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Neuroanatomy Exam 2 > Phys Motor System Components > Flashcards

Phys Motor System Components Flashcards

1
Q

Musculoskeletal contributions to strength reflect what?

A 
o	Length of movement arm of the muscle
o	Length/tension relationship of the muscle
o	Type of muscle fiber 
o	Cross-sectional area of muscle
o	Fiber arrangement
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2
Q

Neural contributions to strength reflect what?

A

o # of motor units recruited
o Discharge frequency
o Type of motor units recruited

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3
Q

What is weakness in the context of neuropathology?

A

o Inability to generate force

o Inability to recruit or modulate motor neurons

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4
Q

neuropathology can lead to what?

A

Loss of movement, loss of power, lack of muscle activity, immobility

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5
Q

Neurologically-induced weakness may result from:

A

o Cortical lesion
o Lesion in descending pathways
o Disruption of impulses from alpha motor neurons
o Peripheral nerve injury
o Synaptic dysfunction at neuromuscular junction
o Damage to muscle tissue

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6
Q

T/F the extent and distribution of weakness depends on extent and location of the lesion

A

True

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7
Q

Paralysis or plegia -

A

total or profound loss of muscle activity

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8
Q

Paresis -

A

mild or partial loss of muscle activity

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9
Q 
How do you name neuromuscular impairments (muscle weakness)?
Mono - 
hemi - 
para - 
tetra -
A 
Named by distribution
mono - One single limb
hemiplegia - one entire side of body
paraplegia/diplegia - both legs
tetraplegia - entire body
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10
Q

Common observations due to underlying weakness in neurologic pathology

A

o Postural abnormalities
o Asymmetrical weight bearing
o Abnormal Synergies

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11
Q

Flexor synergy -

A
  • UE

- scapula retraction and elevation, shoulder abduction and ER, elbow flexion, supination, wrist and finger flexion

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12
Q

Extensor synergy -

A

LE

hip extension, adduction, and IR, knee extension, ankle PF and inversion, toe PF

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13
Q

What is tone?

A

Muscle’s resistance to passive stretch (certain amount of tone is normal)

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14
Q

Hypotonicity vs hypertonicity/spasticity

A

Hypo - flaccid

Hyper - rigid

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15
Q

Neural contributions to normal muscle tone

A
  • Net balance of descending input on motor neurons from corticospinal, rubrospinal, reticulospinal, vestibulospinal tracts
  • Sensitivity of synaptic connections
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16
Q

Non-neural contributions to normal muscle tone

A

 Connective tissue plasticity and viscoelastic properties of the muscles, tendons and joints

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17
Q

What is spasticity/hypertonia?

A

Resistance to movement

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18
Q

Is spasticity dependent/independent of velocity?

A

Dependent - the faster you move muscle, the more tone you will see
-Described as clasp-knife phenomenon

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19
Q

Is hypertonia dependent/independent of velocity?

A

Independent - no matter how fast you move, it will be same tone

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20
Q

Spasticity occurs as result of damage to what part of spinal cord?

A

Pyramidal tract or other nearby descending paths

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21
Q

T/F Spasticity is not associated with clonus

A

False, can be associated with clonus (commonly in distal extremities > proximal)

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22
Q

How do changes in neural contributions lead to spasticity?

A

↓ descending activity -> reduction of inhibitory synaptic input -> increase in tonic excitatory input

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23
Q

T/F Spasticity results in alterations to threshold of golgi tendon reflex

A

False, alterations to stretch reflex

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24
Q

What scale used to measure spasticity?

A

Modified Ashworth Scale

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25
Q

Modified Ashworth Scale:

0 -

A

No increase in muscle tone

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26
Q

Modified Ashworth Scale:

1 -

A
  1. Slight increase muscle tone

2. Catch/release or minimal resistance at end range when moved into flex/ext

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27
Q

Modified Ashworth Scale:

1+ -

A
  1. Slight increase muscle tone

2. Catch followed by minimal resistance throughout remainder (less than half) of ROM

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28
Q

Modified Ashworth Scale:

2 -

A
  1. More increase in muscle tone through most ROM

2. BUT affected part(s) easily moved

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29
Q

Modified Ashworth Scale:

3 -

A
  1. Considerable increase in muscle tone

2. Passive movement difficult

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30
Q

Modified Ashworth Scale:

4 -

A
  1. Affected part rigid in flexion or extension
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31
Q

What is tardieau scale?

