TRIPASS XR تري باس

 • decreased (+)

• present only with reinforcement (+/-)

• absent (0).

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

before striking the tendon.

• 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.

Hoffmann’s reflex

• 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

downwards.

• 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

lying position.

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’

Weak hip extension

‘Lift your left leg’

Hip extension returns to normal

Fig. 7.18 Hoover’s sign.

140 • The nervous system

• Use an orange stick to stroke the upper medial aspect of

the thigh.

• 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

Finger jerk (C8)

• 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.

Plantar response (S1–2)

• 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

• is reproducible.

Abdominal reflexes (T8–12)

• 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

muscle.

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.

Fig. 7.20 Testing the deep tendon reflexes of the lower limb. A Eliciting the knee jerk (note that the patient’s legs should not be in contact with

each other), L3, L4. B Ankle jerk of the recumbent patient, S1.

Fig. 7.21 Eliciting the plantar reflex.

A B C

Fig. 7.19 Testing the deep tendon reflexes of the upper limb. A Eliciting the biceps jerk, C5. B Triceps jerk, C7. C Supinator jerk, C6.

Motor system • 141

7

influence body equilibrium, while each hemisphere controls

ipsilateral coordination.

Examination sequence

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.

Finger-to-nose test

• 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

ataxia.

• 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

nose (Fig. 7.22).

Rapid alternating movements

• 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.

Heel-to-shin test

• 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

(Fig. 7.23).

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

myeloradiculopathy.

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

significance.

Primitive reflexes

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

disease.

Coordination

Performing complex movements smoothly and efficiently depends

on intact sensory and motor function and an intact cerebellum.

Anatomy

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,

7.10 Primitive reflexes

Snout reflex

• Lightly tap the lips. Lip pouting is an abnormal response

Grasp reflex

• Firmly stroke the palm from the radial side. In an abnormal

response, your finger is gripped by the patient’s hand

Palmomental reflex

• Apply firm pressure to the palm next to the thenar eminence with a

tongue depressor. An abnormal response is ipsilateral puckering of

the chin

Glabellar tap

• Stand behind the patient and tap repeatedly between their eyebrows

with the tip of your index finger. Normally, the blink response stops

after three or four taps

142 • The nervous system

Examination sequence

• 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

pentagons or cube).

• 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

movements with their legs.

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.

Sensory system

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

the skin) and localisation.

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

and 7.27 later).

Anatomy

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

and hypotonia.

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

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

or parietal lobes.

Fig. 7.23 Performing the heel-to-shin test with the right leg.

A

1

1

2

2

B

Fig. 7.22 Finger-to-nose test. A Ask the patient to touch the tip of their nose (1) and then your finger (2). B Move your finger from one position to

another, towards and away from the patient (1), as well as from side to side (2).

Sensory system • 143

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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

are defined as follows:

• 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

stimulus

• hyperalgesia: increased sensitivity to a painful stimulus.

Examination sequence