Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

scotomas). Compare subjective colour intensity in four quadrants whilst fixating your eye. Simultaneously holding two red pins either side of the vertical midline (in each eye separately) may help detect bitemporal red desaturation from pituitary tumours or a relative homonymous hemianopia.

7.Test the midperipheral and central field with the red target. ‘Tell me when you first see the red colour, rather than the pin, and tell me if it then disappears or the colour changes at any point.’ Move obliquely in each quadrant from periphery to fixation, equidistant between you and patient. Compare to your own monocular visual field. Look for scotomas.

8.Consider comparing the blind spot size with your own using the red target.

9.It is possible to ascertain the isopter to a small white target such as a 4 mm white hat pin. Failure to detect the white target indicates greater severity of loss than is revealed by the ‘red desaturation’ technique. Similarly, the white target can also be used to plot scotomas and the blind spot.

10.Test the fellow eye.

11.If any defect is detected, draw fields and arrange formal testing. Document the left eye visual field on the left side of the page; the right visual field on the right side of the page (opposite convention to VA).

12.For the interpretation of common field defects, see page 639.

■Colour vision.

Optic nerve damage can result in loss of colour saturation and poor colour discrimination before significant acuity loss is present. This is very helpful in determining the likely cause of visual loss (i.e. refractive, lenticular, retinal, optic nerve, postchiasmal) and is usually tested with Ishihara plates. The procedure is as follows:

1.Patients should wear reading correction if required.

2.Cover one eye and ask patient to read through the book. Allow 2 or 3 seconds per plate only.

3.Patients with VA better than 6/60 can usually complete the test, but do not proceed if they cannot see the first test plate. Test patients before examining them with bright lights

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History and examination

several minutes to recover after such examination. Patients who have had dilating drops can still perform the test but may need to use a +1.00 or +2.00 lens. Consider testing red desaturation instead if VA is very poor (see below).

4.Score the number of plates read out of 13, 17, or 21 depending on which book is used (1/17 or ‘control only’ if only the test plate was read). Record the reading distance and any refractive correction.

5.There are some plates which only some patients with congenital anomalous colour vision (Daltonism) will be able to read. Do not include these when testing for acquired visual loss unless the patient has Daltonsim.

6.Patients who cannot identify numerals (e.g. small children) can be asked to trace the outline of the numbers with their finger or trace the wiggly line across the page in the colour plates at the end of the book.

7.The Ishihara book comes with instructions on how to interpret performance on the missed plates in cases of Daltonism. The missed and misread numbers should be the same using each eye.

■Red desaturation.

Ask the patient to report any difference in the appearance of a red target viewed with each eye in turn.

■Cranial nerves.

I.Rarely formally tested; ask about sense of smell and if food tastes different.

II. Test VA, pupil reactions, visual field and colour vision. III, IV, VI. See eye movements examination (p. 585).

V. Warn the patient then test corneal sensation by lightly touching a wisp of cotton-wool on the peripheral cornea. Sensation may be decreased in contact lens wearers, recurrent herpetic keratitis, or if anaesthetic drops have been instilled to check IOP. Check skin sensation to light touch and pin prick on the face. Ask the patent to clench the teeth together and feel for contraction of the masseter muscles. Ask the patient to open the mouth against the resistance of your hand and look for jaw deviation towards the weaker side.

fingers, raise eyebrows (forehead wrinkling is spared in central/upper motor neurone lesions) and screw up eyes (assess Bell’s phenomenon). Look for loss or asymmetry of nasolabial folds. Assess for lagophthalmos and corneal exposure by asking the patient to close the eyes lightly.

VIII. Ask about hearing loss and vertigo. Cover one ear and whisper a number in the other for the patient to repeat. To test more formally, check that a 256 Hz or 512 Hz tuning fork held on the midline forehead (Weber’s test) is heard equally in both ears, and that air conduction persists after audible bone conduction (with the tuning fork held on mastoid) ceases (Rinné’s test).

IX, X. Ask the patient to open their mouth and say ‘Ahhh!’. Look for symmetrical elevation of the uvula, or deviation away from the affected side. Ask about any choking or problems swallowing. Test the gag reflex with an orange dressed stick if concerned.

XI. Ask the patient to lift both shoulders and press down to check power. Ask the patient to turn the chin towards one shoulder and press against this action with your palm. With the other hand, feel the muscle bulk of sternocleidomastoid.

XII. Observe the patient’s tongue when it is in their mouth for fasciculations or wasting. Ask the patient to stick out their tongue (deviates to the weaker side).

■Cerebellar tests.

1.Listen to the patient’s speech, which may be slurred or interrupted and staccato. Ask them to say ‘British constitution’ or ‘Baby hippopotamus.’

2.Dysdiadochokinesis: Ask the patient to place one hand palm down and then rapidly turn it palm up and palm down again, repeating this about 10 times. Compare with the other side. This is often a little asymmetrical in people who are strongly right or left handed.

3.Ask the patient to touch their nose and then touch your finger held about 50 cm in front of them, then to touch their nose again. Repeat this, moving your own finger further away to make the patient stretch to reach it. In

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History and examination

4.Examine gait, which in cerebellar disease will be broadbased. If uncertain, ask the patient to walk ‘heel-toe’ (as if on a tight rope), which will exaggerate minor degrees of gait ataxia.

