Motor

Motor – Anatomy

Introduction

When one thinks of the motor system it is usually reduced to the direct corticospinal tract and the lower motor neuron (LMN). Although these 2 components are main stage players, it is important to add a few more components to our oversimplified scheme of the motor system.

Control Circuits

First, we need to add two “control circuits” that influence the corticospinal tract- the basal ganglia and the cerebellum.

Brainstem Motor Control Centers

There are also the indirect brainstem motor control centers and their pathways (rubrospinal, vestibulospinal, and reticulospinal) that tonically activate lower motor neurons, especially those that innervate axial and antigravity muscles (those motor neurons that are in the medial part of the ventral horn).

Upper Motor Neuron Lesion

The corticospinal tract has its main influence on the motor neurons that innervate the muscles of the distal extremities- the hand and the foot (motor neurons in the lateral part of the ventral horn). The corticospinal tract also (and this a key point) has collaterals that modulate and control the indirect brainstem motor centers so that we are not a stiff statue opposing gravity but rather we can move at will and have just the right amount of supporting tone. So when there is a lesion of the upper motor neuron (the UMN is the corticospinal tract and it’s collaterals to the brainstem motor nuclei) the clinical findings are a combination of the loss of direct effect of the corticospinal tract on the LMN plus the loss of control and modulation of the indirect brainstem motor control centers.

UMN Lesion Clinical Findings

The clinical findings from a UMN lesion will include loss of distal extremity strength, dexterity and a Babinski sign (loss of direct corticospinal effect) plus increased tone, hyperreflexia, and the clasp-knife phenomenon (from loss of control of the indirect brainstem centers).

LMN Lesion Clinical Findings

Lesions of the LMN, “the final common pathway”, result in loss of strength, tone and reflexes with the denervated muscle showing wasting and denervation hypersensitivity- fasciculations.

UMN Syndrome

Important points to remember:

• The UMN syndrome is a combination of loss of the direct corticospinal tract effect on the LMN and the loss of regulation of the indirect brainstem motor control centers.

Decorticate vs. Decerebrate

• A UMN lesion above the level of the red nucleus will result in decorticate posture (thumb tucked under flexed fingers in fisted position, pronation of forearm, flexion at elbow with the lower extremity in extension with foot inversion) while a lesion below the level of the red nucleus but above the level of the vestibulospinal and reticulospinal nuclei will result in decerebrate posture (upper extremity in pronation and extension and the lower extremity in extension). The reason for this is that the red nucleus output reinforces antigravity flexion of the upper extremity. When its output is eliminated then the unregulated reticulospinal and vestibulospinal tracts reinforce extension tone of both upper and lower extremities. If there is a lesion in the medulla then all the brainstem motor nuclei as well as the direct corticospinal tract would be out and the patient would be flaccid acutely. If the patient were to survive, tone would return because of interneuronal activity at the spinal cord level.

Localizing a UMN Lesion

• An UMN lesion is on the opposite side of the clinical findings for a lesion above the decussation of the pyramids (where the corticospinal tracts cross) whereas it is on the same side as clinical findings if the lesion is in the spinal cord.

Spinal Cord Lesions

• Spinal cord lesions often give UMN signs below the level of the lesion (from effect on the corticospinal tract) and LMN signs at the level of the lesion (from effect on the ventral horn or ventral nerve root).
• LMN signs are good for locating the level of a spinal cord lesion.

Exam Tests

Clinical testing of the motor system:

• Muscle strength
• Tone
• Reflexes
• Pathological reflexes

Motor nerves 9 and 10

These two nerves are clinically lumped together. Motor wise, they innervate pharyngeal and laryngeal muscles. Their sensory component is sensation for the pharynx and taste for the posterior one-third of the tongue.

Potential Traps

Hypertonia can be either spasticity or rigidity. Spasticity is from a UMN lesion. It is rate dependent resistance on range of motion with collapse of the resistance at the end of the range of motion. This is called the clasp-knife phenomena. Rigidity is from basal ganglia disease. The resistance to range of motion is not rate or force dependent and is constant throughout the range of motion. This is often referred to as lead pipe or plastic-like rigidity.

Clinical Pearls

Acute UMN lesions and UMN lesions in infants can produce hypotonia initially with hypertonia occurring later.

Motor – Normal Exam

Upper extremities – Inspection and Palpation

The muscles are inspected for bulk and fasciculations and, when indicated, palpated for tenderness, consistency and contractures.

Tone

Muscle tone is assessed by putting selected muscle groups through passive range of motion. The most commonly used maneuvers for the upper extremities are flexion and extension at the elbow and wrist.

Strength Testing

Muscle strength is tested from the proximal to the distal part of the extremity so that all segmental levels for the extremity are tested (for the upper extremity that is C5 to T1 – see table). Muscle power is graded on a scale of 0-5 (see table).

Stretch or Deep Tendon Reflexes

A brisk tap to the muscle tendon using a reflex hammer produces a stretch to the muscle that results in a reflex contraction of the muscle. The muscles tested, segmental level, and grading of DTR’s is listed below.

Testing for pronator drift

The patient extends their arms in front of them with the palms up and eyes closed. The examiner watches for any pronation and downward drift of either arm. If there is pronator drift this indicates corticospinal tract disease.

