for heterochromia iridis (iris is different, lighter color in
congenital HS due to depigmentation of iris; rarely can occur in acquired
lesions)
- conjunctival injection in acute phase may be seen (loss of vasoconstrictor
activity) as can hemi-facial flushing and nasal stuffiness
+/- reduced intraocular pressure and increased accommodation
2. Ptosis:
- usually subtle (2-3 mm) and may be variable (slight fluctuations)
- due to weakness of Muller's muscle (smooth muscle, involuntary retractor
of upper lid)
- also get upside-down ptosis of lower lid on that side (due to paresis of
inferior tarsal muscle) leading to lower lid drawn up higher (hiding bottom
of cornea) vs other side
- may have apparent enophthalmos (eye looks sunken) with narrowed palpebral
fissure
3. Anhidrosis:
- check sweating (by palpation) on both sides of face, seeing if less on
affected side
- also see if hemibody involved (found with central lesions) vs hemi-face
and neck down to clavicle in pre-ganglionic lesions
Looking for Etiology / Localization:
1. Brainstem testing:
- cranial nerve abnormalities (incl. CN V, VII, IX, X) may be seen in BS
lesions
- ipsilateral ataxia if cerebellum or its connections affected
2. Examination of the Neck:
- palpate for masses, tenderness
- auscultate for carotid bruits and palpate for pulse present (absent if
occlusion)
3. Examination of Limbs:
- look at ipsilateral arm for wasting or weakness suggestive of lower plexus
involvement
- loss of reflexes and sensory loss can also be found
Diagnosis:
- initial clinical suspicion confirmed (if necessary) by pharmacologic
stimulation of sympathetic pathways
1. Cocaine test
- 2 drops of 10% cocaine instilled into each eye
- prolongs action of norepinephrine on dilator muscle by blocking reuptake
(requires its release from nerve terminals by intact oculosympathetic
pathway)
- normal pupil will dilate while HS pupil will fail to dilate after 45
minutes (confirming diagnosis of HS); but still need to examine in dim room
else bright light will overpower effect as PSNS intact - both eyes look
constricted !
NB: metabolites of cocaine will be found in urine for 1-2 days afterwards !
2. 1% Hydroxyamphetamine:
- done only after confirming dx with cocaine test (or clinically) and
waiting 24-28 hrs to allow cornea and pupils to recover
- 2 drops to also create sympathomimetic effect but does so by stimulating
release of norepinephrine from nerve endings, stimulating dilator muscle
- requires that post-ganglionic (3rd-order) neuron be intact and have normal
axoplasmic activity so norepinephrine available for release
- normal pupil will dilate, and also normal or accentuated in HS pupil if
pre-ganglionic (first- or second-order) while incomplete dilatation seen if
post-ganglionic lesion
NB: direct-acting topical adrenergic agents will dilate pupils of HS (eg.
epinephrine solution)
- often becomes larger than unaffected side due to supersensitivity from
denervation (in subacute to chronic, but not acute phase)
Localization:
1. First-order (central):
- MRI of head and cervical spine
2. Second-order (pre-ganglionic)
- Chest x-ray +/- CT of chest
- CT or MRI of neck
3. Post-Ganglionic:
- MRA for carotid dissection
- MRI for cavernous sinus lesions
References:
Kline LB, Bajandas FJ. Neuro-Ophthalmology review manual. 4th ed. 1996.
Miller NR, Newman N. Walsh & Hoyts Clinical Neuro-Ophthalmology. 5th ed.
1999.
Last update: July 2004
Reviewed by: pending
Neurological Medicine Pocketbook
© 2003-2004 UWO Neurology Residents
http://www.uwo.ca/cns/resident
All Rights Reserved
Disclaimer
====================================
LAZY EYE (as opposed to lazy eyelid):

RFW F:
Amblyopia: ammc.8, anag.8, ant-t.8, arn.8, atro.8, bell.8, benz-d., benz-p.,
calc-p.61, caps.8, carbn-s.36, caust.8, chel.8, 3Chin.8, chin-s.8, cich.,
cimic.25, con.36, 2crot-h.8, cycl.8, daph., dros.8, euphr.8, fil., 2gels.,
hyos.8, ign.8, jab.85, lach.8, land., m-aust.85, 2merc.8, 2naphtin.,
nat-m.8, nat-sal.85, nux-v., onos.85, op.8, 2oxyt.77, 2ph-ac.8, 3Phos.8,
puls.8, raph., rob.36, 2ruta8, sac-l., sant., seneg., sil.8, 2stram.8,
sulfonam.149, sulph.8, 2tab.8, 3Ter.8, thiop.149, thuj.8, thyr., 2tub.56,
zinc.8

All About Amblyopia (lazy eye)
by Dr. Jeffrey Cooper & Rachel Cooper (no relation). © 2001-2005

What is Amblyopia (lazy eye)?

