Upper And Lower Motor Neurons And Their Lesions

Front 1

What are extrafusal muscle fibers vs intrafusal? Name function and prevalence.

Back 1

extrafusal- the contractile portion of muscle. they are the majority of the muscle fibers.
intrafusal- the muscle spindles that sit on the extrafusal fibers and detect their stretch

Front 2

Draw the position of the extrafusal fibers, muscle spindle, and golgi tendon organs in the muscle.

Back 2

Front 3

Draw where the alpha motor neurons synapse.

Back 3

Front 4

What receptors are present on the extrafusal fibers at this junction?

Back 4

Nicotinic receptors for ACh.

Front 5

How will the AP travel once the extrafusal fiber is stimulated?

Back 5

It will travel along the entire membrane of the fiber and in through the T tubules.

Front 6

Draw how the fibers coming from the muscle spindles regulate the alpha motor neurons.

Back 6

Front 7

Where are the spiral muscle spindle receptors located?

Back 7

At the very ends of the muscle spindle

Front 8

Describe the muscle spindle reflex in words.

Back 8

When the muscle spindles are stretched, their spiral neuron will go into the dorsal root and stimulate the alpha motor neuron to contract and "protect" the muscle.

Front 9

What other info do muscle spindle neurons give that we will not concern ourselves with now?

Back 9

They will send info up the spinal cord to the cerebellum about proprioception.

Front 10

Draw in and label the neuron that controls muscle spindle contraction. Label the other two neurons as well.

Back 10

Front 11

How does the y-motor neuron lead to contraction of the whole muscle?

Back 11

It contracts the muscle spindle, which stretches it and then activates the stretch reflex to stimulate the a-motor neurons.

Front 12

What is the physiology behind muscle tone?

Back 12

the alpha MN's are being stimulated at a sustained rate by the Ia fiber and this produces the reflexive muscle tone.

Front 13

What OMM technique does this explain?

Back 13

Counterstrain

Front 14

Why is deep tendon reflex a misnomer?

Back 14

because the thing you are stretching is the whole muscle and thus the muscle spindle, not the tendon and the golgi tendon organ.

Front 15

What do doctors do to test the deep tendon reflexes?

Back 15

Tap a reflex hammer lightly to the tendon to quickly and lightly stretch the muscle.

Front 16

What do they expect to see when they stretch the muscle?

Back 16

A reflexive contraction of the muscle.

Front 17

What kind of reflex arc are they testing with the DTR? Name the fibers involved.

Back 17

The muscle stretch reflex arc.
Muscle spindle--> Ia fiber --> + alpha motor neuron --> extrafusal fiber contraction

Front 18

What 5 things have you checked to be normal in a DTR?

Back 18

1. Muscle Spindle
2. 1a fiber
3. Spinal integration
4. Alpha motor neuron
5. Neuromuscular junction

Front 19

Why do you check DTR's in different places?

Back 19

You want to make sure that each spinal level is working.

Front 20

When are golgi tendon organs stimulated?

Back 20

When the tension in the muscles and tendons is so high that it threatens the integrity of the locomotor system.

Front 21

Does the golgi tendon reflex directly inhibit the aMN?

Back 21

No, it involved an inhibitory interneuron.

Front 22

What is happening in ismometric contraction to the muscle and tendon length?

Back 22

Total length stays the same, but muscle shortens and tendon lengthens.

Front 23

What is the action of the golgi tendon reflex if I try to lift too much weight?

Back 23

it will inhibit the muscle and drop everything to protect the muscle from tearing.

Front 24

Draw in and label the fibers involved in the golgi tendon reflex?

Back 24

Front 25

Do upper motor neurons (UMN's) usually synapse directly on aMN's? What path do they take?

Back 25

no, they usually go to interneurons which will inhibit the LMN's.

Front 26

Define the parameters of a LMN lesion.

Back 26

Any kind of disturbance from the cell body of the aMN to it's neuromuscular junction.

Front 27

What are the two fashions in which ACh is release at the NMJ?

Back 27

1. released when aMN is stimulated
2. basally trickling out

Front 28

What is the point of the ACh that trickles out all the time?

Back 28

It is a trophic signal that helps to maintain muscle mass

Front 29

What's the difference between disuse atrophy vs denervation atrophy.

Back 29

Denervation atrophy loses basal ACh as well as AP ACh.

Front 30

What do UMN's do to LMN's?

Back 30

they inhibit them via interneurons (including yMNs)

Front 31

What are the signs you can use to distinguish upper vs lower motor lesions? (5)

Back 31

1. Muscle mass
2. Muscle power
3. Muscle Tone
4. Deep Tendon Reflexes
5. Babinski's sign

Front 32

Back 32

Front 33

So what happens to the muscle mass if there is a LMN? Why?

Back 33

The mass of the muscle will decrease significantly because it will have both disuse and denervation atrophy.

