• Passively move each joint to be tested through as full

a range as possible, both slowly and quickly in all

anatomically possible directions. Be unpredictable with

these movements, in both direction and speed, to prevent

the patient actively moving with you; you want to assess

passive tone. It may be helpful to distract the patient

by asking them to count backwards from 20 while

assessing tone.

Upper limb

• Hold the patient’s hand as if shaking hands, using your

other hand to support their elbow. Assess tone at the

wrist and elbow with supination/pronation and flexion/

extension movements.

• Activation (or synkinesis) is a technique used to

exaggerate subtle increase in tone, and is particularly

useful for assessing extrapyramidal tone increase. Ask the

patient to describe circles in the air with the contralateral

limb while you assess tone. A transient increase in tone

with this manœuvre (Froment’s) is normal.

Lower limb

• Roll the leg from side to side and then briskly flip the knee

up into a flexed position, observing the movement of the

foot. Typically, the heel moves up the bed, but increased

tone may cause it to lift off the bed due to failure of

relaxation.

Ankle clonus

• Support the patient’s leg, with both the knee and the

ankle resting in 90-degree flexion.

• Briskly dorsiflex and partially evert the foot, sustaining the

pressure. Clonus is felt as repeated beats of dorsiflexion/

plantar flexion.

Myotonia

• Ask the patient to make a fist and then to relax and open

their hand; watch for the speed of relaxation.

• Using the tendon hammer, percuss the belly of the thenar

eminence; this may induce contraction of the muscles,

causing the thumb to adduct, and you may witness

dimpling of the muscle belly.

Hypotonia

Decreased tone may occur in lower motor neurone lesions

and is usually associated with muscle wasting, weakness and

hyporeflexia. It may also be a feature of cerebellar disease or

signal the early phases of cerebral or spinal shock, when the

paralysed limbs are atonic prior to developing spasticity. Reduced

tone can be difficult to elicit.

Hypertonia

Increased tone may occur in two main forms: spasticity and

rigidity.

Spasticity is velocity-dependent resistance to passive

movement: it is detected with quick movements and is a feature

of upper motor neurone lesions. It is usually accompanied by

weakness, hyper-reflexia, an extensor plantar response and

sometimes clonus. In mild forms it is detected as a ‘catch’ at

the beginning or end of passive movement. In severe cases

it limits the range of movement and may be associated with

contractures. In the upper limbs it may be more obvious

on attempted extension; in the legs it is more evident on

flexion.

Tremor

Tremor is an involuntary, oscillatory movement about a joint

or a group of joints, resulting from alternating contraction and

relaxation of muscles. Tremors are classified according to their

frequency, amplitude, position (at rest, on posture or movement)

and body part affected.

Physiological tremor is a fine (low-amplitude), fast (highfrequency, 3–30 Hz) postural tremor. A similar tremor occurs in

hyperthyroidism and with excess alcohol or caffeine intake, and

is a common adverse effect of beta-agonist bronchodilators.

Essential tremor is the most common pathological cause of

tremor; it is typically symmetrical in the upper limbs and may

involve the head and voice. The tremor is noted on posture and

with movement (kinetic). It may be improved by alcohol and often

demonstrates an autosomal dominant pattern of inheritance.

Parkinson’s disease causes a slow (3–7 Hz), coarse, ‘pill-rolling’

tremor, worse at rest but reduced with voluntary movement. It is

more common in the upper limbs, is usually asymmetrical and

does not affect the head, although it may involve the jaw/chin

and sometimes the legs.

Isolated head tremor is usually dystonic and may be associated

with abnormal neck postures such as torticollis, antecollis or

retrocollis.

Intention tremor is absent at rest but maximal on movement

and on approaching the target (hunting tremor), and is usually

due to cerebellar damage. It is assessed with the finger-to-nose

test (p. 141).

Other causes of tremor include hereditary or acquired

demyelinating neuropathies (such as Charcot–Marie–Tooth

disease) and are termed neuropathic tremors. Drugs commonly

causing tremor include sodium valproate, glucocorticoids and

lithium.

Movement disorders, including tremor, are common functional

symptoms. They are often inconsistent and distractible, with

varying frequencies and amplitudes, and may be associated

with other functional signs.

Other involuntary movements

These are classified according to their appearance.

Dystonia is caused by sustained muscle contractions, leading to

twisting, repetitive movements and sometimes tremor. It may be

focal (as in torticollis), segmental (affecting two or more adjacent

body parts) or generalised.

Chorea describes brief, jerky, random, purposeless movements

that may affect various body parts, commonly the arms.

Athetosis is a slower, writhing movement, more similar to

dystonia than chorea.

Ballism refers to violent flinging movements sometimes affecting

only one side of the body (hemiballismus).

Tics are repetitive, stereotyped movements that may be briefly

suppressed by the patient.

