CP Part 1 Flashcards
1
Q
what are 5 characteristics of CP path
A
- group of heterogenous etiologies and impairments
- disorders of development
- movement and posture
- attributed to… (not caused by)
- non-progressive
2
Q
what are 6 things that can accompany CP
A
disturbances of:
sensation
cognition
communication
perception
behavior
sz disorder
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
4
Q
what causes CP
A
unknown
- causal pathways uncertain
- usually will say “attributed to” instead of “caused by”
5
Q
what is the significance of movement and posture in CP
A
impacts mobility
- activity limitations
6
Q
what is the significance of CP being a disorder of development
A
impacts trajectory
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
8
Q
what are 4 methods of prevention and dec the incidences of CP
A
- prenatal care
- fetal neuroprotection
- therapeutic hypothermia
- improvements in social determinants of health including disparities
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
10
Q
what is involved with fetal neuroprotection to prevent CP
A
magnesium sulfate w anticipated pre-term delivery
11
Q
what is involved w therapeutic hypothermia
A
brain cooling w/i 6hrs after birth for 2-3 days
12
Q
what are the benefits of therapeutic hypothermia
A
combined dec mortality and morbidity
- esp good for babies at high risk (ex: premature)
13
Q
what is CP associated with (3)
A
- disruption of blood/oxygen supply to developing brain (ie hemorrhage, hypoxia/anoxia)
- malformation (rare)
- hyperbilirubinemia/kernicterus
14
Q
what is a challenge of the etiology of CP
A
difficult to prove causation
15
Q
what are 3 risk factors of CP
A
- maternal infections (ie zika virus, cytomegalovirus, toxoplasmosis)
- prematurity and low birth weight
- possible environmental factors interacting w genetic vulnerabilities
16
Q
at what time can etiologies associated w CP present
A
prenatal, natal, or post natal
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
18
Q
what are 3 classification systems of CP
A
- topography (area of body)
- movement disorder
- function
19
Q
what are the 4 categories of topography
A
hemiplegia
diplegia
triplegia
quadriplegia
20
Q
hemiplegia
A
one side of body, trunk involvement as well
- more often UE than LE
21
Q
diplegia
A
both LE
22
Q
triplegia
A
usually 1 UE is more functional than rest of body
23
Q
quadriplegia
A
entire body involved
24
Q
what are the 3 main types of movement disorder
A
spastic CP
dyskinetic CP
ataxic CP
25
what is the significance of knowing what type of movement disorder
can use to get idea of what part of brain injured
26
what injury does spastic CP reflect
damage/lesion in
- motor cortex
- pyramidal tracts
27
what is spastic overflow
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
28
what are 5 characteristics of spastic CP
1. spasticity/hypertonicity
2. abnormal movement patterns
3. poor movement control
4. poor postural control
5. trunk and neck often hypotonic
29
what is dykinetic CP
involuntary movements; fluctuating tone
30
what are 2 types of dyskinetic CP
dystonia - abnormal posturing
- 1 part or throughout
- twisting, clenching
athetosis - random, writhing-type movement/random
31
dyskinetic CP indicates damage at what location
basal ganglia
32
how can the 2 types of dyskinetic CP present
can be combined or distinctly different
33
how does ataxic CP present (ie in gait)
impaired typing of controlled movements
- inconsistent BOS
- inconsistent step length
tremor
34
ataxic CP indicates damage to what structure
cerebellum
35
how do movement disorders of CP often present
mixed presentation
36
if there is a mixed presentation of CP what is this reflective of and why
reflects damage/lesion to other areas of developing brain
- developing CNS -> multiple presentations
37
what tool is utilized to classify the function of CP
gross motor function classification system (gmfcs)
38
describe the levels of the GMFCS
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
level 2 vs level 3 of the GMFCS
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
what are the 5 primary BSF impairments of CP
1. impaired strength
2. poor selective control of ms activity
3. poor postural control
4. retention of primitive reflexes
5. abnormal ms tone
41
what are the two prime BSF impairment reasons for impaired functions
strength
motor control
42
describe the anatomy of ms in CP which impacts strength
ms are shorter, sarcomeres are shorter and fewer fibers
- inc collagen fibers
- need to think of this bc of alignment and strength
43
what are components that factor into impaired strength (3)
1. insufficient force generation capacity
2. dec neuronal drive
3. inappropriate activation of antagonistic ms groups
44
anwhat factors into a BSF impairment of poor selective control of ms activity
inappropriate sequencing and co-activation
45
what type of postural control is especially impaired in CP
anticipatory
46
what are other primary impairments of CP (4)
1. motor learning