Lazy Eye and Strabismus are not the same condition.

Causes of Amblyopia

Diagnosis of Amblyopia

Treatment of Amblyopia

What is Amblyopia (lazy eye)?
Amblyopia, commonly known as lazy eye, is the eye condition noted by reduced
vision not correctable by glasses or contact lenses and is not due to any
eye disease. The brain, for some reason, does not fully acknowledge the
images seen by the amblyopic eye. This almost always affects only one eye
but may manifest with reduction of vision in both eyes. It is estimated that
three percent of children under six have some form of amblyopia.

Learn more and read the latest research at All About Amblyopia (Lazy Eye).

Lazy Eye and Strabismus are not the same condition.
Many people make the mistake of saying that a person who has a crossed or
turned eye (strabismus) has a "lazy eye," but lazy eye (amblyopia) and
strabismus are not the same condition. Some of the confusion may be due to
the fact that strabismus can cause amblyopia. Amblyopia can result from a
constant unilateral strabismus (i.e., either the right or left eye turns all
of the time). Alternating or intermittent strabismus (an eye turn which
occurs only some of the time) rarely causes amblyopia.

While a deviating eye (strabismus) may be easily spotted by the layman,
amblyopia without strabismus or associated with a small deviation usually
can be not noticed by either you or your pediatrician. Only an eye doctor
comfortable in examining young children and infants can detect this type of
amblyopia. This is why early infant and pre-school eye examinations are so
necessary.

Due to misunderstanding or misuse of the terms for different visual
conditions (i.e., crossed eyes vs. lazy eye), many people are inaccurately
labelled as having a "lazy eye." If you think you or someone you know has
lazy eye, it is recommended that you learn more about Lazy Eye and the
different types of Strabismus. For example, see What is Strabismus?,
Exotropia or Esotropia.

In addition, learn about a much more common visual condition which affects
binocular (two-eyed) vision and is also not easily discernable to the
outside viewer. This condition is also not detected by the standard 20/20
eye test. See What is Convergence Insufficiency?

To complete the picture, find out about the treatment options for amblyopia
and strabismus.

Causes of Amblyopia
Both eyes must receive clear images during the critical period. Anything
that interferes with clear vision in either eye during the critical period
(birth to 6 years of age) can result in amblyopia (a reduction in vision not
corrected by glasses or elimination of an eye turn). The most common causes
of amblyopia are constant strabismus (constant turn of one eye),
anisometropia (different vision/prescriptions in each eye), and/or blockage
of an eye due to trauma, lid droop, etc. If one eye sees clearly and the
other sees a blur, the good eye and brain will inhibit (block, suppress,
ignore) the eye with the blur. Thus, amblyopia is a neurologically active
process. The inhibition process (suppression) can result in a permanent
decrease in the vision in that eye that can not be corrected with glasses,
lenses, or lasik surgery.

Diagnosis of Amblyopia
Since amblyopia usually occurs in one eye only, many parents and children
may be unaware of the condition. Far too many parents fail to take their
infants and toddlers in for an early comprehensive vision examination and
many children go undiagnosed until they have their eyes examined at the eye
doctor's office at a later age.

The most important diagnostic tools are the special visual acuity tests
other than the standard 20/20 letter charts currently used by schools,
pediatricians and eye doctors. Examination with cycloplegic drops can be
necessary to detect this condition in the young.

Treatment of Amblyopia
Amblyopia can be successfully treated up to the age of 17. See a report on
the latest research at National Institutes of Health -- National Eye
Institute. Early treatment is usually simple, employing glasses, drops,
vision therapy and/or patching. Detection and correction before the age of
two offers the best chance for a cure.
According to current research, amblyopia can not be cured -- normal 20/20
stereo vision -- without early detection and treatment. However, treatment
for older children and adults is usually successful in improving vision and
should be attempted. Treatment of amblyopia after the age of 17 is not
dependent upon age but requires more effort including vision therapy. Every
amblyopic patient deserves an attempt at treatment.

