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Neuro Rehab 1 > CP Part 1 > Flashcards

CP Part 1 Flashcards

1
Q

what are 5 characteristics of CP path

A
  1. group of heterogenous etiologies and impairments
  2. disorders of development
  3. movement and posture
  4. attributed to… (not caused by)
  5. non-progressive
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2
Q

what are 6 things that can accompany CP

A

disturbances of:

sensation
cognition
communication
perception
behavior
sz disorder

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3
Q

what does it mean that CP is non-progressive

A

original insult doesn’t worsen
- chronic lesion in CNS won’t change w time

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4
Q

what causes CP

A

unknown
- causal pathways uncertain
- usually will say “attributed to” instead of “caused by”

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5
Q

what is the significance of movement and posture in CP

A

impacts mobility
- activity limitations

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6
Q

what is the significance of CP being a disorder of development

A

impacts trajectory

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7
Q

what does it mean that CP is a group of heterogenous etiologies and impairments

A

one person that has CP isn’t the same reason another person has it

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8
Q

what are 4 methods of prevention and dec the incidences of CP

A
  1. prenatal care
  2. fetal neuroprotection
  3. therapeutic hypothermia
  4. improvements in social determinants of health including disparities
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9
Q

how have advances in medical dx and treatment inc the incidence of CP

A

babies can go home sooner, but inc risk of something/event happening at home that can cause CP

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10
Q

what is involved with fetal neuroprotection to prevent CP

A

magnesium sulfate w anticipated pre-term delivery

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11
Q

what is involved w therapeutic hypothermia

A

brain cooling w/i 6hrs after birth for 2-3 days

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12
Q

what are the benefits of therapeutic hypothermia

A

combined dec mortality and morbidity
- esp good for babies at high risk (ex: premature)

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13
Q

what is CP associated with (3)

A
  1. disruption of blood/oxygen supply to developing brain (ie hemorrhage, hypoxia/anoxia)
  2. malformation (rare)
  3. hyperbilirubinemia/kernicterus
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14
Q

what is a challenge of the etiology of CP

A

difficult to prove causation

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15
Q

what are 3 risk factors of CP

A
  1. maternal infections (ie zika virus, cytomegalovirus, toxoplasmosis)
  2. prematurity and low birth weight
  3. possible environmental factors interacting w genetic vulnerabilities
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16
Q

at what time can etiologies associated w CP present

A

prenatal, natal, or post natal

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17
Q

what is the significance of the associated hyperbilirubinemia

A

untreated jaundice - build up of bilirubin in blood
- BBB not as mature, bilirubin can break thru barrier and cause damage

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18
Q

what are 3 classification systems of CP

A
  1. topography (area of body)
  2. movement disorder
  3. function
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19
Q

what are the 4 categories of topography

A

hemiplegia
diplegia
triplegia
quadriplegia

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20
Q

hemiplegia

A

one side of body, trunk involvement as well
- more often UE than LE

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21
Q

diplegia

A

both LE

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22
Q

triplegia

A

usually 1 UE is more functional than rest of body

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23
Q

quadriplegia

A

entire body involved

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24
Q

what are the 3 main types of movement disorder

A

spastic CP
dyskinetic CP
ataxic CP

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25
Q

what is the significance of knowing what type of movement disorder

A

can use to get idea of what part of brain injured

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26
Q

what injury does spastic CP reflect

A

damage/lesion in
- motor cortex
- pyramidal tracts

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27
Q

what is spastic overflow

A

can see inc tone when excited and see overflow

ex: diplegic spastic - inc tone in legs when excited and then see overflow into one UE when shaking a toy

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28
Q

what are 5 characteristics of spastic CP

A
  1. spasticity/hypertonicity
  2. abnormal movement patterns
  3. poor movement control
  4. poor postural control
  5. trunk and neck often hypotonic
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29
Q

what is dykinetic CP

A

involuntary movements; fluctuating tone

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30
Q

what are 2 types of dyskinetic CP

A

dystonia - abnormal posturing
- 1 part or throughout
- twisting, clenching

athetosis - random, writhing-type movement/random

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31
Q

dyskinetic CP indicates damage at what location

A

basal ganglia

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32
Q

how can the 2 types of dyskinetic CP present

A

can be combined or distinctly different

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33
Q

how does ataxic CP present (ie in gait)

