Ординатура / Офтальмология / Английские материалы / Comprehensive Ophthalmology_Khurana_2007

3.Parietal lobe tumours. These are associated with crossed lower homonymous quadrantanopia due to involvement of the upper fibres of the optic radiations. Other lesions include visual and auditory hallucinations, conjugate deviations of the eyes and optokinetic nystagmus.

4.Occipital lobe tumours. These may produce crossed homonymous quadrantic or hemianopic defect involving the fixation point. Visual agnosia may also be associated.

5.Mid-brain tumours. These may be associated with homonymous hemianopia due to pressure on the optic tracts. Other signs depending upon the site of involvement are as follows:

i.Tumours of the upper part produce spasmodic contraction of the upper lid followed by ptosis and loss of upward conjugate movements. In about 25 percent cases, an upper motor neuron facial paralysis and ipsilateral hemiplegia may also develop.

ii.Tumours of the intermediate level may be associated with the following syndromes: (i) Weber’s syndrome. It is characterised by ipsilateral third nerve palsy, contralateral hemiplegia and facial palsy of upper motor neuron type. (ii) Benedikt’s syndrome. It is characterised by ipsilateral third nerve palsy associated with tremors and jerky movements of the contralateral side which occur due to involvement of the red nucleus.

6.Tumours of the pons. Lesions in the upper part are characterised by ipsilateral third nerve palsy, contralateral hemiplegia and upper motor neuron type facial palsy. While the lesions in the lower part of the pons produce Millard-Gubler syndrome which consists of ipsilateral sixth nerve palsy, contralateral hemiplegia and ipsilateral facial palsy; or Foville’s syndrome is which sixth nerve paralysis is replaced by a loss of conjugate movements to the same side.

7.Cerebellar tumours. Those arising from the cerebellopontine angle produce corneal anaesthesia due to involvement of fifth nerve, early deafness and tinnitis of one side, sixth and seventh cranial nerve paralysis, cerebellar symptoms such as ataxia and vertigo, marked papilloedema and nystagmus.

8.Chiasmal and pituitary tumours. These include: pituitary adenomas, craniopharyngiomas and suprasellar meningiomas. These tumours typically produce chiasmal syndrome which is characterised by bitemporal visual field defects, optic atrophy and sometimes endocrinal disturbances.

DEMYELINATING DISEASES

These include multiple sclerosis, neuromyelitis optica and diffuse sclerosis. Ocular involvement may occur in all these conditions. Their salient features are as follows:

Multiple sclerosis

It is a demyelinating disorder of unknown etiology, affecting women more often than men, usually in the 15-50 years age group. Pathologically, the condition is characterised by a patchy destruction of the myelin sheaths throughout the central nervous system. Clinical course of the condition is marked by remissions and relapses. In this condition, optic neuritis is usually unilateral. Other ocular lesions include internuclear ophthalmoplegia and vestibular or cerebellar nystagmus.

Neuromyelitis optica (Devic’s disease)

It is characterised by bilateral optic neuritis associated with ascending myelitis, entailing a progressive quadriplegia and anaesthesia. Unlike multiple sclerosis, this condition is not characterised by remissions and is not associated with ocular palsies and nystagmus.

Diffuse sclerosis (Schilder’s disease)

It typically affects children and adolescents and is characterised by progressive demyelination of the entire white matter of the cerebral hemispheres. Ocular lesions include: optic neuritis (papillitis or retrobulbar neuritis), cortical blindness (due to destruction of the visual centres and optic radiations), ophthalmoplegia and nystagmus.

OCULAR SIGNS IN HEAD INJURY

Ocular signs related only to the intracranial damage are described here. However, direct trauma to the eyeball and/or orbit is frequently associated with the head injury. Lesions of direct ocular trauma are described in the chapter on ocular injuries (pages 401-414).

A. Concussion injuries to the brain

These are usually associated with subdural haemorrhage and unconsciousness which may produce the following ocular signs.

