Motor system examination

Dr. Rzgar Hamed Abdwl

Supervised by : Dr. Zana A. Mohamad
2019
Motor system examination:

1. Inspection
2. Tone
3. Power
4. Reflexes
5. Co-ordination
1:Inspection: for Muscle wasting, Fasciculation, Abnormal postures, Abnormal movements.

1.1 Muscle wasting and deformity:

• Always compare with the other side
• If there is doubt about muscle wasting, this must be confirmed by measurement procedures at clearly
stated places e.g. 10 cm above or below the olecranon, 18 cm above the patella, and 10 cm below the
tibial tuberosity.

Types of muscle wasting:

1. Global (generalized) wasting: this is commonly seen in systemic diseases and advanced neurological
diseases (myopathies and motor neuron disease)
2. Proximal muscle wasting:
3. Distal muscle weakness:
* Nearly all the conditions mentioned already, if severe enough, will affect the peripheral muscle as well.
a. The forearm and small muscles of the hands
i. Lower motor neuron lesion: Affecting principally the segmental distribution of C7, C8 and T1. This may occur at the following
levels:
• Anterior horn cells (poliomyelitis, motor neuron disease, syringomyelia, cervical cord tumor).
• The anterior root (cervical spondylosis, cervical tumors).
• Brachial plexus (injuries, cervical rib, cervical glandular enlargement, superior pulmonary sulcus tumor).
• Traumatic lesions of the radial, median, and ulnar nerves.
ii.Carpal tunnel syndrome which causes wasting of the thenar eminence.
iii.Ulnar nerve pathology: If it is damaged at or just below the elbow, there will be wasting of most of the small muscles
except opponens pollicis and abductor pollicis brevis. While injuries at the wrist or compression by a ganglion may spare
the hypothenar eminence and sensation.
iv.Muscular lesions: It includes dystrophia myotonica, those due to aging process or rheumatoid arthritis.
v.Contralateral parietal lobe lesions: it occurs very occasionally.
b. The lower leg wasting
1- Peripheral neuropathy (polyneuritis).
2- Extensive cuada equine lesion.
3- Peroneal muscular atrophy.
4- Poliomyelitis.
5- Peripheral nerve trauma, especially the common peroneal nerve e.g. by an inadequately padded plasters or by skin traction
techniques.
6- Wasting of the anterior muscles of the lower leg that follow "syndrome of the anterior tibial compartment“
c. Peripheral wasting in both the lower and upper limbs
Peripheral wasting in all of the 4 extremities is rare except in 2 conditions:
1- Peroneal muscular atrophy (Charcot-Marie-Tooth disease).
2- Chronic polyneuritis.
1.2: Fasciculation
* It is visible irregular flickering over the surface of the affected muscle caused by spontaneous contractions of
individual motor units- suggests that weakness is due to a lower motor neuron lesion.
* They present at rest, stopping during voluntary movements but increased after it.
* They are of 2 types:
a. Physiological fasciculation (benign fasciculation):
* May lasts for years
* There is no weakness, wasting or signs of lower motor neuron lesion.
b. Pathological fasciculation: it is very coarse and repetitive in muscles having the same root supply , indicating chronic
denervation and reinnervations.
 1.3 Abnormal movements
Causes include:
The important involuntary movements are:
1. Motor neuron disease.
1. Epilepsy, myoclonus
2. Early stages of poliomyelitis.
2. Tremor.
3. Progressive spinal muscular atrophy.
3. Athetosis, psedoathtosis
4. Syringobulbia.
5. Prolapsed intervertebral disc. 4. Chorea.

