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Neuroscience (By Chapter) > Ch. 10: Motor System: Motor Neurons > Flashcards

Ch. 10: Motor System: Motor Neurons Flashcards

1
Q

Ongoing Voluntary Movement

A

sensory info (from spindles, tendon organs, skin rec etc) may modify movement at level of motor planning area and/or central circuit and/or spinal cord

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2
Q

LMN

A
  • Lower motor neurons
  • “peripheral” motor neurons
  • Start in ventral horn and go to Mm
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3
Q

UMN

A
  • “central”/upper motor neurons
  • from brainstem/cortex to spinal cord
  • 2 types: medial and lateral
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4
Q

Lateral UMN

A
  • Fine motor tracts
  • control peripheral Mm
  • connect to LMN that go to peripheral Mm
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5
Q

:Active Stiffness:

UMN

A

UMN–>activation of LMG
-conscious & intentional
or
-unconscious & unintentional

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6
Q

Intrinsic Stiffness

A
  • weak actin-myosin attachment in resting state
  • “velcro”
  • happens after a muscle is immobile for a while
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7
Q

Sarcomere Remodeling

A
  • Mm immobilized in shortened position results in decreased number of sarcomeres=contracture (bad)
  • Mm immobilized in lengthened position results in an increased number of sarcomeres
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8
Q

M Line

A

anchors myosin

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9
Q

Z Line

A

anchors actin

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10
Q

Titin

A
  • Structural protein that connects M line to Z line

- increases structural integrity of sarcomere contributes to stiffness of Mm at end range

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11
Q

:Active Stiffness:

Reflex Activity

A
  • branches of sensory neurons can activate LMN reflexively

- (Patellar tendon reflex)

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12
Q

Passive Stiffness

A
  • Elastic resistance of titin
  • particularly troublesome with contractures
  • muscle shorter than it should be
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13
Q

Medial UMN

A
  • postural/gross motor
  • control midline/proximal Mm
  • connect to LMN that go to midline Mm
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14
Q

4 factors of Mm Stiffness

A
  • Active Stiffness: UMN activating LMN
  • Active Stiffness: reflex activity
  • Intrinsic Stiffness
  • Passive Stiffness
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15
Q

Cocontraction

A
  • “joint stiffness”
  • partial/full contraction of Mm on both sides of a joint or around a body segment
  • Static/Dynamic
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16
Q

Static Cocontraction

A

Stiffly locking a joint

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17
Q

Dynamic Cocontraction

A

control movement of a joint

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18
Q

2 Types of LMN

A
  • Alpha motor neurons (to extrafusal Mm)

- Gamma motor neurons (to intrafusal Mm)

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19
Q

Henneman’s Size Principle

A
  • order of recruitment
  • Slow twitch first, then fast twitch
  • EXCEPTION: when you need explosive/high level force right away
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20
Q

alpha-gamma coactivation

A
  • UMN send parallel signals to alpha and gamma neurons

- contracts Mm (alpha) and keeps spindle sensitive (gamma) to stretch during contraction

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21
Q

Motor Neuron Pools

A
  • Clusters of LMN somas in grey matter of spinal cord arranged in vertical fusal shapes (fusiform)
  • axons project to a single muscle per pool
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22
Q

Motor Unit

A
  • one alpha motor neuron & all the Mm fibers it’s connected to
  • slow OR fast (not mixed)
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23
Q

Size of Motor Units

A
  • Gross Motor Control has many Mm fibers for each motor axon

- Fine Motor Control has few Mm fibers for each motor axon

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24
Q

Convergence of info to alpha motor neuron

A
  • each LMN gets input from a variety of sources

- Sources include: UMN, sensory receptors

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25
Q

Vertical Orginization of Neuron Pools

A
  • single pool may include several spinal levels and myotomes

- every Mm gets innervation from 2+ spinal levels

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26
Q

Horizontal Organization of Neuron Pools

A
  • Medial Pools: axial and proximal Mm
  • Lateral Pools: distal Mm
  • Anterior: Extensor Mm
  • Posterior: Flexor Mm
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27
Q

Muscle Synergies

A

-Many Mm working/contracting together
-activation of multiple UMN
OR
-UMN branching to several UMN
OR
-Interneuron Networks

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28
Q

Phasic Stretch reflex

A
  • Spinal region reflex from Mm spindles to LMN (alpha)
  • Quick stretch to a spindle–>Ia fiber–>monosynaptic connection with alpha motor neuron of same Mm–>brief activation of alpha motor neurons of same Mm
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29
Q

UMN Director Tracts

A
  • Start in cerebral cortex
  • end in ventral horn spinal cord
  • 2 divisions: medial/lateral
  • highest amount of voluntary control of movement
30
Q

UMN Director Tract:

Medial Division

A

-to LMN of proximal arm/leg Mm

31
Q

UMN Director Tract:

Lateral Division

A

-to LMN of distal arm/leg Mm

32
Q

Reciprocal Inhibition

A
  • when 1 Mm contracts the antagonist relaxes
  • connections from UMN to alpha motor neurons
  • connectiosn from Mm spindle afferents to alpha motor neurons
  • uses an interneuron
33
Q

Normal Mm Synergies vs Abnormal

A

-group of Mm that work together under control for a functional outcome
VS
-group of Mm working together w/o control and don’t produce functional outcome

34
Q

Withdrawal Reflex

A
  • spinal region reflex from cutaneous receptors to LMN (alpha)
  • pain–>A delta neurons–>multisynaptic connection with alpha motor neurons–>automatic w/d of painful limb