1.Hutchinson’s pupil. It is characterised by initial ipsilateral miosis followed by dilatation with no light reflex due to raised intracranial pressure. If the pressure rises still further, similar changes occur in the contralateral pupil. Therefore, presence of bilateral fixed and dilated pupils is an indication of immediate cerebral decompression.

2.Papilloedema. When it appears within 48 hours of the trauma, it indicates extra or intracerebral haemorrhage and is an indication for immediate surgical measures. While the papilloedema appearing after a week of head injury is usually due to cerebral oedema.

B. Fractures of the base of skull

Associated ocular signs are as follows:

1.Cranial nerve palsies. These are often seen with fractures of the base of the skull; most common being the ipsilateral facial paralysis of the lower motor neuron type. Extraocular muscle palsies due to involvement of sixth, third and fourth cranial nerves may also be seen.

2.Optic nerve injury. It may be injured directly, indirectly or compressed by the haemorrhage. Primary optic atrophy may appear in 2-4 weeks following injury. Presence of papilloedema suggests haemorrhage into the nerve sheath.

3.Subconjunctival haemorrhage. It may be seen when fracture of the base of skull is associated with fractures of the orbital roof. The subconjunctival haemorrhage is usually more marked in the upper quadrant and its posterior limit cannot be reached.

4.Pupillary signs. These are inconsistent and thus not pathognomonic. However, usually pupil is dilated on the affected side.

ANATOMY AND PHYSIOLOGY OF

THE OCULAR MOTILITY SYSTEM

EXTRAOCULAR MUSCLES

A set of six extraocular muscles (4 recti and 2 obliques) control the movements of each eye (Fig. 13.1). Rectus muscles are superior (SR), inferior (IR), medial (MR) and lateral (LR). The oblique muscles include superior (SO) and inferior (IO).

Origin and insertion

The rectus muscles originate from a common tendinous ring (the annulus of Zinn), which is attached at the apex of the orbit, encircling the optic foramina and medial part of the superior orbital fissure (Fig. 13.2). Medial rectus arises from the medial part of the ring, superior rectus from the superior part and also the adjoining dura covering the optic nerve, inferior rectus from the inferior part and lateral rectus from the lateral part by two heads which join in a ‘V’ form.

All the four recti run forward around the eyeball and are inserted into the sclera, by flat tendons (about 10-mm broad) at different distances from the limbus as under (Fig. 13.3):

The superior oblique muscle arises from the bone above and medial to the optic foramina. It runs forward and turns around a pulley — ‘the trochlea’ (present in the anterior part of the superomedial angle of the orbit) and is inserted in the upper and outer part of the sclera behind the equator (Fig. 13.3C).

The inferior oblique muscle arises by a rounded tendon from the orbital plate of maxilla just lateral to the orifice of the nasolacrimal duct. It passes laterally and backward to be inserted into the lower and outer part of the sclera behind the equator (Fig. 13.3C).

Nerve supply

The extraocular muscles are supplied by third, fourth and sixth cranial nerves. The third cranial nerve (oculomotor) supplies the superior, medial and inferior recti and inferior oblique muscles. The fourth cranial nerve (trochlear) supplies the superior oblique and the sixth nerve (abducent) supplies the lateral rectus muscle.

Actions

The extraocular muscles rotate the eyeball around vertical, horizontal and antero-posterior axes. Medial and lateral rectus muscles are almost parallel to the optical axis of the eyeball; so they have got only the main action. While superior and inferior rectus muscles make an angle of 23o (Fig. 13.4) and reflected tendons of the superior and inferior oblique muscles of 51o (Fig. 13.5) with the optical axis in the primary position; so they have subsidiary actions in addition to the main action. Actions of each muscle (Fig. 13.6) are shown in Table 13.1.

Table 13.1: Actions of extraocular muscles

Superior rectus

Fig. 13.4. Relation of the superior and inferior rectus muscles with the optical axis in primary position.

510 Optical axis

Muscle plane

Superior oblique

Fig. 13.5. Relation of the superior and inferior oblique muscles with the optical axis in primary position.

