Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

Transient visual loss

Transient Visual Loss

Background Transient visual loss has numerous causes. A careful history is crucial.

History Ask about: duration; whether one or both eyes are affected; total blackness (arterial occlusion) or just blurred; patchy grey blobs (spasm of choroidal vessels); cardiovascular risk factors; TIAs or strokes; known carotid disease; headache; migrainous aura; dizziness, hearing, or speech problems; loss of balance; haloes; eye pain; abnormal clotting (DVTs); scalp tenderness; jaw claudication (over 50 years). Specific precipitants may suggest the diagnosis:

■Bright light: chronic retinal ischaemia due to carotid insufficiency.

■Eye movements : space occupying orbital lesions or optic nerve tumour.

■Prolonged reading or evening onset : intermittent angle closure glaucoma.

■Exercise : pigment dispersion syndrome.

■Standing up : usually indicates reduced perfusion pressure including postural hypotension, carotid insufficiency, and giant cell arteritis (precedes nerve infarction). Papilloedema may produce brief monocular or bilateral obscurations with either standing up or stooping down.

Examination Check BP in both arms (sitting and standing if appropriate); radial pulse; cardiac and carotid auscultation; temporal artery palpation (in patients over 50 years); VA; confrontation visual fields; colour vision; RAPD; corneal clarity (oedema or endothelial pigment); iris rubeosis; gonioscopy (is angle closeable?); IOP; dilated fundoscopy (especially retinal vessels for emboli, venous dilation, retinal haemorrhages and optic disc for swelling); assess central retinal artery perfusion pressure (p. 483); other tests as indicated.

Differential diagnosis See Table 14.1.

■The following are the more common or serious causes:

1.Carotid or cardiac emboli: see below.

2.Carotid dissection: may have neck pain and Horner’s syndrome.

3.Migraine: usually hemianopic, positive features, with zig-

Table 14.1: Causes of transient visual loss

Patients often incorrectly describe hemianopic visual loss as being loss from one eye only.

4.Giant cell arteritis: see page 655.

5.Vertebrobasilar ischaemia: page 673.

6.Intermittent angle closure glaucoma: page 325.

■Also consider:

7.Occipital embolus: may cause hemianopic loss or transient blindness.

8.Retinal arterial embolus: typically, a curtain descent to a blackout.

9.Retinal vasospasm: more likely a whiteout.

10.Choroidal vasospasm: vision disappears in patches.

11.Cardiac dysrhythmia: blindness may precede loss of consciousness or occur in isolation.

12.Occipital epilepsy: usually hemianopic with positive symptoms such as coloured circles.

Management Investigation and treatment depends on the likely cause. In the case of transient monocular blindness, emboli usually arise from the aorta, carotids, or heart valves. Most commonly, they are cholesterol, platelet-fibrin, or calcific, but septic, amniotic fluid, air, fat or talc (i.v. drug users) may rarely occur in specific situations. If likely, start oral aspirin 75 mg o.d.

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and check BP, FBC, ESR, glucose, and lipids as a minimum. Arrange carotid Doppler and echocardiogram and refer to a stroke physician. Warn patients that intervention may be indicated if investigations reveal internal carotid artery stenosis or valvular heart disease. A statin is likely to be indicated. In the case of posterior circulation transient blindness, or transient hemianopia, a cardiac source is more likely and atrial fibrillation or a paroxysmal dysrhythmia must be considered.

Nystagmus

Background Nystagmus is a rhythmic, often rapid, involuntary eye movement. If a patient is unaware of oscillopsia (visual field appearing to move) then nystagmus is probably congenital. This includes most causes of pendular nystagmus due to low vision (e.g. albinism, Leber’s congenital amaurosis) and congenital motor nystagmus. The latter is usually horizontal in all directions of gaze, uniplanar, and often accompanied by an abnormal head posture to achieve best vision, usually with a head turn to match gaze direction to the null position of the nystagmus (the eye position that minimizes the nystagmus).

Examination Observe and document whether the nystagmus is pendular or jerk. Document whether vertical or horizontal and the direction of the fast phase. Is it present in primary position? The magnification provided by the direct ophthalmoscope can be used to observe low-amplitude nystagmus in the primary position. Is it always horizontal and uniplanar with a null point (e.g. congenital motor nystagmus)? Is the direction of the fast phase always in the direction of gaze (gaze evoked) or not (vestibular, congenital). Is there a torsional component? Examine the eyes in primary position for several minutes. Does the nystagmus change direction in a regular cycle (periodic alternating nystagmus)? Look for the following patterns.

Gaze evoked nystagmus Jerk nystagmus occurs in the same direction as the patient’s gaze, but is absent in the primary position. Seen in cerebellar and brainstem disease and with some drugs (anticonvulsants, sedatives). A few beats of nystagmus at the extremes of gaze may be normal.

Acquired pendular nystagmus May occur with severe visual loss, brainstem strokes, and MS. Consider gabapentin (100 mg t.d.s. increasing slowly to 300 mg t.d.s.) or baclofen

(5 mg daily increasing to a maximum of 10 mg t.d.s.).

Downbeat nystagmus Often most obvious on downward and lateral gaze, the direction of the fast phase is downwards. Seen with Arnold-Chiari malformations and cerebellar degenerations.

Upbeat nystagmus Seen with intrinsic brainstem disease. Upand downbeat nystagmus will be present in primary position and this distinguishes it from vertical gaze evoked nystagmus.

Convergence retraction nystagmus Test with an optokinetic (OKN) drum rotating the stripes downwards to induce attempted up saccades. This results in convergence and retraction

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rather than up saccades and is typically seen in Parinaud’s syndrome, also called dorsal midbrain syndrome: causes include pinealoma, head trauma, arteriovenous malformation, MS, and basilar artery CVA. Parinaud’s syndrome may have light-near dissociation of pupils, lid retraction, and spasm/paresis of convergence/accommodation. It is not a true nystagmus.

