Ординатура / Офтальмология / Английские материалы / Pickwell's Binocular Vision Anomalies 5th edition_Evans_2007

ing the anomaly.

The complete loss of action of a muscle is called a muscle paralysis. A partial

loss is referred to as paresis. The term palsy is used generically to include

both paralysis and paresis. In incomitant deviations of all kinds, treatment

with spectacles or exercises is very limited in remedying the patient’s devi-

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ation. The first priority is to recognize those cases that require urgent medical

attention. In long-standing static cases, referral should also be considered

INCOMITANT DEVIATIONS

17

PICKWELL’S BINOCULAR VISION ANOMALIES

means that it does not act vertically over the centre of rotation, and this

influences the secondary actions of this muscle. By reference to Figure

17.1A, it can be seen that, when the eye is looking straight ahead, the pri-

mary action must be to elevate the eye, and the secondary actions are

adduction and intorsion. The secondary actions will increase on adduction.

On abduction of the eye, the attachment of the muscle will move out-

wards and the line of pull will be carried directly over the centre of rota-

tion when the eye is abducted by about 25°. In this position, two factors

are obvious: the secondary actions can no longer occur and the primary

action will be at its greatest mechanical advantage. When the eye is turned

out, the superior rectus muscle will be a pure elevator and at its maximum

power will act as an elevator (see Fig. 17.2).

A similar state of affairs applies to the depressor action of the inferior

rectus muscle, as this lies very nearly in the same vertical plane as the

superior rectus. When the eye is turned out by about 25°, the inferior rec-

tus has its strongest action as a depressor and has no secondary actions.

The primary action of the superior rectus muscle opposes that of the infer-

ior rectus: the muscles are antagonists.

The oblique muscles are shown in Figure 17.1B. From its attachment

to the eye, the superior oblique pulls towards the trochlea (T). The line of

pull is also medial to the centre of rotation, and its actions in the primary

position – intorsion, depression and abduction – follow from this one

anatomical detail. Also, as the eye turns inwards its vertical action (depres-

sion) is increased and the other actions are very much reduced. If the eye

were to be adducted by about 50°, the line of pull would lie in the same

plane as the centre of rotation. In this position, its power as a depressor

would be maximum and it would have no other actions.

From the point of view of clinical diagnosis, we can regard the inferior

oblique muscle as lying in the same vertical plane as the superior oblique.

Its actions can therefore be deduced in a similar way and the primary

actions of the two muscles are opposite, so they are antagonists.

The single anatomical detail from which the muscle actions arise is that

the two vertical planes containing the lines of pull of the vertically acting

pairs of muscles cross medially to the centre of rotation of the eye. Once

this is understood, not only can the primary and secondary actions of

these muscles be deduced but incomitant deviation can also be analysed.

Figure 17.2 shows the interaction of the two elevator muscles: the superior

rectus and the inferior oblique. The central diagram shows the eye turned

upwards from the primary position. Its elevation is maintained by the

combined actions of both these muscles. Their individual contributions

to the maintenance of elevation (E) are shown in the vector construction

above the central diagram. The diagrams on the left of the figure show

the way these two muscles contribute to elevation when the eye is turned

outwards (abducted) and those on the right show the contribution of each

when the eye is turned inwards (adducted). In the vector construction

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(Fig. 17.2), the sloping dashed line S–R shows how the power of the superior

rectus to elevate the eye is at its maximum when the eye is abducted and

None

None

Adduction

Adduction

Abduction

Abduction

INCOMITANT DEVIATIONS

17

medial recti and therefore equal innervation to the left lateral and medial

recti. Since the left lateral rectus is paretic, the left eye will be deviated

inwards: the primary deviation. If the left eye takes up fixation of an object

straight ahead, then the left lateral rectus will have to receive much more

innervation than the left medial rectus in order to hold the eye in the pri-

mary position. Hering’s law means that the non-paretic right eye will also

receive a much greater innervation to the right medial rectus causing a very

large secondary deviation

The difference between primary and secondary deviations has several

clinical manifestations. During the cover test in the primary position, the

size of the deviation when each eye is covered can be compared and if the

deviation differs then this indicates that the patient may have an incomi-

tant deviation and can also indicate which eye has the underacting muscle.

Later in this chapter the use of the Maddox rod for comparing primary

and secondary deviations will be discussed. The difference between primary

and secondary deviations also explains why Hess and Lees screen plots are

carried out twice, once with each eye fixating.

Classification of incomitant deviations

Incomitant deviations can be classified as neurogenic (a problem with the

nervous supply), myogenic (a problem with the muscle) or mechanical

(where a muscle is mechanically restricted).

Three cranial nerves control the movements of the extraocular muscles:

the fourth nerve (trochlear) controlling the superior oblique muscle, the

sixth nerve (abducens) controlling the lateral rectus and the third nerve

(oculomotor) controlling the other extraocular muscles. These nerves

have nuclei and neurogenic deviations can be supranuclear, nuclear or

infranuclear depending on whether the lesion occurs above, at or below

the level of the relevant nucleus. Nuclear palsies are rarely isolated,

because of the extensive size of the causative lesion in most cases, so that

the clinical findings are complicated by involvement of adjacent supranu-

clear eye movement control centres (Ansons & Davis 2001, p 357). Figure

17.5 illustrates some sites in the ocular cranial nerve pathways where

lesions are particularly likely to occur.

In myogenic palsies the primary problem affects the muscle itself rather

than influencing its nerve supply or mechanically constricting the muscle.

The most common example is myasthenia gravis.

Incomitancies that result from mechanical restriction are caused by elem-

ents within the orbit that either interfere with muscle contraction or other-

wise prevent free movement of the globe. The restriction may be direct

(e.g. tight or shortened muscle or tendon) or indirect (e.g. large retinal

explant).

Incomitant deviations can also be classified as congenital or acquired.

Acquired neurogenic palsies are of particular significance since they can be

a sign of life-threatening pathology or of trauma (Fig. 17.5). Nearly all myo-

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genic palsies are acquired. Mechanical incomitancies can be congenital