Block 5
Dr. C.R. Houser
SPINAL CORD III. MAJOR PATHWAYS OF THE SPINAL CORD - MOTOR
Goals: After the lecture and reading, you should be able to:
1. Describe a major motor pathway (corticospinal path) of the spinal cord and locate the
pathway in the spinal cord and brainstem.
2. Understand the motor deficits produced by a lesion at any point in the pathway.
3. Describe the difference between upper and lower motor neuron syndromes and give a
specific example of a lower motor neuron and an upper motor neuron.
Reading
Nolte, Chapter 10, Spinal Cord, p. 252; Chapter 18, Overview of Motor Systems, pp. 457-469.
Purves, Upper Motor Neuron Syndrome, pp. 447-449.
Overview
Multiple ascending (sensory) and descending (motor) systems are present within the spinal cord,
and each has a distinctive pathway. Knowledge of the pathways is necessary for determining the
location of lesions within these systems and for understanding their effects. One general principle is
that most motor and sensory pathways cross the midline in some region of the CNS. As a result,
one side of the cerebral cortex will be associated with function on the contralateral side of the body.
The location of a lesion in relation to the crossing will determine whether the lesion produces
clinical signs on the same or opposite side of the body.
I. DESCENDING (MOTOR) PATHWAYS
Several motor pathways exist, and they can be divided into two groups according to their
location and general function:
Lateral Pathways
Medial pathways
Corticospinal (lateral)
Vestibulospinal
Rubrospinal
Reticulospinal - Medullary
"
- Pontine
Tectospinal
A. Lateral Corticospinal (Pyramidal) Tract
1. This pathway originates in the cerebral cortex from neurons in the following cortical areas:
Area 4 (primary motor area); 6 (primarily the supplementary motor region); 3,1,2 (primary
somatosensory area); and 5 (adjacent parietal area).
2. Axons of these neurons leave the cerebral cortex and converge in the posterior limb of the
internal capsule.
3. Upon reaching the midbrain, the fibers are concentrated in the central part of the basis pedunculi
(base of the cerebral peduncle).
4. Upon reaching the pons, the fibers diverge and descend in small bundles (located between the
transversely oriented fibers of the basis pontis that are entering the cerebellum).
5. Within the medulla, the corticospinal fibers again form a compact group of fibers, the pyramid,
that is located on either side of the midline on the ventral surface of the medulla.
6. Near the caudal end of the medulla, the corticospinal fibers of the pyramids cross the midline in
the decussation of the pyramids and assume a more dorsolateral location within the lateral
columns of the spinal cord.
7. The fibers descend within the lateral corticospinal tract until they reach the appropriate level of
the spinal cord for termination. They then move into the gray matter where they form synaptic
contacts with a) motoneurons of the ventral horn; b) interneurons in the intermediate zone
which, in turn, contact motoneurons; or c) neurons in the base of the dorsal horn for modulation
of somatosensory information.
Approximately 85% of the descending fibers in the pyramid cross to form the lateral
corticospinal tract. However, the remaining 15% form the anterior corticospinal tract and continue
to be uncrossed until they reach their level of termination in the spinal cord. Most fibers then cross
to the opposite side, but there may be bilateral termination in the spinal cord. These fibers generally
synapse on motoneurons or interneurons that supply proximal musculature and, thus, are
functionally related to the medial pathways.
Function of the Lateral Corticospinal Tract.
Throughout much of their course, the corticospinal fibers are associated with fibers of other
systems and, thus, cannot be selectively lesioned to determine their function. However, an isolated
lesion can be made at the pyramids. Following such a lesion in monkeys, one finds:
a. Relatively little change in muscle tone (or slightly decreased at early stages after the lesion).
b. Slight weakness (particularly of the flexor muscles); and
c. Loss of the ability to make independent movements of specific muscle groups (loss of
fractionation of movement).
Thus it has been concluded that the lateral corticospinal tract:
a. Has facilitatory effects on flexor muscles;
b. Is necessary for isolated and skilled movements of the digits; and
c. Is primarily concerned with voluntary, goal-directed or skilled movements.
B. Additional Motor Pathways
Be aware that there are several additional motor pathways that are named for the brainstem
components that project to the spinal cord. We will discuss these pathways further as we study the
brainstem and integrate our ideas about the motor system. For now, be familiar with the names of
these tracts and their brainstem origins:




Rubrospinal (red nucleus)
Vestibulospinal - (lateral vestibular nucleus)
Medullary reticulospinal - (reticular formation of the medulla)
Pontine reticulospinal - (reticular formation of the pons)
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II. BASIC CLASSIFICATION OF MOTOR DISORDERS
We will now consider a very general classification of motor disorders that is used clinically. Motor
disorders involve changes not only in the ability to produce desired movements but also in muscle
tone.
