Ординатура / Офтальмология / Английские материалы / Comprehensive Ophthalmology_Khurana_2007

champagne cork. The central cup remains obliterated. Small drusen like crystalline deposits (corpora amylacea) may appear on the disc surface.

Visual fields. Blind spot is enlarged and the visual fields begin to constrict.

4. Atrophic papilloedema

Symptoms. Atrophic papilloedema develops after 6-9 months of chronic papilloedema and is characterized by severely impaired visual acuity.

Pupillary reaction. Light reflex is impaired.

Ophthalmoscopic features (Fig. 12.11D)

It is characterised by greyish white discoloration

and pallor of the disc due to atrophy of the neurons and associated gliosis. Prominence of the disc decreases in spite of persistent raised intracranial pressure. Retinal arterioles are narrowed and veins become less congested. Whitish sheathing develops around the vessels.

Visual fields. Concentric contraction of peripheral fields becomes apparent as atrophy sets in.

Differential diagnosis

Papilloedema should be differentiated from pseudopapilloedema and papillitis. Pseudopapilloedema is a non-specific term used to describe elevation of the disc similar to papilloedema, in conditions such as optic disc drusen, hypermetropia, and persistent hyaloid tissue. The differentiating points between papilloedema, papillitis and pseudopapilloedema (pseudopapillitis) due to hypermetropia are enumerated in Table 12.2.

Treatment and prognosis

It is a neurological emergency and requires immediate hospitalisation. As a rule unless the causative disease is treatable or cerebral decompression is done, the course of papilloedema is chronic and ultimate visual prognosis is bad.

OPTIC ATROPHY

It refers to degeneration of the optic nerve, which occurs as an end result of any pathologic process that damages axons in the anterior visual system, i.e. from retinal ganglion cells to the lateral geniculate body.

Classification

A. Primary versus secondary optic atrophy. It is customary to divide the optic atrophy into primary and secondary.

Primary optic atrophy refers to the simple degeneration of the nerve fibres without any

complicating process within the eye e.g., syphilitic optic atrophy of tabes dorsalis.

Secondary optic atrophy occurs following any pathologic process which produces optic neuritis or papilloedema.

Recently,mostoftheauthorshavediscardedtheuse of this time-honoured but non-informative classification. Further, such a classification is misleading since identical lesion at disc (e.g. papillitis in multiple sclerosis) will produce secondary optic atrophyandwheninvolvingopticnervealittledistance up (e.g. retrobulbar neuritis in multiple sclerosis) will produce an apparently primary optic atrophy.

B. Ophthalmoscopic classification. It is more useful to classify optic atrophy based on its ophthalmoscopic appearance. Common types are as follows:

1.Primary (simple) optic atrophy

2.Consecutive optic atrophy

3.Glaucomatous optic atrophy

4.Post-neuritic optic atrophy

5.Vascular (ischaemic) optic atrophy.

The etiology and salient features of each type will

be considered separately.

C. Ascending versus descending optic atrophy.

Ascending optic atrophy follows damage to ganglion cells or nerve fibre layer due to disease of the retina or optic disc. In it the nerve fibre degeneration progresses (ascends) from the eyeball towards the geniculate body.

Descending or retrograde optic atrophy proceeds from the region of the optic tract, chiasma or posterior portion of the optic nerve towards the optic disc.

Pathological features

Degeneration of the optic nerve fibres is associated with attempted but unsuccessful regeneration which is characterised by proliferation of astrocytes and glial tissue. The ophthalmoscopic appearance of the atrophic optic disc depends upon the balance between loss of nerve tissue and gliosis. Following three situations may occur:

1.Degeneration of the nerve fibres may be associated with excessive gliosis. These changes are pathological features of the consecutive and postneuritic optic atrophy.

2.Degeneration and gliosis may be orderly and the proliferating astrocytes arrange themselves in longitudinal columns replacing the nerve fibres (columnar gliosis). Such pathological features are seen in primary optic atrophy.

3.Degenration of the nerve fibres may be associated with negligible gliosis. It occurs due to progressive decrease in blood supply. Such pathological changes are labelled as cavernous optic atrophy and are features of glaucomatous and ischaemic (vascular) optic atrophy.

Etiology

1.Primary (simple) optic atrophy. It results from the lesions proximal to the optic disc without

antecedent papilloedema. Its common causes are: multiple sclerosis, retrobulbar neuritis (idiopathic), Leber’s and other hereditary optic atrophies, intracranial tumours pressing directly on the anterior visual pathway (e.g. pituitary tumour), traumatic severance or avulsion of the optic nerve, toxic amblyopias (chronic retrobulbar neuritis) and tabes dorsalis.