Fig. 13.6. Action of the extraocular muscles, SR (superior rectus); MR (medial rectus); IR (inferior rectus); SO (superior oblique); LR (lateral rectus); IO (inferior oblique).

OCULAR MOTILITY

Types of ocular movements

A Uniocular movements are called ‘ductions’ and include the following:

1.Adduction. It is inward movement (medial rotation) along the vertical axis.

2.Abduction. It is outward movement (lateral rotation) along the vertical axis.

3.Supraduction. It is upward movement (elevation) along the horizontal axis.

4.Infraduction. It is downward movement (depression) along the horizontal axis.

5.Incycloduction (intorsion). It is a rotatory movement along the anteroposterior axis in which superior pole of the cornea (12 O’clock point) moves medially.

6.Excycloduction (extorsion). It is a rotatory movement along the anteroposterior axis in which superior pole of the cornea (12 O’clock point) moves laterally.

B Binocular movements. These are of two types: versions and vergences.

a Versions, also known as conjugate movements, are synchronous (simultaneous) symmetric movements of both eyes in the same direction. These include:

1.Dextroversion. It is the movement of both eyes to the right. It results due to simultaneous contraction of right lateral rectus and left medial rectus.

2.Levoversion. It refers to movement of both eyes to the left. It is produced by simultaneous contraction of left lateral rectus and right medial rectus.

3.Supraversion. It is upward movement of both eyes in primary position. It results due to simultaneous contraction of bilateral superior recti and inferior obliques.

4.Infraversion. It is downward movement of both eyes in primary position. It results due to simultaneous contraction of bilateral inferior recti and superior obliques.

5.Dextrocycloversion. It is rotational movement around the anteroposterior axis, in which superior pole of cornea of both the eyes tilts towards the right.

6.Levocycloversion. It is just the reverse of dextrocycloversion. In it superior pole of cornea of both the eyes tilts towards the left.

b Vergences, also called disjugate movements, are synchronous and symmetric movements of both eyes in opposite directions e.g.:

1.Convergence. It is simultaneous inward movement of both eyes which results from contraction of the medial recti.

2.Divergence. It is simultaneous outward movement of both eyes produced by contraction of the lateral recti.

Synergists, antagonists and yoke muscles

1.Synergists. It refers to the muscles having the same primary action in the same eye; e.g., superior rectus and inferior oblique of the same eye act as synergistic elevators.

2.Antagonists. These are the muscles having opposite actions in the same eye. For example, medial and lateral recti, superior and inferior recti and superior and inferior obliques are antagonists to each other in the same eye.

3.Yoke muscles (contralateral synergists). It refers to the pair of muscles (one from each eye) which contract simultaneously during version movements. For example, right lateral rectus and left medial rectus act as yoke muscles for dextroversion movements. Other pairs of yoke muscles are: right MR and left LR, right LR and left MR, right SR and left IO, right IR and left SO, right SO and left IR and right IO and left SR.

4.Contralateral antagonists. These are a pair of muscles (one from each eye) having opposite action; for example, right LR and left LR, right MR and leftMR.

Laws governing ocular movements

1.Hering’s law of equal innervation. According to it an equal and simultaneous innervation flows from the brain to a pair of muscles which contract simultaneously (yoke muscles) in different binocular movements, e.g.:

i) During dextroversion: right lateral rectus and left medial rectus muscles receive an equal and simultaneous flow of innervation.

ii) During convergence, both medial recti get equal innervation.

iii) During dextroelevation, right superior rectus and left inferior oblique receive equal and simultaneous innervation.

2.Sherrington’s law of reciprocal innervation.

According to it, during ocular motility increased flow of innervation to the contracting muscle is accompanied by decreased flow of innervation to the relaxing antagonist muscle. For example, during dextroversion, an increased innervation flow to the right LR and left MR is accompanied by decreased flow to the right MR and left LR muscles.

Diagnostic positions of gaze

There are nine diagnostic positions of gaze (Fig. 13.7). These include one primary, four secondary and four tertiary positions.

