Ophthalmoplegia and Paralytic Strabismus Definitions

Ophthalmoplegia can affect one or more ocular muscles at the same time. The condition may be partial (paresis, more common) or complete (paralysis, less common). The result is either gaze palsy or strabismus (paralytic strabismus), depending on the cause (see next section) and severity.

❖ Gaze palsy: Impairment or failure of coordinated eye movements. For example in cyclovertical muscular palsy, the upward and downward gaze movements are impaired or absent.

❖ Paralytic strabismus: Strabismus due to:

- Isolated limited motility in one eye.

- Asymmetrical limited motility in both eyes.

The angle of deviation does not remain constant in every direction of gaze (as in concomitant strabismus) but increases in the direction of pull of the paralyzed muscle. This is referred to as an incomitant angle of deviation.

Opthalmoplegia

Etiology and forms of ocular motility disturbances: Two forms are distinguished.

❖ Congenital ocular motility disturbances may be due to the following causes:

- Prenatal encephalitis.

- Aplasia of the ocular muscles.

- Birth trauma.

❖ Acquired ocular motility disturbances may be due to the following causes:

- Diabetes mellitus.

- Multiple sclerosis.

- Intracranial tumors.

- Arteriosclerosis.

- Central ischemia (apoplexy).

- Trauma and other causes.

Ocular motility disturbances are either neurogenic, myogenic, or due to mechanical causes.

Neurogenic ocular motility disturbances (see also ophthalmoplegia secondary to cranial nerve lesions) are distinguished according to the location of the lesion (Table 17.3):

❖ Lesions of the nerves supplying the ocular muscles. This condition is referred to as an infranuclear ocular motility disturbance and is the most common cause of paralytic strabismus. The following nerves may be affected:

- Oculomotor nerve lesions are rare and cause paralysis of several muscles.

- Trochlear nerve lesions are common and cause paralysis of the superior oblique.

- Abducent nerve lesions are common and cause paralysis of the lateral rectus.

❖ Lesions of the ocular muscle nuclei. This condition is referred to as a nuclear ocular motility disturbance (see Fig. 17.2).

H The oculomotor nuclei supply both sides but the nerves are not close together. Therefore, bilateral palsy suggests a nuclear lesion, whereas unilateral palsy suggests a lesion of one nerve.

❖ Lesions of the gaze centers. This condition is referred to as a supranuclear ocular motility disturbance (see gaze centers, Fig. 17.2). It very often causes gaze palsy.

❖ Another possible but rare condition is a lesion of the fibers connecting two nuclei. This condition is referred to as an internuclear ocular motility disturbance and may occur as a result of a lesion of the medial longitudinal fasciculus (see Figs. 17.2 and 17.13, Internuclear ophthalmoplegia).

Table 17.3 Classification of neurogenic ophthalmoplegia according to the location of the lesion (see Fig. 17.2)

Ocular motility

Causes

Location of lesion

Effects

disturbance

Infranuclear

In younger pa

❖ Lesion in one of

Palsy of one or several

ocular motility

tients:

the nerves sup-

extraocular muscles of

disturbance

- Trauma

plying the ocular

one or both eyes

- Multiple

muscles:

resulting in strabismus

sclerosis

- Oculomotor

or complete gaze

- Infectious dis-

nerve

palsy.

ease

- Trochlear

- Brain tumors

nerve

In older patients:

- Abducent

- Vascular dis-

nerve

ease

- Diabetes

- Hyperten-

sion

- Arterioscle

rosis

Nuclear ocular

Multiple sclero-

Lesion of the ocular

Palsy of the extraocu

motility distur-

sis

muscle nucleus

lar muscles of both

bance

Myasthenia

eyes in varying

gravis

degrees of severity.

Meningo-

encephalitis

Syphilis

AIDS

Supranuclear

ocular motility

disturbance

❖ Horizontal

Diabetes

Lesion in the para-

❖ All conjugate eye

gaze palsy

Apoplexy

median pontine

movements on the

Tumor

reticular formation

side of the lesion

Encephalitis

(PPRF; see Fig. 17.2)

are impaired.

Vascular insult

❖ Peripheral facial

Multiple sclero-

paresis is often also

sis

present.

❖ Both eyes are

Continued ^

Table 17.3 (Continued)

Ocular motility disturbance

Causes

Location of lesion

Effects

❖ Vertical gaze

❖ Midbrain infarc-

Lesion in the medial

❖ Isolated upward or

palsy (Pari-

tions

longitudinal fasci

downward gaze

naud's syn-

❖ Tumors of the

culus (MLF; see

palsy (common).

drome)

quadrigeminal

Fig. 17.2)

❖ Combined upward

region such as

and downward

pineal gland

gaze palsy (rare).

tumors and ger-

❖ Moderately wide

minomas.

pupils.

❖ Impaired accommodation.

❖ Convergence nystagmus.

❖ Jerky upper eyelid retraction.

❖ Medial nerve palsy or impaired adduction in one eye in side gaze with intact near reflex convergence (see Fig. 17.13).