2.Consecutive optic atrophy. It occurs following destruction of ganglion cells secondary to degenerative or inflammatory lesions of the choroid and/or retina. Its common causes are: diffuse chorioretinitis, retinal pigmentary dystrophies such as retinitis pigmentosa, pathological myopia and occlusion of central retinal artery.

3.Postneuritic optic atrophy. It develops as a sequelae to long-standing papilloedema or papillitis.

4.Glaucomatous optic atrophy. It results from the effect of long standing raised intraocular pressure.

5.Vascular (ischaemic) optic atrophy. It results from the conditions (other than glaucoma) producing disc ischaemia. These include: giant cell arteritis, severe haemorrhage, severe anaemia and quinine poisoning.

Clinical features of optic atrophy

1.Loss of vision, may be of sudden or gradual onset (depending upon the cause of optic atrophy) and partial or total (depending upon the degree of atrophy). It is important to note that ophthalmoscopic signs cannot be correlated with the amount of vision.

2.Pupil is semidilated and direct light reflex is very sluggish or absent. Swinging flash light test depicts Marcus Gunn pupil.

3.Visual field loss will vary with the distribution of the fibres that have been damaged. In general the field loss is peripheral in systemic infections, central in focal optic neuritis and eccentric when the nerve or tracts are compressed.

4.Ophthalmoscopic appearance of the disc will vary with the type of optic atrophy. However, ophthalmoscopic features of optic atrophy in general are pallor of the disc and decrease in the number of small blood vessels (Kastenbaum index). The pallor is not due to atrophy of the nerve fibres but to loss of vasculature.

Ophthalmoscopic features of different types of optic atrophy are as described below:

i.Primary optic atrophy (Fig. 12.12A). Colour of the disc is chalky white or white with bluish hue. Its edges (margins) are sharply outlined. Slight recession of the entire optic disc occurs in total atrophy. Lamina cribrosa is clearly seen at the bottom of the physiological cup. Major retinal vessels and surrounding retina are normal.

ii.Consecutive optic atrophy (Fig. 12.12B). Disc appears yellow waxy. Its edges are not so sharply defined as in primary optic atrophy. Retinal vessels are attenuated.

iii.Post-neuritic optic atrophy (Fig. 12.12C). Optic disc looks dirty white in colour. Due to gliosis its edges are blurred, physiological cup is obliterated and lamina cribrosa is not visible. Retinal vessels are attenuated and perivascular sheathing is often present.

iv.Glaucomatous optic atrophy. It is characterised by deep and wide cupping of the optic disc and nasal shift of the blood vessels (for details see page 216 & Fig. 9.10).

v.Ischaemic optic atrophy. Ophthalmoscopic features are pallor of the optic disc associated with marked attenuation of the vessels (Fig. 12.12D).

Differential diagnosis

Pallor of optic disc seen in partial optic atrophy must be differentiated from other causes of pallor disc which may be non-pathological and pathological.

1.Non-pathological pallor of optic disc is seen in: axial myopia, infants, and elderly people with sclerotic changes. Temporal pallor is associated with large physiological cup.

2.Pathological causes of pallor disc (other than optic atrophy) include hypoplasia, congenital pit, and coloboma.

Treatment

The underlying cause when treated may help in preserving some vision in patients with partial optic atrophy. However, once complete atrophy has set in, the vision cannot be recovered.

SYMPTOMATIC DISTURBANCES

OF THE VISION

NIGHT BLINDNESS (NYCTALOPIA)

Night (scotopic) vision is a function of rods. Therefore, the conditions in which functioning of these nerve endings is deranged will result in night blindness. These include vitamin A deficiency, tapetoretinal degenerations (e.g., retinitis pigmentosa), congenital high myopia, familial congenital night blindness and Oguchi’s disease. It may also develop in conditions of the ocular media interfering with the light rays in dim light (i.e. with dilated pupils). These include paracentral lenticular and corneal opacities. In advanced cases of primary open angle glaucoma, dark adaptation may be so much delayed that patient gives history of night blindness.

DAY BLINDNESS (HAMARLOPIA)

It is a symptomatic disturbance of the vision, in which the patient is able to see better in dimlight as compared to bright light of the day. Its causes are congenital deficiency of cones, central lenticular opacities (polar cataracts) and central corneal opacities.

