TRIPASS XR تري باس

 and the patient’s own nose (intention or hunting tremor). The

movement may be slow, disjointed and clumsy (dyssynergia). The

heel-to-shin test is the equivalent test for the legs. It is abnormal

if the heel wavers away from the line of the shin. Weakness may

produce false-positive finger-to-nose or heel-to-shin tests, so

demonstrate that power is normal first.

Dysdiadochokinesis (impairment of rapid alternating movements)

is evident as slowness, disorganisation and irregularity of

movement. Dysarthria and nystagmus also occur with cerebellar

disease. Much less reliable signs of cerebellar disease include

the rebound phenomenon (when the displaced outstretched

arm may fly up past the original position), pendular reflexes

and hypotonia.

In disorders predominantly affecting midline cerebellar

structures, such as tumours of the vermis and alcoholic cerebellar

damage, the tests described may be normal and truncal ataxia

(that is, ataxic gait) may be the only finding. In the most severe

cases this may mean that the patient cannot sit unsupported.

Cerebellar dysfunction occurs in many conditions, and the

differential diagnosis varies with age and speed of presentation.

Apraxia

Apraxia, or dyspraxia, is difficulty or inability to perform a task,

despite no sensory or motor abnormalities. It is a sign of higher

cortical dysfunction, usually localising to the non-dominant frontal

or parietal lobes.

Fig. 7.23 Performing the heel-to-shin test with the right leg.

A

1

1

2

2

B

Fig. 7.22 Finger-to-nose test. A Ask the patient to touch the tip of their nose (1) and then your finger (2). B Move your finger from one position to

another, towards and away from the patient (1), as well as from side to side (2).

Sensory system • 143

7

the patient means lack of sensation rather than weakness or

clumsiness. Neuropathic pain (pain due to disease or dysfunction

of the PNS or CNS) is often severe and refractory to simple

analgesia. Reduced ability to feel pain may be accompanied by

scars from injuries or burns (trophic injuries). Sensory symptoms

are defined as follows:

• paraesthesia: tingling, or pins and needles

• dysaesthesia: unpleasant paraesthesia

• hypoaesthesia: reduced sensation to a normal stimulus

• analgesia: numbness or loss of sensation

• hyperaesthesia: increased sensitivity to a stimulus

• allodynia: painful sensation resulting from a non-painful

stimulus

• hyperalgesia: increased sensitivity to a painful stimulus.

Examination sequence

The aim here is to focus the examination. Look for a sensory

level if the history and examination suggest spinal cord

pathology; a glove and stocking pattern usually starting

distally, caused by a peripheral neuropathy; or sensory

disturbance in a specific nerve territory or dermatome. Be

guided by the history and the examination findings from the

motor system and reflexes. It is useful to ask the patient to

map out their area(s) of sensory disturbance if they can.

Light touch

• While the patient looks away or closes their eyes, use a

wisp of cotton wool (or lightly apply your finger) and ask

the patient to say ‘yes’ to each touch.

• Time the stimuli irregularly and make a dabbing rather than

a stroking or tickling stimulus.

• Start distally in the feet and hands; work proximally for a

neuropathy or focus on a specific nerve distribution or

dermatome.

Superficial pain

• Use a fresh neurological pin, such as a Neurotip, not a

hypodermic needle. Dispose of the pin after each patient.

• Explain and demonstrate (on an area of skin not affected

by the lesion, such as the sternum) that the ability to feel a

sharp pinprick is being tested.

• Map out the boundaries of any area of reduced, absent or

increased sensation. Move from reduced to higher

sensibility: that is, from hypoaesthesia to normal, or normal

to hyperaesthesia.

Temperature

• Touch the patient with a cold metallic object, such as a

tuning fork, and ask if it feels cold. More sensitive

assessment requires tubes of hot and cold water at

controlled temperatures but this is seldom performed.

Vibration

Note that ankle oedema may affect perception. Strike the

tuning fork on your own palm; an average healthy person

should be able to detect the vibration this causes for over 10

seconds.

