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164 • THE NERVOUS SYSTEM
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7.11 Common features of carpal tunnel syndrome
• It is more common in women.
• There is unpleasant tingling in the hand.
• It may not observe anatomical boundaries, radiating up the arm to the
shoulder.
• Weakness is uncommon; if it does occur, it affects thumb abduction.
• Symptoms are frequently present at night, waking the patient from
sleep.
• The patient may hang the hand and arm out of the bed for relief.
• There is thenar muscle wasting (in longstanding cases).
• It is commonly associated with pregnancy, diabetes and hypothyroidism.
Radial nerve
This may be compressed as it runs through the axilla, in the spiral
groove of the humerus (Saturday night palsy) or may be injured in
fractures of the humerus. It typically causes wrist drop.
Examination sequence (Video 16B)
• Test for weakness of brachioradialis (elbow flexor) and the
extensors of the arm (triceps). There will also be weakness of
wrist and finger extension.
• Look for sensory loss over the dorsum of the hand (see
Fig. 7.27B) and loss of triceps tendon jerk.
immobile patients or as a result of repetitive kneeling, squatting
or sitting with the legs crossed at the knees. It typically causes a
foot drop.
Examination sequence
• Test for weakness of ankle dorsiflexion and eversion; test for
extension of the big toe (extensor hallucis longus). Inversion
and the ankle reflex will be preserved.
• Test for sensory loss over the dorsum of the foot (see
Fig. 7.27D).
Lateral cutaneous nerve of the thigh
This purely sensory nerve may be compressed as it passes
under the inguinal ligament, producing paraesthesiae in the
lateral thigh (meralgia paraesthetica, ‘burning numbness’) (see
Fig. 7.27E).
Examination sequence
• Ask the patient to map out the area of disturbance.
• Test for disturbed sensation over the lateral aspect of the
thigh. Palpate the abdomen and groin for masses or inguinal
lymph nodes.
Ulnar nerve
The ulnar nerve is most often affected at the elbow by external
compression as the nerve is superficial in some individuals and
vulnerable to pressure, or by injury, as in elbow dislocation/
fracture. Compression usually occurs as the nerve passes
through the condylar groove behind the medial epicondyle of the
humerus or as it passes through the cubital tunnel.
Examination sequence (Video 16C)
• Examine the medial elbow, palpating the nerve in the ulnar
groove (the most common place of entrapment). Note any
scars or other signs of trauma.
• Look for wasting of the interossei (dorsal guttering).
• Test for weakness of finger abduction with the patient’s fin-
gers on a flat surface, and ask them to spread the fingers
against resistance from your fingers.
• Test adduction by asking them to grip a card placed between
their fingers and pulling it out using your own fingers.
• Assess for sensory loss on the ulnar side of the hand, splitting
the ring finger (see Fig. 7.27C).
Common peroneal nerve
The nerve may be damaged by fractures as it winds around the
fibular head, or it may be compressed, particularly in thin,
Interpretation of the findings
Having completed the history and examination, fi rst decide
whether the symptoms are due to neurological disea se, a
functional neurological disorder or non-ne urologic al causes,
remembering that many neurological symptoms (e.g. fasciculation, intermittent sensory disturbance, hypnic je rks) occur in
normal people. Try to l ocalise the lesion to a single area of th e
nervous system if possible (Is the lesion in the CNS or PNS?)
and then l ocalise in more detail (e.g. if the lesion is in the PNS,
is it in the root, nerves or neuromuscular junction muscle?).
Some conditions, like multiple sclerosis, may give rise to
multiple symptoms and signs because they involv e several
lesions; others, like migraine or functional disorders, do not
follow strict neurological and anatomical rules.
Having localised the lesion, consider the likely underlying
pathology (What is the lesion?). This will depe nd on t he history
(e.g. syncope versus seizure; see Box 7.2), and also epidemiology (sudden-onset leg weakn ess in a 72-year-old man
with diabetes and previous angina is unlikely to have the same
explanation as a new foot drop in a 20-year-old carpet fi tter).
Draw up a differential diagnosis and then consider which (if
any) investigations are pertinent. Sometimes during the summarising process, it may become clear that there are aspects
of the history that have not been adequately addressed. Go
back and resolve these areas. Time spent reviewing the history is never wasted; undertaking unnecessary tests, on the
other hand, is more than just a waste of time.