COLOUR BLINDNESS

An individual with normal colour vision is known as trichromate. In colour blindness, faculty to appreciate one or more primary colours is either defective (anomalous) or absent (anopia). It may be congenital or acquired.

A. Congenital Colour Blindness.

It is an inherited condition affecting males more (3-4%) than females (0.4%). It may be of the following types:

Dyschromatopsia

Achromatopsia

1. Dyschromatopsia

Dyschromatopsia, literally means colour confusion due to deficiency of mechanism to perceive colours. It can be classified into:

Anomalous trichromatism

Dichromatism

a.Anomalous trichromatic colour vision. Here the mechanism to appreciate all the three primary colours is present but is defective for one or two of them. It may be of following types:

Protanomalous. It refers to defective red colour appreciation.

Deuteranomalous. It means defective green colour appreciation.

Tritanomalous. It implies defective blue colour appreciation.

b.Dichromatic colour vision. In this conditon faculty to perceive one of the three primary colours is completely absent. Such individuals are called dichromates and may have one of the following types of defects:

Protanopia, i.e., complete red colour defect.

Deuteranopia, i.e., complete defect for green colour.

Tritanopia, i.e., absence of blue colour

appreciation.

Red-green deficiency (protanomalous, protanopia, deuteranomalous and deuteranopia) is more common. Such a defect is a source of danger in certain occupations such as drivers, sailors and traffic police. Blue deficiency (tritanomalous and tritanopia) is comparatively rare.

2. Achromatopsia

It is an extremely rare condition presenting as cone monochromatism or rod monochromatism.

Cone monochromatism is characterised by presence of only one primary colour and thus the person is truely colour blind. Such patients usually have a visual acuity of 6/12 or better.

Rod monochromatism may be complete or incomplete. It is inherited as an autosomal recessive trait. It is characterized by:

Total colour blindness,

Day blindness (visual acuity is about 6/60),

Nystagmus,

Fundus is usually normal.

B. Acquired Colour Blindness.

It may follow damage to macula or optic nerve, Usually, it is associated with a central scotoma or decreased visual acuity.

Blue-yellow impairment is seen in retinal lesions such as CSR, macular oedema and shallow retinal detachment.

Red-green deficiency is seen in optic nerve lesions such as optic neuritis, Leber’s optic atrophy and compression of the optic nerve.

Acquired blue colour defect (blue blindness) may occur in old age due to increased sclerosis of the crystalline lens. It is owing to the physical absorption of the blue rays by the increased amber coloured pigment in the nucleus.

Tests for Colour Vision

These tests are designed for : (1) Screening defective colour vision from normal; (2) Qualitative classification of colour blindness i.e., protans, deuteran and tritan; and (3) Quantitative analysis of degree of deficiency i.e., mild, moderate or marked.

Commonly employed colour vision tests are as

follows:

1.Pseudo-isochromatic charts. It is the most commonly employed test using Ishihara’s plates (Fig. 12.13). In this there are patterns of coloured and grey dots which reveal one pattern to the normal individuals and another to the colour deficients. It is a quick method of screening colour blinds from the normals. Another test based on the same principle is Hardy-Rand- Rittler plates (HRR).

2.The lantern test. In this test the subject has to name the various colours shown to him by a lantern and the judgement is made by the mistake he makes. Edridge-Green lantern is most popular.

3.Farnsworth-Munsell 100 hue test. It is a spectroscopic test in which subject has to arrange the coloured chips in ascending order. The colour vision is judged by the error score, i.e. greater the score poorer the colour vision.

4.City university colour vision test. It is also a spectroscopic test where a central coloured plate is to be matched to its closest hue from four surrounding colour plates.

5.Nagel’s anomaloscope. In this test the observer is asked to mix red and green colour in such a proportion that the mixture should match the given yellow coloured disc. The judgement about the defect is made from the relative amount of red and green colours and the brightness setting used by the observer.

6.Holmgren’s wools test. In this the subject is

Fig. 12.13. Ishihara’s pseudo-isochromatic chart.

asked to make a series of colour-matches from a selection of skeins of coloured wools.

AMAUROSIS

It implies complete loss of sight in one or both eyes, in the absence of ophthalmoscopic or other marked objective signs.

1. Amaurosis fugax

It refers to a sudden, temporary and painless monocular visual loss occurring due to a transient failure of retinal circulation.

