Motor System Examination
The examination of the motor system includes inspection (for atrophy, hypertrophy, fasciculations, and tremor), palpation (for cutaneous reflexes and tone), percussion (for myotonia and stretch reflexes), full flexion and extension of the elbows and knees (for abnormal tone and non-neurologic restrictions to movement e.g. from contractures and joint disease), and strength testing. See the article on the myotomes for the segmental innervation of the muscles
The following systems participate in the creation and coordination of muscle movement
- Motor system: both in its pyramidal and extrapyramidal components (for power)
- Cerebellar system: for rhythmic movement and posture
- Vestibular system: for balance and coordination of the eye, head, and body movements
- Sensory system: for afferent input to the spinal axis
Motor System Components
The motor system is made up of the pyramidal and extrapyramidal components. The pyramidal and extrapyramidal levels of the motor system converge on the "final common pathways" which are the lower motor neurons of the brain stem (cranial nerves) and spinal cord, whose axons descend to skeletal muscles.
Pyramidal component: this is the corticospinal level of the motor system. It consists of
- Upper motor neurons. These exert direct or indirect supranuclear control over the lower motor neurons. Upper motor neurons are found in the motor cortex and brain stem.
- Pyramidal tracts (i.e. the descending corticospinal pathways)
Extrapyramidal component: The nuclei reside in the basal ganglia and their complex connections. There is a complex neural organisation that works closely with other levels of the motor system to achieve neuromotor control.
Approach to Weakness
- Main article: Weakness
When evaluating weakness the following distinction is made:
- Upper motor neuron lesions (lesion in cerebral cortex, brainstem, or descending motor pathway of spinal cord). Also called pyramidal tract disease, long tract signs, or central weakness. Causes increased tone, increased reflexes, pyramidal pattern of weakness (weak extensors in the arm, weak flexors in the leg)
- Lower motor neuron lesions (lesion in peripheral nerve and anterior horn cells of the spinal cord). Also called denervation disease or peripheral weakness. Causes wasting, fasciculation, decreased tone, and absent reflexes
- Muscle disease: Causes wasting, decreased tone, impaired or absent reflexes
- Neuromuscular junction disorders: Causes fatigable weakness, normal or decreased tone, normal reflexes
- Functional weakness: Causes normal tone, normal reflexes without wasting with erratic power.
|Location of Lesion||Muscle Tone||Atrophy or Fasiculations||Sensory Findings||Muscle Stretch Reflexes||Other Findings|
|Upper motor neuron||Spasticity||No||Sometimes||Increased||Babinski or Hoffman Sign|
|Lower motor neuron||Hypotonia||Yes||Usually‡||Decreased/absent||Depends on lesion, e.g. Tinel's|
|Neuromuscular junction||Normal or hypotonia||No||No||Normal/decreased||Ptosis, diplopia|
|Muscle||Normal||No (except if late)||No||Normal/decreased||Myotonia|
|Functional||Normal||No||Non-anatomical||Normal||Multiple, e.g. Hoover's sign|
|‡ in the distribution of the spinal segment, plexus, or peripheral nerve.|
Atrophy and Hypertrophy
Atrophy: muscular wasting or emaciation caused by damage to the lower motor neurons or their axons. The interruption of flow of trophic factors to muscles leads to atrophy of the dependent myofibres, plus fasciculations can also occur.
Causes of atrophy include:
- Damage to the supplying nerve
- Congenital muscular disease
- Disuse: e.g. from trauma or joint disease
Examples of atrophic muscles:
- Flat thenar eminence of carpal tunnel syndrome and cervical radiculopathy.
- Prominent metacarpals with loss of intrinsic interossei muscles in polyneuropathy
- Calf atrophy in lumbar radiculopathy.
- Scapular winging in long thoracic nerve or spinal accessory nerve palsy.
- Absent anterior neck shadows from atrophic sternocleidomastoid muscles in syringomyelia.
Atrophy is tested by assessing the muscles three S's which are: size, symmetry, and shape. Atrophy, hypertrophy, and abnormal bulging or depressions are important findings in identifying various muscular diseases, especially when it is asymmetric. Significant asymmetry suggests atrophy of the smaller side or oedema of the other side. In sciatica finding ipsilateral calf wasting usually indicates lumbosacral nerve compression. Shape is important for example in tendon rupture.