(one pain fiber splits to many spinal levels)

35
Q

UMN Helper Tracts

A
  • Start: in brain stem
  • End: in ventral horn
  • medal/lateral divisions
  • lowest level of voluntary control (hold me up against gravity/pick up against gravity)
36
Q

UMN Helper Tracts:

Medial Division

A

-to LMN that control prox arm/leg Mm

37
Q

UMN Helper Tracts:

Lateral division

A

-to LMN that control distal leg/arm Mm

38
Q

director UMN help control_______

A

activation of helper UMN in brainstem

39
Q

Paralysis

A

inability to move

40
Q

Atrophy

A
  • shrinking of Mm bulk

- disuse versus denervation

41
Q

Paresis

A
  • weakness

- difficulty moving

42
Q

Myoclonus

A

-rhythmic & repetitive involuntary contraction of the whole muscle

43
Q

3 Descending Motor Tracts

A
  • Lateral activation system
  • medial activation system
  • Nonspecific activation system
44
Q

Motor planning areas send _____

A

movement signals to director and helper UMN

45
Q

7 Involuntary Mm Contractions

A
  1. Mm spasms
  2. Mm Cramps
  3. Fasciculation
  4. Mhyoclonus
  5. Tremor
  6. Firillations
  7. Abnormal Movement from dysfunctional basal ganglia
46
Q

Lateral Activation System

A
  • Axons in Lateral columns connect to LMN in ventral horn

- 2 pathways (lateral corticospinal tract, rubrospinal tract)

47
Q

2 Pathways of Lateral Activation System

A
  • lateral corticospinal tract

- rubrospinal tract

48
Q

Mm Spasms/Cramps

A
  • involuntary Mm contraction

- problem at Mm level

49
Q

Hypotonia

A
  • flaccidity

- decreased muscle tone

50
Q

Fasciculations

A
  • contraction of entire motor unit

- sign of NS irritation

51
Q

Tremor

A
  • shaking back and forth of limb

- at rest (Parkinson’s sign) vs Intention (cerebellar damage)

52
Q

Fibrillations

A
  • spontaneous depol of 1 denervted Mm fiber
  • can’t see
  • evidence of severe nerve damage
53
Q

Hypertonia

A
  • increased tone
  • spasticity (Velocity dependent)
  • Rigidity (nonvelocity dependent)
54
Q

5 S/Sx of LMN Disorder

A
  1. loss of reflexes (stretch and cutaneous)
  2. atrophy of denervation
  3. disorders of Mm tone
  4. paralysis (flaccid)
  5. fibrillations
55
Q

5 S/Sx UMN Disorders

A
  1. Paresis/paralysis
  2. loss fractionated movement
  3. abnormal reflexes
  4. disorders of Mm tone
  5. disorders of Mm contraction
56
Q

Mm Stretch hyperreflexia

A
  • exaggerated Mm response to a quick stretch
  • LMN not getting inhibitory signal from damaged UMN, so post synaptic membrane upregulates more receptors to get a signal and causes increased strength of reflexes
57
Q

Clasp Knife Response

A
  • catch and release

- muscle stretch hyperreflexia (catch) that relaxes (release)

58
Q

Rigid Hypertonia

A
  • UMN damage–>send too many signals all the time
  • nonvelocity dependent
  • ex. Parkinson’s
59
Q

Clonus

A

-repeated stretch hyperreflexia

60
Q

Spastic Hypertonia

A
  • Mm stretch hyperreflexia

- velocity depenent

61
Q

Decerebrate Rigidity

A
  • whole head cut off from brainstem
  • unconscious tonic rigidity in arm and leg extensors
  • Ex. TBI
62
Q

Decorticate Rigidity

A
  • cut off from cortex
  • unconscious tonic flexion of arms and extension of legs
  • ex. TBI
63
Q

6 Disorders of Mm contraction

A
  1. delayed initiation
  2. slow force production
  3. prolonged contraction time
  4. disordered corrdination of agonists and antagonists
  5. decreased fractionation
  6. abnormal (stereotyped) Mm synergies
64
Q

Myoplastic Hyperstiffness

A
  • due to paresis & habitual positioning
  • increased stiffness from increased intrinsic stiffness and connective tightness
  • not due to increased tone
  • decreased sarcomere number (contractures)
  • increased weak binding actin/myosin from decreased movement
  • selective loss fast twitch fibers
65
Q

Mm overactivity

A
  • unconscious
  • excess tone is activity dependent
  • ex. stroke
  • at rest no hypertonia
  • moving increases hypertonia
66
Q

4 types of Mm hyperstiffness

A
  • myoplastic hyperstiffness
  • spasticity
  • rigidity & Mm overactivity
  • Mm overactivity
67
Q

Abnormal Tone

A
  • hypotonia
  • hypertonia
  • shock
68
Q

Shock

A
  • period of time after trauma when motor neurons are unexcitable
  • cerebral–post stroke
  • Spinal–post SCI
  • may wake up again
69
Q

Example of LMN Disorders

A
  • peripheral N injury

- ALS

70
Q

ALS

A
  • Amyotrophic Lateral Sclerosis

- LMN in ventral horn attacked and die all the way out to the periphery

71
Q

2 Types of Rigid Hypertonia

A
  • decerebrate
  • decorticate

(too many signals all the time)

72
Q

3 disorders of Mm tone

A

(hypertonia)

  1. spastic hypertonia
  2. rigid hypertonia
  3. Mm overactivity

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