Front 34

How much will it be reduced in 3 months? (%)

Back 34

70%

Front 35

So what happens to the muscle mass if the UMN has a lesion? Why?

Back 35

It will only be decreased 20-30% because you still have the trophic ACh secretion and the stimulation of the stretch reflex working so you only have disuse atrophy.

Front 36

What happens to the power of a muscle with a LMN vs UMN lesion? Why?

Back 36

LMN lesion- power is completely lost because no ACh at all
UMN- power is slightly lost

Front 37

What is the main fiber that determines tone?

Back 37

the yMN.

Front 38

Is disruption of the yMN involved in a LMN lesion?

Back 38

yes, it can be

Front 39

So what happens to tone in a LMN lesion?

Back 39

total loss of tone in that muscle (because of either aMN and yMN lesion).

Front 40

Define tone.

Back 40

muscle resistance to passive stretch

Front 41

Explain the difference in tone between UMN lesions and LMN lesions.

Back 41

In LMN lesion, there is complete loss of tone.
In UMN lesion, there is hypertonicity because the LMN's have escaped the inhibitory effect.

Front 42

What are the two ways in which hypertonia/rigidity is produced in a UMN lesion? (think about the two types of LMN's they affect)

Back 42

1. yMN overfires and activates the stretch reflex
2. aMN is no longer inhibited and will fire and release basal ACh

Front 43

Draw the pathway by which hypertonia and hypereflexia happens in an upper motor lesion.

Back 43

Front 44

Explain the difference in tendon reflexes between UMN lesions and LMN lesions.

Back 44

1. LMN lesion- loss of reflex because reflex arc is disruption at some point
2. UMN lesion- muscle spindle is already contracting and activating the Ia fibers. more stretch applied will cause a bigger reflex than normal.

Front 45

What is it called when a muscle has longer than normal contraction after a reflex test?

Back 45

clonus

Front 46

What is clonus due to?

Back 46

it can be due to a UMN that results in basal overstimulation of aMN.

Front 47

How do you test for Babinski's sign?

Back 47

You draw a pen down the lateral side of the bottom of the foot and then accross the top.

Front 48

What is the appropriate response for babies?

Back 48

To dorsiflex the foot and effectively withdraw from the irritation.

Front 49

What mechanism is the baby's babinski reflex due to? Why are they different?

Back 49

local motor reflex in the lumbar spinal cord because their upper motor neurons are not completely myelinated yet.

Front 50

What will the upper motor neurons do to the baby's withdrawal reflex when it is myelinated?

Back 50

It will inhibit the withdrawal reflex.

Front 51

Why can't babies walk until thier upper motor neurons are myelinated?

Back 51

If they dorsiflex their feet when they hit the ground in walking, they will fall over.

Front 52

So which kinds of pts have a positive babinski's sign?

Back 52

Babies and people with upper motor lesions

Front 53

How do normal people response to the foot irritation? What action does this help with?

Back 53

They perform plantarflexion, which helps with walking

Front 54

Is there such a thing as a negative babinski's sign?

Back 54

No. That is just called normal plantar flexion reflex.

Front 55

What is another name for a positive babinski's sign?

Back 55

upgoing babinski's sign

Front 56

What happens to the toes in a babinski reflex?

Back 56

they fan out

Front 57

When would I have a upgoing babinski's normally?

Back 57

when I am asleep and my upper motor function is shut down.

Front 58

What determines if a LMN lesion will produce a normal or absent babinski's sign?

Back 58

Only if it is the LMN involved in the reflex will it become absent. Otherwise, it is normal.

Front 59

If you are checking tone, what should their arms do if you let it go? Why?

Back 59

It should drop to the side because they should be relaxed for this exam.

Front 60

What are the three types of hypertonia?

Back 60

1. Clasped knife
2. Lead pipe
3. Cog wheel

Front 61

What exam finding tells you is someone has spascity?

Back 61

Clasp-knife feeling in muscle tone checking

Front 62

What should hypertonia feel like in a clasped knife finding?

Back 62

When you are trying to move them, it is very hard at first and then suddenly it gives.

Front 63

What is the physiology behind why it is so hard to move initially?

Back 63

The yMN's are overactive due to lack of UMN inhibition. The muscle spindles are contracted and any further stretch of the muscle will further exacerbate the stretch reflex.

Front 64

What is the physiology behind why it suddenly gives?

Back 64

The tendons accumulate a lot of tension from all the contraction and then the GTO reflex is activated to inhibit the LMN's.

Front 65

How would a person with a UMN lesion fare in flexing and extending their arm? Which muscle is resisting in each movement?

Back 65

It would be hard at first in both directions and then easy. In extension, it would be the bicep creating the resistance and in flexion it would be the tricep.

Front 66

What kinds of pts get lead pipe hypertonia?

