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

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17 PICKWELL’S BINOCULAR VISION ANOMALIES

A computerized version of the Hess screen is now available (Appendix 11), which allows plots (Fig. 17.7) to be obtained on standard desktop or laptop computers. Head position needs to be carefully monitored and too close a working distance might reduce the ability of the test to detect subtle lateral rectus palsies. The absence of the peripheral points that are present on the standard Hess chart might be a disadvantage with rare cases of subtle mechanical limitations, although in my experience this has not been a significant problem. A prototype of the test was described by Thomson et al (1990).

Lees screen

The Lees screen is a pair of Hess screens mounted at right angles, the markings showing only when internally illuminated. A pair of mirrors mounted back to back bisects the angle between the screens (Fig. 17.8). The patient initially faces the unilluminated screen and views the illuminated right screen with the right eye by reflection in the mirror. The patient is thus fixating with the right eye. The examiner uses a pointer to indicate a test

Illuminated, pointed to by practitioner

Mirror

Patient

Not illuminated,

Apointed to by patient

B

290

Figure 17.8 The Lees screen test. (A) The principle of the test. (B) The test in use (both

panels are illuminated, as they are when the practitioner records the result).

INCOMITANT DEVIATIONS

17

position on the illuminated right screen and the patient uses a pointer to indicate the position to which the right pointer is projected on the left screen. The practitioner then presses a foot switch to briefly illuminate the left screen and plots the result relative to the correct position on a record chart (Fig. 17.8). This procedure is repeated for various test positions, as with the Hess screen. The standard pointers have circular targets but they can be modified to bar targets to aid the investigation of torsional palsies.

Interpretation of Hess or Lees screen plots

It is most important with these techniques that the results are plotted correctly, with the fixating eye recorded as such (Fig. 17.8). With the Hess screen, the fixating eye sees the image projected by the examiner. With the Lees screen, the fixating eye sees the image that is constantly illuminated.

General points (worksheet in Appendix 8)

(1)All counting of squares must be from the centre of the plot (result recorded), not from the centre of the chart (Fig. 17.9).

(2)The test is fundamentally a dissociation test in different positions of gaze. When the central point is plotted this is equivalent to a dissociation test in the primary position and the deviation should be revealed. If the deviation varies when different eyes are fixating, this suggests incomitancy.

(3)The test is based on foveal projection so that the position of the plots indicates the position of the eyes. For example, if the left eye’s plot is higher than the right then there is left hypertropia.

(4)It follows from (3) that the smallest plot will be from the eye with the underacting muscle(s) (Fig. 17.9). If it is difficult to tell which is the smaller plot, concentrate on a comparison of the height of the plot in vertical incomitancies and on the width in horizontal incomitancies.

(5)The paretic muscle(s) can be found by looking for the smallest distance from the centre of the plot.

(6)There should be an overaction of the contralateral synergist to the palsied muscle(s), and this will be very marked in a recent onset incomitancy. This overaction occurs because of Hering’s law of equal innervation.

(7)In a long-standing incomitancy, secondary sequelae will be apparent, as described on page 297.

(8)Sloping fields are indicative of an A- or V-pattern, not a cyclodeviation (although this may be present as well).

(9)In mechanical incomitancies, secondary sequelae (see below) are not likely to be present and the deviation in the primary position does not reflect the extent of the defect.

Localization disturbances

The localization of objects in space is determined visually by a combination

291

of two mechanisms: retinal localization and the motor system’s directional

17 PICKWELL’S BINOCULAR VISION ANOMALIES

A

B

292

Figure 17.9 Example plots from the computerized City University Hess screen test. (A) Right

superior oblique muscle paresis. (B) Mild left lateral rectus underaction.

INCOMITANT DEVIATIONS

17

 

 

 

 

 

C

D

Figure 17.9 (Continued) (C) Recent paresis of left lateral rectus (caused by vascular

hypertension). (D) Same as (C) but partially resolved 1 month later (see also Appendix 13 and 293 CD-ROM).

