Chapter 14: Motor System

Question 1

Motor tracts

Answer 1

Often called upper motor neurons. Starts in the head and ends in the spinal cord.

Either middle front (core and proximal (shoulder and hip)
or Lateral front (distal especially hands and feet).

Question 2

Motor tracts to the spinal cord

Answer 2

Some UMN have cell bodies in cerebral cortex- UMN of cortical origin= greater voluntary control over, the directors (they call the shots).

Some UMN have cell bodies in brainstem- they are of brainstem and subcortical origin. The union laborers (they provide the muscle)

Basal ganglia- stylistically sits in between two groups and says “I have an idea for movement and sends idea up to the cortical neurons and down to the brainstem neurons so the same motor message gets sent both places.

UMN from cortex send axons directly down to the spinal cord, they directly control UMN brainstem group got idea to move but they are only the muscle and need direction. So the cortical neurons also provide direction to the muscle and then the muscle has their own group of UMN that go down to the spinal cord.

Question 3

Medial group

Answer 3

Cortical origin-more direct voluntary control of movement.

Subcortical origin- support voluntary movement.
-Guided by medial and lateral cortical pathways.

Question 4

Lateral group

Answer 4

Cortical origin- Direct voluntary control (distal)
-influences and guides activity of supporting medial group pathways.

Subcortical origin- Supports and complements direct voluntary control

Question 5

Medial group

Answer 5

-Reticulospinal- brainstem in origin (reticular formation) a very busy place- it is the origin of a medial brainstem UMN pathway. Fibers from reticular formation project broadly to upper and lower extremities, especially help with postural muscles and gross limb movements. Lower degree of direct voluntary control due to being brainstem.

Medial Vestibulospinal- projects to neck and upper back postural muscles. Helps maintain upright against gravity. Lower degree of direct voluntary control.
Helps us stay upright against gravity.

Lateral Vestibulospinal- Projects to axial and lower extremity extensors. Helps maintain upright against gravity. Lower degree of voluntary control

Medial Corticospinal- Projects to medial motor neuron pools bilaterally. Voluntary control of neck, shoulder, and trunk muscles. Higher degree of direct voluntary control.

Question 6

Lateral group

Answer 6

Rubrospinal- Small pathway. Minor control of distal extensor muscles of upper extremity

Lateral Corticospinal- Most important pathway for voluntary movement.

• fractionated movement (any muscles in any combination of movement that I want). Direct control of distal muscles/of LMN and it provides guiding control of the brainstem group.
• guiding control of postural support muscles.
• 90% cross and 10% stay on the same side at the pyramids.

Question 7

Nonspecific motor tracts

Answer 7

They are UMN come from brainstem down to spinal cord- job is to lower the threshold for all other motor neuron pathways so that it is easier for UMN to set off LMN. Easier to make action potentials. Turned on by activity of autonomic and emotional systems. Get you ready for action.

• Descend from brainstem
• Broad facilitation of lower motor neurons in spinal cord.
• Turned on by activity of limbic system.

Question 8

Corticobrainstem tracts

Answer 8

Voluntary control of face, tongue, throat and part of neck.
-controls cranial nerves

Start in cerebral cortex and end in brainstem, are the UMN of our cranial nerves, high degree of direct voluntary control. Turns on cranial nerve 7 so we can make faces and use facial muscles.

Question 9

Cortical motor areas

Answer 9

Primary motor cortex (motor homunculus)

Most of our UMN come from the pre-central gyrus (frontal lobe)= home base for majority of our cortical UMN, for medial and lateral corticospinal neurons.

• Face is lateral
• Legs are medial.

Premotor area- anticipatory postural control. in front of primary motor cortex- helps us to plan anticipatory postural control, (reach to get a bottle, premotor area helps to set postural control so we don’t knock ourselves over)

Supplementary motor area- Bimanual activities, activities with sequence
-helps to plan bimanual activities, especially activities that have sequence in them. (sequence while playing a piano, Neurons in this area are active even if we just think about moving.)

Question 10

3 broad condition

Answer 10

• UMN completely cut off from LMN (complete spinal cord injury)
• UMN intact but tonically overactive (Parkinson’s disease or TBI)
• Cortical UMN damages, brainstem UMN OK (stroke- can move gross motor fine cause brainstem is still hooked up, cant move fine motor cause cortical are cut off)

Question 11

Signs of Motor tract lesions

Answer 11

Paralysis- possible sign, all UMN have been cut off, exist in brain but can never make connection with the spinal cord (below the level of injury there is no connection with lower than site of injury)

Paresis- weakness, the cortical UMN have been damaged by a cortical stroke but brainstem UMN still hooked up (brainstem attempts the motion but cortical isn’t there to run the show so they are weak and gross in movement). A weakness that is not well controlled.

