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PT 632 Motor Control > Abnormal Postural Control > Flashcards

Abnormal Postural Control Flashcards

1
Q

what factors contribute to abnormal postural control

A
  • behavior (fear, anxiety)
  • sensory loss
  • age-related changes
  • paresis/plegia
  • pathologic synergy
  • abnormal motor tone
  • cognitive impairment
  • impaired coordination
  • loss of feedforward/feedback
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2
Q

the ability to maintain center of gravity within base of support

A

balance

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3
Q

falls are common across all _______ pathologies due to impairment of sensory, motor and cognitive deficits that impact reactive and proactive postural control

A

neurologic

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4
Q

what percent of falls require medical attention

A

15

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5
Q

what does impaired steady state balance lead to

A
  • unable to stand or sit static without loss of balance
  • limits overall function and ADLs
  • abnormal postural alignment may be a function of disease process
  • abnormal postural alignment may cause abnormal postural reactions
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6
Q

describe the typical stooped posture of a pt with PD

A
  • forward head
  • rounded shoulders
  • excessive T/s kyphosis
  • flattened l/s lordosis
  • ppt
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7
Q

inability to move properly; lesions of the motor cortex or descending motor pathways (UMN) produce significant signs and sx that impact normal motor function and postural control

A

motor dyscontrol

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8
Q

signs and sx of UMN

A
  • abnormal reflexes (palmar/plantar grasps, babinski)
  • hypertonia/spasticity/clonus
  • paresis/plegia
  • abnormal timing/coordination of movement
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9
Q

the ability to generate sufficient muscle tension for the purpose of posture and movement (based on number of motor units recruited, type of units recruited, frequency of action potentials)

A

strength

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10
Q

inability to generate normal levels of force –> what are the two types

A

weakness
- paresis
- plegia

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11
Q

what is the difference between paresis and plegia

A

paresis: mild weakness
plegia: severe to complete loss of strength/paraylsis (hemiplegia, paraplegia, quadriplegia, tetraplegia)

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12
Q

coupling together of muscle groups to produce more efficient movement

A

synergy

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13
Q

mass patterns of movement in stereotypical presentation; limits fractionation; movement outside of a fixed pattern is not possible

A

abnormal/pathological synergy

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14
Q

inability to move single joints without activating movements in other joints

A

limited fractionation

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15
Q

used to rehabiliate pts post stroke; focuses on synergistic muscle patterns progressing through various stages on involuntary and voluntary movement

A

Brunnstrom method

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16
Q

stage I of Brunnstrom’s Stage of Recovery

A

flaccidity
no voluntary or reflex activity present

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17
Q

stage II of Brunnstrom’s Stage of Recovery

A

spasticity begins to develop
synergy pattern begins to develop, may appear as associated reactions

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18
Q

stage III of Brunnstrom’s Stage of Recovery

A

spasticity reaches peak
movement synergies can be performed voluntarily

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19
Q

stage IV of of Brunnstrom’s Stage of Recovery

A

spasticity begins to decrease
deviation from movement synergy is possible, limited combo of movement

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20
Q

stage V of Brunnstrom’s Stage of Recovery

A

spasticity essentially absent
isolated and combo movement evident, coordination may be impaired

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21
Q

stage VII of Brunnstrom’s Stage of Recovery

A

return to normal function
return of fine motor skills

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22
Q

describe UE and LE flexor synergy patterns

A
  • UE: scapular retraction and elevation, shoulder ER and abd to 90, elbow flexion, FA supinated, wrist and finger flexion
  • LE: hip flexion and abd and ER, knee flexion to 90, ankle Df and inversion, toe extension
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23
Q

describe UE and LE extensor synergy

A

UE: scapular protraction, shoulder IR and add, full elbow extension, FA pronation, wrist and finger flexion
LE: hip extension and add and IR, knee extension, ankle PF and inversion, toe flexion

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24
Q

what is the name for full body extensor tone

A

decerebrate

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25
Q

amount of stiffness in a muscle noted during PROM

A

muscle tone

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26
Q

hypotonicity is associated with deficits in

A

cerebellum, T21, developmental delay or LMN lesion

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27
Q

hypertonicity is associated with deficits in

A

motor cortex or descending motor pathways (UMN)

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28
Q

two types of hypertonicity

A

rigidity and spasticity

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29
Q

what is rigidity

A

coactivation of antagonists that result in resistance in PROM t/o the range that is not velocity dependent (ex: PD)

