CP Flashcards
Possible Prenatal causes of CP
developmental brain malformation, genetic/chromosomal abnormalities, intrauterine exposure (radiation, drugs, infection), neurological event
possible perinatal causes of CP
prematurity, birth asphyxia (stuck in birth canal bc no O2), trauma, meconium aspiration
Factors that affect extent of injury
timing
duration
individual variability
Levels of CP (GMCS)
- Walk no limitation
- Walk with limitation
- Walk using hand held mobility device
- Self mobility with limitation may use powered mobility
- Transported in manual WC
Lesion in brain, usually BILAT, caused by ischemia which results in necrosis of white matter around lateral ventricles
Periventricular leukomalacia (PVL)
What is the leading known cause of CP / cognitive impiarments in premature infants?
PVL
what is PVL caused by
reduction in blood flow
lack of O2 to the brain due to reduced blood flow
hypoxic - ischemic encephalopathy
Clinical presentation of perinatal stroke (hemi CP)
one sided UE and LE involvement
UE typically more involved
initial symptom may be when fam notices decreased use of UE
presents as
delayed response to visual stimuli
visual field preference
attraction to color/light
difficulty with visual novelty
cortical visual impairment (not acuity, visual processing)
CV / pulmonary complications of CP
- bronchopulmonary dysplasia, vent dependency
- Secondary to scoliosis
- aerobic capacity (increased weight/decreased strength)
- energy expenditure in relationship to ambulatory status
MSK impairments
strength (unable to generate normal vol force, poor neural drive, co activation)
ROM (spasticity/decreased m control, m tightening)
high incidence of scoliosis, hip instability, bone torsion/version
common ROM measurements
popliteal angle, DF, hip flexion, hip IR/ER, hip ADD/ABD
examination CP red flags
atypical movement patterns, delayed milestones, retained primitive reflexes, hyper-reflexive DTRs, clonus, abnormal m tone
Examples of atypical movement patterns
early appearance of skills (standing, head control–increased m tone)
cramped synchronized movements (appear rigid, all limb/trunk m contract and relax almost sync.) highly predictive (98%)
atypical performance: rolling
does not progress past segmental roll, extremities get stuck, reflexed interfere (ATNR)
atypical performance: sitting up
always fall to one side
no protective ext
do not use one side to prop and/or keeps UE postured
thrusts backwards
atypical performance: crawling
only uses one side
no or limited LE use
does not progress past army crawling
“bunny hop”
common gait patterns to CP
toe walking
hemiparesis
scissoring
crouched
ataxic
type of gait pattern:
retraction of involved side, including pelvis
little to no heel rise
genu recurvatum
hemiparesis
type of gait pattern:
common with spastic diplegia
due to increased tone in med hamstrings/adductors
characterized by: hip flexion, IR, ADD, PF
accompanied with trunk compensations
scissoring
type of gait pattern:
excessive hip and knee flexion ankle DF due to decreased strength (initially, then decreased ROM as well)
crouched
type of gait pattern:
over/undershooting
poor foot placement
wide BOS
ataxic
