L-25 Suprasegmental Motor Control I

Front 1

Feedback control

Back 1

Compare sensory inputs to desired state.

Generates error signal that goes to controller - brain areas - and eventually goes to actuators that produce a movement.

Front 2

Feedforward control

Back 2

Sensory inputs are fed to feed-forward controller. Generates anticipatory command that is passed to actuator muscles.

Feedback signaling necessary to adjust.

Front 3

EMG activity at biceps, triceps, wrist flexor, and wrist extensor when catching ball

Back 3

Bicep and wrist extensor EMG activity rises tens of milliseconds before ball arrives at hand - anticipatory activity to resist impact.

Movement peaks only after ball hits hand.

Front 4

Basic of motor control for face and body

Back 4

Corticospinal tract upper motor neurons travel down ventral horn and synapse on lower motor neurons and spinal interneurons.

Control of face - brainstem motor nuclei, not spinal cord lower motor neurons.

Front 5

Position of axial and appendicular

Back 5

Lower motor neurons for axial muscles are in venteromedial, limb muscles are in dorsolateral part of ventral horn.

Front 6

Short propriospinal interneurons

Back 6

Spinal cord's own interneurons

Go up and down several segments. Can be responsible for abnormal movements in just a few segments.

Front 7

Medial brainstem pathways

Back 7

Project to venteromedial axial musculature lower motor neurons.

Includes vestibulospinal tract, tectospinal tract, and reticulospinal tract.

Front 8

Tectospinal tract

Back 8

Tectum - primitive visual area that forms tectospinal tract. Connections go bilaterally to medial lower motor neurons although tectum fibers do cross over.

Front 9

Reticulospinal tract

Back 9

Tectum also projects to medial reticular formation, which forms reticulospinal tract that is involved in postural control.

Front 10

Vestibulospinal tract

Back 10

Input from inner ears feed into vestibular nuclei which controls ability of neck and body to resist changes in posture.

Front 11

Lateral brain stem pathways

Back 11

Projects to dorsolateral appendicular musclature lower motor neurons.

Front 12

Rubrospinal tract

Back 12

lateral pathway. Projects from red nucleus, midbrain motor projection, contralaterally (just like motor cortex) down rubrospinal tract to control proximal musculature.

Front 13

Rubrospinal tremor

Back 13

Multiple sclerosis, coarse "wing-beating" tremor - if hold hands near nose, elbows tremor uncontrollably.

Front 14

Ventral corticospinal tract

Back 14

Goes contralaterally through internal capsule, cerebral peduncles, pons. Ends in brainstem and lower axial motor neurons. May cross over at spinal cord level.

Front 15

Distinguishing hand area of precentral gyrus

Back 15

"Hand knob"

Seen as upside down omega or episilon. Highly folded and expanded because of importance of hands.

Front 16

Precentral gyrus Brodmann areas

Back 16

Area 4, more anterior is Brodmann area 6.

Broddman area 4 has Betz cells which control LMN through projections to corticospinal tract.

Brodmann area 6 primarily project to propriospinal interneurons, not lower motor neurons.

Front 17

Lateral corticospinal tract

Back 17

Input from precentral gyrus (Brodmann 4 and 6) plus postcentral gyrus sensory areas.

Almost completely crosses over at pyramidal decussation, innervates LMNs for limbs/appendicular.

Front 18

Where are Betz cells located?

Back 18

Primarily Brodmann area 4, but a few in Brodmann area 6 and some in postcentral gyrus as well.

Front 19

Comparison of corticospinal tract in human and rat

Back 19

Rat has dorsal corticospinal tract instead of lateral corticospinal tract

Still has ventral corticospinal tract

Front 20

Cross section of human spinal cord

Back 20

Lateral corticospinal tract

Rubrospinal tract below it

Ventral corticospinal tract in completely different location

Front 21

UMN lesion symptoms

Back 21

Weakness

Spasticity - increased motor output with stretch or constantly, because loss of inhibitory input from UMN to LMN, increase in reflexes, and increase in LMN excitability in absence of UMN input

Increase in reflexes

Loss of fine motor control - measured by inability to tap finger and thumb together

Front 22

Causes of UMN Lesion Symptoms

Back 22

Loss of descending inhibition

Increased gain of spinal reflexes

Front 23

Extrapyramidal lesions

Back 23

Not in pyramidal tract but in basal ganglia. Leads to abnormal motor output in form of:

Rigidity - Increased activity in multiple muscles

Tremors - Patterns of abnormal motor activity

Slowness

Postural instability - Inability to compensate for postural changes.

Front 24

Rigidity vs spasticity

Back 24

Spasticity is increased motor output in response to stretch, Rigidity is increased activity in multiple muscles

Front 25

Babinski reflex

Back 25

Normal plantar reflex - if stroke bottom of foot, toes flex down.

Positive Babinski reflex - Big toe goes up and other toes fan down. Normal in babies but suppressed by upper motor neurons throughout most of life. Reliable sign of damage to corticospinal tract.

Back 26

Lower motor neurons for face are in brainstem - facial nucleus contains motor neurons for lower and upper face.

For upper face, facial nucleus gets input from both motor cortices.

For lower face, facial nucleus gets input from contralateral motor cortex.

Front 27

Upper motor lesion on one side of facial nucleus

Back 27

Preserved strength in upper face usually because facial nucleus for upper face gets input from both motor cortices.

Lower face gets facial droop because input from only contralateral cortex.

Front 28

How can spinal reflexes be modified?

Back 28

Development (Babinski)

Experience/conditioning

Front 29

Learning postural reflexes - move platform backwards

Back 29

Gastrocnemius (plantar flexor that extends ankle)

Place subject on platform that suddenly moves backwards, causing subject to lean forward. Activity in gastrocnemius seen in EMG becomes earlier and increases. Body sway goes down.

Result of upregulating reflex that is usually inhibited when walking.

Front 30

Learning postural reflexes - move platform forwards

Back 30

Must use tibialis anterior to respond, not gastrocnemius.

Gastrocnemius is activated at first but activation decreases with successive repetitions.

Front 31

Concussions and sway

Back 31

Concussions affect postural control. Football players with concussions have sway similar to MS or peripheral neuropathy.

Worse when eyes are closed.

Front 32

Adaptation of posture

Back 32

Walk on turntable - must take longer steps on side moving faster to stay in same place.

After walking on turntable with eyes closed, walk on circle. Effect lasts for several minutes.

Does not occur with person in wheelchair - adaptation is not to circling environment but to specific motor activity of walking.

Front 33

Central pattern generation

Back 33

Network of neurons with inhibitory connections where one type of movement inhibits another.

Output goes into patterning network that produces motor pattern via motor neurons.

Exists for a variety of activities.

Front 34

Where in brain is CPG for walking?

Back 34

Cannot pin down one place

Front 35

Stimulating motor activity in people with spinal cord injury.

Back 35

Can implant or place sticky electrodes to activate rhythmic activity in spinal cord

Continuous high frequency stimulation of increasing intensity can yield increasing muscle activity.

Can generate gait like patterns of activity in multiple muscles with combination of stimulation and treadmill stepping.

Front 36

Cortical role in motor control

Back 36

Neuroinfraspectroscopy - look at brain activity while walking.

Multiple areas including primary sensory, primary motor, and supplemental motor area (brodmann area 6, head of prefrontal cortex) are activated while walking.

Brodmann area 6 is a midline area important in bilateral control.

Front 37

Effect of counting or chewing gum while walking

Back 37

Higher cortical activation