A
Investigations • 165
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Do not place undue emphasis on an isolated sign that fails to
fit with the history, such as an apparently isolated extensor
plantar response in a patient with typical migraine. It is more likely
that this is a false-positive sign due to an inept examination/
interpretation of a ticklish patient rather than an indication of
underlying pathology.
Investigations
Initial investigations
Not all patients require investigation. Most patients with headache,
for example, need no tests, but some do (such as a 75-year-old
man with new-onset headache and temporal tenderness on
examination, who should have urgent measurement of the
erythrocyte sedimentation rate and C-reactive protein and a
temporal artery biopsy). Unfortunately, the increasing availability of
tests means that many patients are investigated unnecessarily,
which creates new problems (such as what to do with the incidental finding of an unruptured intracranial aneurysm identified in a
patient with migraine). Avoid doing tests because you can or
because you do not know what else to do; further investigations
should be guided by the history and physical examination. Magnetic resonance imaging (MRI) of the brain may unearth incidental
findings of no clinical relevance in up to 20%, depending on age,
and there is an irony – usually lost on your patient – in attempting
reassurance with a scan only to identify an incidental ‘abnormality.’
Sometimes a single carefully chosen test is all that is necessary to
confirm a diagnosis. For example, a patient with chorea whose
father died of Huntington’s disease will almost certainly have the
diagnosis confirmed with genetic testing without the need for
imaging or other tests.
Consider your diagnosis and start with any necessary simple blood tests ( such as exclusion of metabo lic disturbance,
including diabetes); the n work upwards. If imaging is required,
decide what to image using which modality (computed tomography, MRI, ultrasound or functional imagi ng) and whet her
any special sequences or techniques are necessary (like
intravenous contrast; Figs 7.28– 7.30). Discuss the case with
the radiologists if you are unsure. For some PNS disorders,
nerve conduction studies and electromyography may be
helpful. Electroencephalography is perhaps the most misused
test in neurology. Think carefully about whether it will add
anything to what you already know; it should not be used to
diagnose epilepsy. The more invasive tests (lumbar puncture,
nerve/muscle/brain biopsy) all require careful consideration
and should be guided by specialists. Last ly, knowledge of
antibody-mediated and genetic diseases is evolving rapidly, so
you may need to have a discussion with the relevant experts
about which specialised test might be most appropriate.
Specific investigations
Lumbar puncture
Lumbar puncture is a key investigation in a number of acute and
chronic neurological conditions. Always measure the CSF
opening pressure (in a lying position, not sitting), using an
atraumatic (blunt) needle. CSF is routinely examined for cells,
protein content and glucose (compared to simultaneously taken
blood glucose); it is also stained and cultured for bacteria. Other
specific tests may be carried out, such as analysis for oligoclonal
bands, meningococcal and pneumococcal antigens, polymerase
chain reaction (PCR) for certain viruses or cytology for malignant
cells.
7
Fig. 7.28 Imaging of the head. A DaTscan showing uptake of tracer (dopamine receptors) in the basal ganglia on cross-section of the brain. B Magnetic
resonance scan showing ischaemic stroke. T2 imaging demonstrates bilateral occipital infarction and bilateral hemisphere lacunar infarction.
computed tomogram showing subarachnoid blood in both Sylvian fissures (white arrows) and early hydrocephalus. The temporal horns of the lateral ventricles are
visible (black arrows).
B C
C Unenhanced
A
166 • THE NERVOUS SYSTEM
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A B
C
Fig. 7.29 Imaging of the head. A Computed tomogram (CT) showing a cerebral abscess. B Magnetic resonance scan showing multiple sclerosis with white
demyelinating plaques.
C CT scan showing a large meningioma arising from the olfactory groove.
B
Fig. 7.30 T2 magnetic resonance images showing a large left paracentral L4–5 disc protrusion (arrowed) compressing the L5 nerve root. A
Sagittal section.
B Axial section.
Neurophysiological tests
Electroencephalography (EEG) records spontaneous electrical
activity of the brain, using scalp electrodes. It is employed in the
investigation of epilepsy, encephalopathies or dementia. Modifications to standard EEG improve sensitivity and include sleepdeprived studies, prolonged videotelemetry and invasive EEG
monitoring.
Electromyography (EMG) involves needle electrodes inserted
into muscle. Electrical activity is displa yed on an oscilloscope
and an audio monitor, allowing the neurophysiologist to see and
hear the pattern of activity. Neurogenic and myopathic pathology
causes characteristic EMG abnormalities.
Nerve conduction studies involve applying electrical stimuli
to nerves an d measuring the speed of impulse conduction.