 

17

 

PICKWELL’S BINOCULAR VISION ANOMALIES

 

 

 

 

mechanism. The position of the image on the retina determines the direc-

 

 

 

 

tion in which it is perceived: its visual location. Because the eyes and

 

 

 

 

head move, the brain must also take these movements into account in

 

 

 

 

localizing an object with respect to the egocentre. Eccentric fixation can

 

 

 

 

cause a disturbance of the retinal system when the fixation point moves

 

 

 

 

away from the centre of localization at the fovea: past pointing occurs

 

 

 

 

(Ch. 13).

 

 

 

 

The motor localization system uses two types of information to register

 

 

 

 

eye position. One of these is feedback from the extraocular muscles them-

 

 

 

 

selves (inflow), which is called muscle proprioreception. The other is

 

 

 

 

information that is copied within the brain from the centres that control

 

 

 

 

movement to those that monitor eye position (efferent copy: outflow). Pro-

 

 

 

 

prioreception is a back-up to efferent copy (Bridgeman & Stark 1991). If

 

 

 

 

the eyes do not move correctly in response to the nerve impulses sent to

 

 

 

 

the muscles, as in paretic strabismus, then the motor localization system

 

 

 

 

will be disturbed.

 

 

 

 

The past pointing test may be used to demonstrate these motor disturb-

 

 

 

 

ances. The test is applied monocularly to each eye in turn, as described in

 

 

 

 

Chapter 13. Past pointing will be demonstrated in the eye having the

 

 

 

 

affected muscle and in the field of action of this muscle. The degree of past

 

 

 

 

pointing will increase as the eye turns further into the direction of its

 

 

 

 

action, and will not occur in the opposite direction of gaze. This test can be

 

 

 

 

made more effective by holding a card horizontally (for horizontal devia-

 

 

 

 

tions) at the level of the patient’s chin, so that it occludes the patient’s

 

 

 

 

pointing hand from view while the target appears above the card. Past

 

 

 

 

pointing only occurs with paresis of recent onset and lessens as the patient

 

 

 

 

adapts to the deviation. Past pointing can also occur in eccentric fixation

 

 

 

 

(p 196), where it is typically of a lesser degree than in incomitant deviations

 

 

 

 

of recent onset.

 

 

 

 

Testing the vestibular system

 

 

 

 

In supranuclear lesions the vestibulo-ocular reflex (VOR) will be maintained

 

 

 

 

but in those caused by infranuclear lesions it will not. The VOR is phylo-

 

 

 

 

genetically the oldest slow eye movement system and, because it does not

 

 

 

 

require visual feedback, it has a short latency. Horizontal VOR is well

 

 

 

 

developed at birth; the vertical VOR develops a little later.

 

 

 

 

The VOR can be tested to investigate whether a gaze palsy is supranuclear

 

 

 

 

or infranuclear, and to investigate a lack of abduction in an infant. The two

 

 

 

 

most common ways of testing the VOR are as follows. In the doll’s head

 

 

 

 

test, the patient is asked to fixate an object while the examiner rapidly rotates

 

 

 

 

the patient’s head, first in the horizontal and then in the vertical plane. A

 

 

 

 

normally functioning VOR will result in eye movements equal and opposite

 

 

 

 

to head movements. In the spinning baby test the infant is held upright by

 

 

 

 

the practitioner sitting on a rotating chair. The practitioner rotates him/

 

 

294

 

herself and the baby through 180° or 360°, observing the patient’s eyes. The

 

 

 

eyes make a conjugate movement in the direction opposite (compensatory)

INCOMITANT DEVIATIONS

17

to that of the body rotation and then, after about 30°, they make a fast

 

 

movement to the primary position; the cycle repeating. Once the rotation

 

 

is stopped there may be some postrotational nystagmus, but only for a few

 

 

seconds in a sighted infant. An older infant may maintain fixation on the

 

 

examiner’s face, in which case the test can only be done in the dark with

 

 

eye movement recording equipment.

 

 

Algorithms for aiding the diagnosis of vertical muscle

 

 

pareses

 

 

The diagnosis of the paretic muscle(s) is fairly straightforward in horizon-

 

 

tal deviations but is more complicated in cyclovertical deviations (Spector

 

 

1993). Some workers have developed algorithms (e.g. three-steps tests) to

 

 

help practitioners detect the paretic muscle(s) in cyclovertical deviations,

 

 

and three of these will now be described. The principles behind the vari-

 

 

ous tests in these methods can be understood from the earlier sections of

 

 

this chapter.

