1. Organization of the
Motor System

2. Motor Organization – The Big Picture
There are several systems that enable smooth and exact purposeful movements. The
corticospinal and corticobulbar systems are the
most important voluntary motor systems. The motor signals generated in the cerebral cortex are relatively coarse and need modulation, however, as facilitated by the basal ganglia and the cerebellum.
Other voluntarily regulated motor pathways are the rubrospinal and the reticulospinal tracts. The two vestibulospinal tracts receive sensory input from the vestibular nuclei but are not directly influenced by the cerebral cortex. They are thus largely involuntary motor pathways. The motor system receives also
somatosensory input via the muscle spindles, the dorsal column/medial lemniscus pathways, the somatosensory cortex, the anterolaleral system (ALS), and thereticulospinal tracts.

3. Start of the Motor Pathways
The lateral corticospinal tract is a long motor pathway
between the cortex and the spinal cord, several long motor
Pathways also start in the brainstem and end in the spinal cord.
Start of the Motor Pathways

4. End of the Motor Pathways
The descending motor tracts (at spinal levels) are subdivided into the ventromedial (also called anteromedial) and the
lateral pathways.
The ventromedial tracts are:
· Pontine (medial) reticulospinal
· Lateral vestubulospinal
· Medial vestibulospinal
The lateral tracts are:
· Lateral corticospinal
· Rubrospinal
· Medullary (lateral) reticulospinal

5. Location of Motor Neurons in Relation to Function
In the ventral horn of the spinal
cord, flexor and adductor
neurons lie dorsal to the
extensor and abductor
neurons. Cells for distal
muscles lie laterally to those
for trunk structures (i.e.,
proximal muscles).
Relations between Motor Neurons and Spinal Pathways
Lateral Pathways are Biased for Flexion of the Limbs
Medial Pathways are Biased for Extension of
the Limbs

6. Corticospinal Tract Initiation and Control of Motor Activity
The corticospinal tract is the
most important motor
pathway. Prefrontal areas
(motor planning) project to
the premotor cortex
(production of motor
programs), which then
communicates with the
primary motor cortex
(execution of excitatory
drive for motor activity).
(Brodmann’s area 4)
Brodmann’s area 4 is often
called the primary motor cortex.
Premotor and Supplementary Cortices (Brodmann’s area 6)

7. Homunculus
Each distinct area in the primary motor cortex is responsible for the motor control
of a particular part
of the body. The
representation of
the body that can
be functionally
mapped against
such a region is
called a
“homunculus.”

8. Predominant Role of the Lateral Corticospinal Tract
The main function of the lateral corticospinal tract is voluntary contraction of distal flexor muscles of the limbs (e.g., it is thus integral to reaching and walking).
Sensory input from the periphery
is processed by the cortex, which constantly modifies the signals transmitted by this tract. Inputs into the cortex from the basal
ganglia and cerebellum via the thalamus also always modulate lateral corticospinal output.

9. Start of Lateral Corticospinal Tract
The origin of the corticospinal
tract is the pyramidal cell
bodies located in layer 5 of
the precentral gyrus and
anterior paracentral lobule.
End of Lateral
Corticospinal Tract
The end of the corticospinal
tract is the contralateral
anterior horn of the spinal
cord, where the axons of the
upper motor neurons
synapse with alpha and
gamma lower motor neurons

10. Route of Corticospinal Tract
· corona radiata
· internal capsule
(posterior limb)
· crus cerebri
· basilar pons
· corticospinal tracts in
spinal cord
· synapses on alpha and
gamma neurons in
spinal anterior horn

11. Approximately 90% of the fibers from motor cortex cross over at the pyramidal decussation (caudal medulla) to form the lateral corticospinal tract.
Ten percent remain ipsilateral to enter the cord as the ventral (anterior) corticospinal tract.
Damage to the lateral corticospinal tract rostral to the pyramidal decussation
produces contralateral hemiparesis.
Damage to the lateral corticospinal tract caudal to the decussation produces
ipsilateral hemiparesis at and below the lesion.

12. Upper Motor Neurons
· Upper motor neurons forming the corticospinal and corticobulbar tracts arise from cell bodies located in layer 5 of the primary motor cortex. The corticospinal fibers project through the corona radiata, internal capsule, crus cerebri, basal pons, and pyramid, entering the spinal cord to terminate (largely) in the contralateral
anterior (ventral) horn. Direct or indirect excitatory synaptic contact is made with a second order motor neuron (lower motor neuron).
Lower Motor Neurons
· The cell bodies of the lower motor neurons dwell in the ventral horn of the spinal cord (receiving inputs from corticospinal fibers) and the motor nuclei of the brainstem (receiving inputs from corticobulbar fibers). They send axons directly to skeletal muscle fibers to effect muscular contractions.

