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

17 PICKWELL’S BINOCULAR VISION ANOMALIES

is indicated in these cases when there is poor cosmesis, symptoms (principally diplopia), a recent onset within the sensitive period or marked ocular torticollis that could cause permanent neck problems. The aims of surgery are to straighten the visual axes and, if possible, to restore binocular vision. Eye exercises, patching, prisms and refractive correction may be required in addition to surgery (Ch. 15).

A recent review found two randomized controlled trials of strabismus surgery for adults, suggesting that the intervention is reasonably safe and effective at improving ocular alignment (Mills et al 2004). Surgical correction of acquired strabismus can also result in recovery of stereoacuity, particularly if surgery occurs within 12 months of the onset of strabismus (Fawcett et al 2004).

Before surgery, the surgeon should carry out the forced duction test to investigate the influence of the extraocular muscles, Tenon’s capsule and other non-muscular tissues on globe rotation in different positions of gaze (Bruenech 2001).

Presurgical prism adaptation test

The presurgical prism adaptation test is different to the short-term prism adaptation test that is used to investigate the usefulness of prescribing prisms in heterophoria (p 106). The presurgical prism adaptation test is useful for determining the presence of binocular vision and for planning surgery (Rutstein et al 1991), commonly in esotropia (Moore & Drack 2000). It is still useful for adults who are considering surgery for esotropia of childhood onset (Kutschke & Scott 2004). The patient should have equal or nearly equal visual acuities and an angle of deviation not exceeding 40 (Ansons & Spencer 2001).

The deviation is completely corrected or slightly overcorrected with prisms, which are usually split between the two eyes. These are prescribed, typically as Fresnel prisms, and the patient is reassessed 1 week later. If the patient has adapted to the prisms so that there is a manifest deviation greater than 8 Δ,the prism strength is increased. The process is repeated until the deviation is 8 or less, or the magnitude of the prism exceeds 50 .

There are three possible responses to the test (Ansons & Spencer 2001):

(1)the visual axes become straight and binocular single vision is confirmed

(2)there is a residual microtropia with a good sensory adaptation (Ch. 16)

(3)the visual axes keep reconverging (‘eating up the prisms’).

If options (1) or (2) occur then the patient is described as a ‘prism responder’ and surgery is performed to correct the maximum angle measured (Ansons & Spencer 2001). If the test results in option (3), the patient is classed as a non-responder and any surgery performed is based on the angle of deviation first measured.

Prism testing for diplopia

reasons. In these cases the possibility of postoperative diplopia must be considered (Ansons & Spencer 2001) and Kushner (2002) advocated testing for diplopia with prisms in all adults before strabismus surgery. Diplopia can occur even in the presence of very poor acuity (see Case study 14.2).

The patient is asked to view a fixation target at distance and near through prisms (base-out for esotropia and base-in for exotropia). The prism is introduced and the strength is slowly increased until the patient notices diplopia (Ansons & Davis 2001). The range of prismatic strength that elicits diplopia should be recorded and will help the surgeon in planning the surgery. If diplopia is likely to occur, the patient should be informed and the diplopia should be demonstrated with prisms so that they can decide whether to have the operation (Ansons & Spencer 2001). The surgeon may use botulinum toxin to correct the strabismus temporarily and provide additional information about postoperative diplopia risk and its probable tolerance.

Overview of surgical techniques

The decision to surgically undercorrect, fully correct or overcorrect the strabismus is influenced by whether there is potential binocular single vision and the duration of the strabismus (Ansons & Spencer 2001). Adjustable sutures can be used in certain cases to improve the results of strabismus surgery. A detailed description of surgical procedures is beyond the scope of this book, but the main procedures (Kanski 1994, pp 449–453, Bruenech 2001) are summarized below:

(1)Weakening procedures, which decrease the pull of a muscle:

(a)Recession, where the insertion of a muscle is moved posteriorly. It can be used on any extraocular muscle

(b)Marginal myotomy, which lengthens a muscle without moving its insertion. It is used to weaken a previously fully recessed rectus muscle

(c)Myectomy, which involves severing a muscle from its insertion without re-attachment. It is most commonly used in weakening an overactive inferior oblique muscle

(d)Posterior fixation suture (Faden procedure), which is used mainly to treat dissociated vertical deviation.