Tone

Tone is the resistance felt by the examiner when moving a joint

passively.

Examination sequence

• Ask the patient to lie supine on the examination couch

and to relax and ‘go floppy’. Enquire about any pain or

limitations of movement before proceeding.

138 • The nervous system

Examination sequence

• Do not test every muscle in most patients; the commonly

tested muscles are listed in Box 7.9.

• Ask about pain that might interfere with testing.

• Observe the patient getting up from a chair and walking.

• Test upper limb power with the patient sitting on the edge

of the couch. Test lower limb power with the patient

reclining.

• Ask the patient to lift their arms above their head.

• Ask them to ‘play the piano’. Check movements of the

fingers; asymmetric loss of fine finger movement may be a

very early sign of cortical or extrapyramidal disease.

• Observe the patient with their arms outstretched and

supinated (palms up) and their eyes closed for ‘pronator

drift’, when one arm starts to pronate.

7.8 Medical Research Council grading of muscle power

Grade Description

0 No muscle contraction visible

1 Flicker of contraction but no movement

2 Joint movement when effect of gravity eliminated

3 Movement against gravity but not against resistance

4a Movement against resistance but weaker than normal

5 Normal power

a

May be further classified as 4+ or 4−.

7.9 Nerve and muscle supplies of commonly tested movements

Movement Muscle Nerve and root

Shoulder abduction Deltoid Axillary C5

Elbow flexion Bicepsa Musculocutaneous C5a

/6

Brachioradialis (supinator reflex)a Radial C6a

Elbow extension Tricepsa Radial C7

Wrist extension Extensor carpi radialis longus Posterior interosseous C6

Finger extension Extensor digitorum communis Posterior interosseous C7

Finger flexion Flexor pollicis longus (thumb)

Flexor digitorum profundus (index and middle fingers)

Anterior interosseous C8

Flexor digitorum profundus (ring and little fingers) Ulnar C8

Finger abduction First dorsal interosseous Ulnar T1

Thumb abduction Abductor pollicis brevis Median T1

Hip flexion Iliopsoas Iliofemoral nerve L1/2

Hip extension Gluteus maximus Sciatic L5/S1

Knee flexion Hamstrings Sciatic S1

Knee extension Quadricepsa Femoral L3a

/4

Ankle dorsiflexion Tibialis anterior Deep peroneal L4/5

Ankle plantar flexion Gastrocnemius and soleusa Tibial S1a

/2

Great toe extension (dorsiflexion) Extensor hallucis longus Deep peroneal L5

Ankle eversion Peronei Superficial peroneal L5/S1

Ankle inversion Tibialis posterior Tibial nerve L4/5

a

Indicates nerve root innervation of commonly elicited deep tendon reflexes.

Rigidity is a sustained resistance throughout the range of

movement and is most easily detected when the limb is moved

slowly. In Parkinsonism this is classically described as ‘lead

pipe’ rigidity. In the presence of a Parkinsonian tremor there

may be a regular interruption to the movement, giving it a jerky

feel (‘cog wheeling’).

Clonus

Clonus is a rhythmic series of contractions evoked by a sudden

stretch of the muscle and tendon. Unsustained (<6 beats) clonus

may be physiological. When sustained, it indicates upper motor

neurone damage and is accompanied by spasticity. It is best

elicited at the ankle; knee (patella) clonus is rare and not routinely

tested.

Myotonia

Myotonia refers to the inability of muscles to relax normally and

characterises a group of neuromuscular disorders, the most

common of which is myotonic dystrophy. Patients may notice

difficulty in letting go of things with their hands, or a stiff gait.

Power

Strength varies with age, occupation and fitness. Grade muscle

power using the Medical Research Council (MRC) scale (Box

7.8). Record what patients can do in terms of daily activities;

for example, whether they can stand, walk and raise both arms

above their head. Lesions at different sites produce different

clinical patterns of weakness; examination will help discriminate

upper from lower motor neurone lesions.

Motor system • 139

7

weakness. This is helpful both diagnostically and therapeutically,

as you can show patients that their leg is not actually weak

using this sign.

Deep tendon reflexes

Anatomy

A tendon reflex is the involuntary contraction of a muscle in

response to stretch. It is mediated by a reflex arc consisting

of an afferent (sensory) and an efferent (motor) neurone with

one synapse between (a monosynaptic reflex). Muscle stretch

activates the muscle spindles, which send a burst of afferent

signals that lead to direct efferent impulses, causing muscle

contraction. These stretch reflex arcs are served by a particular

spinal cord segment that is modified by descending upper motor

neurones. The most important reflexes are the deep tendon

and plantar responses, whereas others, such as abdominal and

cremasteric reflexes, are rarely tested and of questionable value.

Dermatomal involvement may further help localise a lesion; for

example, pain going down one leg, with an absent ankle jerk

(S1) and sensory loss on the sole of the foot (S1 dermatome),