Back 66

Pt's with parkinson's.

Front 67

Describe what lead pipe hypertonia feels like. Why is it called this?

Back 67

There is resistance to passive movement throughout the movement with no give point. Feels like you are bending a lead pipe.

Front 68

Are extrapyrimidal or pyrimidal tracts damaged in Parkingson's?

Back 68

extrapyrimidal

Front 69

When these are damaged, do you get a lot or a little loss of LMN inhibition?

Back 69

Only a little.

Front 70

Why only a little?

Back 70

Because the extrapyrimidal tracts are mostly supportive tone neurons and don't have as great of an effect on the LMN's.

Front 71

So why is there a lead pipe effect in a extrapyrimidal UMN lesion?

Back 71

Since there is only slight contraction from the stretch reflex, you don't put enough tension on the GTO's to stiimulate the golgi reflex.

Front 72

Describe cogwheel rigidity.

Back 72

It feel like a cog where there is alternating give and resistance as you passively try to move the muscle

Front 73

What pathology would give you cogwheel rigidity?

Back 73

When you heave lead pipe rigidity plus tremors.

Front 74

Are the nicotinic receptors on the extrafusal fibers all over the fiber? Where are they?

Back 74

No, they are only under the neuromuscular junction.

Front 75

So are there many nicotinic channels on a regular muscle cell?

Back 75

no

Front 76

What happens to the number of any receptors when they are overstimulated?

Back 76

They are downregulated

Front 77

So what happens to the number and distribution of nicotinic receptors in denervation?

Back 77

they increase drastically in number and become distributed all throughout the muscle.

Front 78

What is this upregulation of nicotinic receptors in skeletal muscle called?

Back 78

dennervation hypersensitivity

Front 79

What happens when you tap on a regular muscle?

Back 79

Nothing really

Front 80

What happens when you tap on a muscle with tons of upregulated nicotinic receptors on it?

Back 80

Some will open and cause mini action potentials and contractions.

Front 81

What is this phenomenon called?

Back 81

fasiculations

Front 82

What type of neural lesion would produce fasiculations?

Back 82

A chronic dennervation LMN lesion

Front 83

What is the difference between fasiculations and fibrillations?

Back 83

fibrillations are like fasiculations except that they can only be stimulated and detected by electromyography.

Front 84

What is electromyography?

Back 84

That test where they stick electrode prods into your muscle and stimulate it electrically to measure it's AP conduction.

Front 85

Is there any fasiculation/fibrillation in UMN lesions?

Back 85

No

Front 86

Draw a section of a spinal cord and indicate where the sensory, motor, and autonomic grey matter is.

Back 86

Front 87

Back 87

1- dorsal spinocerebellar
2- ventral spinocerebellar
3- lateral spinothalamic
4- corticospinal pyrimidal tract

Front 88

Back 88

lesion at left fasiculus cuneatus -
loss of fine touch, proprioception, 2 point discrim, and vibration on the left side below the level of lesion.

Front 89

Back 89

lesion at dorsal horn-
loss of all sensation on right side at that level. loss of spinoolivary input on right. loss of crude touch, pain, and temperature on that side for several levels above and below.

Front 90

What are the two questions you should ask when trying to dx a spinal cord injury?

Back 90

What is happening at that level?
What is happening below that level?

Front 91

Back 91

lesion at dorsal lateral tract (dorsal spinocerebellar)
right ipsilateral lower leg dystaxia

Front 92

Back 92

lesion at ventral lateral tract (dorsal spinocerebellar)
left/contralateral lower leg loss of coordination

Front 93

Where is the pyrimidal motor tract located in the lateral column?

Back 93

Front 94

Back 94

loss of voluntary motor function below this level.

Front 95

Back 95

lesion of right pyrimidal column and ventral horn-
loss of right UMN function below that level and LMN function at that level

Front 96

What kind of symptoms would you see in the previous example?

Back 96

flacidity etc at the damaged levels
spasticity etc at all the levels below.

Front 97

Where would the lesions be if you were checking a body from top to bottom and found:
1. normal reflexes
2. no reflexes
3. hyperreflexia

Back 97

at the level of no reflexes

Front 98

Back 98

lesion at right anterior column
contralateral loss of axial motor movement below that level
contralateral loss of crude touch 3-4 levels below and beyond

Front 99

Which sensory systems cross anteriorly on their second order neurons? Which one is more anterior?

Back 99

anterolateral sensory system
posterior- pain and temperature
anterior- crude touch

Front 100

What does the anterior white commisure cross through?

Back 100

The anterior column

Front 101

What would disrupt the anterior commisure?

Back 101

anterior dilation of the spinal cord

Front 102

What would be the first sx if you dilated the spinal cord anteriorly at one section? Why?

Back 102

bilaterally loss of temperature, and pain at those sections only because the anterior white commissure is the first neurons it will hit.