 

 

The Lindblom 70 cm rod method

 

 

A very simple method of qualitatively investigating cyclovertical incomi-

 

 

tancies is to use a 70 cm rod held horizontally 1 m in front of the patient

 

 

(Lindblom et al 1997). This test can be carried out with most patients using

 

 

a normal 30 cm ruler. The patient is asked to describe whether the rod is

 

 

single or double and if double whether tilted (indicating faulty oblique

 

 

muscle(s)) or parallel (indicating faulty vertical recti muscle(s)). If tilted

 

 

then the patient’s perception typically resembles an arrow (e.g. ) that

 

 

points towards the side of the eye with the paretic muscle. The muscle can

 

 

be further identified by investigating the effect of upand down-gaze on the

 

 

patient’s perception. If the patient reports a shape resembling an X then it

 

 

suggests that there may be a double oblique paresis, usually both superior

 

 

obliques. This method is surprisingly easy to use and is included in the

 

 

worksheet in Appendix 8.

 

 

This test is delightfully straightforward and a modified version can be used

 

 

in patients who have more subtle deviations and who are not diplopic in

 

 

the primary position. For these cases, the Lindblom method can be carried

 

 

out with two Maddox rods, one in front of each eye placed so that the

 

 

patient sees two horizontal lines when viewing a spot-light.

 

 

Parks’ method

 

 

There are three questions that are considered in Parks’ method, each of

 

 

which narrows down the paretic extraocular muscle. These questions are

 

 

summarized in Box 17.1: each question is followed by a list of the muscles

 

 

that are suggested as possibly paretic by the answer to the question. A right

 

 

hypotropia is treated as a left hypertropia and a left hypotropia as a right

 

 

hypertropia. A clinical worksheet that is designed to help practitioners carry

295

 

out this test and to interpret the result is reproduced in Appendix 8. Vazquez

 

17 PICKWELL’S BINOCULAR VISION ANOMALIES

described a simple graphical method of recording and analysing the results (Vazquez 1984).

Box 17.1

1.

Is the deviation a right hyperdeviation (or left hypodeviation), or left

 

hyperdeviation (right hypodeviation)?

 

 

R/L: RSO, RIR, LIO, LSR

L/R: RIO, RSR, LSO, LIR

2.

Is the hyperdeviation greater in right or left gaze?

 

R gaze: RSR, RIR, LIO, LSO

L gaze: LSR, LIR, RIO, RSO

3.

Is the vertical deviation greater with head tilt to R or L?

 

R tilt: RSO, RSR, LIO, LIR

L tilt: RIO, RIR, LSO, LSR

When the results of the three questions are combined, the paretic muscle should be identified. The last question utilizes the Bielschowsky head tilt test, which should be carried out with the patient seated upright fixating at 3 m (Finlay 2000). When the head is tilted to the right, normally the right eye intorts from actions of the right superior oblique and right superior rectus. With weakness of the right superior oblique, the right superior rectus acts alone to accomplish intorsion and this causes a marked elevation of the right eye. The elevation occurs because the superior rectus receives a larger signal than usual, has a primary action of elevation and receives less opposition than usual from the superior oblique.

Parks’ method is not infallible, and the result is confounded by several factors (Spector 1993): contracture of vertical recti muscles; paresis of more than one muscle, where there is a restrictive (mechanical) aetiology; skew deviation; previous strabismus surgery; myasthenia gravis; dissociated vertical divergence; and small non-paretic vertical deviations with horizontal strabismus. Many, if not all, of these factors will also affect the result of Scobee’s method, described below.

Scobee’s method:

 

 

 

Another three-step method was described by Scobee (1952), particularly for

 

 

 

hyperphoria, and is given in Box 17.2. Again, each question is followed by a

 

 

 

list of the muscles that are suggested as possibly paretic by the answer to the

 

 

 

question. The clinical worksheet in Appendix 8 includes Scobee’s method.