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30
Q

what is spasticity and what is it characterized by

A
  • velocity dependent resistance to PROM; overactive stretch reflex
  • tendon jerks, excessive coactivation of muscles, associated movements, abnormal synergies, abnormal posturing of the limbs or trunk
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31
Q

spasticity is involuntary and occurs due to injury to what structures and is often associated with what injuries

A
  • cortex, basal ganglia, thalamus, brainstem, central white matter, spinal cord
  • TBI, stroke, MS, SCI, CP
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32
Q

spasticity is the loss of higher level inhibitory influence due to pathology that leads to lower level movement strategies and reflexes to appear such as

A
  • abnormal synergy patterns
  • primitive reflexes
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33
Q

what is used to grade spasticity

A

MAS

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34
Q

looking at center of pressure excursion (how much the body moves in quiet standing); typically assessed using force platforms (A-P and M-L speed and excursion); increased with pathology

A

postural sway

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35
Q

what pathologies can impact postural sway

A

CP, CVA, TBI

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36
Q

types of sway associated with locations of cerebellar lesions

A
  • upper vermal/intermediate ant lobe: increased A-P sway
  • lower vermis: increased omnidirectional sway
  • lesion of spinocerebellar afferents (Friedreich’s disease): large amplitude lateral sway
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37
Q

what conditions lead to increased sway area, velocity and asymmetry

A

PD, down syndrome

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38
Q

balance reactions in postural sway deficits lead to LOB due to ______ and toward ____ side

A
  • delay in response
  • toward the affected side
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39
Q

what are 4 things associated with impaired response to perturbation

A
  • delayed motor recruitment in response to perturbation
  • co-activation (results in stiffness - unable to recover following perturbation)
  • delayed activation of postural responses (slower sequencing, timing and amplitude of postural muscles in paretic limb)
  • impaired stepping strategy (delayed activation of postural muscles or lateral or cross stepping)
40
Q

what part of the body needs to be controlled before anything else

A

head
- HAT: head –> arms –> trunk

41
Q

what is a good prognostic indicator for functional outcomes with TBI/CVA and what are good measures to be used with stroke

A

sitting balance
- postural assessment scale for stroke patients (PASS)
- function in sitting test (FIST)

42
Q

recovery of function in sitting follows ______ sequence

A

top-down

43
Q

coordination deficits develop due to what with impaired postural control

A
  • sequencing
  • timely activation
  • adaptation
44
Q

neurological deficits can impair sitting/standing postural reactions

A

impaired postural reactions

45
Q

describe sequencing problems associated with coordination issues with impaired postural control

A

inability to sequence proper muscle firing due to weakness or increased tone

46
Q

describe timely activation coordination issues with impaired postural control

A

activation time may be longer and amplitude smaller on affected side

47
Q

described impaired adaptation with coordination issues with impaired postural control

A

inability to adapt sequencing and amplitude based on demand; altered feedback and feedforward control mechanisms due to deficits

48
Q

what is anticipatory postural control reliant on and what structures does it involve

A
  • reliant on experience and ability to learn
  • involves supplementary motor cortex, basal ganglia, and cerebellum
49
Q

an example would be not being able to tell how much force/energy is needed to pick up an object (using too much or too little force)

A

impaired anticipatory postural control

50
Q

what conditions with impaired anticipatory postural control will be altered with changes in movement (abnormal tone, weakness, coordination deficits)

A

TBI, CVA, MS, PD, CP

51
Q

what conditions that have perception or sensory system affected will alter anticipatory postural control

A

dementia, TBI, PN, MS, vestibular, lack of vision/hearing

52
Q

coordination and timing problems are associated with lesion to

A

cerebellum and basal ganglia

53
Q

uneven movement trajectory, not smooth, loss of coordinated synergy, difficulty with movement error correction would suggest lesion where

A

cerebellum

54
Q

sx/outcomes of cerebellar lesion

A
  • ataxia
  • dysdiadochokinesia (inability to do rapid alternating movements)
  • dysmetria (inability to judge forces)
  • delated reaction time
  • inability to stop/start/change directions
  • inadequate force generation, intention tremor
55
Q

tremor that only occurs with movement and a lesion where would lead to this

A
  • intention tremor
  • cerebellum
56
Q

hypokinetic disorders due to lesion to basal ganglia

A

PD (bradykinesia, rigidity, resting temor)

