• present only with reinforcement (+/-)
Principal (deep tendon) reflexes
• Ensure that both limbs are positioned identically with the
same amount of stretch. This is especially important for
the ankle reflex, where the ankle is passively dorsiflexed
• Compare each reflex with the other side; check for
symmetry of response (Figs 7.19 and 7.20).
• Use reinforcement whenever a reflex appears to be absent.
For knee and ankle reflexes, ask the patient to interlock
their fingers and pull one hand against the other on
command (‘Have a tug of war with yourself’), immediately
before you strike the tendon (Jendrassik’s manœuvre).
• To reinforce upper limb reflexes, ask the patient to make a
fist with the contralateral hand.
• Place your right index finger under the distal
interphalangeal joint of the patient’s middle finger.
• Use your right thumb to flick the patient’s finger
• Look for any reflex flexion of the patient’s thumb.
• Assess individual muscles depending on the history. Ask
the patient to undertake a movement. First assess whether
they can overcome gravity. For example, give the
instruction ‘Lift your right leg off the bed’ to test hip
flexion. Then apply resistance to this movement, testing
across a single joint; for instance, apply resistance to the
thigh in hip flexion, not the lower leg.
• To test truncal strength, ask the patient to sit up from a
Upper motor neurone lesions produce weakness of a relatively
large group of muscles, such as a limb or more than one limb.
Lower motor neurone damage can cause paresis of an individual
and specific muscle, so more detailed examination of individual
muscles is required (Ch. 13). Look for patterns of weakness that
may suggest a diagnosis. In pyramidal weakness – after a stroke,
for example – the extensors in the upper limbs are weaker than
the flexors, and vice versa in the lower limbs. Myopathies tend
to cause proximal weakness and neuropathies often give rise to
more distal patterns, while mononeuropathies or radiculopathies
lead to discrete focal weakness (such as a foot drop caused by
a common peroneal nerve palsy or L5 radiculopathy).
Patients may find it difficult to sustain maximum power for
reasons other than weakness, most commonly pain. You need
only show that the patient can achieve maximum power briefly
to be satisfied that the weakness is not neurological. Very
few organic diseases cause power to fluctuate; the fatigable
weakness of myasthenia is the chief exception. Wildly fluctuating
or sudden ‘give-way’ weakness suggests a functional explanation.
Hoover’s sign (Fig. 7.18) refers to the improvement of apparently
weak hip extension when it is tested at the same time as
contralateral hip flexion (as hip flexion is associated with reflex
contralateral hip extension), and is often present in functional leg
‘Push down with your right heel’
Hip extension returns to normal
• Use an orange stick to stroke the upper medial aspect of
• Normally the testis on the side stimulated will rise briskly.
Hyper-reflexia (abnormally brisk reflexes) is a sign of upper
motor neurone damage. Diminished or absent jerks are most
commonly due to lower motor neurone lesions. In healthy
older people the ankle jerks may be reduced or lost, and in the
Holmes–Adie syndrome, myotonic pupils (p. 162) are associated
• Place your middle and index fingers across the palmar
surface of the patient’s proximal phalanges.
• Tap your own fingers with the hammer.
• Watch for flexion of the patient’s fingers.
• Run a blunt object (orange stick) along the lateral border
of the sole of the foot towards the little toe (Fig. 7.21).
• Watch both the first movement of the great toe and the
other leg flexor muscles. The normal response is plantar
flexion of the great toe (downward movement).
• A true Babinski sign, signifying an abnormal reflex due to
an upper motor neurone lesion:
• involves activation of the extensor hallucis longus
tendon (not movement of the entire foot, a common
‘withdrawal’ response to an unpleasant stimulus)
• coincides with contraction of other leg flexor muscles
• The patient should be supine and relaxed.
• Use an orange stick and briskly but lightly stroke the
upper and lower quadrants away from the midline of the
relaxed abdomen, watching for a contraction.
• The normal response is contraction of the underlying
Cremasteric reflex (L1–2): males only
• Explain what you are going to do and why it is necessary.
• Abduct and externally rotate the patient’s thigh.
each other), L3, L4. B Ankle jerk of the recumbent patient, S1.
Fig. 7.21 Eliciting the plantar reflex.
influence body equilibrium, while each hemisphere controls
Test cerebellar function by assessing stance and gait (p. 134),
including tandem gait (walking in a straight line, heel to toe),
eye movements (looking for nystagmus; p. 164), speech
(dysarthria; p. 125) and limb coordination.
• Ask the patient to touch their nose with the tip of their
index finger and then touch your fingertip. Hold your finger
at the extreme of the patient’s reach (you should make the
patient use the arm outstretched).
• Ask them to repeat the movement between nose and
target finger as quickly as possible.
• Make the test more sensitive by changing the position of
your target finger. Timing is crucial; move your finger just
as the patient’s finger is about to leave their nose,
otherwise you will induce a false-positive finger-to-nose
• Some patients are so ataxic that they may injure their eye/
face with this test. If so, use your two hands as the
targets or ask the patient to touch their chin rather than
• Demonstrate repeatedly patting the palm of your hand
with the palm and then the back of your opposite hand as
quickly and regularly as possible.
• Ask the patient to copy your actions.
• Repeat with the opposite hand.
• Alternatively, ask the patient to tap a steady rhythm rapidly
with one hand on the other hand or table, and ‘listen to
the cerebellum’; ataxia makes this task difficult, producing
a slower, more irregular rhythm than normal.