They are used for both motor and sensory nerves, and are
helpful in diagnosing peripheral nerve disorders, such as nerve
compressions or polyneuropathies. They are also helpful in
distinguishing between axonal and demyelinating neuropathies, the underl ying causes and management of which are
very different.
Investigations • 167
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OSCE example 1: Headache history
Miss Das, 32 years old, presents acutely with a severe global headache, associated with vomiting and feeling dreadful.
Please take a history from this patient
Confirm:
• Onset – gradual or sudden
• Site – lateralised or global
• Severity
• Aggravating and relieving factors, such as bright light
• Associated symptoms, such as vomiting, photophobia, neck pain or visual disturbance
• Relevant family history.
Summarise your findings
This 32-year-old woman’s headache began gradually last night and is worse today; she has been in bed in a darkened room trying to sleep. She has vomited
the analgesic she took. She often has headaches at the time of her period, but this is the worst headache she has ever experienced. She recalls having one or
two migraines as a child, and her mother had migraines. She is otherwise well and takes no medication other than the oral contraceptive. The examinationis
normal, although she looks tired and distressed.
Suggest a differential diagnosis
The most likely diagnosis is migraine; the headache evolved and worsened over a few hours, with no ‘red flags,’ on a background of a predisposition to
migraine. The differential includes more sinister causes such as meningitis, cerebral venous sinus thrombosis or intracranial haemorrhage, but there are no
features to support these. The headache is likely to resolve in the next day or two.
Suggest initial investigations
She does not need any tests, as there are no features to suggest she needs brain imaging or lumbar puncture to exclude a subarachnoid haemorrhage or
meningitis.
7
OSCE example 2: Tremor
Mr Anderson, 76 years old, presents with a tremor of his arm.
Please examine his arms
• Introduce yourself and clean your hands.
• Observe the patient sitting at rest; note any tremor, abnormal postures, facial expression, jaw/chin tremor or drooling.
• Listen to his speech.
• Ask him to raise both arms above his head, then to stretch them out in front of him; observe any tremor on posture.
• Ask him to perform piano-playing movements; look carefully for asymmetry and reduced fine finger movements.
• Assess tone, looking specifically for asymmetry, and cog wheeling or lead pipe rigidity in the affected right arm.
• Test power in shoulder abduction, elbow flexion/extension and finger extension.
• Test upper limb deep tendon reflexes (biceps, supinator and triceps).
• Omit sensory testing, as this is unlikely to add anything.
• Test finger-to-nose movements.
• Ask him to walk, observing what happens to the tremor and right arm swing.
• Thank the patient and clean your hands.
Summarise your findings
The patient has an asymmetric pill-rolling rest tremor of the right arm, which briefly disappears on movement but quickly returns (re-emergent tremor). He
also has a tremor affecting the jaw/chin. There is a lack of facial expression; drooling; monotonous, hypophonic speech; bradykinesia (reduced fine finger
movements, difficulty with repetitive movements); increased tone with cog wheeling; and loss of right arm swing and increased tremor when walking, with
short stride length.
Suggest a diagnosis
These findings are typical of Parkinson’s disease.
Suggest initial investigations
A diagnosis of Parkinson’s disease is usually based on the clinical features, and investigation is unnecessary. In selected cases, structural imaging (MR or CT)
to rule out the rare mimics of Parkinson’s disease or functional imaging (DaTscan) may be appropriate. Blood tests are rarely helpful, but a strong family
history may precipitate consideration of genetic testing.
168 • THE NERVOUS SYSTEM
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Integrated examination sequence for the nervous system
A complete neurological examination is demanding for both doctor and patient and in many cases will not be necessary. The history will dictate a more
targeted examination, and time spent on the history is always more productive than an amateur neurological examination.
Cranial nerve examination
• Ask about sense of smell and taste (I).
• Assess visual acuity (using a Snellen chart) and visual fields (by confrontation) (II).
• Observe pupils and test pupillary reactions bilaterally: direct and consensual (II).
• Observe both eyes in the neutral position. Are they orthotropic (both pointing in the same direction)? Test eye movements, observing for completenessof
movement in pursuit and looking for nystagmus (III, IV, VI).
• Test facial sensation (V) and corneal reflex (V and VII).
• Observe for facial asymmetry and test facial muscles of the upper and lower parts of the face (VII).
• Perform a bedside test of hearing (VIII).
• Assess speech, swallow and palatal movement (IX, X, XI).