2. cognitive
3. communication
4. primary sensory
47
how is motor learning is impaired and how can we address this
motor learning especially impaired when using intrinsic feedback
- need more explicit feedback
- inc amt of practice
48
how can cognition be impaired in CP and how common is this
attention
decision making
learning
memory
problem solving
30-50% of children w CP
49
how can communication be impaired and why
speech fluency/proficiency
language skills
d/t oral motor skills
- dysphagia
- spit production issues
50
what are primary sensory impairments associated w CP
vision
hearing
51
what are the 3 main secondary impairments of CP
abnormal bone growth
ROM
joint instability
52
what are 8 secondary impairments of BSF in CP
reduced fitness
impaired aerobic capacity
pain
disuse atrophy
reduced bone density
abnormal bone growth
ROM
joint instability
53
what are 5 things that fit under the umbrella of fitness as a secondary impairment
aerobic capacity
strength
flexibility
balance
bone mineral density
54
what is a consideration about a secondary impairment of pain
common
- may not be understood
- may be reason they see you
- may not be able to articulate well
55
what is an important consideration of reduced bone density as a secondary impairment
seen even in GMSF levels 1 and 2 (amb patients)
56
describe 5 pathophys steps that lead to secondary lever arm dysfunction
bony deformity
abnormal skeletal forces
ms contractures
inability to stretch via active play
impaired motor control
57
what is the typical expectation for an anatomical lever arm
optimal ms function occurs w normal bony alignment
- bony alignment achieved via normal ms pull, positioning
58
what happens when there is poor alignment
poor ms function -> different responses to WTB, movement -> more issues
59
what are 3 characteristics of CP that lead to secondary lever arm dysfunction
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
what are 3 things that can be thought of as lever arm dysfunction
abnormal bone growth
abnormal ROM
abnormal joint instability
61
what is an example of lever arm dysfunction typically seen in CP
excessive femoral anteversion
62
how does excessive femoral anteversion impact the lever arms in LE
compromises lever arm of hip ABD
poor lever arm @ push-off / terminal stance
63
what compensations and deformities are seen d/t excessive femoral anteversion
causes hip IR
- more ADD than ABD
compensatory tibial ER
plantovalgus foot deformity
- calcaneal ABD, forefoot pronation
64
what function is impacted by excessive femoral anteversion
loading - knee and foot
65
what is hip remodeling and what facilitates it
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
what is the risk with the hip not being remodeled by 5yo
dec hip stability and inc risk of post hip subluxation and dislocation
- ant can happen but not typical d/t mechanism
67
what is the downward spiral effect associated with a secondary impairment of fitness
mobility issues + dec strength + pattern of disuse -> greater impairments -> deconditioning -> dec activity -> inc disability -> mobility issues ...
68
what is the two-pronged approach that is critical for intervening with a secondary impairment of fitness
1. dec sedentary behavior
2. inc mod to vig levels of intensity of physical activity
69
what should be considered when determining activity limitations of CP
GMFCS levels
- ambulatory
- primarily wheeled mobility
- dependent mobility
70
what are early motor development activity limitations
head control
sitting
creeping
71
what should be focused on of the activity limitations possible in CP and why
ambulation/gait
- wide variation of impairments, focus on gait bc how you get around
72
what is consideration of ambulation in people w CP vs someone TD
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
what are deviations in gait d/t in people w CP (4)
weakness
spasticity
abnormal alignment
contractures
74
what are 4 common gait patterns seen in CP
crouched gait
stiff knee / true equinus gait
hemiplegic gait
ataxic gait
75
what are 5 contributing factors to a crouched gait
knee flexion contractures
hip flexion contractures
weak extensors
weak PFs
planovalgus feet
76
what are 6 things that a crouched gait leads to
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
what is a contributing factor to equinus ("stiff knee") gait
LE spasticity
- PFs (+) co-contraction HS/Quads
78
why might you see genu recurvatum in someone with CP
d/t spasticity of PFs
79
what are 5 things that equinus gait leads to
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
what are 3 contributing factors to a hemiplegic gait pattern
1. asymmetry
2. hypertonia and/or spasticity - unilateral
3. weakness - affected limb
81
what are 7 things that hemiplegic gait leads to
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
what is the role of gastroc-soleus group in gait and how can this lead to genu recurvatum
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