A

impaired typing of controlled movements
- inconsistent BOS
- inconsistent step length
tremor

34
Q

ataxic CP indicates damage to what structure

A

cerebellum

35
Q

how do movement disorders of CP often present

A

mixed presentation

36
Q

if there is a mixed presentation of CP what is this reflective of and why

A

reflects damage/lesion to other areas of developing brain
- developing CNS -> multiple presentations

37
Q

what tool is utilized to classify the function of CP

A

gross motor function classification system (gmfcs)

38
Q

describe the levels of the GMFCS

A

1 - walks w/o limitations
2 - walks w limitations (AD)
3 - walks using hand-held mobility device
4 - self mobility w limitations, may use powered mobility
5 - transported in manual wc (fully dependent on others)

39
Q

level 2 vs level 3 of the GMFCS

A

level 2
- might have difficulties when carrying objects, uneven terrain and w speed
- better ability w walking longer distances

level 3
- often wc to get around
- need assistance or stable support surface to get out of sitting
- can walk indoors, but probably need wc outdoors

40
Q

what are the 5 primary BSF impairments of CP

A
  1. impaired strength
  2. poor selective control of ms activity
  3. poor postural control
  4. retention of primitive reflexes
  5. abnormal ms tone
41
Q

what are the two prime BSF impairment reasons for impaired functions

A

strength
motor control

42
Q

describe the anatomy of ms in CP which impacts strength

A

ms are shorter, sarcomeres are shorter and fewer fibers
- inc collagen fibers
- need to think of this bc of alignment and strength

43
Q

what are components that factor into impaired strength (3)

A
  1. insufficient force generation capacity
  2. dec neuronal drive
  3. inappropriate activation of antagonistic ms groups
44
Q

anwhat factors into a BSF impairment of poor selective control of ms activity

A

inappropriate sequencing and co-activation

45
Q

what type of postural control is especially impaired in CP

A

anticipatory

46
Q

what are other primary impairments of CP (4)

A
  1. motor learning
  2. cognitive
  3. communication
  4. primary sensory
47
Q

how is motor learning is impaired and how can we address this

A

motor learning especially impaired when using intrinsic feedback
- need more explicit feedback
- inc amt of practice

48
Q

how can cognition be impaired in CP and how common is this

A

attention
decision making
learning
memory
problem solving

30-50% of children w CP

49
Q

how can communication be impaired and why

A

speech fluency/proficiency
language skills

d/t oral motor skills
- dysphagia
- spit production issues

50
Q

what are primary sensory impairments associated w CP

A

vision
hearing

51
Q

what are the 3 main secondary impairments of CP

A

abnormal bone growth
ROM
joint instability

52
Q

what are 8 secondary impairments of BSF in CP

A

reduced fitness
impaired aerobic capacity
pain
disuse atrophy
reduced bone density
abnormal bone growth
ROM
joint instability

53
Q

what are 5 things that fit under the umbrella of fitness as a secondary impairment

A

aerobic capacity
strength
flexibility
balance
bone mineral density

54
Q

what is a consideration about a secondary impairment of pain

A

common
- may not be understood
- may be reason they see you
- may not be able to articulate well

55
Q

what is an important consideration of reduced bone density as a secondary impairment

A

seen even in GMSF levels 1 and 2 (amb patients)

56
Q

describe 5 pathophys steps that lead to secondary lever arm dysfunction

A

bony deformity
abnormal skeletal forces
ms contractures
inability to stretch via active play
impaired motor control

57
Q

what is the typical expectation for an anatomical lever arm

A

optimal ms function occurs w normal bony alignment
- bony alignment achieved via normal ms pull, positioning