57
Q

hyperkinetic disorders associated with lesion to basal ganglia

A

chorea, athetosis, dystonia

58
Q

lack of coordination of movement; typically described as undershooting or overshooting of arm, leg or eyes; unable to judge distance or scale

A

dysmetria

59
Q

involuntary, jerky movements; appear random, continuous and unpredictable

A

chorea

60
Q

involuntary writhing movement; typically slow; does not have sustained postures

A

athetosis

61
Q

repetitive twisting or writhing movement that are repeated and frequently held

A

dystonia

62
Q

inability to maintain postural control while performing multiple tasks (increased sway, LOB reactions, poor quality of movement, decreased accuracy, change in BOS, diminished cognitive performance, loss of attention to task)

A

dual task interference

63
Q

what is posture second strategy

A

prioritization of cognitive task over posture

64
Q

what conditions is dual task interference tested in

A

PD, TBI, post stroke, dementia, Alzheimers, CP, developmental coordination disorder

65
Q

postural control and aging

A
  • sensory and motor processes decline (depends on genetics, lifestyle, environment)
  • we are what we eat and do (cannot change genetics)
  • aging is not homogenous
66
Q

is aging homo or heterogenous

A

heterogenous

67
Q

____ max force production loss by 65, ___ muscle mass loss each decade after 30

A
  • 40%
  • 3-5%
68
Q

what MSK factors are influenced by aging

A

muscle strength, muscle mass, elasticity of contractile tissue, bone density, BALANCE

69
Q

loss of hearing

A

presbycusis

70
Q

declining visual acuity

A

presbyopia

71
Q

minimum amount of light needed to see - how does it change in aging

A
  • visual threshold
  • increases due to decline in retinal function
72
Q

lose of central vision

A

macular degeneration

73
Q

clouding of lens of eye

A

cataracts

74
Q

____ changes result in increased postural sway in quiet standing and difficulty when environmental lighting changes

A

visual

75
Q

visual changes with age

A
  • increased visual threshold
  • visual field changes
  • visual acuity changes (macular degeneration, cataracts, loss of peripheral vision
  • loss of depth perception
76
Q

cardiac changes with age

A
  • decreased cardiac output
  • decreased max HR
  • decreased stroke volume
  • increased resting BP
  • increased exercise BP
77
Q

amount of blood pumped from heart per minute

A

cardiac output

78
Q

amount of blood pumped from L ventricle per beat

A

stroke volume

79
Q

older adults with and without balance problems show changes in the motor system that limit their ability to adapt to changes in the environment leading to

A

increased fall risk

80
Q

older adults often have ______ when holding something else in their hand; give example

A
  • delayed reaching response
  • no attempt to reach for a handrail if holding an assistive device
81
Q

vibratory threshold at the great toe _____ 3-fold by age 90 –> suggests loss of protective sensation in the foot and ankle

A

increases

82
Q

tactile sensation decreases as a result of diminished quality and quality of what

A

meissner end organs and pacinian corpuscles

83
Q

at what age is 40% loss of vestibular hair cells

A

70

84
Q

___ loss of vestibular nuclei cells per decade between 40-90 y/o

A

3%

85
Q

vestibular changes in older age limits the ability of the vestibular system to act as a corrective system when there is conflicting information from visual and somatosensory system leading to

A

dizziness and unsteadiness in busy environments

86
Q

greater _____ of positional vertigo and dizziness with aging

A

increase

87
Q

by age 80, _____ likelihood of having vestibular dysfunction

A

85%

88
Q

pulmonary changes in older adults

A
  • increased residual volume
  • increased respiratory frequency
  • decreased vital capacity
89
Q

volume of air still in lungs after max expiration

A

residual volume

90
Q

max amount of air that can be exhaled

A

vital capacity

91
Q

endocrinologic changes in older adults

A
  • decreased metabolic rate
  • decreased lean body mass
  • increased body fat
92
Q

are balance problems just a result of aging

A

NO

93
Q

what sensory systems do older adults use as input for balance

A

vision and somatosensory

94
Q

changes in posture with aging

A
  • forward head
  • increased TS kyphosis
  • flattened lordosis
  • decreased knee and hip flexibility
  • loss of strength
  • decreased ankle flexibility and strength
  • changes in gait patterns causing less toe off and floor clearance
95
Q

gait changes with aging

A
  • cautious
  • cadence, velocity, stride length reduce
  • stride width increases
  • double support time increases
  • delayed initiation
  • increased difficulty stepping over objects
  • dual tasks problems

PT 632 Motor Control (9 decks)

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