• With the patient lying supine, ask them to lift the heel into
the air and to place it on their opposite knee, then slide
their heel up and down their shin between knee and ankle
The finger-to-nose test may reveal a tendency to fall short of
or overshoot the examiner’s finger (dysmetria or past-pointing).
with loss of some reflexes. Isolated loss of a reflex suggests a
mononeuropathy or radiculopathy, such as loss of ankle jerk with
L5/S1 lumbosacral disc prolapse compressing the S1 nerve root.
Reflex patterns are helpful in localising neurological lesions and
you should know the nerve roots that serve the commonly tested
reflexes (Box 7.9). There are several reflex grading systems but
interobserver agreement is poor; record reflexes as present (and,
if so, whether normal, increased or decreased) or absent. Never
conclude that a reflex is absent until you have used reinforcement.
An ‘inverted’ biceps reflex is caused by combined spinal cord
and root pathology localising to a specific spinal level. It is most
common at the C5/6 level. When elicited, the biceps reflex is
absent or reduced but finger flexion occurs. This is because the
lesion at the C5/6 level affects the efferent arc of the biceps jerk
(C5 nerve root), causing it to be reduced or lost, and also the
spinal cord, increasing reflexes below this level (including the
finger jerks, C8). It is most commonly seen in cervical spondylotic
A Hoffmann’s reflex and increased finger jerks suggest
hypertonia; they may occur in healthy individuals but can be
informative if asymmetric. In cerebellar disease the reflexes may
be pendular and muscle contraction and relaxation tend to be
slow, but these are not sensitive or specific cerebellar signs.
An extensor plantar (Babinski) response is a sign of upper
motor neurone damage and is usually associated with other upper
motor neurone signs, such as spasticity, clonus and hyper-reflexia.
Fanning of the toes is normal and not pathological.
Superficial abdominal reflexes (T8–12) are lost in upper motor
neurone lesions but are also affected by lower motor neurone
damage affecting thoracic roots T8–12. They are usually absent
in the obese and the elderly or after abdominal surgery, and are
not part of the routine examination.
The cremasteric reflex in males (L1, 2) may be absent on
the side of spinal cord or root lesions but this is of little clinical
These are present in normal neonates and young infants but
disappear as the nervous system matures (p. 305). People
with congenital or hereditary cerebral lesions and a few healthy
individuals retain these reflexes, but their return after early
childhood is often associated with brain damage or degeneration.
Although often referred to as frontal, the primitive reflexes (snout,
grasp, palmomental and glabellar tap) have little localising value
and in isolation are of little significance, but in combination suggest
diffuse or frontal cerebral damage (Box 7.10). Unilateral grasp and
palmomental reflexes may occur with contralateral frontal lobe
pathology. The glabellar tap is an unreliable sign of Parkinson’s
Performing complex movements smoothly and efficiently depends
on intact sensory and motor function and an intact cerebellum.
The cerebellum lies in the posterior fossa and consists of two
hemispheres with a central vermis. Afferent and efferent pathways
convey information to and from the cerebral motor cortex, basal
ganglia, thalamus, vestibular and other brainstem nuclei and the
spinal cord. In general, midline structures, such as the vermis,
• Lightly tap the lips. Lip pouting is an abnormal response
• Firmly stroke the palm from the radial side. In an abnormal
response, your finger is gripped by the patient’s hand
• Apply firm pressure to the palm next to the thenar eminence with a
tongue depressor. An abnormal response is ipsilateral puckering of
• Stand behind the patient and tap repeatedly between their eyebrows
with the tip of your index finger. Normally, the blink response stops
• Ask the patient to perform an imaginary act, such as
drinking a cup of tea, combing their hair, or folding a letter
and placing it in an envelope.
• Ask the patient to copy movements you make with your
fingers, such as pointing or making a V sign.
• Ask the patient to copy a geometric figure (interlocking
• Ask the patient to put on a pyjama top or dressing gown,
one sleeve of which has been pulled inside out.
• Ask the patient to lie on the couch and perform cycling
The patient may be unable to initiate a task or may perform
it in an odd or bizarre fashion. Constructional apraxia (difficulty
drawing a figure) is a feature of parietal disturbance. Dressing
apraxia, often associated with spatial disorientation and neglect,
is usually due to parietal lesions of the non-dominant hemisphere.
Patients with gait apraxia have difficulty walking but are able to
perform cycling movements on the bed surprisingly well.
The sensory system comprises the simple sensations of light
touch, pain, temperature and vibration, together with joint position
sense (proprioception) and higher cortical sensations, which
include two-point discrimination, stereognosis (tactile recognition),
graphaesthesia (identification of letters or numbers traced on
Detailed examination of sensation is time-consuming and
unnecessary unless the patient volunteers sensory symptoms
or you suspect a specific pathology, such as spinal cord
compression or mononeuropathy. In patients without sensory
symptoms, assessing light touch of all four limbs as a screening
process may suffice. It is useful to have a working knowledge
of the dermatomal distribution (a dermatome is an area of skin
innervated by a single nerve root) and sensory distribution of
the more commonly entrapped peripheral nerves (see Figs 7.26
Proprioception and vibration are conveyed in large, myelinated
fast-conducting fibres in the peripheral nerves and in the posterior
In more severe cases there may be a tremor (or an increase in
amplitude of tremor) of the finger as it approaches the target finger
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
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, 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
Fig. 7.23 Performing the heel-to-shin test with the right leg.
another, towards and away from the patient (1), as well as from side to side (2).
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
• 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
• hyperalgesia: increased sensitivity to a painful stimulus.
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