58
Q

what happens when there is poor alignment

A

poor ms function -> different responses to WTB, movement -> more issues

59
Q

what are 3 characteristics of CP that lead to secondary lever arm dysfunction

A
  1. abnormal forces on bones d/t spastic ms -> poor alignment
  2. weak ms provide sub-optimal force on bones
  3. both contribute to contractures -> abnormal biomechanics / alignment
60
Q

what are 3 things that can be thought of as lever arm dysfunction

A

abnormal bone growth
abnormal ROM
abnormal joint instability

61
Q

what is an example of lever arm dysfunction typically seen in CP

A

excessive femoral anteversion

62
Q

how does excessive femoral anteversion impact the lever arms in LE

A

compromises lever arm of hip ABD
poor lever arm @ push-off / terminal stance

63
Q

what compensations and deformities are seen d/t excessive femoral anteversion

A

causes hip IR
- more ADD than ABD
compensatory tibial ER
plantovalgus foot deformity
- calcaneal ABD, forefoot pronation

64
Q

what function is impacted by excessive femoral anteversion

A

loading - knee and foot

65
Q

what is hip remodeling and what facilitates it

A

hip is remodeled by 5yo
- in newborn/toddlers common to have relative anteversion and inc femoral angle

facilitated by active flex, hip ABD, WB-ing

66
Q

what is the risk with the hip not being remodeled by 5yo

A

dec hip stability and inc risk of post hip subluxation and dislocation
- ant can happen but not typical d/t mechanism

67
Q

what is the downward spiral effect associated with a secondary impairment of fitness

A

mobility issues + dec strength + pattern of disuse -> greater impairments -> deconditioning -> dec activity -> inc disability -> mobility issues …

68
Q

what is the two-pronged approach that is critical for intervening with a secondary impairment of fitness

A
  1. dec sedentary behavior
  2. inc mod to vig levels of intensity of physical activity
69
Q

what should be considered when determining activity limitations of CP

A

GMFCS levels
- ambulatory
- primarily wheeled mobility
- dependent mobility

70
Q

what are early motor development activity limitations

A

head control
sitting
creeping

71
Q

what should be focused on of the activity limitations possible in CP and why

A

ambulation/gait
- wide variation of impairments, focus on gait bc how you get around

72
Q

what is consideration of ambulation in people w CP vs someone TD

A

high physical strain
- resulting in slower walking speeds

walking for someone w CP has same physical strain as TD person running @75% of max capacity

73
Q

what are deviations in gait d/t in people w CP (4)

A

weakness
spasticity
abnormal alignment
contractures

74
Q

what are 4 common gait patterns seen in CP

A

crouched gait
stiff knee / true equinus gait
hemiplegic gait
ataxic gait

75
Q

what are 5 contributing factors to a crouched gait

A

knee flexion contractures
hip flexion contractures
weak extensors
weak PFs
planovalgus feet

76
Q

what are 6 things that a crouched gait leads to

A
  1. dec step length
  2. dec knee ext at terminal swing
  3. ant pelvic tilt
  4. inc knee and hip flex in stance
  5. inc ankle DF in stance
  6. cont quad firing to prevent knee collapse
77
Q

what is a contributing factor to equinus (“stiff knee”) gait

A

LE spasticity
- PFs (+) co-contraction HS/Quads

78
Q

why might you see genu recurvatum in someone with CP

A

d/t spasticity of PFs

79
Q

what are 5 things that equinus gait leads to

A
  1. dec knee/hip flex throughout gait
  2. poor foot clearance
  3. may include scissoring - ADD, inc tone
  4. equinus at ankle; pronation or supination of forefoot
  5. often compensatory genu recurvatum - midstance
80
Q

what are 3 contributing factors to a hemiplegic gait pattern

A
  1. asymmetry
  2. hypertonia and/or spasticity - unilateral
  3. weakness - affected limb
81
Q

what are 7 things that hemiplegic gait leads to

A
  1. poorly aligned trunk/pelvis
  2. dec hip ext
  3. risk of genu recurvatum
  4. lack of toe clearance
  5. vaulting on contralateral side
  6. limited UE swing on hemi side
  7. short step length
82
Q

what is the role of gastroc-soleus group in gait and how can this lead to genu recurvatum

A

gastroc-soleus controls forward progression of tibia over foot, ext of knee, and orientation of ground vector
- drive to keep foot planted and fully in WB

when spasticity of gastroc-soleus group, genu recurvatum is a way to do the gastrocs job listed above

Neuro Rehab 1 (27 decks)

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