Strabismus is responsive to treatments at all ages. Therefore, as explained
earlier, it is important to make careful distinction between amblyopia and
strabismus.

While no recent scientific studies have been done on treatment of amblyopia
after the age of 17, the optometrists in our network collectively report
decades of clinical success with adult amblyopia. [This editor hopes for an
NEI study on adult amblyopia and neuroplasticity].

To quote one of our members, Dr. Leonard J. Press, FAAO, FCOVD: "It's been
proven that a motivated adult with strabismus and/or amblyopia who works
diligently at vision therapy can obtain meaningful improvement in visual
function. As my patients are fond of saying: "I'm not looking for
perfection; I'm looking for you to help me make it better". It's important
that eye doctors don't make sweeping value judgments for patients. Rather
than saying "nothing can be done", the proper advice would be: "You won't
have as much improvement as you would have had at a younger age; but I'll
refer you to a vision specialist who can help you if you're motivated."

In conclusion, improvements are possible at any age, but early detection and
treatment offer the best outcome. If not detected and treated early in life,
amblyopia can cause a permanent loss of vision with associated loss of
stereopsis (two eyed depth perception). Better vision screenings are needed
for young children. The 20/20 eye chart screening is not adequate.

Amblyopia causes more visual loss in the under 40 group than all the
injuries, and diseases combined in this age group.

=========================================
WANDERING EYE/SQUINT/CROSS-EYE/STRABISMUS/DEVIATING/CONVERGENT/DIVERGENT

RFW F:
Strabismus/squint/wandering/cross-eyed/deviating/divergent/convergent:
acon.5, aeth.5, agar.5, aloe102, 2alum.5, alumn.8, amyg-am.54, anan.8,
androc.222, ant-t.5, apis5, apoc.102, arg-n., arn.5, ars.5, art-v.5, bac.,
2bell.5, benz-d.102, benz-n.36, berb.8, bufo5, buth-aust.85, 2calc.5,
calc-p.5, camph.8, cann-i.36, cann-s.5, canth., caras., carb-an.8, caust.5,
cent.36, chel.8, chin., chin-b.139, chin-s.8, 3Cic.5, cic-m.36, cina5,
coca8, coloc.5, con.5, conin.139, cub.36, cupr.5, cupr-acet.102, cur.137,
3Cycl.5, dig.5, diphtox., electr.85, ery-a.8, euph.54, euphr.8, gels.5,
glon.36, graph., hell.8, 2hyos.5, iod.36, 2jab.8, kali-bi.8, kali-br.8,
kali-i.5, kali-p.8, lac-lox-a., lach.8, lepro.197, lil-t., lyc.8, lyss.8,
mag-p.5, meny.5, merc.5, merc-c.5, merc-i-f., merc-s.54, mim-p., morph.8,
morph-m., nat-ar., 2nat-m.5, nat-p.5, nat-sal.85, nuph.8, nux-m.36, nux-v.8,
olnd., op.5, oxyu-s., par.8, phos.8, phys.5, pin-s.85, plb.5, podo.5,
psor.56, puls.5, raph.36, rhod., rhus-t.5, ruta, sant., sapin.85, sec.5,
seneg.8, sil.5, 2spig.5, spig-m.36, 2stram.5, sulph.5, syph.8, 2tab.5,
tanac.36, tarent.54, thuj.5, tub.54, tung.252, ust.54, valer.54, verat.5,
verat-v.54, zinc.5
===========
http://www.strabismus.org/all_about_strabismus.html

All About Strabismus
by Dr. Jeffrey Cooper & Rachel Cooper (no relation). © 2001-2005

Development, Causes, Diagnosis,
Types, and Treatments.

