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Neuroanatomy and Physiology > Lecture 12- Motor Examination > Flashcards

Lecture 12- Motor Examination Flashcards

1
Q

What are the 6 parts of the ICF Model?

A
  • Health Condition
  • Impaired Body Functions and Structures
  • Activity Limitation
  • Participation Restrictions
  • Environmental Factors
  • Personal Factors
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2
Q

What is the organization of examination?

A
  • Pathophysiology
  • Impairements
    • Sensory/Perceptual
    • Cognitive/Behavioral
    • Motor
  • Functional Limitations
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3
Q

Primary neuromuscular impairements, with time, can often lead to ________ effects.

A

secondary

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4
Q

What part of the examination do we most often see secondary sequelae?

A

motor portion

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5
Q

Paresis and spasticity are ________ effects of a stroke.

A

primary

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6
Q

With time, paresis and spasticity from a stroke can lead to ___________ effects.

A

secondary

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7
Q

What is the primary things we are looking for in a motor exam?

A

strength (muscle weakness)

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8
Q

Musculoskeletal contributions to strength reflect:

  • Length of _________ arm of the muscle
  • ______/_______ relationship of the muscle
  • Type of muscle fiber
  • ___________ area of muscle
  • Fiber arrangement
A
  • movement
  • length/tension
  • cross-sectional
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9
Q

Neural contributions to strength reflect:

  • Number of _________ recruited
  • Discharge __________
  • Type of motor units recruited
A
  • motor units

- frequency

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10
Q

What is weakness in the context of neuropathology?

A
  • inability to generate force

- inability to recruit or modulate motor neurons

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11
Q

Neurologically induced weakness may result from:

  • _______ lesion
  • Lesion in ________ pathways
  • Disruption of impulses from _______ motor neurons
  • Peripheral nerve injury
  • Synaptic dysfunction at __________
  • Damage to muscle tissue
A
  • cortical
  • descending
  • alpha
  • NMJ
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12
Q
  • What is paralysis or plegia?

- What is dense hemiplegia?

A
  • total or profound loss of muscle activity

- nothing in muscles involved (even twitch)

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13
Q

What is paresis?

A

mild or partial loss of muscle activity

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14
Q

Muscle Weakness by Distribution

  • What is monoplegia?
  • What is hemiplegia?
  • What is paraplegia?
  • What is tetraplegia?
A
  • isolated region that has muscle weakness
  • one-sided
  • spinal cord injuries, half (lower or upper)
  • full body (quad)
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15
Q

What are some common observations we will see due to underlying weakness in neurologic pathology?

A
  • Postural abnormalities
  • Asymmetrical weight bearing
  • Abnormal synergies
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16
Q

Postural abnormalities can present both at rest and with ________.

A

activity

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17
Q

Asymmetrical weight bearing produces big differences in ______ time of gait.

A

stance (weak side less time)

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18
Q

What is abnormal synergies?

A
  • result of loss of ability to recruit a limited number of muscles that are supposed to control a movement
  • muscle weakness can produce mass pattern of movement
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19
Q

What are the most common synergies we see and where do we see them?

A
  • Flexor synergy - UE

- Extensor synergy - LE

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20
Q

What is flexor synergy characterized by?

A
  • scapular retraction and elevation
  • shoulder abduction and ER
  • elbow flexion
  • supination
  • wrists and finger flexion
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21
Q

What is extensor synergy characterized by?

A
  • hip extension, adduction, and IR
  • knee extension
  • ankle PF and inversion
  • toe PF
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22
Q

Can you have extensor synergies in the UE and flexor synergies in the LE?

A

Yes, just less likely

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23
Q

What is muscle tone?

A

muscles resistance to passive stretch

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24
Q

Is a certain amount of muscle tone normal?

A

Yes

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25
Q

Normal tone is high enough to resist the effects of ______ but low enough to allow our muscles to move freely.

A

gravity

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26
Q

What is hypotonicity?

A

flaccid muscle (floppy)

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27
Q

What is hypertonicity/spasticity?

A

rigid (stuck)

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28
Q

Tone is both _______ and non-________ components.

A

neural

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29
Q
  • Neural contributions to muscle tone come from a net balance of ___________ input on motor neurons from corticospinal, rubrospinal, reticulospinal, vestibulospinal tracts.
  • Descending info coming from these tracts are _________.
A
  • descending

- inhibitory

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30
Q

Neural contributions to muscle tone also come from the sensitivity of ________ connections.

A

synaptic

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31
Q

Non-neuronal contributions to muscle tone come from connective tissue plasticity and __________ properties of the muscles, tendons and joints

A

viscoelastic

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32
Q

What is the difference between spasticity and hypertonia?

A
  • Both are resistant to movement

- Spasticity is velocity dependent while hypertonia is not.