• Inspect the tongue and assess movement (XII).
Neurological examination of the upper limbs
• Expose the upper limbs, ensuring maintenance of dignity and privacy; request a chaperone if appropriate.
• Inspect for wasting, fasciculations, abnormal movements and contractures/other deformities.
• As a screening test, ask the patient to hold their arms out (palms up) and close their eyes. Watch for pronator drift.
• Assess tone.
• Test muscle power: shoulder abduction (axillary nerve C5), elbow flexion (musculocutaneous nerve, C5, C6) and extension (radial nerve, C7), finger
extension (posterior interosseus nerve, C7), index finger abduction (ulnar nerve, T1), little finger abduction (ulnar nerve, T1) and thumb abduction (median
nerve, T1).
• Assess reflexes at biceps (C5), triceps (C7) and supinator (brachioradialis, C6).
• Test coordination with finger-to-nose test and look for dysdiadokinesia.
• Test sensory modalities: pinprick, temperature, vibration sense, joint position sense.
Neurological examination of the lower limb
• Undress the patient to expose both lower limbs fully, ensuring maintenance of dignity and privacy; request a chaperone if appropriate.
• Carry out a general inspection, noting walking aids and other associated neurological signs, such as facial droop or ipsilateral arm flexion.
• If the patient is able to do so, ask them to stand and walk so that you can assess stance and gait. Assess tandem gait.
• Inspect both legs, noting any scars, muscle wasting or fasciculations, abnormal postures or movements.
• Assess tone at the hip, knee and ankle. Test for ankle clonus.
• Test muscle power. As a simple screen, assess hip flexion (iliofemoral nerve, L1, 2) and extension (sciatic, L5/S1), knee flexion (sciatic, S1) and extension
(femoral, L3, 4), and ankle plantar flexion (tibial, S1, 2) and dorsiflexion (deep peroneal, L4, 5).
• Assess reflexes at the knee (L3) and ankle (S1), comparing sides. Test the plantar response.
• Test coordination via heel-to-shin tests.
• Test sensory modalities: pinprick, temperature, vibration and joint position sense. Map out any symptomatic areas of disturbed sensation.
Shyamanga Borooah
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Naing Latt Tint
The visual system
8
Anatomy and physiology 170
Eye 170
Extraocular muscles 170
Refractive elements of the eye 171
Visual pathway 172
Pupillary pathways 172
Patient history 173
Common presenting symptoms 173
Past ocular history 178
Past medical history 178
Drug and allergy history 178
Family history 178
Social history 178
The physical examination 179
General examinati on 179
Visual acuity 179
Orbit and periorbital examination 180
Pupils 180
Visual fields 182
Ocular alignment and eye movements 183
Ophthalmoscopy 184
Retinopathies 186
Investigations 188
Ophthalmic examination and COVID-19 189
OSCE example 1: Gradual visual loss 191
OSCE example 2: Double vision 191
Integrated examination sequence for ophthalmology 192
170 • THE VISUAL SYSTEM
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Anatomy and physiology
The eye lies in the bony orbit of the skull and is covered by the
eyelid, which protects it from foreign bodies and keeps the
anterior surface moist by maintaining the tear film. The upper lid
is elevated by two muscles: the levator palpebrae superioris,
innervated by cranial nerve III; and Müller’s muscle, innervated by
sympathetic nerves. The orbicularis oculi muscle closes both
upper and lower eyelids and is innervated by cranial nerve VII.
The orbit also contains the six extraocular muscles responsible
for eye movement; the lacrimal gland; blood vessels; autonomic
nerve fibres; and cranial nerves II, III, IV and VI, cushioned by
orbital fat (Fig. 8.1).
The conjunctiva is a thin mucous membrane lining the inner
aspects of the eyelids and the anterior surface of the eyeball. It is
reflected at the superior and inferior fornices. The conjunctiva is
coated in a tear film that protects and nourishes the ocular
surface.
Eye
The eyeball is normally approximately 25 mm in diameter and
comprises three layers (see Fig. 8.1). These are:
• Outer fibrous layer: this includes the white sclera and the clear
cornea anteriorly.
• Middle vascular layer (uveal tract): anteriorly, this consists of
the ciliary body and the iris, and posteriorly, the choroid.