Table of Contents

Evolution of Two-eyed Vision:

* Two Eyes to the Side
* Two Eyes in Front
* Benefits of Two Eyes in Front
* What is Stereopsis (3D Vision)?
* Benefits of Stereopsis
What is Strabismus?
When two-eyed vision breaks down.
Is It Lazy Eye?
Is strabismus a lazy eye condition?
What Causes Strabismus?
Eye muscles or the brain?
What Does Strabismus Cause?
What does my child with strabismus see?
Early Detection and Treatment.
When should my child have the first eye exam?
When is it too late for treatment?
What is the "critical period?
Why does my eye doctor say it is "too late?"
What are basic treatment options?
Types of Strabismus and their Recommended Treatments
References
Welcome to this Table of Contents. Dr. Jeffrey Cooper is the author of
All About Strabismus. Check out the fun bits on the evolution of two-eyed
vision.
Learn about Treatment Options
Two-Eyed Vision
Some vision problems can't be improved with just glasses or surgery.
Vision therapy treats the entire visual system and changes reflexes to make
a lasting cure. Learn more...
Constant? Intermittent?
What is Convergence Insufficiency?
What is Double Vision?
What is Lazy Eye?
What is Optometric Vision Therapy?
What is Strabismus or Lazy Eye Surgery?

Patient Testimonials
Successful Treatment
Evolution of Two-eyed Vision
Two Eyes to the Side
Nature has given animals the physical attributes necessary for survival.
Lateral placement of the eyes is essential to the survival of hunted animals
or herbivorous animals (e.g., horse, rabbit, cow) as it allows them to
increase side or peripheral vision.

Side vision (increased by lateral placement) is a sensitive detector for
motion or movement. Peripheral vision allows creatures to effectively scan
for danger. The rabbit must be constantly aware of its natural enemies while
it eats your garden greens. At the first sign of danger, peripheral vision,
the motion detector system, alerts the rabbit that there is danger. The
immediate reflexive response is for the rabbit to run.
Two Eyes in Front
Faster moving carnivorous hunters do not need as much peripheral vision as
the hunted. It is more important for hunters to locate their prey and
accurately determine the distance from themselves to that prey. Therefore,
animals that hunt (carnivorous or meat eating animals, e.g. lion, cat) as
well as humans have frontal placement of the two eyes in order to determine
the exact location of their prey. The hunters sacrifice the large peripheral
motion detection system afforded by side placement of the eyes in favor of
the incredibly accurate depth perception system created by frontal placement
of the eyes. To make up for the loss of peripheral vision, most carnivorous
animals have also developed a sophisticated, pivoting system which extends
the range of side vision...that is, the neck.
The Benefits of Two Eyes in Front
Frontal placement of the eyes allows for a remarkable visual phenomenon
called stereopsis. Stereopsis is the 3D perception that occurs as a result
of both eyes working together to create relative depth perception.

Many of you have experienced exaggerated demonstrations of stereoscopic
depth by viewing I-Max 3D movies or old stereoscopes. Or, perhaps, you have
seen photos of theatergoers in the 1950's wearing special Polaroid glasses
in order to view 3D movies.

What is Stereopsis?
Stereopsis results from the combination of the two images received by the
brain from each eye. Each eye views the world from a slightly different
vantage point (See Fig 1).

Figure 1

The fusion of these two slightly different pictures from our two "cameras"
(the eyes) gives us the sensation of strong three-dimensionality or relative
depth.

At near, there is a greater difference in what the two eyes view as compared
to far. Thus, stereopsis is strongest and most important at near distances.
At near is where man uses accurate hand-eye coordination to make tools and
other items!

The Benefits of Stereopsis
Stereopsis has been very important in human development. Keen and accurate
two-eyed depth perception has allowed man to develop tools and the
manufacture of goods, a central aspect of modern civilization. Stereopsis
plays a role in many other human activites, such as, catching a ball,
parking a car, threading a needle, performing surgery, or any other activity
that requires accurate depth perception at close distances.

Animals that have lateral position of the eyes and individuals who have
constant strabismus (eye turn) lack stereopsis. This does not mean that they
have absolutely no depth perception. There are many one-eyed (monocular)
depth perception cues that allow us to make reasonably accurate depth
judgements. These monocular depth perception cues may be familiar to you and
include: perspective, overlay, shadowing, aerial perspective (color of the
sky), relative motion, relative size, etc.

Binocular vision cues (from two eyes), such as stereopsis and parallax, are
dependent on accurate alignment of the eyes and appropriate unification of
the two images by the brain. People with only monocular or one-eye depth
perception skills can do fine in many situations. However, they are not
allowed to fly a rocket ship, drive the trains in New York city subways, and
they definitely should not be surgeons. They may have trouble catching a fly
ball or becoming a NBA point guard. However, many jobs do not require
stereopsis and thus the lack of stereopsis does not preclude a successful
life.