 

 

 

The second question in Scobee’s method is based on the fact that the

 

 

 

vertical recti have a greater effect when the eyes are abducted, as during

 

 

 

distance vision, and the vertical actions of the oblique muscles are max-

 

 

 

imal when the eyes are adducted, as during near vision. The third question

 

296

 

is based on a point discussed on page 278: the secondary deviation is greater

 

 

than the primary deviation.

 

 

INCOMITANT DEVIATIONS

17

Box 17.2

 

 

1.

Is the deviation a right hyperdeviation (or left hypodeviation), or left

 

 

hyperdeviation (or right hypodeviation)?

 

 

R/L: RSO, RIR, LIO, LSR

L/R: RIO, RSR, LSO, LIR

 

2.

Is the dissociated deviation (e.g. with Maddox rod) greater at distance

 

 

(when the visual axes are looking straight ahead) or at near (when the

 

 

visual axes are adducted)?

 

 

 

D: RSR, RIR, LSR, LIR

N: RSO, RIO, LSO, LIO

 

3.With the Maddox rod test, which eye is fixating when there is the greatest deviation?

R: RSR, RIR, RSO, RIO

L: LSR, LIR, LSO, LIO

Evaluation

Muscle sequelae of palsies

Clearly, a muscle palsy will result in an underaction of the affected muscle (the primary deviation). When the patient is fixating with the affected eye (or binocularly), there will also invariably be an overaction of the contralateral synergist (the secondary deviation; see Fig. 17.4), as predicted by Hering’s law. This is the largest overaction in the sequelae and occurs at onset, increasing over the first week (Stidwill 1998).

Over a period of time, other muscles become affected: motor secondary sequelae occur. It is important to accurately recognize secondary sequelae, since they help the practitioner to decide whether an incomitancy is new or old. In a long-standing incomitancy, one of the following two secondary sequelae may also occur (Mallett 1988a).

(1)If the non-paretic eye is used for everyday fixation, the ipsilateral antagonist to the palsied muscle will be in a permanently contracted state. Consequently, some of the elastic tissue in this muscle may be replaced by fibrous tissue. This results in contracture, which occurs within days to weeks (Finlay 2000) or about 4 weeks (Stidwill 1998, p 151) after the original palsy. This exaggerates the original deviation and manifests as an enlargement of the Hess plot in the field of action of the ipsilateral antagonist (Fig. 17.9). If possible, this contracture should be avoided, for example by prescribing alternate occlusion.

(2)If the patient fixates with the paretic eye in everyday vision then Hering’s law may result in a constant overaction of the contralateral synergist to the palsied muscle (the secondary deviation; Fig. 17.4). There may also be an inhibitional palsy of the contralateral antagonist. To give a common example, if a patient has a right superior oblique

palsy and fixates with the right eye then there will be an inhibition of

 

the ipsilateral antagonist (right inferior oblique) and a consequent inhib-

297

ition (by Hering’s law) of the contralateral synergist to this (left superior

 

17

 

PICKWELL’S BINOCULAR VISION ANOMALIES

 

 

 

 

rectus). This inhibitional palsy can be greater than the original palsy

 

 

 

 

(Stidwill 1998, p 151) and the effect of this may be to make the patient’s

 

 

 

 

ocular motility less incomitant with time. This is sometimes referred to

 

 

 

 

as a ‘spreading of the comitance’ and occurs between 2 and 9 months

 

 

 

 

after the original palsy (Stidwill 1998, pp 151–152).

 

 

 

 

If the patient sometimes fixates with either eye, then secondary sequelae

 

 

 

 

are less frequently found (Mallett 1969). The literature is not clear about

 

 

 

 

the situation when the patient has a palsy but is most of the time het-

 

 

 

 

erophoric, as often happens with superior oblique palsies. It seems likely

 

 

 

 

that these cases exhibit less marked secondary sequelae, possibly following

 

 

 

 

the scenario outlined in (2) above.

 

 

 

 

Differentiating incomitancies that are long-standing

 

 

 

 

from those of recent onset

 

 

 

 

The first priority with incomitant deviations is to decide if there is an active

 

 

 

 

pathological cause requiring immediate medical attention, or if it is a long-

 

 

 

 

standing deviation. Table 17.2 summarizes the factors that help in this

 

 

 

 

evaluation.