• Inner neurosensory layer (retina): the retina is a thin layered
structure responsible for transducing light to neurological
signals. There are two main types of photoreceptors: cones
function maximally under photopic (light) conditions and
enable colour vision while rods are primarily used in scotopic
(dark) conditions. Cones are concentrated at the centre of the
retina and are most highly concentrated at the centre of the
macula (the fovea). Photoreceptors transduce light into
neuronal signals that pass via bipolar cells and ganglion cells
to the nerve fibre layer of the inner retina before entering the
optic nerve.
Extraocular muscles
Six extraocular muscles are responsible for eye movement: (1)
the superi or rectus, (2) medial rectus, (3) latera l rectus, (4)
inferior rectus, (5) superior oblique and (6) inferior oblique. Each
muscle is responsible for a specific v ector of eye movement
(Fig. 8.2). They work together to move the eye in other
directions.
Cranial nerve III innervates th e sup eri or r ect us, me dia l re ctu s,
inferior oblique and inferior rectus muscles. Cranial nerve IV
innervates the superior oblique muscle, and cranial nerve VI
innervates the lateral rectus muscle. The cranial nerves originate in the midbrain and pons and pass through the cavernous
sinus (Fig. 8.3). Examining for eye movement deficits reveals
cranial nerve deficits. For instance, a complete loss of cranial
nerve III results in a loss of function of the superior rectus,
Skin
Frontalis muscle
Orbital fat
Septum
Ora serrata
Orbicularis oculi muscle
Zonules
Iris
Cornea
Pupil
Anterior chamber
Meibomian glands
Tarsal plate
Ciliary body
Sclera
Inferior oblique
Lens
Fig. 8.1 Cross-section of the eye and orbit (sagittal view).
Frontal sinusMüller’s muscle
Vitreous body
Hyaloid canal
Levator palpebrae superioris muscle
Superior rectus muscle
Retina
Fovea centralis
Central retina vein
Central retina artery
Optic nerve
Inferior rectus muscle
Optic disc
Anatomy and physiology • 171
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Lateral
rectus
Superior
rectus
Inferior
rectus
Right eye
Inferior
oblique
Superior
oblique
Medial
rectus
Inferior
oblique
Superior
oblique
Left eye
Superior
rectus
Inferior
rectus
Lateral
rectus
Fig. 8.2 Control of eye movements. The direction of displacement of the
pupil by normal contraction of a particular muscle can be used to work out
which eye muscle is paretic.
inferior oblique, medial rectus and inferior rectus. If cranial
nerves IV and VI are intact, the lateral rectus and the superior
rectus continue to pull the eye inferiorly and laterally. This gives
the classical ‘do wn and out ’ resting position of an eye with
cranial nerve III palsy.
Refractive elements of the eye
The major refractive elements of the eye are the tear film, cornea
and crystalline lens. The cornea accounts for approximately twothirds of the refractive power of the eye while the lens provides
additional controllable refraction, allowing light to focus onto the
retina at varying focal lengths. When light is precisely focused at
the retina, the eye is called emmetropic (Fig. 8.4A). When the
focus point falls behind the retina, the result is hypermetropia (see
Fig. 8.4B, long-sightedness). When the focal point is in front of the
retina, the result is myopia (see Fig. 8.4C, short-sightedness).
These refractive errors can be corrected with lenses or partially
corrected with a pinhole (see Fig. 8.4D).
Third ventricle Optic tracts
Anterior pituitary
A
B
C
D
Fig. 8.4 Normal and abnormal refraction by the cornea and lens. A
Emmetropia (normal refraction). Cornea and lens focus light on the retina.
B Hypermetropia (long-sightedness). The eye is t oo short and the image
focuses behind the retina. A convex (plus) lens focuses the image on the
C Myopia (short-sightedness). The eye is too long and the image
retina.
focuses in front of the retina. A concave (minus) lens focuses the image on
the retina.
D Myopia corrected using a pinhole, which allows only rays not
requiring refraction to pass to the retina.
Anterior cerebral arteries
8
Subarachnoid space
Arachnoid mater
Cavernous sinus
Fig. 8.3 Cavernous sinus (coronal view). Neuroanatomy of cranial nerves III, IV and VI.
Sphenoidal air sinuses
Internal carotid arteries
Oculomotor nerve
Trochlear nerve
Temporal
lobe
Ophthalmic division
of trigeminal nerve
Maxillary division
of trigeminal nerve
Dura mater
Abducens nerve
A
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Visual pathway
The visual pathway connects the eye to the brain and consists of
the retina, optic nerve, optic chiasm, optic tracts, lateral geniculate bodies, optic radiations and visual cortex. Deficits in the
visual pathway lead to specific field defects (Fig. 8.5).