❖ Jerk nystagmus in the abducted eye as long as the palsy persists.

❖ In bilateral INO, fine vertical nystagmus in the direction of gaze.

Myogenic ocular motility disturbances are rare. These include palsies due to the following causes:

❖ Graves' disease is the most common cause of myogenic ocular motility disturbances. Because it alters the contractility and ductility of the ocular muscles, it can result in significant motility disturbances (see Chapter 15).

❖ Ocular myasthenia gravis is a disorder of neuromuscular transmission characterized by the presence of acetylcholine receptor antibodies. Typical symptoms of ocular myasthenia gravis include fluctuating weakness

Internuclear ocular motility disturbance (INO)

Younger patients with bilateral INO: multiple sclerosis

Older patients with unilateral INO: brain stem infarction

Lesion in the medial longitudinal fasciculus (see Fig. 17.2)

Right internuclear ophthalmoplegia.

a

b

c

d

Fig. 17.13 a Parallel visual axes. b Normal right gaze. c In left gaze, the right eye cannot be adducted because the medial longitudinal fasciculus is interrupted. d Convergence is preserved in both eyes.

that is clearly attributable to any one cranial nerve. The weakness typically increases in severity during the course of the day with fatigue. Important diagnostic aids include the following tests.

- Simpson test: The patient is asked to gaze upward for one minute. Gradual drooping of one of the patient's eyelids during the test due to fatigue of the levator palpebrae strongly suggests myasthenia gravis.

- Tensilon (edrophonium chloride) test: This test is used to confirm the diagnosis. The patient is given 1-5 mg of intravenous Tensilon (edrophonium chloride). Where myasthenia gravis is present, the paresis will disappear within a few seconds. (Refer to a textbook of neurology for a detailed description of this test.)

❖ Chronic progressive external ophthalmoplegia (CPEO) is a usually bilateral, gradually progressive paralysis of one or more extraocular muscles. In the final stages it results in complete paralysis of both eyes. Because the paralysis is symmetric the patient does not experience strabismus or double vision.

❖ Ocular myositis is inflammation of one or more extraocular muscles. The pathogenesis is uncertain. Ocular motility is often limited not so much in the direction of pull of the inflamed muscle as in the opposite direction. While there is paresis of the muscle, it is characterized primarily by insufficient ductility. Often additional symptoms are present, such as pain during eye movement.

Mechanical ocular motility disturbances include palsies due to the following causes:

❖ Fractures. In a blowout fracture for example, the fractured floor of the orbit can impinge the inferior rectus and occasionally the inferior oblique. This can interfere with upward gaze and occasionally produce strabismus.

❖ Swelling in the orbit or facial bones, such as can occur in an orbital abscess or tumor.

Symptoms: Strabismus: Paralysis of one or more ocular muscles can cause its respective antagonist to dominate. This results in a typical strabismus that allows which muscle is paralyzed to be determined (see Diagnostic considerations). This is readily done especially in abducent or trochlear nerve palsy as the abducent nerve and the trochlear nerve each supply only one extraocular muscle (see Fig. 17.1).

Example: abducent nerve palsy (Fig. 17.14). A lesion of the abducent nerve paralyzes the lateral rectus so that the eye can no longer by abducted. This paralysis also causes the muscle's antagonist, the medial rectus, to dominate. Because this muscle is responsible for adduction, the affected eye remains medially rotated.

Gaze palsy. Symmetrical paralysis of one or more muscles of both eyes limits ocular motility in a certain direction. For example, vertical gaze palsy orPari-naud's syndrome, which primarily occurs in the presence of a pineal gland tumor, involves a lesion of the rostral interstitial nucleus of the medial longitudinal fasciculus (see Fig. 17.12). Paralysis of all extraocular muscles leads to complete gaze palsy. Gaze palsy suggests a supranuclear lesion, i.e., a lesion in the gaze centers. Examination by a neurologist is indicated in these cases.

Double vision. Loss of binocular coordination between the two eyes due to ophthalmoplegia leads to double vision. Normal vision may be expected in patients with only moderate paresis. As the onset of paresis is usually sudden, double vision is the typical symptom that induces patients to consult a phys

Left abducent nerve palsy. -

Fig. 17.14 The left eye remains immobile in left gaze (arrow).

Left abducent nerve palsy. -

ician. Some patients learn to suppress one of the two images within a few hours, days, or weeks. Other patients suffer from persistent double vision. Children usually learn to suppress the image quicker than adults.

Causes. Double vision occurs when the image of the fixated object only falls on the fovea in one eye while falling on a point on the peripheral retina in the fellow eye. As a result, the object is perceived in two different directions and therefore seen double (Fig. 17.15 a and b). The double image of the deviating eye is usually somewhat out of focus as the resolving power of the peripheral retina is limited. Despite this, the patient cannot tell which is real and which is a virtual image and has difficulty in reaching to grasp an object.

The distance between the double images is greatest in ophthalmoplegia in the original direction of pull of the affected muscle.

