Transcript The Motor System

The
Motor Control System
Learning Module
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Overview describes the module content &
learning objectives
Please complete this section first!
Contents overview of the Motor System under
normal conditions and 3 interactive examples of
lesion effects.
Case-based practice provides practice
with feedback using patient cases.
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Overview
Introduction
Learning Objectives
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Introduction
• This module reviews the Motor Control System.
• Module organization consists of three components. Overview
consists of this Introduction and the Learning Objectives. Contents
consists of Navigation Instructions, a Legend, Review of the normal
structure and function of the motor control system, and 3 interactive
lesion lessons. Cases consists of Instructions and 2 interactive
patient cases with feedback.
• At the bottom of each page a navigation bar contains options to
move throughout the module.
• Material is presented at both the behavioral level and the
neuroanatomical level.
• The behavioral level is presented first and depicts a patient’s clinical
presentation.
• The neuroanatomical level depicts the detailed anatomy of first-order,
second-order and third-order neurons.
• The neuroanatomical level accounts for the patient’s behavioral
presentation on examination under normal and lesioned conditions.
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Learning Objectives
After completing this module you should be able to:
• describe, in detail, the structure and function of the
corticospinal tract.
• given a lesion, identify the signs and symptoms that
would be expected.
• given a patient case (examination results and chief
complaint), identify the location of the lesion causing
the signs and symptoms .
• correlate neurology information between the
behavioral and neuroanatomical levels.
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Contents
Read these Instructions!
Legend: symbols used throughout the module
Overview of the Motor Control System
Lesion lessons
Corticospinal tract lesion
Lateral corticospinal tract lesion
Ventral horn lesion
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Instructions
• This module contains 3 interactive lesion lessons with animation.
• Lesson lessons begin with a question about the symptoms
produced by that particular lesion.
• Clicking the answer button will reveal the answer to the question.
• Clicking the explanation button will lead to both behavioral and
neuroanatomical explanations of the lesion.
•
Each presentation is launched by clicking the animation button.
The same button serves to replay the animation if desired.
• Any of the lessons may be accessed by simply clicking on the
lesion title on the Contents page.
• Please refer to the Legend that defines the symbols used
throughout the module.
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Legend
Mechanism of injury
Upper motor neuron
Lesion
Lower motor neuron
Stimulus
Motor impairment
Function intact
Function lost
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Voluntary Knee Extension:
Behavioral Description
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Voluntary movement is controlled by a
system of brain and spinal motor centers
linked by neuronal pathways. The primary
motor pathway (Corticospinal tract) is
crossed such that the left hemisphere
controls movement of the right half of the
body and vise versa. Motor pathways
consist of upper and lower motor neurons.
Upper motor neurons originate in the
precentral gyrus, decussate in the medulla,
descend in the lateral column of the spinal
cord, and terminate on lower motor neurons
in the ventral horn. Lower motor neurons
exit the CNS and innervate skeletal muscles
via the peripheral nervous system.
Stimulus
UMN
LMN
Neuroanatomical Explanation
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Legend
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Voluntary Knee Extension:
Neuroanatomical Description
The cell body of the upper motor neuron is
located in he precentral gyrus
(somatotopically organized). The axon
descends through the internal capsule,
decussates in the medulla, descends
through the lateral column of the spinal cord
and terminates in the ventral horn.
The cell body of the lower motor neuron is
located in the ventral horn. The axon exits
the CNS via ventral rootlets of
spinal nerves and
innervates skeletal muscle
via a peripheral nerve.
Skeletal muscles contract
to produce the force to
extend the knee.
Stimulus
UMN
LMN
Behavioral Explanation
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Legend
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Voluntary Knee Extension:
Neuroanatomical Description
The cell body of the upper motor neuron is
located in he precentral gyrus
(somatotopically organized). The axon
descends through the internal capsule,
decussates in the medulla, descends
through the lateral column of the spinal cord
and terminates in the ventral horn.
The cell body of the lower motor neuron is
located in the ventral horn. The axon exits
the CNS via spinal nerves and
innervates skeletal muscle
via a peripheral nerve.
Skeletal muscles contract
to produce the force to
extend the knee.
Behavioral Explanation
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Stimulus
UMN
LMN
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Legend
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Lesion of the left corticospinal
tract (at the level of the cortex)
produces what impairment?
Click for answer
Cortical damage to the left corticospinal tract causes
upper motor neuron signs on the right face and body
(arm, leg, and trunk, contralateral). Stroke is the most
common cause of supraspinal damage to the
corticospinal tract.
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Legend
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Corticospinal Tract Lesion: Behavioral Explanation
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Damage to the corticospinal
tract, prior to the decussation,
produces UMN signs and
symptoms to the contralateral
face and body.
UMN signs:
• Weakness (Spastic paralysis)
• Hyperreflexia (+ Babinski, clonus)
• Hypertonia
Lesion
UMN
LMN
Lost function
Impairment
Neuroanatomical Explanation
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Legend
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Corticospinal Tract Lesion:
Neuroanatomical Explanation
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Impairment is seen in the
contralateral face because
CN VII is crossed and the
contralateral body because the
UMN decussated in the
medulla.
Impairment is
generalized to all
body parts below the
lesion level because
the lateral
corticospinal tract is
an efferent pathway.
Lesion
UMN
LMN
Lost function
Impairment
Behavioral Explanation
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Legend
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Lesion of the right lateral
corticospinal tract produces
what impairment?
Click for answer
Damage to the right lateral corticospinal tract causes UMN
signs and symptoms in the right (ipsilateral) side of the
body, generalized below the lesion level.
Impairment is ipsilateral because the pathway decussated
in the medulla. Impairment is generalized below the lesion
level because it is an efferent pathway. The lateral
corticospinal tract exists only at the level of the spinal cord.