Stereopsis does enhance quality of life and life choices, however! Some eye
doctors might tell you that it is a luxury, but it is part and parcel of our
evolution and human potential. 3D vision is a human skill we all want and
deserve. Every attempt should be made to develop this visual-motor skill in
a child [and it's not too late for many adults!]

What is the "critical period?"
In the early 1960's, two Nobel Prize winners from Harvard , Hubel and
Weisel, did research on the development of vision. They studied monkeys and
cats who have stereoscopic vision similar to humans. This led to conclusions
regarding a "critical period" of development for stereopsis.

What is the "critical period" and what does it mean in regards to you or
your child and your treatment options. Explore this controversial topic by
reading the following two articles by Dr. Jeffrey Cooper and Dr. Paul
Harris, two different experts on strabismus. Dr. Harris refers to the famous
1960s Hubel and Weisel study as well as later studies by Hubel and Weisel
and others. Many of the more recent studies call into question the idea of a
finite "critical period." Dr. Cooper explains the Hubel and Weisel study and
its implications in detail.

The Myth of the Critical Period
by Dr. Paul Harris

Development of Vision (Critical Periods)
by Dr. Jeffrey Cooper

Why does my eye doctor say it is "too late?"
Whenever an eye doctor tells you that it is "too late" to treat your child's
loss of binocular vision (or eye turn or "lazy eye"), he or she is probably
referring to his or her earlier education regarding the "critical period."
He or she might even be directly or indirectly referring to the
aforementioned research dating from the 1960s.

Remember, a great deal has been learned about the human brain since the
1960s! For example, a new ground-breaking study on the brain's plasticity
(its ability to change and grow) was released to broad media fanfare in the
year 2000.

We recommend that you find a doctor who is more up-to-date on the latest in
developmental vision and the brain (neuronal plasticity).

When is it too late to treat strabismus or lazy eye?
It is often asked at what age should treatment no longer be attempted. The
answer is, everyone deserves a chance! Age should not be a deterrent, though
treatment under age 6 (especially before 2) is ideal and allows better
results than later treatment. After age 6, age is not important.
------------------------------------------------------------------------
"... every attempt should be made to improve strabismus and lazy eye."
------------------------------------------------------------------------

The best chance of success in eliminating the effects of the most difficult
conditions, amblyopia or constant strabismus, occurs before the age of two.
However, this does not preclude excellent success in many older patients and
at least partial success in most patients older than 6 years of age. There
are numerous studies that demonstrate that treatment after the age of 6 is
very successful. One study compared treatment before age 6 to treatment
after age 6. They found no statistical difference between the two groups. As
a matter of fact, loss of an eye in patients over the age of 65 who were
never treated for their amblyopia experienced a spontaneous improvement in
vision in over one-third of the cases.

Thus, every attempt should be made to improve strabismus and lazy eye,
though treatment might not be as effective after the age of six, and
definitely requires more work. Also, remember that if an eye turn occurs
only some of the time (intermittent), the cells of the brains do not develop
the changes associated with the more challenging cases of constant eye
turns.
------------------------------------------------------------------------
"It is never too late to try!!"
------------------------------------------------------------------------

An analogy to understanding the relationship of age in regards to the
treatment of eye muscle anomalies would be to consider the relationship of
one's age in learning to speak a second language. During the period of
neurological development, around the first year of life, language
development is natural and spontaneous. Children raised in families that
speak two languages from birth automatically learn both languages. However,
if the second language is introduced in later school years, language
development takes a longer time and is more arduous. Yet, remember, people
learn languages well into their sixties and seventies. The very same is true
of visual development. It is easier to develop normal vision during the
critical period, but with work, many people can develop normal binocular
vision in later years.

See the following relevant sections:

"What is the "critical period?"

About eye muscle surgery for strabismus.
What are basic treatment options?
Types of Strabismus and their Recommended Treatments
References

© Copyright 1996-2005, Optometrists Network

============
(see for pictures):
http://www.eyemdlink.com/EyeProcedure.a ... edureID=59

Strabismus surgery
Strabismus is a general term referring to ocular misalignment due to
extraocular muscle imbalance. In short, the eyes are "crooked". Strabismus
occurs in approximately 2% of children under 3 years of age and about 3% of
children and young adults. The condition affects males and females equally.
Strabismus has an inherited pattern, i.e., it is much more likely to occur
if one or both parents are affected. However, many cases occur without any
family history of the disorder.

