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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. |
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Control
Circuits
First, we need to add two "control circuits" that influence the corticospinal
tract- the basal ganglia and the cerebellum. |
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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).
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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. |
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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). |
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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. |
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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.
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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.
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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.
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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.
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Exam Tests
Clinical testing of the motor system:
- Muscle strength
- Tone
- Reflexes
- Pathological reflexes
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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. |
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Pearls
Acute UMN lesions and UMN lesions in infants can produce hypotonia initially
with hypertonia occurring later. |
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