• Ask the patient to shrug their shoulders, then apply
downward pressure with your hands to assess the
• Test power in the left sternomastoid by asking the patient
to turn their head to the right while you provide resistance
with your hand placed on the right side of the patient’s
chin. Reverse the procedure to check the right
• Test both sternocleidomastoid muscles simultaneously by
asking the patient to flex their neck. Apply your palm to
Isolated XI nerve lesions are uncommon but the nerve may
be damaged during surgery in the posterior triangle of the neck,
penetrating injuries or tumour invasion. Wasting of the upper fibres
of trapezius may be associated with displacement (‘winging’) of the
upper vertebral border of the scapula away from the spine, while
the lower border is displaced towards it. Wasting and weakness
of the sternomastoids are characteristic of myotonic dystrophy.
Weakness of neck flexion or extension, the latter causing head
drop, may occur in myasthenia gravis, motor neurone disease
and some myopathies. Dystonic head postures causing antecollis
(neck flexed), retrocollis (neck extended) or torticollis (neck twisted
to one side) are not associated with weakness.
The XII nerve innervates the tongue muscles; the nucleus lies
in the dorsal medulla beneath the floor of the fourth ventricle.
The nerve emerges anteriorly and exits the skull in the hypoglossal
canal, passing to the root of the tongue (see Fig. 7.5).
• Ask the patient to open their mouth. Look at the tongue at
rest for wasting, fasciculation or involuntary movement.
Fig. 7.14 Left hypoglossal nerve lesion. From Epstein O, Perkin GD, de
Bono DP, et al. Clinical Examination. 2nd edn. London: Mosby; 1997.
The group of muscle fibres innervated by a single anterior
horn cell forms a ‘motor unit’. A lower motor neurone lesion
causes weakness and wasting in these muscle fibres, reduced
tone (flaccidity), fasciculation and reduced or absent reflexes.
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.
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