Hypertrophy: the opposite of atrophy, an enlargement of a muscle.
Causes of hypertrophy include:
- Overuse and conditioning
- Congenital myopathy (paradoxical hypertrophy), associated with weakness not strength in this case. For example bilateral calf hypertrophy in Duchenne's
- Wide variety of neuromuscular disease
Fasciculations are visible, involuntary, and irregular muscle flickering due to spontaneous contraction of individual motor units. These muscle twitches are too weak to move a limb but are easily felt by patients and clinicians.
Fasciculations are usually benign, especially when they occur in the calf or eyelid muscles. Most healthy people have fasciculations at some point in their life.
When accompanied by weakness or atrophy, fasciculations reflect lower motor neuron denervation. Interruption of the nerve supply makes the muscle hyperexcitable. The lesion is usually in the anterior horn cell or proximal peripheral nerve.Tongue fasciculations occur in about one third of patients with amyotrophic lateral sclerosis.
The patients symptoms guide which muscles are tested. For simple screening one can test one extensor and one flexor in each arm and leg, both proximally and distally. E.g. biceps, triceps, wrist extensors, arm grip for upper extremities; iliopsoas, hamstrings, anterior tibial, gastrocnemius for lower extremities.
Strength is graded on a 6 point scale, which comes from the British Medical Research Council (MRC) during World War II.
|0/5||no muscle contraction and no joint movement|
|1/5||visible contraction of a muscle without sufficient strength to move a joint|
|2/5||strength sufficient to move a joint but not to overcome the resistance of gravity|
|3/5||strength sufficient to move against gravity but not to withstand active resistance|
|4/5||strength sufficient to move against gravity and to overcome some resistance by the examiner|
There are some important limitations of the MRC muscle strength grading. One limitation is the reference point. In unilateral disease the reference is the contralateral healthy limb. In bilateral disease the reference standard is the examiners experience. The 3/5 has flaws because only few patients can move against gravity yet be unable to offer any active resistance. For example the biceps muscle uses only 2% of its full power to overcome gravity (grade 3 strength), and so the remaining 98% is grade 4 and above. The 4/5 is too broad for clinical use and so it is often segmented as follows
- 4-/5: offers little resistance
- 4/5: offers moderate resistance
- 4+/5: offers strong resistance (almost full power).
In upper motor neuron disease, the above simple test of strength can underestimate the severity of deficit. Therefore special tests are necessary
- Upper limb drift: downdrift and pronation of the affected arm when the patient is instructed to keep them both outstretched with eyes closed
- Forearm rolling test: rapid rotation of forearms around each other. In hemispheric disease there is an inability to do this with the forearm contralateral to the lesion.
- Rapid finger (or foot) tapping: rapid sequential tapping of the index finger and thumb together. The hand is slower contralateral to the lesion.
There is also a limitation with testing the powerful antigravity muscles. Simple testing of resisted movement can miss significant weakness at the hips and knees. Using the patients body weight is a better method of testing these muscles.
- Arising from a chair on the symptomatic leg: tests the quadriceps muscles. More accurate than manually resisting the patient's attempt to extend the knee
- Trendelenburg: tests the hip abductors
- Rise up from a chair and sit down 10 times: patients without weakness accomplish this in under 20 seconds if 50 years old and under 25 seconds if 75 years old. If it takes longer then there is either proximal leg weakness or joint/bone disease.
Muscle tone is the involuntary muscle tension that is perceived by the clinician with the repeated passive flexion and extension of a patient's limbs. The patient must be relaxed with no bone or joint limitations to movement. Tell the patient to "relax, let me do all the work."
- Hypertonia: seen in upper motor neuron disease. There may be spasticity, rigidity, or paratonia
- Hypotonia: seen in lower motor neuron disease. There may be flaccidity.
Spasticity is the hypertonia of pyramidal tract disease. There are three characteristics of increased muscle tone of spasticity
- Velocity-dependence: the amount of muscle tone is dependent on the velocity of movement. With more rapid passive motion, there is greater resistance, and vice versa.
