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.

Motor System

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

1. 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.
2. 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.

Upper and Lower Motor Neuron Signs

When evaluation weakness there is a fundamental distinction with separation of upper motor neuron lesions (lesion in cerebral cortex, brainstem, or descending motor pathway of spinal cord), from lower motor neuron lesions (lesion in peripheral nerve and anterior horn cells of the spinal cord).

Upper motor neuron dysfunction: weak and flaccid muscles that eventually become spastic, hypertonic, and hyperreflexive. There is an association with pathologic reflexes (such as Babinski's and Hoffmann) and induced clonus of the ankle or wrist. Spasticity is prominent in the antigravity muscles (flexors of the upper extremities and extensors of the lower extremities). Spasticity is associated with clasp-knife finding due to a variable degree of resistance to passive motion.

Upper motor neurons cross over to the contralateral side at the decussation of the pyramids (between the brainstem and spinal cord). Therefore upper motor neuron type weakness can result from:

• Ipsilateral spinal cord lesion: In spinal cord lesions there may be both upper and lower motor neuron type weakness. Lower motor neuron type weakness occurs at the level of the lesion, and upper motor neuron type weakness occurs below the level of the lesion.
• Contralateral brainstem lesion
• Contralateral cerebral hemisphere lesion

Lower motor neuron dysfunction: weakness and paralysis of affected muscles. Flaccidity, hypotonia, diminished or absent stretch reflexes, and eventually atrophy. Fasciculations occur which are visible twitches of small groups of muscle fibres. There are no pathologic reflexes.

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

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.

See Also

• Reflex Testing
• Pain Oriented Sensory Examination
• Spinal Cord Anatomy