Lower extremities – Inspection and Palpation

The muscles are inspected for bulk and fasciculations and, when indicated, palpated for tenderness, consistency and contractures.

Tone

Muscle tone is assessed by putting selected muscle groups through passive range of motion. The most commonly used maneuvers for the lower extremities are flexion and extension at the knee and ankle.

Strength Testing

Muscle strength is tested from the proximal to the distal part of the extremity so that all segmental levels for the extremity are tested (for the lower extremity that is L2 to S1 – see table). Muscle power is graded on a scale of 0-5 (see table)

Stretch or Deep Tendon Reflexes

A brisk tap to the muscle tendon using a reflex hammer produces a stretch to the muscle that results in a reflex contraction of the muscle. The muscles tested, segmental level, and grading of DTR’s is listed below.

Plantar Reflex

The plantar reflex is a superficial reflex obtained by stroking the skin on the lateral edge of the sole of the foot, starting at the heel advancing to the ball of the foot then continuing medially to the base of the great toe. The normal response is flexion of all the toes. The abnormal response is called a Babinski sign and consists of extension of the great toe and fanning of the rest of the toes.

Pathological reflexes- frontal release signs- snout, root, palmomental

These patterned behavior reflexes appear when there is damage to the frontal lobes, which inhibits these primitive reflexes. In the normal person these reflexes are absent. Pressing a tongue blade on the lips tests for the snout reflex. The abnormal response is a pouting of the lips. The root reflex is tested for by gently stroking the lateral upper lip. The abnormal response is movement of the mouth towards the stimuli. Stroking the palm of the hand while watching for contraction of the ipsilateral mentalis muscle of the lower lip tests for the palmomental reflex.

Strength testing using squat & rise, heel & toe

The strength of the powerful muscles of the lower extremities is often best assessed by using the patient’s own weight. Having the patient squat and rise tests the pelvic girdle and upper leg muscles while heel and toe walking tests the muscles of the foreleg.

Motor – Abnormal

Upper extremities – Inspection and Palpation

In this patient there are fasciculations (spontaneous contraction of a motor unit) noted in the deltoid muscle as well as atrophy. There is also atrophy of the interosseous muscles of the hands. These findings can be seen in motor neuron disease such as amyotrophic lateral sclerosis.

Tone

There is increased tone in the right upper extremity that is rate dependent with the clasp-knife phenomena noted when the arm is flexed. This is spasticity from an upper motor neuron lesion.

Strength Testing

With an UMN lesion the fine, fractionated movements of the fingers and hand are lost. Distal extremity weakness is greater than proximal weakness. With greater effort to move the paretic hand, there is overflow activation of proximal muscles and even of the contralateral hand, which produces mirror or synkinetic movements.

Stretch or Deep Tendon Reflexes

It is always important to compare right vs. left. The first patient shown has hyperreflexia or 3+ DTR’s of the right biceps, triceps and brachioradialis. The second patient has hyperreflexia of the right finger flexors. Hyperreflexia is one of the signs of a UMN lesion.

Testing for pronator drift

With an UMN lesion there is pronation and downward drift of the outstretched supinated arm. This is because the pronators overpower the weaker supinators. Another name for this sign is a pronator Babinski.

Lower extremities – Inspection and Palpation

There is hypertrophy of this patient’s left leg. Closer inspection of that extremity shows hyperpigmented skin lesions suggesting segmental neurofibromatosis. A thorough skin search can provide important clues to diagnosis especially in the neurocutaneous syndromes.

Tone

There is spasticity on passive range of motion of the patient’s right ankle with decrease range of motion and clonus which is caused by repetitive contraction of the stretched gastrocnemius muscle. Range of motion at the knee would also demonstrate spasticity. These findings are part of the UMN syndrome.

Strength Testing

Testing of the muscle strength in this patient shows 1/5 weakness of dorsiflexion, plantar flexion, inversion and eversion of the right ankle with normal proximal strength.

Stretch or Deep Tendon Reflexes

There is hyperreflexia of the right knee jerk (3+) with a rightsided crossed adductor response (the crossed adductor contraction occurred because of the increased right leg tone which resulted in reflex contraction of the adductor magnus with the very slight stretch of this muscle caused by tapping the opposite knee). There is also hyperreflexia with clonus (4+ DTR) of the right ankle. The second patient demonstrates a 4+ ankle jerk on the left with sustained clonus. Hyperreflexia is one of the signs of the UMN syndrome.

Plantar Reflex

The patient has a Babinski sign on the right with an up going great toe and dorsiflexion and fanning of the other toes. This is an important indication of UMN disease.

Pathological reflexes- frontal release signs- snout, root, palmomental

These patterned behavior reflexes appear when there is damage to the frontal lobes, which normally inhibits these primitive reflexes.

• A snout reflex occurs when a tongue blade is pressed on the lips and there is pouting of the lips.
• A root reflex occurs when gently stroking the lateral upper lip causes the mouth to moves toward the stimuli.
• A palmomental reflex occurs when stroking the palm of the hand causes the ipsilateral mentalis muscle of the lower lip to contract.

Strength testing using squat & rise, heel & toe

This patient has proximal pelvic girdle weakness which is demonstrated by his using his hands to climb the wall and then pushing on his thighs to get his trunk upright. When a patient uses his hands to climb up his legs to get to a standing position is this called a Gowers’ sign.