Fig. 7.16 Basal ganglia. A Anatomical location. B Coronal view.

7.7 Common gait abnormalities

Gait disturbance Description Causes

Parkinsonian Stooped posture

Shuffling (reduced

stride length)

Loss of arm swing

Postural instability

Freezing

Parkinson’s disease

and other Parkinsonian

syndromes

Gait apraxia Small, shuffling steps

(marche à petits pas)

Difficulty in starting to

walk/freezing

Better ‘cycling’ on bed

than walking

Cerebrovascular

disease

Hydrocephalus

Spastic Stiff ‘walking-throughmud’ or scissors gait

Spinal cord lesions

Myopathic Waddling (proximal

weakness)

Bilateral

Trendelenburg signs

Muscular dystrophies

and acquired

myopathies

Foot drop Foot slapping Neuropathies

Common peroneal

nerve palsy

L5 radiculopathy

Central ataxia Wide-based, ‘drunken’

Tandem gait poor

Cerebellar disease

Sensory ataxia Wide-based

Positive Romberg sign

Neuropathies

Spinal cord disorders

Functional Variable, often bizarre,

inconsistent

Knees flexed, buckling

Dragging immobile leg

behind

Functional neurological

disorders

© Crown Copyright.

136 • The nervous system

such as professional sports players, may have physiological

muscle hypertrophy. Pseudohypertrophy may occur in muscular

dystrophy but the muscles are weak.

Fasciculation

Fasciculations are visible irregular twitches of resting muscles

caused by individual motor units firing spontaneously. This occurs

in lower motor neurone disease, usually in wasted muscles.

Fasciculation is seen, not felt, and you may need to observe

carefully for several minutes to be sure that it is not present.

Physiological (benign) fasciculation is common, especially in the

calves, but is not associated with weakness or wasting. Myokymia

– fine, involuntary fascicular contractions – involves rapid bursts

of repetitive motor unit activity that often affects orbicularis oculi

or the first dorsal interosseus, and is rarely pathological.

Abnormal movements

Myoclonic jerks

These are sudden, shock-like contractions of one or more muscles

that may be focal or diffuse and occur singly or repetitively.

Healthy people commonly experience these when falling asleep

(hypnic jerks). They may also occur pathologically in association

with epilepsy, diffuse brain damage and some neurodegenerative

disorders such as prion diseases. Negative myoclonus (asterixis)

is seen most commonly in liver disease (liver flap).

gait with bilateral Trendelenburg signs (see p. 259 and Fig. 13.37).

Bizarre gaits, such as when patients drag a leg behind them,

are often functional but some diseases, including Huntington’s

disease, produce unusual and chaotic gaits.

Inspection and palpation of the muscles

Examination sequence

• Completely expose the patient while maintaining their

comfort and dignity.

• Look for asymmetry, inspecting both proximally and

distally. Note deformities, such as flexion deformities or

pes cavus (high foot arches).

Inspect for wasting or hypertrophy, fasciculation and

involuntary movement.

Muscle bulk

Lower motor neurone lesions may cause muscle wasting. This

is not seen in acute upper motor neurone lesions, although

disuse atrophy may develop with longstanding lesions. A motor

neurone lesion in childhood may impair growth (causing a smaller

limb or hemiatrophy) or lead to limb deformity, such as pes

cavus. Muscle disorders usually result in proximal wasting (the

notable exception is myotonic dystrophy, in which it is distal,

often with temporalis wasting). People in certain occupations,

A Spastic hemiparesis

One arm held immobile and

 close to the side with elbow,

wrist and fingers flexed

Leg extended with plantar

flexion of the foot

On walking, the foot is

dragged, scraping the toe

in a circle (circumduction)

Caused by upper motor

neurone lesion, e.g. stroke

B Steppage gait

 Foot is dragged or lifted high

 and slapped on to the floor

 Unable to walk on the heels

 Caused by foot drop owing to

 lower motor neurone lesion

C Sensory or cerebellar ataxia

 Gait is unsteady and wide-

 based. Feet are thrown forward

 and outward and brought down

 on the heels

In sensory ataxia, patients watch

 the ground. With their eyes

 closed, they cannot stand

 steadily (positive Romberg sign)

 In cerebellar ataxia, turns are

 difficult and patients cannot

 stand steadily with feet together

 whether eyes are open or

 closed

 Caused by polyneuropathy or

 posterior column damage, e.g.

 syphilis

D Parkinsonian gait

 Posture is stooped with head

 and neck forwards

 Arms are flexed at elbows and

 wrists. Little arm swing

 Steps are short and shuffling

 and patient is slow in getting

 started (festinant gait)

 Caused by lesions in the basal

 ganglia

Fig. 7.17 Abnormalities of gait.

Motor system • 137

7

• 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.

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