The basal ganglia are connected structures within the cerebral
hemispheres and brainstem (Fig. 7.16). They include the caudate
nucleus and putamen (collectively known as the striatum), globus
pallidus, thalamus, subthalamic nucleus and substantia nigra
(the latter in the brainstem). The basal ganglia receive much
information from the cortex and are involved in regulating many
activities, principally control of movement, but are also involved
in eye movement, behaviour and executive function control.
Disorders of the basal ganglia may cause reduced movement
(typically Parkinsonism; p. 135) or, less commonly, excessive
movement such as ballism or tics (p. 137).
Assess the motor system using the following method:
• assessment of stance and gait
• inspection and palpation of muscles
Stance and gait depend on intact visual, vestibular, sensory,
corticospinal, extrapyramidal and cerebellar pathways, together
with functioning lower motor neurones and spinal reflexes.
Non-neurological gait disorders are discussed in on page 259.
Certain abnormal gait patterns are recognisable, suggesting
diagnoses (Box 7.7 and Fig. 7.17).
• Ask the patient to stand with their (preferably bare) feet
• Swaying, lurching or an inability to stand with the feet
together and eyes open suggests cerebellar ataxia.
• Ask the patient to close their eyes (Romberg’s test) but be
prepared to steady/catch them. Repeated falling is a
Fig. 7.15 Principal motor pathways.
7.6 Features of motor neurone lesions
Inspection Usually normal (may
Weakness Preferentially affects
Deep tendon reflexes Increased Decreased/absent
Plantar response Extensor (Babinski
the nervous system, such as the basal ganglia and cerebellum,
have important modulating effects on movement. It is important
to distinguish upper from lower motor neurone signs to help
localise the lesion (Box 7.6).
If the lesion affects the CNS pathways, the lower motor neurones
are under the uninhibited influence of the spinal reflex. The motor
units then have an exaggerated response to stretch with increased
tone (spasticity), clonus and brisk reflexes. There is weakness but
not wasting (although atrophy may develop with longstanding
lesions). Primitive reflexes, such as the plantar extensor response
(Babinski sign), may be present.
Motor fibres, together with input from other systems involved in
the control of movement, including extrapyramidal, cerebellar,
vestibular and proprioceptive afferents, converge on the cell
bodies of lower motor neurones in the anterior horn of the grey
matter in the spinal cord (Fig. 7.15).
behind the patient, deliver a brisk push forwards or pull
backwards. You must be ready to catch them if they are
unable to maintain their balance. If in doubt, have an
assistant standing in front of the patient.
• Look at the patient’s shoes for abnormal wear patterns.
• Time the patient walking a measured 10 metres, with a
walking aid if needed, turning through 180 degrees and
• Note stride length, arm swing, steadiness (including
turning), limping or other difficulties.
• Look for abnormal movements that may be accentuated
by walking such as tremor (in Parkinson’s disease) or
• Listen for the slapping sound of a foot-drop gait.
• Ask the patient to walk first on their tiptoes, then heels.
Ankle dorsiflexion weakness (foot drop) is much more
common than plantar flexion weakness, and makes
walking on the heels difficult or impossible.
• Ask the patient to walk heel to toe in a straight line
(tandem gait). This emphasises gait ataxia and may be the
only abnormal finding in midline cerebellar (vermis) lesions.
Unsteadiness on standing with the eyes open is common in
cerebellar disorders. Instability that only occurs, or is markedly
worse, on eye closure (Romberg’s sign) indicates proprioceptive
sensory loss (sensory ataxia) or bilateral vestibular failure. Cerebellar
ataxia is not usually associated with a positive Romberg test.
Hemiplegic gait (unilateral upper motor neurone lesion) is
characterised by extension at the hip, knee and ankle and
circumduction at the hip, such that the foot on the affected
side is plantar flexed and describes a semicircle as the patient
walks. The upper limb may be flexed (Fig. 7.17A).
Bilateral upper motor neurone damage causes a scissor-like gait
due to spasticity. Cerebellar dysfunction leads to a broad-based,
unsteady (ataxic) gait, which usually makes walking heel to toe
impossible. In Parkinsonism, initiation of walking may be delayed;
the steps are short and shuffling with loss/reduction of arm
swing (Fig. 7.17D). A tremor may become more apparent. The
stooped posture and impairment of postural reflexes can result
in a festinant (rapid, short-stepped, hurrying) gait. As a doorway
or other obstacle approaches, the patient may freeze. Turning
involves many short steps, with the risk of falls. Postural instability
on the pull test, especially backwards, occurs in Parkinsonian
syndromes. Proximal muscle weakness may lead to a waddling
positive result. Swaying is common and should not be
• The ‘pull test’ assesses postural stability. Ask the patient
to stand with their feet slightly apart. Inform them that you
are going to push them forwards or pull them backwards.
They should maintain their position if possible. Standing
Fig. 7.16 Basal ganglia. A Anatomical location. B Coronal view.
Gait disturbance Description Causes
Gait apraxia Small, shuffling steps
Spastic Stiff ‘walking-throughmud’ or scissors gait
Foot drop Foot slapping Neuropathies
Central ataxia Wide-based, ‘drunken’
Functional Variable, often bizarre,
such as professional sports players, may have physiological
muscle hypertrophy. Pseudohypertrophy may occur in muscular
dystrophy but the muscles are weak.
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.
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
• Completely expose the patient while maintaining their
• Look for asymmetry, inspecting both proximally and
distally. Note deformities, such as flexion deformities or
• Inspect for wasting or hypertrophy, fasciculation and
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,
Foot is dragged or lifted high
C Sensory or cerebellar ataxia
based. Feet are thrown forward
In sensory ataxia, patients watch
steadily (positive Romberg sign)
In cerebellar ataxia, turns are
stand steadily with feet together
and patient is slow in getting
Caused by lesions in the basal
Fig. 7.17 Abnormalities of gait.
• 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
• 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/
• 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.
• 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
• 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/
• 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
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.
Increased tone may occur in two main forms: spasticity and
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
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)
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
Isolated head tremor is usually dystonic and may be associated
with abnormal neck postures such as torticollis, antecollis or
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
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
Movement disorders, including tremor, are common functional
symptoms. They are often inconsistent and distractible, with
varying frequencies and amplitudes, and may be associated
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
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
Ballism refers to violent flinging movements sometimes affecting
only one side of the body (hemiballismus).
Tics are repetitive, stereotyped movements that may be briefly
Tone is the resistance felt by the examiner when moving a joint
• 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.
• 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
• 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
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
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
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)
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
Ankle dorsiflexion Tibialis anterior Deep peroneal L4/5
Ankle plantar flexion Gastrocnemius and soleusa Tibial S1a
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
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
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
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.
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.
weakness. This is helpful both diagnostically and therapeutically,
as you can show patients that their leg is not actually weak
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),
localises to the S1 root, most commonly due to a prolapsed
intervertebral disc (sciatica).
• Ask the patient to lie supine on the examination couch
with the limbs exposed. They should be as relaxed and
comfortable as possible, as anxiety and pain can cause an
• Extend your wrist and allow the weight of the tendon
hammer head to determine the strength of the blow. Strike
your finger that is palpating the biceps and supinator
tendons (otherwise it is painful for the patient), or the
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