Common causes of amaurosis fugax are: carotid transient ischaemic attacks (TIA), embolization of retinal circulation, papilloedema, giant cell arteritis, Raynaud’s disease, migraine, as a prodromal symptom of central retinal artery or carotid artery occlusion, hypertensive retinopathy, and venous stasis retinopathy. An attack of amaurosis fugax is typically described by the patients as a curtain that descends from above or ascends from below to occupy the upper or lower halves of their visual fields.

Clinical characteristics. The attack lasts for two to five minutes and resolves in the reverse pattern of progression, leaving no residual deficit. Due to brief duration of the attack, it is rarely possible to observe the fundus. When observed shortly after an attack, the fundus may either be normal or reveal signs of retinal ischemia such as retinal oedema and small superficial haemorrhages. In some cases, retinal emboli in the form of white plugs (fibrin-platelet aggregates) may be seen.

2. Uraemic amaurosis

It is a sudden, bilateral, complete loss of sight occurring probably due to the effect of certain toxic materials upon the cells of the visual centre in patients suffering from acute nephritis, eclampsia of pregnancy and renal failure. The visual loss is associated with dilated pupils which generally react to light. The fundi are usually normal except for the coincidental findings of hypertensive retinopathy, when associated. Usually, the vision recovers in 12-48 hours.

AMBLYOPIA

It implies a partial loss of sight in one or both eyes, in the absence of ophthalmoscopic or other marked objective signs. It may be either congenital or acquired. Acquired amblyopia may be organic (toxic

amblyopia; page 296) or functional.

Functional amblyopia results from the psychical suppression of the retinal image. It may be anisometropic, strabismic or due to stimulus deprivation (amblyopia ex anopsia) (see page 319).

CORTICAL BLINDNESS

Cortical blindness (visual cortex disease) is produced by bilateral occipital lobe lesions. Unilateral occipital lobe lesions typically produce contralateral macular sparing congruous homonymous hemianopia.

Causes of cortical blindness include:

Vascular lesions producing bilateral occipital infarction are the commonest cause of cortical blindness (e.g., embolisation of posterior cerebral arteries).

Head injury involving bilateral occipital lobes is the second common cause.

Tumours, primary (e.g., falcotentorial meningiomas, bilateral gliomas) or metastatic are rare causes.

Other rare causes of cortical blindness are migraine, hypoxic encephalopathy, Schilder’s disease and other leukodystrophies.

Clinical features. Cortical blindness is characterized by:

Bilateral loss of vision,

Normal pupillary light reflexes,

Visual imagination and visual imagery in dream are preserved

Anton syndrome i.e., denial of blindness by the patients who obviously cannot see.

Riddoch phenomenon i.e., ability to perceive kinetic but not static targets.

Management. A thorough neurological and cardiovascular investigative workup including MRI and MRI angiography should be carried out. Treatment depends upon the underlying cause. Partial or complete recovery may occur in patients with stroke progressing from cortical blindness through visual agnosia, and partially impaired perceptual function to recovery.

MALINGERING

In malingering a person poses to be visually defective, while he is not. The person may do so to gain some undue advantage or compensation. Usually, one eye is said to be blind which does not

show any objective sign. Rarely, a person pretends to be completely blind. In such cases, a constant watch over the behaviour may settle the issue.

Differential diagnosis

Before diagnosing malingering following conditions (which produce visual loss with apparantly normal anterior segment and a normal fundus) should be ruled out:

1.Amblyopia. Many a time an individual may suddenly notice poor vision in one eye though the onset is usually in early childhood. It is important to identify an amblyogenic factor (see page 319).

2.Cortical blindness must be ruled out from its characteristic features(see page 306).

3.Retrobulbar neuritis a common cause of visual loss with normal fundus. Presence of a definite or relative afferent pupillary defect (RAPD) and VER are diagnostic.

4.Cone rod dystrophy is characterized by a positive family history, photophobia in bright light, abnormal dark adaptation and abnormal cone dystrophy electroretinogram.

5.Chiasmal tumours may sometimes present with visual loss and normal fundus (before the onset of optic atrophy). Sluggish pupillary reactions to light with characteristic visual field defects may be noted.

Tests for malingering

1.Convex lens test. Place a low convex or concave lens (0.25 D) before the blind eye and a high

convex lens (+10 D) before the good eye. If the patient can read distant words, malingering is proved.

2.Prism base down test. Place a prism with its base downwards before the good eye and tell the person to look at a light source. If the patient admits seeing two lights, it confirms malingering.