• Place a vibrating 128-Hz tuning fork over the patient’s

sternum.

• Ask the patient, ‘Do you feel it buzzing?’

• Place the fork on the patient’s big toe. If vibration is not

felt, then move it proximally to the medial malleolus; if this

is not perceived, move to the patella, then the anterior iliac

spine, lower chest wall or clavicle. Repeat on the other

(dorsal) columns of the spinal cord. Pain and temperature

sensation are carried by small, slow-conducting fibres of the

peripheral nerves and the spinothalamic tract of the spinal cord.

The posterior column remains ipsilateral from the point of entry

up to the medulla, but most pain and temperature fibres cross to

the contralateral spinothalamic tract within one or two segments

of entry to the spinal cord. All sensory fibres relay in the thalamus

before sending information to the sensory cortex in the parietal

lobe (Fig. 7.24).

Common presenting symptoms

Sensory symptoms are common and it is important to discern

what the patient is describing. Clarify that, by ‘numbness’,

Medial lemniscus

and spinothalamic

tract

Medial lemniscus

Spinothalamic tract

Spinothalamic tract

Lentiform

nucleus

Thalamus

Pain

Temperature

1/2 touch

Vibration

Position

1/2 touch

Posterior columns

(no relay)

Nucleus gracilis

Nucleus cuneatus

V nerve sensory

nucleus

Internal capsule

Caudate nucleus

Cerebral hemisphere

A

B

C T L S

Pons

Medulla

Spinal cord

Fig. 7.24 The sensory system. A Main sensory pathways.

B Spinothalamic tract: layering of the spinothalamic tract in the cervical

region. C represents fibres from cervical segments, which lie centrally;

fibres from thoracic, lumbar and sacral segments (labelled T, L and S,

respectively) lie progressively more laterally.

144 • The nervous system

Sensory inattention

• Only test if sensory pathways are otherwise intact.

• Ask the patient to close their eyes.

• Touch their arms/legs in turn and ask which side has been

touched.

• Now touch both sides simultaneously and ask

whether the left side, right side or both sides were

touched.

Sensory modalities

In addition to the modalities conveyed in the principal ascending

pathways (touch, pain, temperature, vibration and joint position

sense), sensory examination includes tests of discriminative

aspects of sensation, which may be impaired by lesions of the

sensory cortex. Assess these cortical sensory functions only if

the main pathway sensations are intact. Consider abnormalities

on sensory testing according to whether the lesion (or lesions)

is in the peripheral nerve(s), dorsal root(s) or spinal cord, or is

intracranial.

Peripheral nerve and dorsal root

Many diseases affect peripheral nerves, generally resulting

in peripheral neuropathies or polyneuropathies. Peripheral

neuropathies tend to affect the lower limbs, first starting in the

toes. In these length-dependent neuropathies the upper limbs may

become involved once the symptoms extend above the knees.

Symptoms first affecting the upper limbs suggest a demyelinating

rather than axonal neuropathy or a disease process in the nerve

roots or spinal cord. In many cases, touch and pinprick sensation

are lost in a ‘stocking-and-glove’ distribution (Fig. 7.25A). There

side. Record the level at which vibration is detected by the

patient.

• Repeat the process in the upper limb. Start at the distal

interphalangeal joint of the forefinger; if sensation is

impaired, proceed proximally to the metacarpophalangeal

joints, wrist, elbow, shoulder and finally clavicle.

• If in doubt as to the accuracy of the response, ask the

patient to close their eyes and to report when you stop

the fork vibrating with your fingers.

Joint position sense (proprioception)

• With the patient’s eyes open, demonstrate the

procedure.

• Lightly hold the distal phalanx of the patient’s great toe at

the sides. Tell the patient you are going to move their toe

up or down, demonstrating as you do so.

• Ask the patient to close their eyes and to identify the

direction of small movements in random order.

• If perception is impaired, move to more proximal joints –

ankle, knees and hips. Repeat for the other side.