A. Muscle Tone
Normal muscle tone can be considered operationally as the normal resistance of a muscle to active or
passive stretch. It is due to at least two factors:
1. Inherent viscoelastic properties of the muscle;
2. Tension set up by contraction of a small number of skeletal muscle fibers. To avoid fatigue,
different groups of muscle fibers within a muscle are brought into action at different times. The
muscle fibers contract in response to the asynchronous firing of motor neurons.
Normal postural tone of skeletal muscle is dependent not only on the integrity of the reflex arc, but
also on the summation of impulses received by the motor neurons from other regions of the nervous
system.
Clinical terms for alterations in muscle tone include
1. Atonia, hypotonia, flaccidity - absent or decreased tone
2. Hypertonia - increased muscle tone (spasticity or rigidity - to be discussed later)
B. Motor Syndromes
A lower motor neuron syndrome (or motor neuron syndrome) is a group of signs that occurs when
there is direct damage to motor neurons (specifically alpha motor neurons) that innervate skeletal muscle.
Examples of clinical conditions that lead to lower motor neuron syndromes are poliomyelitis that affects
the anterior horn cells themselves, and peripheral nerve injuries that interrupt the axons of the motor
neurons.
Upper motor neuron syndromes result from damage or abnormalities of neurons that constitute
the multiple descending pathways of the motor system. The motor abnormalities may be quite different
from those of a lower motor neuron syndrome. Cerebral vascular accidents (stroke) and multiple
sclerosis are clinical conditions that may produce "upper motor neuron syndromes". Some of the
signs in each type of syndrome are listed in table form for comparison.
Lower Motor Neuron Syndrome
Paralysis or paresis
Hyporeflexia
Hypotonia (flaccidity)
Atrophy of muscles
Fibrillations & fasciculations
--
Upper Motor Neuron Syndrome
Paralysis or paresis
Hyperreflexia
Hypertonia (spasticity)
Minimal (disuse) atrophy
-Babinski sign, i.e. extensor plantar response (usually)
A distinction between hypotonia and hypertonia is clearly important for the above
classification. While it is relatively easy to understand why one could have hypotonia as a result of motor
neuron damage, it is less clear why one frequently sees hypertonia in the form of spasticity
following damage to the descending pathways. As a generality, anything that could lead to increased
excitation (facilitation) or decreased inhibition of the  or  motor neurons could produce hypertonia
and spasticity.
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Spasticity is a clinical condition that is characterized by:
1. Increased sensitivity of the stretch reflex (hyperreflexia).
2. Increased muscle tone (hypertonia) that results in increased resistance to passive stretch. This increased
resistance to passive movement is generally:
a. Greater on one side of the joint than on the other;
b. Greatest in antigravity muscles, i.e. flexors of the upper limb and
extensors of the lower limb;
c. Velocity dependent - the more rapid the movement, the greater the resistance.
3. Clasp-knife (lengthening) reaction that can be elicited toward the end of the range of movement.
4. Clonus (variable). This is a series of rhythmic alternating contractions that can occur following a
single stimulus such as a tendon tap or stretch of the muscle in other ways.
5. Finally, when spasticity is present, movements typically occur in stereotyped patterns, and these
patterns cannot be voluntarily fractionated into the "normal" patterns of movement.
III. DEFINITIONS
A. Fibrillations
1. Spontaneous contraction of single muscle fibers
2. Results from sensitization of single muscle fibers that are denervated and contract
individually. Because single fibers contract asynchronously, fibrillations are not visually
detectable (except in the tongue), but they can be revealed by electromyographic (EMG)
recording
B. Fasciculations
1. Spontaneous contraction of groups of skeletal muscle fibers resulting in
localized twitching which can be seen under the skin
2. Caused by spontaneous discharges of irritated motor neurons. They involve motor units as a whole
and, thus, are visible. Twitching of groups of muscle fibers is seen most often in patients with
chronic disease that affects the motor neurons, such as progressive muscular atrophy.
C. Babinski sign (Extensor Plantar Response)
1. Dorsiflexion of the great toe instead of the normal plantar flexion in response to plantar
stimulation (stroking the sole of the foot with a blunt instrument).
2. Indicative of abnormalities (or incomplete development) of descending motor pathways. Some
clinicians/investigators believe that the Babinski sign is indicative of a lesion of the
corticospinal tract, but others think that the precise pathways and mechanisms are unknown.
Purves 17.16
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Practice Drawing the Corticospinal (and Somatosensory) Pathways
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