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Legend
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Lateral Corticospinal Tract Lesion: Behavioral Explanation
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Damage to the lateral
corticospinal tract, after to the
decussation, produces
ipsilateral UMN signs and
symptoms, generalized below
the lesion level.
Lesion
UMN
LMN
Lost function
Impairment
Neuroanatomical Explanation
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Legend
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Lateral Corticospinal Tract Lesion:
Neuroanatomical Explanation
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Because the lesion involves
UMNs that have already
decussated, impairment is
ipsilateral to the lesion.
Impairment is generalized to all
body parts below the
lesion level because
the lateral corticospinal
tract is an efferent
pathway.
Lesion
UMN
LMN
Lost function
Impairment
Behavioral Explanation
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Legend
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Lesion of the right ventral horn at
L2-4 produces what impairment?
Click for answer
Lesion of the right ventral horn at L2-4 produces LMN
signs (weakness and atrophy) of the right hip flexion,
adduction, and knee extension muscles.
Lesion of the ventral horn will damage the cell bodies of
LMNs. L2-4 is the origin of femoral and obturator nerves
which innervate the muscles of hip flexion, adduction, and
knee extension. Because LMNs are uncrossed the
impairment will be seen ipsilateral to the lesion.
Click for explanation
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Legend
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Ventral Horn Lesion: Behavioral Explanation
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Damage to the ventral horn
produces ipsilateral LMN signs
and symptoms, in a myotomal
distribution.
LMN signs:
•
•
•
•
•
Weakness (Flaccid paralysis)
Hyporeflexia
Hypotonia
Atrophy
Fasciculations
Lesion
UMN
LMN
Lost function
Impairment
Neuroanatomical Explanation
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Legend
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Ventral Horn Lesion:
Neuroanatomical Explanation
Click to animate
Damage to the ventral horn (cell
body of LMNs) produces
ipsilateral LMN signs and
symptoms, in a myotomal
distribution. Signs are ipsilateral
because LMNs project to skeletal
muscles via spinal and
peripheral nerves that
remain uncrossed. The
distribution is myotomal
because skeletal
muscles are innervated
by peripheral nerves that
originate from selected
levels of the spinal cord.
Lesion
UMN
LMN
Lost function
Impairment
Behavioral Explanation
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Legend
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Case-based Practice
Read these instructions!
Patient Case #1
Patient Case #2
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Case Instructions
• These patient cases are intended to facilitate the
integration and clinical application of information
about the Motor Control System by coupling the
findings on examination and patient interview with
their neuroanatomical correlates.
• Cases are presented from two perspectives.
What lesion would account for a given set of
examination results and patient history?
For a given lesion, what signs and symptoms would
be expected on examination?
• Click on a Case number to begin the exercise.
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Review Questions: Case 1
In the emergency room the patient’s wife reports her husband had a sudden
onset slurring of speech, inability to stand from a chair because of the inability
to accept body weight onto his right leg, and the inability to feed himself or
drink with his right hand. On examination the right side of his face was
hypotonic, he was drooling from the drooping right corner of his mouth, and
he had lost the nasal labial fold on the right.
Damage to what system(s) is causing this patient’s problems?
Answer
Lesion of the left corticospinal tract above the level of the brainstem.
Lesion of the left corticospinal tract, prior to the decussation (corticobulbar
tract): removed cortical input to cranial nerves serving the face which are
crossed (hypotonia and drooping of right face with drooling).
Lesion of the left corticospinal tract, after the decussation: removal of cortical
input to cervical (inability to feed himself or drink with his right hand) and
lumbar regions of the cord (inability to stand from a chair because of the
inability to accept body weight onto his right leg).
Pathophysiology: stroke involving the perfusion territory of the left middle
Show lesion
cerebral artery (primary motor and sensory cortical areas).
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Corticospinal Tract Lesion: Behavioral Explanation
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Damage to the corticospinal
tract, prior to the
decussation, produces UMN
signs and symptoms to the
contralateral face and
contralateral body.
UMN signs:
• Weakness (Spastic paralysis)
• Hyperreflexia (+ Babinski,
clonus)
• Hypertonia
Lesion
UMN
LMN
Lost function
Impairment
Neuroanatomical Explanation
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Case Menu
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Corticospinal Tract Lesion:
Neuroanatomical Explanation
Click to animate
Impairment is seen in the
contralateral face because the
cranial nerves serving the face are
crossed. Impairment is seen in the
contralateral body because the
UMN decussated in the medulla.
Impairment is
generalized to all
body parts below
the lesion level
because the
lateral
corticospinal tract
is an efferent
pathway.
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Case Menu
Lesion
UMN
LMN
Lost function
Impairment
Exit
Review Questions: Case 2
Imaging report: The CT image reveals a mass producing impingement of the
lateral region of the right lateral column of the spinal cord at L1.
What signs and symptoms would be expected from this lesion?
Answer
A mass impinging the right lateral column at L1 would affect the lateral
corticospinal tract. The size of the mass will determine the extent of damage.
The lesion will produce UMN signs in the right leg from L1 down involving all
leg muscles from the hip flexors down. If the lesion is complete, there will be
paralysis. If the lesion is incomplete there will be paresis. In addition to
weakness (paralysis or paresis), there will be hyperreflexia and hypertonia.
Show lesion
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Right Lateral Corticospinal Tract Lesion
UMN
Click to animate
R
L
L2-4
Lateral corticospinal tract lesion
Ipsilateral upper motor neurons signs
generalized below the lesion level
UMN signs
Weakness (Spastic paralysis)
Hyperreflexia (+ Babinski, clonus)
Hypertonia
Common causes
include penetrating
injuries, lateral
compression from
tumors, and MS.
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The End
D. Michael McKeough, PT, EdD
 2008