Strabismus is important to recognize, primarily because, in childhood, it is
often associated with the development of amblyopia, or lazy eye. Amblyopia
refers to reduced vision, uncorrectable with glasses or contact lenses, due
to failure or incomplete development of the visual cortex of the brain. For
more on amblyopia, the reader is referred to discussion of that condition
elsewhere in this library.

Strabismus is not only important from the standpoint of amblyopia, however.
It is also important for other functional and cosmetic reasons. Strabismus
is associated with reduction of depth perception and, if onset is in
adulthood, double vision. Furthermore, strabismus presents a cosmetic
concern, especially for school-age children.

When an individual's eyes are straight, they are said to have orthotropia.
This indicates that both eyes are aimed at the same spot. The brain fuses
the two separate images into one three-dimensional image. This allows a high
degree of depth perception. If the eyes are misaligned, depth perception is
substantially reduced. Furthermore, when one eye is deviated in early
childhood, the brain may learn to ignore the image from that eye, and
amblyopia (lazy eye) often results. It is important to understand that it is
usually not just one eye that is deviated, but rather, the eyes are
misaligned in relation to one another. In essence, both eyes are usually at
fault, although one eye may appear to be the "crooked" one. If strabismus
develops for the first time in adulthood, the affected individual usually
experiences double vision. This occurs because the brain, which no longer
has the "plasticity" of early childhood, is unable to ignore the image from
the deviated eye.

Top of page

The cause of strabismus is usually unknown. However, strabismus is certainly
more common in families with a history of the disorder. Several neurological
conditions are more commonly associated with strabismus, including Down¹s
syndrome, cerebral palsy, hydrocephalus, and brain tumors. The great
majority of children who present with strabismus, however, have no other
associated neurological abnormalities. A cataract, eye tumor, or other eye
disorder associated with reduced vision may also present with strabismus.

Signs and Symptoms of Strabismus

Strabismus can often be recognized by a casual observer as a ³crooked eye².
In fact, most cases of strabismus are first noted by a parent or the child¹s
pediatrician prior to examination by an ophthalmologist. All children should
have their vision examined between 3 and 4 years of age. The pediatrician¹s
office usually evaluates visual acuity in toddlers; however, the acuity can
also by evaluated by a family doctor or ophthalmologist. If there is a
family history of strabismus, children should have an eye exam by an
ophthalmologist at an earlier age, perhaps by twelve to eighteen months of
age. In some cases, amblyopia (reduced vision) may occur when there is
minimal misalignment of the eyes (microtropia). This type of deviation may
be difficult to recognize in a young, uncooperative child, even for the
highly experienced pediatric ophthalmologist. This type of deviation becomes
important if amblyopia develops, which can only be discovered with
evaluation of visual acuity.

Treatment for Strabismus

Treatment of strabismus may include patching of one eye (if amblyopia is
present), glasses, or strabismus surgery to realign the eyes. It is
important to understand that strabismus surgery does not resolve amblyopia
(poor vision), and that this can only be corrected with patching and/or
glasses. In some cases, realignment of the eyes occurs with proper
prescription eyeglasses. However, the majority of children with strabismus
will eventually require strabismus surgery to better align the eyes.
Strabismus surgery commonly entails recessions of eye muscles if weakening
of muscles is required, and resections of eye muscles when strengthening of
eye muscles is required. Recession of an eye muscle requires disinsertion of
one of the six muscles attached to the eye, and reattachment of the muscle
further back on the eye, thereby causing weakening. Resection of an eye
muscle requires disinsertion of the muscle from the eye, excising a portion
of the distal end of the muscle, and subsequent reattachment to the eye,
thereby resulting in a stronger muscle. The amount that a muscle is recessed
or resected is based on the pre-operative degree of misalignment of the
eyes, which is measured by the ophthalmologist using prisms. In general,
once a child develops manifest strabismus (obviously crooked eyes), there is
no treatment which will ³perfectly² straighten the eyes. The goal of
surgery, therefore, is to realign the eyes as close to normal as possible,
typically erring on the side of undercorrection.