Pupillary pathways
The pupil controls the amount of light entering the eye. The
intensity of light determines the pupillary aperture through autonomic reflexes. The parasympathetic pathway controlling pupillary constriction is shown in Fig. 8.6A; the sympathetic pathway
controlling pupillary dilatation is shown in Fig. 8.6B.
Fig. 8.5 Visual field defects. 1; Total loss of vision in one eye because of a lesion of the optic nerve. 2; Bitemporal hemianopia due to compression of the
optic chiasm.
3; Right homonymous hemianopia from a lesion of the optic tract. 4; Upper right quadrantanopia from a lesion of the lower fibres of the optic
radiation in the temporal lobe. 5; Lower quadrantanopia from a lesion of the upper fibres of the optic radiation in the anterior part of the parietal lobe. 6; Right
homonymous hemianopia with sparing of the macula due to a lesion of the optic radiation in the occipital lobe.
B
Light source
Short ciliary nerve
Ciliary ganglion
Optic nerve
III nerve
Edinger–Westphal nucleus
Lateral geniculate body
Posterior commissure
Midbrain
Superior
colliculus
Müller’s muscle
Pupil dilator
Long ciliary
Trigeminal nerve
Carotid plexus
Posterior
hypothalamus
First-order neuron
nerve
Fig. 8.6 Pupillary innervation. A Parasympathetic pathway. B Sympathetic pathway.
Internal carotid artery
Superior cervical ganglion
External carotid artery
Ciliospinal centre of Budge
(C8–T2)
Second-order neuron
A
Patient history • 173
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Patient history
To guide your ophthalmic history, remember the anatomy of the
eye. This will enable you to work from ‘front to back’ to include or
exclude differential diagnoses.
Common presenting symptom s
Start the ophthalmic history with open questions so the patient
can describe their symptoms in their own words. Use the patient’s description to inform more directed questions later.
Specificvisualsymptomspromptspecific sets of directed
questions. The most common symptoms are described
below.
Change in vision
Loss or reduced vision is the most common change. Patients
often describe blurred vision. Ocular disease is the most common cause of a change in vision. Any intraocular condition that
prevents light from activating retinal photoreceptors or the signal
from photoreceptors reaching the optic nerve can cause altered
vision. Rarely, damage to the extraocular visual pathway may
cause altered vision (see Fig. 8.5).
When patients present with a change in vision, ask:
• Was the onset of visual change sudden or gradual? Sudden
or gradual visual loss leads to specific differential diagnoses
(Box 8.1 and Fig. 8.7; Box 8.2 and Fig. 8.8). If sudden, then
enquire about possible causes (e.g. trauma, foreign body,
chemical injury).
• Does the vision change affect one or both eyes? Sudden onset
of bilateral change in vision suggests a post chiasmal cause.
• Is the change in vision associated with any additional features
(e.g. haloes, flashing lights, floaters, distortion, discharge, red
eye, pain)? Haloes are bright or rainbow-coloured rings seen
surrounding a light source. They occur when there is corneal
oedema and are most commonly associated with angleclosure glaucoma. Flashes and floaters result from a disturbance of the vitreous–retinal interface, most commonly due to
a posterior vitreous detachment. This usually occurs with age
as the vitreous degenerates, liquefies and peels away from the
retina, resulting in floaters. Detachment sometimes causes
retinal traction, resulting in flashing lights. More rarely, posterior
vitreous detachment causes a retinal tear (releasing cells seen
as floaters), which may progress to retinal detachment with
visual field loss. Distortion is most commonly seen in diseases
of the macula, such as age-related macular degeneration,
epiretinal membrane, vitreous traction on the retina or central
serous retinopathy.
• Does the change in vison affect part or whole of the visual
field? If part, which part? Specific types of visual field loss
may point to retinal disease, such as macular degeneration,
optic nerve disease such as glaucoma or visual pathway
defects (see Fig. 8.5).
Pain
Ask:
• Can you describe the nature of the pain?
• How severe is it?
• Did anything cause the pain?
8
D
Fig. 8.7 Common causes of an acute change in vision. A Central retinal vein occlusion. B Retinal detachment. Elevation of the retina around the
‘attached’ optic disc; the retina may even be visible on viewing the red reflex.
related macular degeneration. F Swollen optic nerve head in acute optic neuritis.
B
E
C Central retinal arterial occlusion. D Herpes simplex virus keratitis. E Wet age-
C
F
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