• Repeat for the upper limbs. Start with movements at the

distal interphalangeal joint of the index finger; if the

movements are not accurately felt, move to the first

metacarpophalangeal joint, wrist, elbow and finally

shoulder.

Stereognosis and graphaesthesia

• Ask the patient to close their eyes.

• Place a familiar object, such as a coin or key, in their hand

and ask them to identify it (stereognosis).

• Use the blunt end of a pencil or orange stick and trace

letters or digits on the patient’s palm. Ask the patient to

identify the figure (graphaesthesia).

Distribution

of sensory

impairment

A B

Light touch causes

exquisite pain

(hyperpathia)

Impaired light touch

and vibration sense

Pyramidal weakness

Increased tendon reflexes in left

leg and extensor plantar response

Impaired pain and

temperature sense

Fig. 7.25 Patterns of sensory loss. A Length-dependent peripheral neuropathy. B Brown–Séquard syndrome. Note the distribution of corticospinal,

posterior column and lateral spinothalamic tract signs. The cord lesion is in the left half of the cord.

Sensory system • 145

7

T2

T1 T1

T2

T2

Fig. 7.26 Dermatomal and sensory peripheral map innervation. Points (shown in blue) for testing cutaneous sensation of the limbs. By applying

stimuli at the points marked, both the dermatomal and main peripheral nerve distributions are tested simultaneously. A Anterior view. B Posterior view.

may also be autonomic involvement, causing symptoms affecting

sweating, sphincter control and the cardiovascular system (such

as orthostatic hypotension). In mononeuritis multiplex, different

nerves in the upper and lower limbs can be affected in a stepwise

fashion.

In ‘large-fibre’ neuropathies, such as Guillain–Barré syndrome,

vibration and joint position sense may be disproportionately

affected (reduced vibration sense at the ankle may be normal in

people over 60 years). Patients may report staggering when they

close their eyes during hair washing or in the dark (Romberg’s

sign, p. 135). When joint position sense is affected in the arms,

pseudoathetosis may be demonstrated by asking the patient to

close their eyes and hold their hands outstretched; the fingers/arms

will make involuntary, slow, wandering movements, mimicking

athetosis. Interpretation of sensory signs requires knowledge of

the relevant anatomy of sensory nerves and dermatomes (Figs

7.26 and 7.27). In ‘small-fibre’ neuropathies, in which pain and

temperature sensation are mainly affected, the only finding may

be reduced pinprick and temperature sensation; there may also

be autonomic involvement. The most common causes worldwide

are diabetes mellitus and HIV infection.

Spinal cord

Traumatic and compressive spinal cord lesions cause loss or

impairment of sensation in a dermatomal distribution below the

level of the lesion. A zone of hyperaesthesia may be found in

the dermatomes immediately above the level of sensory loss.

Syringomyelia (a fluid-filled cavity within the spinal cord) can

result in a dissociated pattern of altered spinothalamic (pain

and temperature) sensation and motor function, with sparing

of dorsal column (touch and vibration) sensation.

When one-half of the spinal cord is damaged, the Brown–

Séquard syndrome may occur. This is characterised by ipsilateral

upper motor neurone weakness and loss of touch, vibration and

joint position sense, with contralateral loss of pain and temperature

(see Fig. 7.25B).

Intracranial lesions

Brainstem lesions are often vascular, and you must understand

the relevant anatomy to determine the site of the lesion. Lower

brainstem lesions may cause ipsilateral numbness on one side

146 • The nervous system

Examination sequence

• Look for wasting of the thenar eminence.

• Test thumb abduction with the patient’s hand held

palm up on a flat surface. Ask the patient to move their

thumb vertically against your resistance (abductor pollicis

brevis).

• Test opposition by asking the patient to touch their thumb

and ring finger together while you attempt to pull them

apart (opponens pollicis).

• Test for altered sensation over the hand involving the

thumb, index and middle fingers and the lateral half

of the ring finger – splitting of the ring finger (see

Fig. 7.27A).