- Flexor and extensor tones difference. There is an imbalance in the tone of the flexors and extensors. This often causes abnormal resting postures of the limb
- Associated weakness. The spastic muscle is also weak. If untreated then the spastic muscle becomes shortened and develops a fixed contracture.
Abnormal resting postures:
- Hemiplegia: excess tone in the flexors of the arms and extensors of the legs. The arm is flexed, internally rotated, and fixed against the chest. The leg is extended with a pointed foot.
- Complete spinal cord lesion: Some patients with complete spinal cord lesions have excess tone in the flexors of the legs causing paraplegia-in-flexion which is when the legs flex up into the abdomen.
These postures reflect the developmental kinesiology of normal infants. Paraplegia-in-flexion resembles the initial posture of babies, with their legs flexed against their chests. The infant is eventually able to extend their legs and stand which resembles the extensor tone of hemiplegia. This occurs when the descending pathways from the brainstem are mature enough to overcome the spinal reflexes responsible for the flexed position. The infant is then able to walk when cerebral connections are mature enough to provide fine motor control. When the cerebral hemispheres are damaged for example in stroke, there is disruption of the fine motor control which uncovers the extensor posture. Damage to the spinal cord such as in severe multiple sclerosis or complete spinal cord transection removes all supraspinal input and uncovers the original flexed posture of the legs.
Up to half of patients with spasticity also have the clasp-knife phenomenon. This is usually seen in the knee extensors, and less commonly in the elbow flexors. The clinician extends the patient's knee with a constant velocity. As the patient's knee nears full extension the muscle tone of the quadriceps muscle dramatically increases and completes the movement. This is just like the blade of a pocket knife opening under the influence of its spring. This phenomenon occurs because muscle tone is dependent on muscle length. The tone diminishes with stretching and increases with shortening.
The severity of spasticity is poorly correlated with the severity of associated weakness or hyperreflexia. Slowly developing cerebral hemisphere lesions result in concordant development of spasticity and weakness. However in sudden onset lesions such as stroke or spinal cord injury, there is immediate weakness and flaccidity, but spasticity appears days to weeks later. Some elderly patietns with large strokes have persistent flaccid hemiplegia: here the paralysed muscles never actually develop increased muscle tone but are nevertheless hyperreflexic.
Rigidity is the hypertonia of extrapyramidal disease (Parkinson's). There are three characteristic features
- No velocity-dependence: The resistance to movement is the same with both slow and rapid movements
- Flexor and extensor tones are the same
- No associated weakness.
There is no clasp-knife phenomenon. Cogwheel rigidity is the rigidity that gives way intermittently like the limb is a lever pulling over a ratchet.
Paratonia is increased tone that occurs not at rest but when the affected limb contacts another object. It is a sign of bilateral frontal lobe disease, usually associated with demenita.
There are two forms of paratonia
- Gegenhalten (oppositional paratonia): There is a stiffening of the limb with every applied movement. However unlike rigidity the stiffening is dependent on contact and the force is proportional and opposite to the examiners movements (proportional to how quickly the limb is moved). There is diminishing of resistance when movement is slowed.
- Mitgehen (fascilatory paratonia): movement is actively aided by the patient.
Both forms are associated with frontal lobe diseases (Alzheimers and head trauma).
Hypotonia is reduced or absent muscle tension and is a feature of lower motor neuron disease and cerebellar disease.
Flaccidity is unusual floppiness i.e. an extreme form of hypotonia. It is a sign of cerebellar disease or damage to lower motor neurons.
Striking a muscle with a reflex hammer can elicit two abnormal findings, percussion myotonia and myoedema.
Percussion myotonia is a prolonged muscle contraction lasting several seconds with a sustained dimple appearing on the skin. On the thenar eminence the thumb may draw into sustained opposition with the fingers. It is a feature of some myotonic syndromes such as myotonia congenita and myotonic dystrophy
Myoedema is a focal mounding of a muscle lasting seconds at the point of percussion. Myoedema causes a lump rather than a dimple as seen in myotonia. The lump may be oriented crosswise or diagonal to the direction of the muscle fibres. Myoedema is a normal physiologic response. In undernourished patients this normal response may be more visible.