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33
Q

In ________ we will see the same results whether we move the muscle fast or slowly.

A

hypertonia

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34
Q

Spasticity

  • _________ dependent increase in resistance to passive movement
  • Sometimes described as _________ phenomenon
  • Occurs as a result of damage to _________ tract or other nearby descending paths (ex: corticoreticulospinal)
  • Can be associated with ________ (commonly in distal extremities > proximal)
A
  • velocity
  • clasp-knife
  • pyramidal
  • clonus
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35
Q

What is clonus?

A
  • quick stretch causing bouncing of muscle

- more common distal

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36
Q

Clonus is indicative of a _____ injury.

A

UMN

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37
Q

What 2 main things happen after acute CNS damage?

A
  • paresis

- CNS plastic rearrangements

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38
Q

What is thought to be the main reason we see muscle overactivity?

A

CNS plastic rearrangements after acute CNS damage

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39
Q

What are the 2 spasticity mechanisms?

A
  • changes in neural contributions

- results in alterations to threshold of stretch reflex

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40
Q

Decrease in descending activity leads to a _________ in inhibitory synaptic input which leads to _______ in tonic excitatory input

A
  • decrease

- increase

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41
Q

What scale is used to assess muscle tone?

A

Modified Ashworth Scale

42
Q

What is the scale of the Modified Ashworth Scale?

A

0-4
0= no increase in muscle tone
4= affected part(s) rigid in flexion or extension

43
Q

Does the Modified Ashworth Scale look at hypotonicity?

A

No, 0 means normal

44
Q

What is another, lesser used scale to assess muscle tone?

A

Tardieau Scale

45
Q

Different tests performed for the Tardieau Scale.

A

V1 (PROM)= slow as possible
V2 (spasticity)= speed of limb falling under gravity
V3 (spasticity)= fast as possible

46
Q

Which muscle tone scale accounts for clonus?

A

Tardieau Scale

47
Q

Hypertonia is _________ independent.

A

velocity

48
Q

Hypertonia is predominantly seen in flexors or extensors?

A

flexors

49
Q

What are the 2 main presentations of hypertonia?

A
  • Leadpipe

- Cogwheel

50
Q

What is leadpipe hypertonia?

A

constant resistance to movement throughout entire ROM

51
Q

What is cogwheel hypertonia?

A

alternating episodes of resistance and relaxation

52
Q

Hypertonia can present as ________ at rest. What are the two types?

A

Posturing

  • decorticate
  • decerebrate
53
Q

Decorticate posturing is a result of lesions ______ the red nucleus while decerebrate posturing is a result of lesions ______ the red nucleus.

A
  • above

- below

54
Q

How does decorticate posturing present itself?

A
  • UE flexion

- LE extension/IR/PF

55
Q

How does decerebrate posturing present itself?

A

-UE and LE extension

56
Q

We tend to see ________ much more with cortical involvement.

A

spasticity (pyramidal)

57
Q

We tend to see _______ much more with basal ganglia involvement.

A

rigidity (extrapyramidal)

58
Q

Brainstem involvement above/below the red nucleus can result in what?

A 
above= decorticate posturing
below= decerebrate posturing
59
Q

In regards to chronicity, increases in non-neuronal changes results in increased “__________”

A

stiffness

60
Q

What are some common pathologies with hypertonicity?

A
  • CVA, TBI, MS

- Parkinsons Disease (rigidity)

61
Q

People with hypotonicity have a _____________ in resistance to lengthening.

A

reduction

62
Q

How is hypotonicity different from flaccidity?

A

Flaccidity is a complete loss of muscle tone while hypotonicity isn’t a full loss

63
Q

Hypotonicity is a disruption of ________ input from stretch reflex resulting in a lack of cerebellar efference influence resulting in decreased input to _______ motor neurons.

A
  • afferent

- gamma

64
Q

What are some common pathologies with hypotonicity?

A
  • cerebellar lesions, DS, muscular dystrophies, late stage ALS, post-polio
  • ACUTE CNS injuries -> hypertonicity/spasticity once subacute/chronic
65
Q

Functional implications of an INCREASE in muscle 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, increased risk for contractures)
66
Q

Functional implications of a DECREASE in muscle tone:

A
  • fall into gravity

- high risk for injury during dynamic tasks

67
Q

What is coordination?

A
  • the ability to use different parts of the body together smoothly and efficiently
  • affects quality of movement
68
Q

What kind of velocity curve should we see with coordination?

A

bell shaped velocity curve

69
Q

What are the 3 critical componenets of coordination?

A
  • sequencing
  • timing
  • grading
70
Q

What is incoordination?