• Tinel’s sign is elicited by tapping the distal wrist crease

with the tendon hammer, which may produce tingling in

the median nerve territory. Although often used, it has

poor sensitivity and specificity.

• Phalen’s test is forced flexion of the wrist for up to 60

seconds, to induce symptoms; it also has limited

sensitivity and specificity.

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

• Test for weakness of brachioradialis (elbow flexor) and the

extensors of the arm (triceps), wrist and fingers.

• Look for sensory loss over the dorsum of the hand (see

Fig. 7.27B) and loss of triceps tendon jerk.

Ulnar nerve

The ulnar nerve is most often affected at the elbow by external

compression as the nerve is exposed, 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.

of the face (V nerve nucleus) and contralateral body numbness

(spinothalamic tract).

Thalamic lesions may cause patchy sensory impairment on

the opposite side with unpleasant, poorly localised pain, often

of a burning quality.

Cortical parietal lobe lesions typically cause sensory inattention

but may also affect joint position sense, two-point discrimination,

stereognosis (tactile recognition) and localisation of point touch.

Two-point discrimination and touch localisation are not helpful

signs and tests are not performed routinely.

Peripheral nerves

Peripheral nerves may be damaged individually (mononeuropathy)

or multiply (peripheral neuropathy or mononeuritis multiplex).

Certain nerves (median nerve at the wrist, common peroneal

nerve at the knee) are particularly prone to compression.

Median nerve

The medial nerve may be compressed as it passes between the

flexor retinaculum and the carpal bones at the wrist (carpal tunnel

syndrome). This is the most common entrapment neuropathy

and initially produces sensory symptoms and pain in the hands,

occasionally radiating up the arm – typically at night. Carpal

tunnel syndrome occurs commonly during pregnancy (Box 7.11).

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

Fig. 7.27 Sensory and motor deficits in nerve lesions. A Median. B Radial. C Ulnar. D Common peroneal. E Lateral cutaneous of the thigh.

Investigations • 147

7

(for example, syncope versus seizure; see Box 7.2), and also

epidemiology (sudden-onset leg weakness 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 fitter).

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.

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-yearold 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 unexpected, and quite 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. 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 metabolic disturbance, including

diabetes); then work upwards. If imaging is required, decide

what to image using which modality (computed tomography,

MRI, ultrasound or functional imaging), and whether 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.

Lastly, the worlds of antibody-mediated and genetic diseases

are changing rapidly, and you may need to have a discussion with

the relevant experts about which specialised test might be most

appropriate.

Examination sequence

• 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

fingers 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,

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, which means 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.

Interpretation of the findings

Having completed the history and examination, first decide

whether the symptoms are due to neurological disease, a

functional neurological disorder or non-neurological causes. Try

to localise the lesion to a single area of the nervous system if

possible (Is the lesion in the CNS or PNS?) and then localise in

more detail (for example: 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 involve 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 depend on the history

148 • The nervous system

A B C

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.

C Unenhanced 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).

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.

A 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.

Investigations • 149

7

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.

Neurophysiological tests

Electroencephalography (EEG) records spontaneous electrical

activity of the brain, using scalp electrodes. It is employed in

OSCE example 1: Headache history

Miss Bolton, 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, 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 analgesia 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 migraine. She is otherwise well and takes no medication other than the oral

contraceptive. The examination is 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.

the investigation of epilepsy, encephalopathies or dementia.

Modifications to standard EEG improve sensitivity and include

sleep-deprived studies, prolonged videotelemetry and invasive

EEG monitoring.

Electromyography (EMG) involves needle electrodes inserted

into muscle. Electrical activity is displayed 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 and 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 is

distinguishing between axonal and demyelinating neuropathies,

the underlying causes and management of which are very

different.

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, 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.

Continued

150 • The nervous system

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 completeness of 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 limb

• Expose the upper limbs ensuring maintenance of dignity and privacy; request a chaperone if appropriate.

• Inspect for wasting, fasciculations.