1.Primary position of gaze. It is the position assumed by the eyes when fixating a distant object (straight ahead) with the erect position of head (Fig. 13.7e).

2.Secondary positions of gaze. These are the positions assumed by the eyes while looking straight up, straight down, to the right and to the left (Figs. 13.7b, d, f and h).

3.Tertiary positions of gaze. These describe the positions assumed by the eyes when combination of vertical and horizontal movements occur. These include position of eyes in dextroelevation, dextrodepression, levoelevation and levodepression (Figs. 13.7a, c, g and i).

4.Cardinal positions of gaze. These are the positions which allow examination of each of the 12 extraocular muscles in their main field of action. There are six cardinal positions of gaze, viz, dextroversion, levoversion, dextroelevation, levoelevation, dextrodepression and levodepression (Figs. 13.7 a, c, d, f, g and i).

SUPRANUCLEAR CONTROL OF EYE MOVEMENTS

There exists a highly accurate, still not fully elucidated, supranuclear control of eye movements which keeps the two eyes yoked together so that the image of the object of interest is simultaneously held on both fovea despite movement of the perceived object or the observer’s head and/or body.

Following supranuclear eye movement systems have been recognized:

1.Saccadic system

2.Smooth pursuit system

3.Vergence system

4.Vestibular system

5.Optokinetic system

6.Position maintenance system

All these systems perform specific functions and

each one is controlled by a different neural system but share the same final common path the motor neurones that supply the extraocular muscles.

1. Saccadic system. Saccades are sudden, jerky conjugate eye movements, that occur as the gaze

shifts from one object to another. Thus, they are performed to bring the image of an object quickly on the fovea. Though normally voluntary, saccades may be involuntary aroused by peripheral, visual or auditory stimuli.

2.Smooth pursuit eye movement system. Smooth pursuit movements are tracking movements of the eye as they follow moving objects. These occur voluntarily when the eyes track moving objects but take place involuntarily if a repetitive visual pattern is displayed continuously. When the velocity of the moving object is more, the smooth pursuit movement is replaced by small saccades (catchup saccades).

3.Vergence movement system. Vergence movements allow focussing of an object which moves away from or towards the observer or when visual fixation shifts from one object to another at a different distance. Vergence movements are very slow disjugate movements.

4.Vestibular eye movement system. Vestibular movements are usually effective in compensating for the effects of head movements in disturbing visual

fixation. These movements operate through the vestibular system.

5.Optokinetic system. The system helps to hold the images of the seen world steady on the retinae during sustained head rotation. This system becomes operative, when the vestibular reflex gets fatigued after 30 seconds. It consists of a movement following the moving scene, succeeded by a rapid saccade in the opposite direction.

6.Position maintenance system. This system helps to maintain a specific gaze position by means of rapid micromovements called ‘flicks’ and slow micromovements called ‘drifts’. This system coordinates with other systems. Neural pathway for this system is believed to be the same as for saccades and smooth pursuits.

BINOCULAR SINGLE VISION

Definition

When a normal individual fixes his visual attention on an object of regard, the image is formed on the fovea of both the eyes separately; but the individual perceives a single image. This state is called binocular single vision.

Visual development

Binocular single vision is a conditioned reflex which is not present since birth but is acquired during first 6 months and is completed during first few years. The process of its development is complex and partially understood.

Important mile stones in the visual development are:

At birth there is no central fixation and the eyes move randomly.

By the first month of life fixation reflex starts developing and becomes established by 6 months.

By 6 months the macular stereopsis and accommodation reflex is fully developed.

By 6 year of age full visual acuity (6/6) is attained and binocular single vision is well developed.

Prerequisites for development of binocular single vision

1.Straight eyes starting from the neonatal period with precise coordination for all directions of gaze (motor mechanism).

2.Reasonably clear vision in both eyes so that similar images are presented to each retina (sensory mechanism).

3.Ability of visual cortex to promote binocular single vision (mental process).