6. Chronic nerve entrapment. 5. Dyskinesia.

7. Polyneuropathies. 6. Dystonias.
8. Collagen diseases. 7. Hemiballismus.
9. Myositis. 8. Torticollis.
10. Thyrotoxic myopathy. 9. Tics.
11. Syphilitic amyotrophy. 10. Myokymia.
12. Peroneal muscular atrophy. 11. Tetany.
12. Titubation.
1.4 Abnormal postures
Pyramidal posture: the arm on the affected side is usually held flexed and adducted while the leg is usually extended and
inverted , due to cortico-spinal lesion.
Foot drop: Failure of the dorsiflexion of foot due to common peroneal nerve lesion, root lesion at (L5) or rarely due to central
lesion.
Wrist drop: Due to radial nerve injury or root lesion at (C7).
Claw hand: Due to ulnar nerve lesion or root lesionat (C8, T1).
Pes cavus: High plantar arch which may be associated with inherited peripheral neuropathy.
* Other sustained postures like dystonias, torticollis
Two : Muscle Tone
Testing the tone in the upper limb:
* First pick up the patient's hand and forearm as if to take the pulse, holding his fingers in the right hand.
* Then proceed to passive flexion and extension of the wrist, elbow and the shoulder, all movement must be gentle.
* Now raise each arm in turn and left it fall back onto the bed, comparing (on the 2 sides) the checking movement which
usually breaks the fall.
Testing the tone in the lower limb:
* First gently role the limbs with the palms of the hands on the shins.
* Then proceed to passive flexion and extension of the hip, knee and ankle.
* Lastly raise the lower leg as one piece and allow it to fall, noting the normal checking movement.
Findings :
I. Hypertonia: two types of increased tone can be distinguished:
1- Spasticity
* the resistance is usually most noticeable when the movement is first made and then suddenly overcome, producing the so
called "clasp knife" Spasticity.
* The increase in tone is velocity dependent, so that passive movement at a high velocity (sudden, unpredicted flexion,
of a big joint) may be met with increased resistance.
* Spasticity is caused by an upper motor neuron lesion.
2- Rigidity
* Rigidity consists of increased resistance to passive movement that affects agonist and antagonist muscle group equally ((lead
pipe" rigidity))
* In "cogwheel" rigidity there are interruptions in the passive movement which probably relate to the underlying tremor.
* In general, rigidity indicates extra-pyramidal dysfunction and is due to a lesion of the basal ganglia e.g. Parkinson’s
disease.
II. Hypotonia (flaccidity)
• excessive floppiness-a reduced resistance to passive movement
• there are hyperextended joints and the muscle belly may look flattened and feels less firm than usual.
Causes :
- Lesions of the muscle itself: Myopathies, benign infantile hypotonia, myasthenia gravis.
- State of neurological shock: It occurs in the earliest stages of a severe cord lesion, or profound hemiplegia. It is
temporary unless destruction is extreme.
- Cerebellar lesions: ipsilateral hypotonia is common, but rarely very marked.
- Chorea: As in Sydenham's chorea, Huntington's disease.

III. Paratonia :The patients give the impression of being unable to relax, occurs in patients with frontal lobe or diffuse cerebral
disease.
Three :Muscle Power
Examination of the upper limbs
I. Ask the patient to hold his arm outstretched in front of him and then to close his eyes. This is useful as a screen for:
a. Weakness of the shoulder abduction (C5)-the arm will drift down.
b. Cerebellar lesion: the arm on the affected side tends to hyperpronate and to rise above the other arm.
c. Loss of joint position sense: The affected arm tends to drift away from
the other.
d. Pronator sign: now ask the patient to hold his arm outstretched and
supinated in front of him. The arm on the affected side tends to hyperpronate and drift down. This indicates pyramidal
weakness.
II. Now proceed rapidly, through the muscle groups, starting proximally from the shoulder downwards, remembering
that for each of the basic movement there is single root value and peripheral nerve supply.
Testing specific nerves of the upper arms:
Examination of the lower limbs:
* Start proximally , most muscles have a nerve supply derived from 2 roots, so weakness is often
difficult to detect in an individual root lesion.
Testing specific nerves in the lower limbs
Testing for weakness of shoulder girdle muscles
Patterns of muscle weakness
1- Pyramidal weakness:
- weakness of the abductors and extensors of the upper limbs, and flexors of the lower limbs.
- Distribution is more distal than proximal, particularly in the upper limb, where hand movements are affected earliest.

2- Proximal weakness: This pattern is commonly encountered in myopathies like:

a. Polymyositis, Myasthenia gravis.
b. Metabolic myopathies (hypokalemia, thyrotoxicosis, hypocalcaemia).
c. Muscular dystrophy like pelvic girdle dystrophy.
d. Radiculopathies (C5 in the upper limb, L1-L2 in the lower limb, diabetic amyotrophy).
E. Carcinomatous neuromyopathy.
3-Distal weakness:
- encountered in peripheral neuropathies and radiculopathies that involve the distal parts like C8, T1 lesions in the upper limb, or
cauda equina lesions in the lower limb.
4-Radicular weakness:
- It means that the weakness is limited to the muscles having that segmental supply e.g. disc prolapse at L5, S1 level lead to
weakness which respect S1 root.
- This involves weakness of plantar flexion, loss of sensation at S1 dermatome and loss of ankle jerk.
5-Isolated peripheral nerve weakness:
- It means loss of the function of that nerve (mononeuropathy).
- This is commonly encountered in vasculitis, trauma, entrapment and inflammatory neuropathies e.g. are: foot drop, wrist drop
due to radial nerve and peroneal nerve lesion respectively.
Four : Reflexes
1- Tendon reflexes
* These are monosynaptic stretch reflexes, elicited by tapping the tendon of a lightly stretched muscle with a reflex hammer.
Prior requisites:
1- A good percussion hammer.
2- An examiner with flexible wrists who allows the weight of the hammer to decide the strength of the blow.
3- A patient who is warm, comfortable and relaxed.
4- A muscle placed in the optimum position, slightly on stretch, but with plenty of space for contraction.
5- When examining the tendon reflexes in the legs, care is taken to allow the patient's genitalia to be properly covered.
Types of Reflexes :
Some other reflexes other than spinal reflexes
Examination with reinforcement
* This maneuver must be done whenever the reflexes are absent, because absent reflexes is not necessarily pathological.
* This situation is often found in patients involuntarily tensing themselves, and those very relaxed, such as a happy young child,
and probably in very muscular individual. If other muscles are placed under strain, it often becomes possible to obtain a normal
reflex.
* For the upper limbs, the patient should clench his teeth tightly, or while one arm is being examined, he should clench the fist of
the other.
* For the lower limbs these measures can still be used, but the well tried method of Jendrassek is more reliable.
* The patient interlocks the flexed fingers of the two hands and pulls one against the other at the moment the reflex is
stimulated.
* Whatever the method used, the patient should make the movement at the moment that the reflex is tested and relax
afterwards.
Clonus
* This phenomenon must be done whenever the reflexes are exaggerated as a result of cortico-spinal lesion.
* is an involuntary to-and-fro (5-8-cycles per second (cps) with the frequency slowing, but stabilizing by the 4-5th beat)
rhythmic movement of essentially any muscle, elicited by a quick stretch, but at times occurring without such a movement
Technique for eliciting clonus
a. ankle clonus:
- flex the Pt’s knee slightly to relax the triceps surae muscle.
- Hold the Pt’s foot and Gently but briskly jerk the foot upward and a little outward. After the upward jerk, maintain finger
pressure against the sole of the Pt’s foot.
B- wrist clonus: simply jerk quickly up on the Pt’s hand.
c. patellar clonus:
Abnormalities of tendon reflexes
a. Areflexia: causes
i. When there is a pathology in any part of the reflex arc for example:
- Lesion of the afferent part as in polyneuritis, tabes dorsalis
- The anterior horn cells (poliomyelitis)
- The anterior root (spinal compression)
- The efferent part (trauma, peripheral neuropathy)
- The muscle itself (myopathies, periodic muscle paralysis).
i. Spinal shock.
iii. Advanced rigidity, Spasticity, or muscle contracture..
iv. Cerebellar disease.
v. Deep coma.
b. Hyper-reflexia
* This occurs with UMN lesions at all levels above the anterior horn cells. It may occur with anxiety or nervousness, in
thyrotoxicosis, and as a manifestation of tetanus.
* Hyper-reflexia is therefore only of pathological significance, if it is asymmetrical or associated with other signs of upper motor
neuron lesion.
c. Reflex asymmetry
Several points can be made regarding reflex asymmetries:
1- Lateralized asymmetries of response i.e. the reflexes that are brisker on one side of the body than on the other side. It usually
indicates upper motor neuron disturbance.
2- Focal reflex deficit often related to root, plexus, or peripheral nerve lesion, e.g. unilateral depression of the ankle jerk
commonly reflect an S1 radiculopathy resulting from a lumbosacral disc lesion.
3- Loss of distal tendon reflexes (especially the ankle jerk) with preservation of more proximal ones is common in
polyneuropathy.
D- Other important reflex abnormalities:
1- The inverted supinator jerk: With lesions at C5 c6, the supinator reflex or biceps reflex may be lost, but, when it is tested,
brisk flexion of the finger is seen. In practice, this is usually associated with exaggerated triceps reflex.

2- Extended pyramidal reflexes: In hyper-reflexic states, there may be spread of the region from which a particular reflex
response can be elicited. For example, elicitation of the biceps or triceps reflexes may be accompanied by reflex finger flexion.
This indicates that the lesion is above the level of the reflex which is tested, in this example it is above C5.

3- Cross adduction: It means that the reflexes are more exaggerated on the side where adduction occurs
Normal variations and flexion reflex in response to a plantar stimulus
* If there is little or no toe or leg movement after a plantar stimulus, a so-called mute sole.
Causes: Arthritic changes, trauma, or previous toes surgery.

* Most adult persons tend to withdraw their feet from a plantar stimulus and flex their toes,
normal plantar reflex or flexor response.

* But dorsiflexion of the ankle and flexion of the knee and hip is called a triple flexion reflex.
Which is a sign of UMN lesion but occurs several days after injury.
* the synergistic extension of the great toe can occur with an exaggerated triple flexion of the
ankle, knee, and hip, considered as abnormal planter reflex.

* The small toes may fan, but this does not constitute a consistent or clinically important part
of the plantar reflex.