3.Prism base out test. Ask the patient to look at a light source. Then a prism of 10 D is placed before the alleged blind eye with its base outwards. If the eye moves inwards (to eliminate diplopia) malingering is proved.

4.Snellen’s coloured types test. It has letters printed

in red and green. Place a red glass before the good eye. If the person can read all the letters, it confirms malingering because, normally one can see only red letters through red glass.

HYSTERICAL BLINDNESS

It is a form of psychoneurosis, commonly seen in attention-seeking personalities, especially females. It is characterised by sudden bilateral loss of vision (cf. malingering). The patient otherwise shows little concern for the symptoms and negotiates well with the surroundings (c.f. malingering). There may be associated blepharospasm and lacrimation. Visual fields are concentrically contracted. One can commonly find spiral fields as the target moves closer to the fixation point. Pupillary responses are essentially normal and so is the blink response. Optokinetic nystagmus is intact. Its treatment includes psychological support and reassurance. Placebo tablets may also be helpful. A psychiatrist’s help should be sought for, if these fail.

DISORDERS OF HIGHER VISUAL FUNCTIONS

Visual agnosia

Definition. Visual agnosia refers to a rare disorder in which ability to recognise the objects by sight (despite adequate visual acuity) is impaired while the ability to recognize by touch, smell or sound is retained.

Types of visual agnosia include :

Prosopagnosia. In it patient cannot recognize familiar faces.

Object agnosia. In it patient is not able to name and indicate the use of a seen object by spoken or written words or by gestures.

Site of lesion in visual agnosia is bilateral inferior (ventromedial) occipitotemporal junction.

Associated features include :

Bilateral homonymous hemianopia.

Dyschromatopsia (disturbance of colour vision).

Visual hallucinations

Visual hallucinations refers to the conditions in which patient alleges of seeing something that is not evident to others in the same environment.

Types. Visual hallucinations are of two types:

Elementary (unformed) hallucinations include flashes of light, colours, luminous points, stars, multiple lights and geometric forms. They may be stationary or moving.

Complex (formed) hallucinations include objects, persons or animals.

Causes of visual hallucinations include:

Occipital and temporal lobe lesions. Elementary hallucinations are considered to have their origin in the occipital cortex and complex ones in the temporal cortex.

Drug induced. Many drugs acting on the CNS in high doses are hallucinogenic.

Bilateral visual loss in elderly individuals may be associated with formed hallucinations (Charles Bonnet syndrome).

Migraine is a common cause of unformed hallucinations.

Optic nerve diseases and vitreous traction are reproted to produce unformed hallucinations.

Psychiatric disorders are not the causes of isolated visual hallucinations.

Alexia and agraphia

Alexia means the inability to read (despite good vision). It is commonly associated with agrphia (inability to write).

Causes. Alexia associated with agraphia is produced by lesions of the angulate gyrus of the dominant hemisphere.

Alexia without agraphia is usually caused by lesions that destroy the visual pathway in the left occipital lobe and also interrupt the association fibres from the right occipital lobe that have crossed in the splenium of corpus callosum.

Visual illusions

In visual illusions patients perceive distortions in form, size, movement or colour of the objects seen. Some of the visual illusions are:

Palinopsia (visual perservation) is an illusion whereby the patient continues to perceive an image after the actual object is no longer in view.

Optic anaesthesia refers to false orientation of objects in space.

Cerebral dyschromotopsia may occur as disappearance of colour (achromatopsia) or illusional colouring (e.g., erythropsia)

Cerebral diplopia or polyopia are also reported to occur as rare symptoms of central nervous system disease.

Causes. Visual illusions are reported to occur in lesions of the occipital, occipitoparietal or occipitotemporal regions, and the right hemisphere appears to be involved more often than the left.

OCULAR MANIFESTATIONS OF DISEASES OF CENTRAL NERVOUS SYSTEM

Ocular involvement in diseases of the central nervous system is not infrequent.Afew common ocular lesions of these diseases are mentioned here.

INTRACRANIAL INFECTIONS

These include meningitis, encephalitis, brain abscess and neurosyphilis.

1.Meningitis. It may be complicated by papillitis, and paralysis of third, fourth and sixth cranial nerves. Chronic chiasmal arachnoiditis may produce bilateral optic atrophy. Tuberculous meningitis may be associated with choroidal tubercles.