Distribution of lost strength (hemiplegia, paraplegia, tetraplegia) tell us the pattern of the paralysis or paresis.

Loss of fractionated movement (if cortical UMN, especially the lateral corticospinal- weak and will lose fractionated movement, moving muscles in any combo and pattern we want). Corticospinal not able to control distal body part

Question 12

Abnormal cutaneous reflexes

Answer 12

After UMN are cute, spinal level reflexes below that level of damage get stronger. Hyperactivity of spinal level reflexes.
Babinski response- toes will extend and whole limb may withdraw- when UMN cut off that reflex grows stronger

Question 13

Muscle stretch hyperreflexia

Answer 13

Exaggerated reflex response to stretch when descending connection is missing or much reduced.
-Stretch- typically quick stretch is stimulus (velocity dependent hypertonia-requires the stretch to stimulate it)

Stretch a muscle- response is contraction of the same muscle that is stretched, when UMN cut off, the strength of the contraction response is stronger.

When UMN doesn’t connect to the synapse in spinal cord, normal stimulus brings an abnormally large response.

Question 14

Clonus

Answer 14

Rhythmic, repeating (usually involuntary) contraction of single muscle group
-Can be unsustained (happen for a few beats and die out) or sustained (always pathologic- can keep going and keep going)

A series of muscle contractions in response to a quick stretch, velocity dependent hypertonia that repeats itself.

We don’t know what the source is.

Question 15

Clasp-knife response

Answer 15

initial resistance to stretch that fades over time. Hard to start and about halfway it fades and becomes easier.
-All evidence of a stronger than normal stretch reflex.

Enhanced phasic stretch

Question 16

Myoplasticity

Answer 16

Changes/remodeling of the muscles themselves because they are not contracting normally. (adaptive changes within the muscle itself)
-Atrophy- atrophy of disuse not the atrophy of denervation (still connected to its nerve supply that never turns on), loss of neuromuscular excitation.

• Increased “stiffness”- actin and myosin sticking due to lack of movement. Need to be broken up by movement (passive or active)
• Contracture- when muscle is chronically shortened it adapts by taking out sarcomeres so that it is right length for contracting, When we try to stretch it out it cannot. resists.

Question 17

Atrophy

Answer 17

If LMN- atrophy of denervation-muscle will wither away

If UMN- atrophy of disuse

Question 18

Abnormal muscle tone

Answer 18

Temporary hypotonia (spinal shock) 
-LMN will temporarily go to sleep

For a short period of time there are no spinal reflexes because the reflex loop is in shock, overtime it gets over its shock and becomes hypersensitive because it realizes it lost its UMN supple. No messages from above.

Stroke may have some cerebral shock due to damage of UMN in brain (may be very plegic and then become more responsive and more paretic)

Question 19

Hypertonia

Answer 19

3 different kinds of hypertonia (in spinal cord injury, in Parkinson’s disease, and post stroke)

Hypertonia can be velocity dependent (muscle stretch reflex can be overactive), hypertonia related to the stretch which brings a hyper response= muscle flex hyperreflexia (most often after spinal cord injury)

Spasticity- exaggerated response of a muscle to a stretch- any disorder of tone that leads to extra tone, we will use it only to refer to muscle stretch hyperreflexia.

Hypertonia (velocity independent)- UMN being present but abnormally active (Parkinson’s and TBI) because of damage to the brain the UMN don’t work well and send too many signals all the time.
Rigidity-they will always fight back against the stretch (all the time, too much tone)

Decerebrate- without the head, tonically active with extension of the arms and extension of the legs. UMN too active to contract extensors of arms and legs.
-indicative of more sever injury cause more of the head is cut off but decorticate is more common.

Decorticate- without cortex- the patient is in flexion of the arms and extension of the legs, UMN that flex that arms are tonically overactive and UMN that extend the legs are tonically overactive.

Both are more representative of post trauma to the brain. Not Parkinson’s disease.

Question 20

Muscle overactivity (reduction of cortical control)

Answer 20

activity dependent- last type of hypertonia- muscle overactivity- typically what we see in patients who have had a stroke, blue ball means the cortex is gone, the stroke has damaged the corticospinal neurons, brainstem is still there. Basil ganglia says “lets move” and brain stem says got it and the cortex is not there to control it. Wasn’t there when they were sitting down, only when they went to move/active. Hypertonia really shows up when they try to move.

Abnormal synergy of the leg is extension and for the arm it is flexion. move in abnormal patterns because the brainstem is doing its job but the cortex isn’t there to say relax and do your job.

Question 21

muscle overactivity

Answer 21

reduction of cortical control. author calls it “reticulospinal tract overactivity. brainstem overactivity