• As a screening test ask the patient to hold the 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), thumb abduction

(median nerve, T1).

• Assess reflexes at biceps (C5), triceps (C7) and supinator (brachioradialis, C6).

• Test coordination with finger – nose test and look for dysdiodokinesia.

• 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.

OSCE example 2: Tremor – cont’d

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 the 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 unnecessary. In selected cases, structural imaging (MR or

CT) to rule out the rare mimics of PD, or functional imaging (DaTscan) may be appropriate. Blood tests are rarely helpful, but a strong family history

may precipitate consideration of genetic testing.

8

The visual system

Shyamanga Borooah

Naing Latt Tint

Anatomy and physiology 152

Eye 152

Extraocular muscles 152

Refractive elements of the eye 153

Visual pathway 153

Pupillary pathways 153

The history 155

Common presenting symptoms 155

Past ocular history 159

Past medical history 159

Drug and allergy history 159

Family history 159

Social history 159

The physical examination 160

General examination 160

Visual acuity 160

Orbit and periorbital examination 161

Pupils 161

Visual fields 162

Ocular alignment and eye movements 163

Ophthalmoscopy 164

Retinopathies 165

Investigations 165

OSCE example 1: Gradual visual loss 168

OSCE example 2: Double vision 169

Integrated examination sequence for ophthalmology 169

152 • The visual system

Eye

The eyeball is approximately 25 mm in length and comprises

three distinct layers. From outside in (Fig. 8.1), these are the:

• Outer fibrous layer: this includes the sclera and the clear

cornea. The cornea accounts for two-thirds of the

refractive power of the eye, focusing incident light on to

the retina.

• 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 the structure

responsible for converting light to neurological signals.

Extraocular muscles

The six extraocular muscles are responsible for eye movements

(Fig. 8.2). Cranial nerve III innervates the superior rectus, medial

rectus, 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

Anatomy and physiology

The eye is a complex structure situated in the bony orbit. It is

protected by the eyelid, which affords protection against injury

as well as helping to maintain the tear film. The upper lid is

elevated by the levator palpebrae superioris, innervated by cranial

nerve III, and Müller’s muscle, innervated by the sympathetic

autonomic system. Eyelid closure is mediated by the orbicularis

oculi muscle, innervated by cranial nerve VII.

The orbit also contains six extraocular muscles: the superior

rectus, medial rectus, lateral rectus, inferior rectus, superior

oblique and inferior oblique. In addition, the orbit houses the

lacrimal gland, blood vessels, autonomic nerve fibres and cranial

nerves II, III, IV and VI. The contents are cushioned by orbital

fat, which is enclosed anteriorly by the orbital septum and the

eyelids (Fig. 8.1).

The conjunctiva is a thin mucous membrane lining the posterior

aspects of the eyelids. It is reflected at the superior and inferior

fornices on to the surface of the globe. The conjunctiva is coated

in a tear film that protects and nourishes the ocular surface.

Retina

Fovea centralis

Central retina vein

Central retina artery

Optic nerve

Optic disc

Inferior rectus muscle

Superior rectus muscle

Levator palpebrae superioris muscle

Cornea

Orbicularis oculi muscle

Septum

Skin

Frontalis muscle

Orbital fat

Müller’s muscle Frontal sinus

Iris

Pupil

Sclera

Inferior oblique

Lens

Anterior chamber

Meibomian glands

Tarsal plate

Ciliary body

Vitreous body

Zonules

Ora serrata

Hyaloid canal

Fig. 8.1 Cross-section of the eye and orbit (sagittal view).

Right eye

Superior

rectus

Lateral

rectus

Lateral

rectus

Inferior

rectus

Inferior

rectus

Superior

oblique

Superior

oblique

Inferior

oblique

Inferior

oblique

Medial

rectus

Superior

rectus

Left eye

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. For

example, a patient whose diplopia is maximal on looking down and

to the right has either a weak right inferior rectus or a weak left

superior oblique muscle.