13. Lower Motor Neuron Lesion
– Symptoms occur ipsilateral to site of the lesion
-- Flaccid paralysis (loss of movement)
– Hyporeflexia/areflexia(due to interruption of the
efferent (motor) limb of the sensory-motor reflex arcs.
– fasciculations  Wasting of muscles,
-- atonia or hypotonia(muscle tone reflects sustained partial contraction of muscular fibers and depends directly on the monosynaptic reflex arc that connects the muscle spindles to the lower motor neurons)
Damage to lower motor
neuron cell bodies or their
peripheral axons yields
paralysis (loss of
movement) or paresis
(weakness) of the affected
muscles. In addition to
paralysis and/or paresis, the
lower motor neuron
syndrome includes a loss or
decrease of reflexes
(areflexia or hyporeflexia)
due to interruption of the
efferent (motor) limb of the
sensory-motor reflex arcs.
Damage to lower motor neurons also produces a loss of muscle tone (atonia or
hypotonia – muscle tone reflects sustained partial contraction of muscular fibers
and depends directly on the monosynaptic reflex arc that connects the muscle
spindles to the lower motor neurons). Later, because of denervation
(disconnection of muscle from nerve cells), atrophy and finally the wasting of
the affected muscles occur. The involved muscles may also express
fasciculations, spontaneous twitches characteristic of muscles innervated by
sick or dying lower motor neurons. These spontaneous contractions can be
recognized in an electromyogram (EMG) as fibrillations. The symptoms occur
ipsilaterally to the site of the damage
Examples of diseases that involve LMN syndrome are:
· Amyotrophic lateral sclerosis
· Peripheral nerve damage (traumatic)

14. Diseases of the Lower Motor Neuron
Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease)
It is a progressive neuromuscular disease that initially affects and later destroys lower motor neurons and eventually also parts of the pyramidal tract and the precentral gyrus (and the anterior portion of the paracentral lobule)
ALS patients usually develop
muscle weakness and difficulty
speaking and/or swallowing.
Sphincter control, sensory
function, intellectual ability, and
skin integrity are not commonly
affected.

15. Upper Motor Neuron Lesion
– Lesion above decussation: symptoms contrlateral to the lesion
– Lesion below the decussation: symptoms ipsilateral to the lesion
– Hyperreflexia
– Extensor plantar response
– First flaccid paralysis, later spastic paralysis
– No wasting of muscles (because 2nd motor neuron is not impaired)

16. Brown–Sequard Syndrome -->Hemisection of the spinal cord

17. Paraplegia
Paraplegia occurs after a
bilateral spinal cord injury. In
most cases, a traumatic
event impairs the cells within
the spinal cord or cuts or
crushes the fibers of the long
tracts (through bruising,
compression, or laceration).
The symptoms of
paraplegia are:
· flaccid paralysis below
the level of the lesion (i.e., related to spinal shock), followed days-to-weeks later by spasticity.
· increased deep tendon reflexes and clonus.
· extensor plantar response (Babinski sign).
· early retention of urine with painless distension of the bladder and overflow, as pressure overcomes the reflex closure of bladder sphincters. Reflexive emptying of bladder accompanies the lifting of spinal shock.
· paraplegia in flexion (physiotherapy is warranted).
· loss of all somatosensation from below the lesion.

18. Other Motor Pathways 1. Rubrospinal Tract (Flexor Muscles)
Start: Red nucleus in midbrain
End: Alpha and gamma
motor neurons in the anterior horn of the spinal cord.
Function- stimulation of flexors of upper limb.
2. Medullary (Lateral) Reticulospinal Tract (Flexor Muscles)
-originates in the nuclei of medulla and ends in anterior horn of spinal cord.
- Most fibers of the medullary
reticulospinal pathway facilitate contraction of flexor muscles of the
limbs.

19. 3. Pontine (Medial) Reticulospinal Tract (Extensor Muscles)
originates in the nuclei of medulla and ends in anterior horn of spinal cord.
End: anterior horn of the spinal cord.
Most fibers in this pathway facilitate
contraction of extensor muscles of the limbs.
4. Lateral Vestibulospinal Tract (Extensor Muscles)
Start: Lateral vestibular nucleus.
End: anterior horn of the spinal cord
5. Medial Vestibulospinal Tract (Extensor Muscles)-simillar to lateral vestibulospinal tract.

20. Decorticate Posturing
A lesion rostral to the red nucleus that impairs corticospinal, produces decorticate posturing. After a noxious stimulus or spontaneously, the affected patient will flex the upper limbs and extend the lower limbs.
corticospinal tract
interrupted – mainly flexion impaired
rubrospinal tract intact – flexion of the arms
· medullary reticulospinal tract intact – flexion of extremities
· pontine reticulospinal tract intact – extension of extremities
· vestibulospinal tracts intact – extension of extremities
Arms
In the arms, the flexor input of the rubrospinal tract is still intact. Hence, there is strong flexor innervation, which is much greater than the extensor input of pontine reticulospinal and vestibulospinal tracts.
Legs
For the lower limbs rubrospinal tract has almost no impact, hence the extensor innervation is much more relevant, so the lower limbs are extended.

21. Decerebrate Posturing
A lesion below the red nucleus that impairs the
corticospinal, corticobulbar, and rubrospinal
Fibers produces decerebrate posturing. After
a noxious stimulus or spontaneously, the patient
will extend the upper and lower limbs.
· corticospinal tract
interrupted – mainly flexion impaired
· corticobulbar tract
interrupted – paralysis of motor CNs
· rubrospinal tract interrupted – no flexion of arms
· medullary reticulospinal tract intact – flexion of extremities
· pontine reticulospinal tract intact – extension of extremities
· vestibulospinal tracts intact – extension of extremities
In the upper and lower limbs, there is flexor input from only the medullary
reticulospinal tract, which is overruled by the extensor innervation of the pontine reticulospinal and vestibulospinal tracts.