Babinski mimickers
1- Pseudo Babinski sign
* This sign may be encountered in patients with
choreoathetosis where the upgoing toe is a manifestation
of hyperkinesia.
2- Inversion of the plantar reflex
If the short flexors of the toe are paralysed, or the flexor
tendons have been severed, an extensor plantar response
may be obtained even in the absence of UMN lesions and
is termed inversion of the plantar reflex of peripheral origin.
3- Withdrawal response
* It is basically a voluntary movement or withdrawal due to a ticklish or unpleasant
sensation.
* It is encountered in sensitive individuals or patients with plantar hyperaesthesia due to
peripheral neuritis,
* In such a situation, it is important to repeat the stimulus more gently and hold the foot at
the ankle, or try
alternative stimuli.
Pathologic variations in the plantar reflexes
* After interruption of the UMNs to the lumbosacral cord, the great toe extends instead of
flexing, a result called an extensor (plantar) response, extensor toe sign, or Babinski sign.

* Although anatomically the upward toe movement is called extension and is mediated by
the extensor hallucis longus, but physiologically the movement shortens the joint angle and,
hence, is regarded as flexion, and the movement belongs to the overall flexion reflex of the
leg.
* A true extensor toe sign meets four criteria:
a. The toe usually begins to extend only after the plantar stroke has moved a few centimeters
along the sole
b. The toe remains tonically extended as the plantar stroke continues.
c. Just after release of the stroke, the toe then promptly but slowly returns to the neutral
position

d. Some degree of a triple flexion reflex always occurs, best monitored by inspection or
palpation of the tensor fascia lata muscle (Brissaud reflex).
(((some Pts with UMN lesions will fail to show an extensor toe sign or other features of the
UMN syndrome)))
* the extensor toe response is a sign of anatomic or pathophysiologic interruption of the
pyramidal tract .
* However, experimental studies suggest it results from dysfunction of the cortico-
reticulospinal tract that lies close to the corticospinal tract ,consequently can be damaged
with it and normally suppresses the flexor reflexes.
* Causes of Reversible and transient extensor toe signs:
1- toxic-metabolic coma
2- postictal hemiparesis after epileptic seizures (Todd paralysis)
3- trauma with concussion or contusion
4- transient ischemic attacks
5- hemiplegic migraine.
Ways to elicit
Babiniski sign:
Five: Coordination
* Coordinate movement needs intact motor, sensory, cerebellar, extra pyramidal, proprioceptive, vestibular and
visual functions.
Tests of coordination (cerebellar functions) in the upper limbs
1- Finger-nose test:
Look for the following cerebellar signs:
i. Intention tremor: It is more evident as the finger approaches the nose.
ii. Dysmetria: It means overshooting of the target. In this test, the patient will shoot the finger past the nose, to the
cheek or the ear.
iii. Dyssynergia: It denotes the breakdown of complex actions into the individual movements composing them; the
patient may first flex the elbow and then bring the hand up to the nose instead of combining the movements into
one action.
2- Rapid alternating movements:
• Ask the patient to strike his thighs rhythmically.
• Ask him to flex his elbows to a right angle and then alternatively to supinate and prorate his forearms as rapidly
as possible as though screwing in a light bulb.
* Other many maneuvers, which may include rapid alternating
movement between palms and back of the hands, rapidly touching the
thumb to each finger in succession.
• Dysdiadochokinesia: It is the technical term for dysrhythmia in
performing any of these tasks.
3- Rebound phenomenon:
- The patient flexes an arm as strongly as possible, or holds his arm
extended against resistance.
- The examiner then suddenly lets go, if the arm flies up towards the face,
this signifies that the patient is unable to check the abrupt imbalance
between flexors and extensors (This is a solid cerebellar sign)
4- The finger-tapping test: Listen for dysrhythmia and slowness
Cerebellar signs in the upper limbs
They are divided into specific and non specific signs.

I. Specific signs:
• Intention tremor.
• Dysmetria.
• Dyssynergia.
• Dysdiadochokinesia.
• Rebound phenomenon.

II. Non specific signs:

*Hypotonia
*Hyporeflexia
Tests of coordination in the lower limbs
1- Heel-Knee-Shin test:
* Ask the patient to left one leg high in the air, to place the heel on this leg on the opposite knee, and then to slide the heel down
his shin towards the ankle.
2- Gait examination:
a. If the patient is able to walk, a good test of lower limb coordination consists of asking him to walk along a straight line.
b. Tandem walk: Ask the patient to walk along straight line on the floor placing the heel of one foot immediately adjacent to the
toe of the one behind.
3. Combus test:
Ask the patient to walk to a known point and then to return back to the original place. In patient with cerebellar lesion he will
continuously deviate to the side of the lesion until he finally makes a combus.
Thanks