(2)Strengthening procedures, which enhance the pull of a muscle:

(a)Resection, which shortens the length of a muscle to enhance its effective pull; it is suitable only for a rectus muscle

(b)Tucking of a muscle or its tendon is usually reserved to enhance the action of the superior oblique muscle in cases of fourth nerve palsy

(c)Advancement, which moves the insertion of a muscle nearer to the limbus to enhance the action of a previously recessed rectus muscle.

(3)Transposition procedures, which change the direction of action of a muscle:

(a)Vertical transposition of the horizontal recti, to correct A and V patterns

17 PICKWELL’S BINOCULAR VISION ANOMALIES

(b) Hummelsheim’s procedure, to improve abduction in sixth nerve palsy

(c) Jensen’s procedure, also to improve abduction in sixth nerve palsy, in conjunction with recession of the medial rectus or injection of botulinum toxin.

Clinical Key Points

■In incomitant deviations, the angle varies in different positions of gaze and according to which eye is fixating

■An understanding of the actions of the extraocular muscles is essential to be able to diagnose incomitant deviations

■The actions of the muscles change as the eyes move into different positions of gaze

■Incomitant deviations can be classified as neurogenic, myogenic or mechanical

■Primary care practitioners need to refer all new or changing incomitancies

■Symptoms and signs usually make it clear whether an incomitancy is longstanding or recent (Table 17.2)

■Superior oblique muscle pareses are difficult to diagnose from motility testing and testing of the angle of torsion is helpful

■Ideally, incomitancies should be quantified with a Hess screen (e.g. computerized Hess screen)

■Algorithm methods (Lindblom, Parks’ or Scobee’s) are useful but require practice

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NYSTAGMUS 18

Introduction

Nystagmus is a regular, repetitive, involuntary movement of the eye whose direction, amplitude and frequency is variable. It is rare: Stayte et al (1990) found manifest nystagmus and latent nystagmus in 0.15% and 0.015%, respectively, of 2-year-old children and Abadi et al (1991) gave a prevalence of congenital bilateral nystagmus of 0.025%. Physiological nystagmus can occur with certain types of visual (optokinetic nystagmus) or vestibular stimulation (e.g. by rotating the subject or by introducing warm or cold water into the ear). End-point nystagmus can also occur during motility testing, particularly if the child is tired (Grisham 1990) and if the target is held in the end point position for 15–30 s. This chapter will concentrate on non-physiological nystagmus.

There are several factors, listed below, that cause the investigation of nystagmus to be complicated. The aim of this chapter is to provide an overview of the subject for clinicians who may only encounter nystagmus occasionally and who need to know when to refer and what optometric management, if any, is appropriate. A more detailed review of nystagmus can be found in Harris 1997a. Other eye movement disorders are reviewed by Harris 1997b.

Problems in the evaluation of nystagmus

(1)Nystagmus is not a condition but a sign. Many different ocular anomalies can cause nystagmus, or nystagmus can be idiopathic, with no apparent cause.

(2)Attempts to classify the type of nystagmoid eye movement by simply watching the patient’s eye movements often do not agree with the results of objective eye movement analysis (Dell’Osso & Daroff 1975).

(3)The pattern of nystagmoid eye movements cannot be used with certainty to predict the aetiology of the nystagmus (Dell’Osso & Daroff

NYSTAGMUS 18

giving the appearance of a lateral rectus palsy and resulting in an anomalous head posture (Grisham 1990).