A

Measuring spasticity that takes into account resistance to passive movement at both slow and fast speeds

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32
Q

Tardieau scale:
V1 -
V2 -
V3 -

A

V1 - Slow as possible
V2 - Speed of limb falling under gravity
V3 - Fast as possible

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33
Q

Tardieau scale:

0 -

A

No resistance in passive movement

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34
Q

Tardieau scale:

1 -

A

slight resistance with passive movement

No clear catch at precise angle

35
Q

Tardieau scale:

2 -

A

Clear catch at precise angle interrupting passive movement followed by release

36
Q

Tardieau scale:

3 -

A

Fatigable clonus (<10 seconds when maintaining pressure) occurring at precise angle

37
Q

Tardieau scale:

4 -

A

Infatigable clonus (> 10 sec when maintaining pressure) occurring at precise angle

38
Q

What is rigidity?

A

heightened resistance to passive movement of the limb, independent of velocity of the stretch

39
Q

Where is rigidity predominantly seen?

A

Flexors

40
Q

What is leadpipe rigidity?

A

constant resistance to movement throughout entire ROM

41
Q

What is cogwheel rigidity?

A

Alternating episodes of resistance and relaxation

42
Q

Do you see posturing during movement or at rest?

A

At rest

43
Q

What is decorticate posturing? Where would you expect a lesion to be?

A

-UE flexion
-LE ext/IR/PF
Lesion = brainstem above red nucleus

44
Q

What is decerebrate posturing?

A

UE and LE extension

Lesion = below the red nucleus

45
Q

T/F Tone characteristics depend on type and location of pathology

A

True

46
Q

If you have a cortical lesion where would you expect the lesion and what type of tone would it cause?

A

Pyramidal (change in descending inputs of alpha motor neurons)
Spasticity (dep of velocity)

47
Q

If you have a basal ganglia lesion where would you expect the lesion and what type of tone would it cause?

A 
Extrapyramidal 
Rigidity (type of hypertonia - ind of velocity)
48
Q

If you have a Brainstem lesion where would you expect the lesion and what type of tone would it cause?

A

Above/below red nucleus

Decorticate/decerebrate posturing (type of hypertonia - ind of velocity)

49
Q

What is chronicity in regard to tone characteristics?

A

Increase nonneural changes -> increased stiffness

50
Q

What are some common pathologies with hypertonicity?

A

CVA, TBI, MS, PD (rigidity)

51
Q

What is hypotonicity?

A

o Reduction in resistance to lengthening; reduction in “stiffness”

52
Q

Floppy hypotonicity -

A

collapse into gravity, harder to excite

53
Q

Flaccidity -

A

complete loss of muscle tone

54
Q

Hypotonicity is cause by:

A

Disruption of afferent input from stretch reflex -> lack of cerebellar efferent influence -> decreased input to gamma motor neurons

55
Q

Common pathologies of hypotonicity

A

 Cerebellar lesions, down syndrome, muscular dystrophies, late stage ALS, post-polio
 ACUTE CNS injuries -> hypertonicity/spasticity once subacute/chronic

56
Q

What are functional implications of increased tone?

A

 Abnormal posturing
 Misalignment
 High risk for injury during prolonged rest (skin breakdown)
 Bias with recruitment - Increased likelihood of synergistic movement
 Destabilization with changes in position (clonus, ↑ risk for contractures)

57
Q

What are functional implications of decreased tone?

A

 Fall into gravity

 High risk for injury during dynamic tasks

58
Q

What is coordination?

A

the ability to use different parts of the body together smoothly and efficiently

59
Q

What are 3 critical components of coordination?