Example: trochlear nerve palsy (Fig. 17.16). The superior oblique supplied by the trochlear nerve is primarily an intorter and depressor in adduction (see Table 17.1); it is also an abductor when the gaze is directed straight ahead. Therefore, the limited motility and upward deviation of the affected eye is most apparent in depression and intorsion as when reading. The distance between the double images is greatest and the diplopia most irritating in this direction of gaze, which is the main direction of pull of the paralyzed superior oblique.

Compensatory head posture. The patient can avoid diplopia only by attempting to avoid using the paralyzed muscle. This is done by assuming a typical compensatory head posture in which the gaze lies within the binocular visual field; the patient tilts his or her head and turns it toward the shoulder opposite the paralyzed eye.

488 17 Ocular Motility and Strabismus Crossed and uncrossed diplopia. -

Uncrossed double images Crossed double images

Virtual image Real image

Virtual image Real image

a Esotropic eye

Fig. 17.15 a Esotropia in the left eye (LE) with uncrossed images. The right eye (RE) is the leading eye, and the left eye is esotropic. The visual image falling on the fovea in the leading eye falls on the nasal retina next to the fovea (PLE) in the esotropic eye and is perceived in space in a temporal location. The object is seen as two uncrossed or homonymous images.

a Esotropic eye

Fig. 17.15 a Esotropia in the left eye (LE) with uncrossed images. The right eye (RE) is the leading eye, and the left eye is esotropic. The visual image falling on the fovea in the leading eye falls on the nasal retina next to the fovea (PLE) in the esotropic eye and is perceived in space in a temporal location. The object is seen as two uncrossed or homonymous images.

Virtual image Real image

Virtual image Real image

b Exotropic eye b Exotropia in the left eye (LE) with crossed images. The right eye (RE) is the leading eye, and the left eye is ex-otropic. The visual image falling on the fovea in the leading eye falls on the temporal retina next to the fovea (PLE) in the exotropic eye and is perceived in space in a nasal location. The object is seen as two crossed or heteronymous images.

b Exotropic eye b Exotropia in the left eye (LE) with crossed images. The right eye (RE) is the leading eye, and the left eye is ex-otropic. The visual image falling on the fovea in the leading eye falls on the temporal retina next to the fovea (PLE) in the exotropic eye and is perceived in space in a nasal location. The object is seen as two crossed or heteronymous images.

The Bielschowsky head tilt test uses this posture to confirm the diagnosis of trochlear or fourth cranial nerve palsy (Fig. 17.17). In this test, the examiner tilts the patient's head toward the side of the paralyzed eye. If the patient then fixates with the normal eye, the paralyzed eye will deviate. When the patient's head is tilted toward the normal side, there will be no vertical deviation (see Diagnostic considerations for further diagnostic procedures).

Ocular torticollis. The compensatory head posture in trochlear nerve palsy is the most pronounced and typical of all cranial nerve palsies. Congenital trochlear nerve palsy can lead to what is known as ocular torticollis.

Incomitant angle of deviation. The angle of deviation in paralytic strabismus also varies with the direction of gaze and is not constant as in concomitant strabismus. Like the distance between the double images, the angle of deviation is greatest when the gaze is directed in the direction of pull of the paraLang, Ophthalmology © 2000 Thieme

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Right trochlear nerve palsy. -

Fig. 17.16 Vertical deviation of the right eye in left downward gaze (arrow).

1

if ' -^wm pi ^

iHirrv " ■ ■f* W1 - w

IB. tI

IP

pl i

à 1 s

h. '

— Bielschowsky head tilt test.

— Bielschowsky head tilt test.

Her Head The Right
Fig. 17.17 a When the patient tilts her head to the left (toward the normal side), the right eye does not deviate upward when the normal left eye fixates.

b When the patient tilts her head to the right (toward the side of the paralyzed muscle), the right eye deviates upward when the normal left eye fixates.

lyzed muscle. The angle of deviation may be classified according to the which eye fixates.

- A primary angle of deviation is the angle of deviation when fixating with the normal eye. This angle is small.

- A secondary angle of deviation is the angle of deviation when fixating with the paralyzed eye. This angle is large.

H The secondary angle of deviation is always larger than the primary angle. This is because both the paralyzed muscle and its synergist in the fellow eye receive increased impulses when the paralyzed eye fixates. For example when the right eye fixates in right abducent nerve palsy, the left medial rectus will receive increased impulses. This increases the angle of deviation.

Cranial nerve palsies: The commonest palsies are those resulting from cranial nerve lesions. Therefore, this section will be devoted to examining these palsies in greater detail than the other motility disturbances listed under Etiology. It becomes evident from the examples of causes listed here that a diagnosis of ophthalmoplegia will always require further diagnostic procedures (often by a neurologist) to confirm or exclude the presence of a tumor or a certain underlying disorder such as diabetes mellitus.

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Responses

  • Giuseppa Siciliano
    Is complete opthalmoplegia concomitant strabismus?
    2 years ago

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