Therefore, pathologic states disturbing any of the above mechanisms during the first few years of life will hinder the development of binocular single vision and may cause squint.

Grades of binocular single vision

There are three grades of binocular single vision, which are best tested with the help of a synoptophore.

Grade I — Simultaneous perception. It is the power to see two dissimilar objects simultaneously. It is tested by projecting two dissimilar objects (which can be joined or superimposed to form a complete picture) in front of the two eyes. For example, when a picture of a bird is projected onto the right eye and that of a cage onto the left eye, an individual with presence of simultaneous perception will see the bird in the cage (Fig. 13.8a).

Grade II—Fusion. It consists of the power to superimpose two incomplete but similar images to form one complete image (Fig. 13.8b).

The ability of the subject to continue to see one complete picture when his eyes are made to converge or diverge a few degrees, gives the positive and negative fusion range, respectively.

Grade III— Stereopsis. It consists of the ability to perceive the third dimension (depth perception). It can be tested with stereopsis slides in synoptophore (Fig. 13.8c).

Anomalies of binocular vision

Anomalies of binocular vision include suppression, amblyopia, abnormal retinal correspondence (ARC), confusion and diplopia.

Suppression

It is a temporary active cortical inhibition of the image of an object formed on the retina of the squinting eye. This phenomenon occurs only during binocular vision (with both eyes open). However, when the fixating eye is covered, the squinting eye fixes (i.e., suppression disappears). Tests to detect suppression include Worth’s 4-dot test, four dioptre base out prism test, red glass test and synoptophore test (see page 327-329).

Amblyopia

Definition.Amblyopia, by definition, refers to a partial loss of vision in one or both eyes, in the absence of any organic disease of ocular media, retina and visual pathway.

Pathogenesis. Amblyopia is produced by certain amblyogeneic factors operating during the critical period of visual development (birth to 6 years of age). The most sensitive period for development of amblyopia is first six months of life and it usually does not develop after the age of 6 years.

Amblyogenic factors include :

Visual (form sense) deprivation as occurs in anisometropia,

Light deprivation e.g., due to congenital cataract, and

Abnormal binocular interaction e.g., in strabismus. Types. Depending upon the cause, amblyopia is of following types:

1. Strabismic amblyopia results from prolonged uniocular suppression in children with unilateral constant squint who fixate with normal eye.

2. Stimulus deprivation amblyopia (old term: amblyopia ex anopsia) develops when one eye is totally excluded from seeing early in life as, in congenital or traumatic cataract, complete ptosis and dense central corneal opacity.

3. Anisometropic amblyopia occurs in an eye having higher degree of refractive error than the fellow eye. It is more common in anisohypermetropic than the anisomyopic children.

Even 1-2D hypermetropic anisometropia may cause amblyopia while upto 3D myopic anisometropia usually does not cause amblyopia.

4.Isoametropic amblyopia is bilateral amblyopia occurring in children with bilateral uncorrected high refractive error.

5.Meridional amblyopia occurs in children with uncorrected astigmatic refractive error. It is a selective amblyopia for a specific visual meridian.

Clinical characteristics of an amblyopic eye are:

1.Visual acuity is reduced. Recognition acuity is more affected than resolution acuity.

2.Effect of neutral density filter. Visual acuity when tested through neutral density filter improves by one or two lines in amblyopia and decreases in patients with organic lesions.

3.Crowding phenomenon is present in amblyopics i.e., visual acuity is less when tested with multiple letter charts (e.g., Snellen’s chart) than when tested with single charts (optotype).

4.Fixation pattern may be central or eccentric. Degree of amblyopia in eccentric fixation is proportionate to the distance of the eccentric point from the fovea.

5.Colour vision is usually normal, may be affected in deep amblyopia with vision below 6/36.

Treatment of amblyopia should be started as early as possible (younger the child, better the prognosis). Occlusion therapy i.e., occlusion of the sound eye, to force use of amblyopic eye is the main stay in the treatment of amblyopia. However, before the