A
  1. Sequencing
  2. Timing
  3. Grading
60
Q

What is incoordination?

A

o Movements that are awkward, uneven, inaccurate

o Disruption of sequencing, timing, grading

61
Q

Find incoordination with what type of lesions?

A

o Found with motor cortex, basal ganglia, cerebellar lesions (Also tied to proprioceptive lesions)

62
Q

What is dysmetria?

A

general term for problems judging path to get to ultimate location (get to path ultimately)

63
Q

Hypermetria -

A

overestimate/shoot the target

64
Q

Hypometria -

A

undershoot the target

65
Q

What are the functional timing difficulties with incoordination?

A

 Increased reaction times
 Slowed movement times
 Difficulties terminating movement

66
Q

What is the rebound phenomenon?

A
  • Incoordination
  • cerebellum lesions
  • difficulty halting movement when resistance is removed
67
Q

Dysdiadochokinesia

A

inability to perform rapid alternating movement

68
Q

What is coactivation?

A
  • Firing of both extensors and flexes at same time

- Decrease degrees of freedoms patient can move through

69
Q

What is impaired inter-joint coordination?

A
  • Cerebellum lesions

- Move one joint at a time sequentially

70
Q

How do you examine incoordination?

A 
- Multi joint movements
	Finger to nose
	Alternating pronation/supination (Dysdiadochokinesi)
	Hand or foot tapping 
	Heel to shin
71
Q

What are 4 involuntary movements?

A
  1. Dystonia (twisting/repetitive movements)
  2. Tremors
  3. Choreiform (jerky/rapid movements)
  4. Athetosis (slow twisting movements)
72
Q

What is dystonia? Lesion to what area of brain? Affects what part of body?

A

o Basal ganglia
o Syndrome dominated by sustained muscle contractions
o Causes twisting, repetitive movements, abnormal postures
o Coactivation agonist/antagonist
o Focal, segmental, hemibody, or generalized/whole

73
Q

What are tremors?

A

o Rhythmic, involuntary oscillatory movement of a body part

o Can be intermittent or constant, sporadic or as a sequelae to disease or injury

74
Q

What is a resting tremor?

A

 Occurs in body part that is not voluntary activated, relaxed

75
Q

What is an action tremor?
Postural -
Intention -

A

 Any tremor that is produced by voluntary contraction of a muscle
• Postural Tremor: person maintains a part of body against gravity (hold a lifted arm)
• Intention Tremor: produced with purposeful movement (sliding or lifting arm)

76
Q

What is choreiform?

Seen in what syndromes?

A

o Involuntary, rapid, irregular and jerky movements

o Seen with Huntington’s Disease; side effect of PD medications

77
Q

What is athetosis?
Is UE or LE move affected?
Common in what syndrome?

A

o Slow, writing and twisting movements
o UE>LE
o Common in Cerebral Palsy

78
Q

Neuromuscular impairments can secondarily cause what issues?

A
  1. ROM and alignment issues
  2. Endurance issues
  3. Pain
79
Q

Spasticity and hypertonia can lead to (decrease/increase) ROM?

A

Decrease (contractures)

80
Q

Immobilization of joint can lead to (decrease/increase) stiffness?

A

Increased stiffness
 ↑ resistance to stretch, ↓ in sarcomeres -> ↑ in connective tissues
 ↓ rate of protein synthesis -> atrophy

81
Q

Changes in length/tension relationship can do what 2 things?

A

 Contributes to further weakness

 Alters mechanical advantage

82
Q

Endurance issues with neuromuscular impairments -

A

o Decrease in central drive to spinal cord motor neurons
o Decrease in activity level/immobility
o Presence of comorbidities - Afib, CAD, COPD, DM, etc…

83
Q

Musculoskeletal pain due to:

A

 Synergistic movements resulting in overworking of certain muscles
 Muscle asymmetries causing abnormal loading through joints
 ROM and alignment issues
 Decreased efficiency of movements leading to increased workload required to complete tasks

Neuroanatomy Exam 2 (7 decks)

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