See–saw nystagmus One eye elevates and intorts whilst the other depresses and extorts then vice versa. Occurs with suprasellar lesions. May have a fast phase or be a variant of pendular nystagmus.

Periodic alternating nystagmus Horizontal jerk nystagmus that changes direction every few minutes. May be congenital or occur in a variety of vestibulocerebellar diseases and occasionally following severe bilateral visual loss. Consider gabapentin (100 mg t.d.s. increasing slowly to 300 mg t.d.s.) or baclofen (5 mg daily increasing to a maximum of 10 mg t.d.s.). Try baclofen first.

Peripheral vestibular nystagmus Unidirectional, uniplanar with a torsional element, and greatest amplitude with gaze in the direction of the fast component. Associated with paroxysmal vertigo, tinnitus, and hearing loss. Occurs in acute labyrinthitis, Menière’s disease, and benign positional vertigo.

Central vestibular nystagmus Chronic jerk nystagmus, unior bidirectional, that varies with the direction of gaze. Often but not always torsional. Pure torsional nystagmus is of central vestibular origin. Vertigo, deafness, and tinnitus are less of a feature than in peripheral vestibular nystagmus. Caused by a variety of brain stem diseases, e.g. MS, CVA, tumour.

Visual Field Defects

Background The accurate delineation of visual field defects is critical to the diagnosis of visual pathway lesions. Visual field defects are frequently asymptomatic and may be detected on routine screening (usually by an optometrist) or when field tests are preformed for some other reason. An awareness of the various artefactually produced field defects is important.

Symptoms Patients are less likely to notice field defects from optic nerve or visual pathway lesions if these spare the central field. Retinal lesions often produce positive scotomas with patients aware of photopsia within the visual field defect.

History Ask when and how the field defect was first noticed. Sudden onset or gradual? Any recovery? Ask about cardiovascular risk factors, photopsia, pain, headache and other neurological symptoms, and symptoms of pituitary disease (amenorrhoea, hypothyroidism, loss of libido, headache, and acromegaly).

Examination Check BP, cranial nerves, VA, colour vision, RAPD, formal fields, eye movements, IOP, assess angle, and dilated fundoscopy. Exclude ptosis, and disc cupping, pallor, or swelling. Many field defects are relative, and not absolute.

Differential diagnosis Abnormal visual fields may be caused by retinal pathology (e.g. retinal detachment or vein occlusion). Cataract may cause a globally decreased field but not focal defects. A homonymous hemianopia should not cause a decreased VA. Glaucoma can cause a range of field defects but confirm that the field defect corresponds to the sectoral neuroretinal rim thinning; colour vision is relatively well preserved until late in the disease, unlike optic nerve disease.

■Left homonymous hemianopia (Fig. 14.4): consider a right postchiasmal lesion such as occipital lobe CVA or tumour. The more congruous the field defect, the nearer to the occipital lobe, but a large lesion affecting both temporal and parietal lobes (the entire optic radiation) could also cause this.

■Left superior homonymous quadrantanopia (Fig. 14.5): probably right inferior occipital cortex but consider right temporal lobe lesion. Inferior homonymous quadrantanopia may be caused by a parietal lobe lesion. The defect may be relative or absolute. The vertical meridian will be absolutely respected but usually not the horizontal meridian.

■Bitemporal superior quadrantanopia (Fig. 14.6): typically caused by pituitary tumours but will be relative; the defect will

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Fig. 14.4: Left homonymous hemianopia.

Fig. 14.5: Left superior homonymous quadrantanopia.

Fig. 14.6: Bitemporal superior quadrantanopia.

Fig. 14.7: Complete bitemporal hemianopia.

Fig. 14.8: Central scotoma.

■Complete bitemporal hemianopia (Fig. 14.7): may occur with compressive lesions of the chiasm but such a clear-cut deficit is typically only seen in cases of traumatic chiasmal transection.

■Central scotoma (Fig. 14.8): the commonest cause is agerelated macular degeneration. In the case of optic nerve disease, such a symmetrical picture is more likely to be toxic, nutritional, or an inherited condition. Cone dystrophy can produce a similar picture.

■Superior altitudinal heminaopia in the left eye (Fig. 14.9): typically seen with nonarteritic anterior ischaemic optic neuropathy but also normal pressure glaucoma (usually bilateral and with arcuate defects in the lower field also), hemicentral vein occlusion, branch retinal artery occlusion, ptosis (less severe), sector panretinal photocoagulation (PRP) laser, and inferior retinal detachment.

■Concentric peripheral field loss (Fig. 14.10): may be seen in retinitis pigmentosa, chronic atrophic papilloedema (e.g.

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Fig. 14.9: Superior altitudinal heminaopia in the left eye.

Fig. 14.10: Concentric peripheral field loss.

PRP, central retinal artery occlusion with cilioretinal artery sparing (usually unilateral), optic neuropathies, and in vigabatrin toxicity.

Investigations Most afferent visual system deficits affect the central 10º of the visual field. A Humphrey 24–2 threshold field is therefore suitable for most indications, including subtle chiasmal lesions. Review the reliability indices (p. 284). Goldmann kinetic perimetry (Fig. 14.11) may be preferable for medically unexplained visual loss (p. 677), patients who cannot adequately perform a Humphrey test, and conditions such as idiopathic intracranial hypertension and vigabatrin-associated visual field loss where peripheral loss may be outside the area tested by a Humphrey. Goldmann field tests are also useful for patients with very large central scotomas (e.g. severe optic neuritis) who may see nothing on a Humphrey. The remaining peripheral field can still be used to assess progression or improvement of the condition in such patients.