TRIPASS XR تري باس

 

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.