5.If gait is unsteady, perform Romberg’s test of dorsal column function (proprioception). Ask the patient to stand still with feet together and eyes open. If the patient cannot do this, abandon the test. See how steady the patient is for 15 seconds then ask the patient to close their eyes. In cerebellar disease there should be little difference in balance whether the eyes are closed or open, whilst in dorsal column disease the patient will become more unsteady when the eyes are shut. Do not let the patient fall!

6.If the patient has binocular double vision, consider patching one eye for steps 3 to 5.

Investigations

Computed tomography (CT)

See page 75.

Magnetic Resonance Imaging (MRI)

Useful for imaging the anterior and posterior visual pathways (including optic nerve, chiasm, optic tracts, optic radiation and visual cortex), brain, soft tissue or vascular masses, and nonorganic, nonmetallic foreign bodies (FB). Does not show bone or calcium well. More expensive and less readily available than CT, and less useful for some orbital disease. Contraindications include a pacemaker and possible metal FB. Patients with clipped intracranial aneurysms need documentation to show that their clip is not ferromagnetic.

■Commonly used sequences:

a.T1 image : best for structural definition of anatomy. Water (vitreous and CSF) appears black (hypointense), fat is hyperintense, which degrades orbital images (Fig. 14.1).

b.T2 image : best for identifying diseased tissue. Water appears white, so pathological oedema shows as a high signal; fat is also hyperintense (Fig. 14.2).

c.Fat suppression : Suppression of high signal from orbital fat allows clear definition of the optic nerve and extraocular muscles (Fig. 14.3).

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plaques. Contrast enhancement can be seen on T1 weighted images but not on T2 weighted images.

■Common examples:

a.Optic nerve disease : judge size on coronal sections. Acute

optic neuritis shows high signal on T2 imaging and gadolinium enhancement. The acute phase, anterior ischaemic optic neuropathy shows no abnormality. Both will show high signal chronically due to Wallerian degeneration.

b.Vascular imaging : blood flow produces a ‘flow void’ on MRI, appearing as low signal in most of the above sequences. Lack of flow void implies complete or partial

occlusion. Consider axial T2 cuts to look for dural sinus thrombosis or carotid artery dissection. MR angiography (MRA): can confirm blood flow without contrast injection, but may fail to detect very slow flow. MRA excludes

clinically significant intracranial arterial aneurysms of

>3 mm but has not yet completely replaced intra-arterial angiography, e.g. in acute, painful 3rd nerve palsy with pupillary involvement. CT angiography and MR venography are also available.

c.Stroke : early (within 1–8 days) CT excludes clinically significant haemorrhage and allows early aspirin use. CT may be normal for the first 24 hours after a nonhaemorrhagic cerebral infarct. MRI may not detect acute intracerebral haemorrhage but is more sensitive for diagnosing small infarcts such as brainstem lesions. Diffusion weighted images (DWI) on MRI and FLAIR imaging are the most sensitive way of detecting early ischaemic CVAs.

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Anisocoria

Anisocoria

History Ask who first noticed the anisocoria (difference in pupil size) and attempt to establish the duration. Review of old photos such as a bus pass may help. Magnification may be required to assess pupil size. Exclude a history of neck or chest surgery/ injury, limb weakness, difficulty focusing, diplopia, and ptosis.

Examination Identify which pupil is abnormal by examining first in the dark then in the light. Greater anisocoria in the dark indicates impaired dilatation (sympathetic dysfunction): greater anisocoria in the light indicates impaired constriction (parasympathetic dysfunction). Physiological anisocoria is usually ≤2 mm and the difference is the same at all light levels. Examine the pupils (p. 623) and the iris on the slit lamp.

Differential diagnosis of an abnormally large pupil Consider Adie’s pupil (below), 3rd nerve palsy, dilating drops, traumatic mydriasis, iris rubeosis, Urrets-Zavalia syndrome (iris atrophy following corneal graft), and physiological anisocoria.

■Adie’s tonic pupil (Holmes-Adie pupil) : Presumed postviral denervation of the sphincter pupillae and ciliary muscle produces anisocoria and difficulty focusing. Owing to reinervation, accommodation recovers in a few weeks but the sphincter pupillae becomes partially innervated by lens fibres. Signs thereafter include light-near dissociation (slow or absent constriction to light but prompt constriction on attempted near vision), segmental sphincter palsy on slit lamp examination which gives rise to so-called vermiform movements of the iris, and absent limb reflexes. Slow dilation following accommodation (tonic constriction) differentiates it from Argyll Robertson pupils. Exclude ptosis and diplopia (3rd nerve palsy). Whereas normal pupils do not usually constrict to G. pilocarpine 0.125%, Adie’s pupil does (denervation hypersensitivity), but this test has only moderate specificity, as preganglionic lesions do likewise. Further investigations are not normally required. Arrange routine referral to a neuroophthalmologist. Long-term follow-up is not required. It is often bilateral but asymmetric. The affected pupils eventually become small.

Differential diagnosis of an abnormally small pupil Consider Horner’s syndrome (below), pilocarpine drops, uveitis/posterior synechiae, chronic unilateral aphakia, and physiological anisocoria.