A
  • movements that are awkward, uneven, inaccurate

- disruption of sequencing, timing, grading

71
Q

Does incoordination cause a lack in the bell-shape velocity curve? Why or why not?

A

Yes, loss of coupling between synergistic joints and muscles

72
Q

What lesions cause incoordination?

A
  • motor cortex, basal ganglia, cerebellar lesions

- also tied to proprioceptive lesions

73
Q

What are the 3 terms used to describe the grading/scaling of incoordination?

A
  • dysmetria
  • hypermetria
  • hypometria
74
Q

What is dysmetria? (C)

A

-problems judging path to get to a location

75
Q

What is hypermetria?

A

-overshooting target they are reaching for

76
Q

What is hypometria?

A

-undershooting target they are reaching for

77
Q

Coordination deficits can cause timing difficulties as well:

  • ________ reaction times
  • ________ movement times
  • Difficulties ___________ movement
  • Rebound phenomenon
  • Dysdiadochokinesia
A
  • increased
  • slowed
  • terminating
78
Q

What is rebound phenomenon?

A
  • difficulty checking/halting movement when resistance is moved
  • more common in cerebellar lesions
79
Q

What is dysdiadochokinesia?

A

inability to perform rapid alternating movements

80
Q

Coordination deficits can cause activation and sequencing difficulties as well:

  • abnormal _________
  • coactivation
  • impaired inter-joint ________
A
  • synergies

- coordination

81
Q

Coactivation may cause contraction of both ________ and _________ during walking.

A

flexors and extensors

82
Q

What is impaired inter-joint coordination?

A
  • can only move 1 joint at a time

- may have to elevate shoulders, then flex shoulder, then extend elbow to reach

83
Q

What are the tests we perform to examine coordination deficits?

A
  • finger to nose
  • alternating supination/pronation
  • hand or foot tapping
  • heel to shin
84
Q

All tests performed for coordination look at _____ joint movements and we observe the patients performing them.

A

-multi

85
Q

What are involuntary movements?

A

movements we aren’t performing on purpose

-dystonia
-tremors
-athetosis
choreiform

86
Q

What is dystonia a disorder of?

A

basal ganglia

87
Q

Dystonia

  • Basal ganglia
  • Syndrome dominated by __________ muscle contractions
  • Causes twisting, repetitive movements, abnormal postures
  • Coactivation ________/_________
  • Focal, segmental, hemibody, or generalized/whole
A
  • sustained

- agonist/antagonist

88
Q

What are tremors?

A
  • Rhythmic, involuntary oscillatory movement of a body part

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

89
Q

Where are tremors most often seen?

A

hands

90
Q

What is the difference between resting tremor and action tremor?

A

Resting Tremor
-occurs in body part that is not voluntarily activated, relaxed

Action Tremor
-any tremor that is produced by voluntary contraction of a muscle

91
Q

What are the 2 most common subcategories of action tremors?

A
  • postural tremor- person maintains a part of body against gravity (put arms up)
  • intential tremor- produced with a purposeful movement (reaching across table or up)
92
Q

Choreiform and Athetosis are both linked to dysfunction of what?

A

basal ganglia

93
Q
  • What is athetosis?
  • Does it affect UE or LE more?
  • What is it common in?
A
  • slow, writing and twisting movements
  • UE>LE
  • common in cerebral palsy
94
Q
  • What is choreiform?

- What can cause this?

A
  • involuntary, rapid, irregular and jerky movements

- seen with Huntington’s Disease; side effects of PD medicine

95
Q

Spasticity and hypertonia can lead to loss of ____, contractures

A

ROM

96
Q

Immobilization of joints can lead to increased _________.

  • Increase resistance to stretch, decrease in sarcomeres can lead to ________ in connective tissue.
  • Decrease rate of protein synthesis can lead to ________.
A

-stiffness

  • increase
  • atrophy
97
Q

When we have ROM issues, we see a change in ______/________ relationship.

  • This leads to further weakness
  • alters mechanical advantage
A

length/tension

98
Q

Endurance issues can be both _______ and ________.

A

primary and secondary

99
Q

Endurance Issues:

  • Decrease in central drive to spinal cord motor neurons
  • Decrease in activity level/immobility
  • Presence of _________
A

comorbities (Afib, CAD, COPD, DM, etc…)

100
Q

Can neuromuscular impairements cause musculoskeletal pain?

A

Yes, should always keep an eye out for it.

101
Q

Musculoskeletal Pain Main Reasons:

  • ___________ movements resulting in overworking of certain muscles
  • Muscle __________ causing abnormal loading through joints
  • ____ and alignment issues
  • Decreased efficiency of movements leading to increased __________ required to complete tasks
A
  • synergistic
  • asymmetries
  • ROM
  • workload

Neuroanatomy and Physiology (19 decks)

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