 

 

 

 

The aetiology of the incomitancy

 

 

 

 

It will be seen that one of the differences between deviations of recent patho-

 

 

 

 

logical cause and more long-standing deviations is that there may be other

 

 

 

 

symptoms of the general pathological condition. It is therefore useful to be

 

 

 

 

aware of the primary conditions that can give rise to incomitant deviations

 

 

 

 

and of the other signs and symptoms that may accompany them. There is a

 

 

 

 

very large number of these conditions and they are summarized in Table

 

 

 

 

17.3. In this table, the conditions are divided into three categories to make

 

 

 

 

them easier to remember rather than as a strict taxonomic classification.

 

 

 

 

Some of these aetiologies may have incomitant diplopia as an early sign

 

 

 

 

before the patient is really aware of the seriousness of other signs and

 

 

 

 

symptoms. This is not a very frequent occurrence but means that we must

 

 

 

 

be all the more vigilant and continue to bear the possibility in mind. In

 

 

 

 

other conditions, the deviation may occur as part of the possible progress

 

 

 

 

of the disease for which the patient is already under treatment. The

 

 

 

 

patient’s medical adviser needs to be made aware of this development. An

 

 

 

 

awareness of relevant anatomy is helpful (Evans 2004e, h).

 

 

 

 

Some of the most common of the conditions that may have ocular mus-

 

 

 

 

cle palsy as an early sign or as part of the progress of the condition are

 

 

 

 

described below. The other general symptoms that can accompany the

 

 

 

 

diplopia are also given as a means of helping to confirm the diagnosis of

 

 

 

 

the deviation as of recent pathological cause.

 

 

 

 

(1) Diabetes: ocular palsy from diabetes usually affects the third cranial

 

 

 

 

nerve and may sometimes involve the pupil reflex and reduce the

 

 

298

 

amplitude of accommodation. The symptoms of diabetes may include,

 

 

 

 

 

 

in addition to the diplopia, generalized headache, increased thirst and

 

 

 

 

INCOMITANT DEVIATIONS

17

Table 17.2 Summary of main factors to be considered in assessing incomitant deviations for active pathology

 

Factor

Congenital or

Recent onset

 

 

long-standing

 

 

 

 

 

 

 

 

Diplopia

Unusual

Usually present in at least

 

 

 

one direction of gaze

 

 

 

 

 

 

Onset

Patient does not know when

Usually sudden and

 

 

the deviation began

distressing

 

 

 

 

 

 

Amblyopia

Often present

Absent (almost always)

 

 

 

 

 

 

Comitance

More comitant with time

Always incomitant

 

 

 

 

 

 

Secondary sequelae

Usually present

Absent, except for

 

 

 

overaction of

 

 

 

contralateral synergist

 

 

 

 

 

 

Fusion range

May be large in vertical

Usually normal

 

 

incomitancies

 

 

 

 

 

 

 

 

Facial asymmetry

May be present

Absent, unless from

 

 

 

trauma

Abnormal head

Slight, but persists on

posture (if present)

covering paretic eye;

 

patient often unaware

 

of reason for it

More marked; the patient is aware of it (to avoid diplopia); disappears on covering paretic eye

 

Past pointing in field

Absent

Present

 

 

of paretic muscle

 

 

 

 

 

 

 

 

 

Old photographs

May show strabismus or

Normal

 

 

 

anomalous head posture

 

 

 

 

 

 

 

 

Other symptoms

Unlikely

May be present as a result

 

 

 

 

of the primary cause

 

 

 

 

 

 

urination, increased appetite with loss of weight, constipation, boils or other skin conditions. The older patients are mostly overweight.

(2)Thyroid eye disease: this can occur with muscle palsy and is described on page 311.

(3)Vascular hypertension: the chance of hypertension being accompanied by ocular palsy increases with age as the blood supply to the cranial nerves becomes involved. In addition to the vascular changes seen on the fundus, symptoms may include headache, dizziness, breathlessness and ringing in the ears.

(4)Aneurysms: the ocular palsy may be accompanied by frontal pain on the same side. The symptoms of hypertension may also be present.

(5)Temporal (giant cell) arteritis: marked temporal pain and tenderness is present with intermittent diplopia, loss of appetite and general lassitude.

The pain may be noticed on brushing the hair or chewing and there

299