2.Encephalitis. It may be complicated by papillitis and/or papilloedema. Cranial nerve palsies are usually incomplete. Diplopia and ptosis are often present.

3.Brain abscess. It is frequently associated with papilloedema. Focal signs depend upon the site of the abscess, and are thus similar to tumours.

4.Neurosyphilis. Ocular involvement is quite frequent. Gummatous meningitis may be associated with papillitis, papilloedema or postneuritic optic atrophy and cranial nerve palsies. (Third nerve is paralysed in nearly 30 per cent cases, less frequently the fifth and sixth, and least frequently the fourth.) Tabes dorsalis and generalised paralysis of insane may be associated with primary optic atrophy, Argyll Robertson pupil, and internal and/or external ophthalmoplegia.

INTRACRANIAL ANEURYSMS

Intracranial aneurysms associated with ocular manifestations are located around the circle of Willis

Intracranial aneurysms may produce complications by following mechanisms:

1. Pressure effects. i Aneurysms of circle of Willis and internal carotid artery (supraclenoid, infraclenoid i.e., intracavernous, and anterior communicating artery) may produce following pressure effects :

Central and peripheral visual loss due to pressure on intracranial part of optic nerve and chiasma.

Slowly progressive ophthalmoplegia, due to pressure, on motor nerves in the cavernous sinus.

Facial pain and paraesthesia associated with corneal anaesthesia due to pressure on the branches of trigeminal nerve.

Horner’s syndrome due to pressure on sympathetic fibres along the carotid artery.

ii.Posterior communicating artery aneurysm typically presents with isolated painful third nerve palsy.

iii.Vertebrobasilar artery aneurysms may also be associated with third nerve palsy.

2. Production of arteriolar venous fistula. Carotidcavernous fistula may be produced by rupture of a giant aneurysm of the intracavernous part of the internal carotid artery. Pulsating exophthalmose is a typical presentation of carotid-cavernous fistula.

3. Subarachnoid haemorrhage. Subarachnoid haemorrhage is a life-threatening complication associated with sudden rupture of aneurysm of the circle of Willis. It is characterized by:

Sudden violent headache.

Third nerve palsy with pupillary dilatation.

Photophobia, signs of meningial irritation, vomiting and unconsiousness.

Terson syndrome refers to the combination of bilateral intraocular haemorrhages (intraretinal, subhyaloid and vitreous haemorrhage) and subarachnoid haemorrhage due to aneurysmal rupture.

INTRACRANIAL HAEMORRHAGES

Ophthalmic signs of intracerebral haemorrhage are tonic conjugate and dysconjugate deviations.

Subarachnoid haemorrhage may produce retinal haemorrhages (especially subhyaloid haemorrhage of the posterior pole), papilloedema, and ocular palsies.

INTRACRANIAL SPACE-OCCUPYING LESIONS (ICSOLS)

These include primary and secondary brain tumours, haematomas, granulomatous inflammations and parasitic cysts. Clinical features of the ICSOLs may be described under three heads:

I. General effects of raised intracranial pressure. These include headache,vomiting, papilloedema, drowsiness, giddiness, slowing of pulse rate and rise in blood pressure.

II. False localising signs. These occur due to the effect of raised intracranial pressure and displacement or distortion of the brain tissue. False localising signs of ophthalmological interest are as follows:

1.Diplopia: It occurs due to pressure palsy of the sixth nerve.

2.Sluggish pupillary reflexes and unilateral mydriasis may occur due to pressure on the 3rd nerve.

3.Bitemporal hemianopia: It results from downward pressure of the distended third ventricle on the chiasma.

4.Homonymous hemianopia: It may result from occipital herniation through the tentorium cerebelli with compression of the posterior cerebral artery.

III. Focal signs of intracranial mass lesions. These depend upon the site of the lesion. Focal signs of ophthalmological interest are as follows:

1.Prefrontal tumours, particularly meningioma of the olfactory groove, are associated with a pressure atrophy of the optic nerve on the side of lesion and papilloedema on the other side due to raised intracranial pressure (Foster-Kennedy syndrome).

2.Temporal lobe tumours. These may produce incongruous crossed upper quadrantanopia due to pressure on the optic radiations. Visual hallucinations may occur owing to irritation of the visuo-psychic area. Third and fifth cranial nerves may be involved due to downward pressure. Impairment of convergence and of superior conjugate movements may occur in late stages due to prolapse of the uncus through the tentorium cerebelli into the posterior fossa, with resulting distortion of the ventral part of midbrain.