(2) Latent nystagmus (fusion maldevelopment nystagmus syndrome) is characteristically only present, or greatly increased, on monocular occlusion. However, it is very occasionally found in monocular individuals. The fast phase of the eye movement always beats towards the uncovered eye. Therefore, the direction of the nystagmus always reverses when the cover is moved from one eye to the other and this is pathognomonic of latent nystagmus (Repka 1999). Dell’Osso (1994) stated that both types of latent nystagmus (see below) are always accompanied by strabismus and that a cyclotorsional element is usually present, together with dissociated vertical deviation (Guyton 2000).

(a)Latent latent nystagmus, or true latent nystagmus, only becomes apparent on monocular occlusion.

(b)Manifest latent nystagmus is present without occlusion.

(3)Acquired (neurological) nystagmus occurs usually after the first few months of life, owing to some pathological lesion or trauma affecting the motor pathways (e.g. multiple sclerosis, closed head trauma). All uninvestigated cases, except voluntary nystagmus, should be referred.

(a)Gaze paretic (evoked) nystagmus, a jerk nystagmus, appears on eccentric gaze and beats in the direction of the gaze. It is associated with cerebellar disorders (Harris 1997a) or sedative or anticonvulsant medication or alcohol.

(b)Acquired pendular nystagmus is associated with brain stem or cerebellar disease, or demyelinating diseases (Averbuch-Heller & Leigh 1996). Rarely, acquired pendular nystagmus occurs in the first few months of life (Harris 1997a).

(c)Acquired jerk nystagmus is usually associated with cerebellar or brain stem disease. Down-beating nystagmus is strongly suggestive of Arnold–Chiari malformation, where vertical pursuit and the vestibulo-ocular reflex also may be abnormal.

(d)Convergence-retraction nystagmus (induced convergence-retraction) is caused by co-contraction of the extraocular muscles, particularly the medial recti. There is a jerk nystagmus (with discomfort) stimulated by attempted up-gaze in which the fast phase brings the two eyes together in a convergence movement with retraction of the globe.

(e)Vestibular nystagmus is usually acquired and has a ‘saw tooth’ waveform where a slow constant velocity drift takes the eyes off target, followed by a quick corrective saccade (Grisham 1990).

(f)See-saw nystagmus: one eye elevates and usually intorts as the other depresses and extorts. It is rare and is usually associated with parasellar or chiasmal lesions; there may be bitemporal hemianopia.

(g)Dissociated nystagmus, with eye movements that are dissimilar in direction, amplitude or speed, may occur in internuclear

NYSTAGMUS 18

movement

A

time

B

C

Figure 18.1 Schematic eye movement traces to illustrate (A) pendular nystagmus and (B, C) jerk nystagmus with (B) an accelerating slow phase and (C) a decelerating slow phase. Faster eye movements are represented by lines that are close to vertical: the eyes are stationary when the trace is horizontal.

Dell’Osso & Daroff (1975) presented a thorough review of eye movement types in CN and a classification of waveforms into 12 different types. The situation is complicated by the fact that most people with CN exhibit more than one type of waveform and the waveform shape cannot be used to determine the type of nystagmus, as classified in the previous section (Abadi & Dickinson 1986). Indeed, the waveform in a given person with CN may evolve with time to develop adaptations that increase the foveation period, as described below (Abadi & Dickinson 1986).

The foveation period is the proportion of time that the object of regard is imaged at or very close to the fovea and during which the image is moving slowly enough for useful information to be assimilated. The precision of foveation is a better predictor of acuity than the intensity of the nystagmus (Abadi & Dickinson 1986). Dell’Osso (1994) argued that the ability to use a foveation period explains why patients with congenital and manifest latent nystagmus do not experience oscillopsia. However, Waugh & Bedell (1992) found that people with nystagmus sample visual information continuously, not just during one phase of the nystagmus. Extraretinal signals are likely to play a role in alleviating the perception of motion smear from the eye movements in CN, in the same way as they do during eye movements in normal observers (Bedell 2000). Chung & Bedell (1997) noted that it is not just the duration of the foveation period that is important in CN but also the period of temporal integration of the visual system. These researchers showed an interaction between these two variables and luminance.

Investigation

Symptoms and history