Nature and Characteristics of CP Flashcards
CP
describes a group of permanent disorders of the development of mvmt and posture, causing activity limitations that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain
Although brain lesion is static, progressive MSK impairments is seen in most children
Secondary issues
mm contractures, boney torsion, hip displacement and spinal deformity
all can contribute to functional deterioration
problems develop throughout life d/t physical growth, mm spasticity/weakness, aging and other factors
Impairments
Motor Impairments often accompanied by disturbances in cognition, behavior, communication, sensation, epilepsy, and perception
Increased prevalence of impaired, speech, hearing, vision, seizure disorders, urinary incontinence, constipation
tactile sensory impairments: stereognosis, proprioception, two point discrimination
visuospatial or visuoperceptual deficits
children with significant motor impairments experience high rates of associated impairments
Classification
Look at GMFCS levels
Topographic Classification:
- Diplegia (LE more affected than UE)
- Hemiplegia or Hemiparesis (ue and le on one side of body)
- Quadriplegia or Tetraplegia (all limbs)
- -involvement of head and trunk also typical in all types of CP
Movement differences also noted and reflect location of brain damage:
- spastic- involvement of motor cortex or white matter projections to/from cortical sensorimotor areas of the brain–> results in abnormal patterns of movement and postures, exaggerated reflexes
- dyskinetic- involvement of BG, atypical patterns of posture and involuntary/uncontrolled/ recurring and occasionally stereotyped mvmts of specific body parts, dominated by involuntary sustained or intermittent mm contraction with repetitive mvmts and abnormal postures
- athetosis = slow, continuous, writhing mvmts that prevent maintenance of stable posture
- ataxic- cerebellar lesion, in ability to generate normal or expected voluntary mvmt trajectory that cannot be attributed to weakness or involuntary mm activity aout affected joints–> results in general instability, abnormal postures, and lack of orderly coordinated rhythmic movements
- mixed- some spasticity and dyskinesia may be present
Origin and Pathophysiology
events associated with CP: hypoxic, ischemic, infectious, congenital, or traumatic insults affecting the brain
premature birth, atypical uterine growth, multiple births, and genetic factors
Insults to CNS contributing to CNS: perinatal > prenatal > postnatal
1st and 2nd trimesters = brain pathology is characterized by genetic or acquired impairments
Late 2nd trimester onward = disturbances are more often caused by infectious or hypoxic-ischemic mechanisms that result in lesions
Most cases of CP diagnosed with CP were born at term and result of prenatal influences
CP is most often caused by more than a single event
Single events makes up small proportion of cases- uterine rupture, core prolapse, or major placental abruption resulting in hypoxic insult
hypoxic damage is typically bilateral and widespread including the BG and gray/white matter resulting in total body involvement with spastic and dyskinetic features
***Cerebral vascular events occurring within 28 days after birth are significant cause of CP
Imaging important for dx bc neonates with stroke do not present the same as adults
Infections: toxoplasmosis, rubella, CMV, herpes virus, hep B, syphilis, HIV, and Strep B–> all can be transmitted from mother to infant affecting brain and result in CP
- placental inflammation also linked with adverse neuro outcomes
- children with CP often have congenital abnormalities (brain malformatin, cleft palate/lip, gut atresia)
- -Maternal trauma resulting in direct fetal injury, placental abruption, or prenatal vascular insult can also cause CP
- —mechanisms include reduced placental blood flow and/or placental embolization
- -Maternal thyroid disease also linked with CP
Progress in Prevention
perinatal strategies help to prevent CP
Decreased incidence of bilirubin associated encephalopathy– due to treatment of jaundice and prevention of isoimmunization
Continuous fetal monitoring during labor
hypothermia shown to significantly decrease combined outcome of infant mortality and major neurodevelopmental disability in term infants with neonatal encephalopathy— further research needed
Trials of administering magnesium sulfate for fetal neuroprotection in women in premature labor have shown potential for decreased moderate to severe CP, but not death in very premature infants
social class gradient noted in prevalence of CP associate of btwn birth weight and socioeconomic status
avoid multiple implantations during IVF could decrease incidence of CP due to multiple births
Diagnosis
Neuroimaging and prenatal risk factors assist in dx Cp
CP remains a clinical dx when a child does not reach early motor milestones
PT can play important role in dx of CP- assessment of asymmetry, involuntary mvmts, and abnormal primitive reflexes and late development of postural responses can contribute to clinical dx
3D analysis of spontaneous general mvmts in 1st month of life has sown potential to objectively differentiate normal from atypical mvmts in healthy and at risk infants– more sensitive and specific
AIMS- good for corrected age 4m-10m to compare infant development to normative data
TIMP and NeuroSensort Motor Development Assessment (NSMDA) can be used before and after term
Prechtl’s General Mvmts (GM) has best combo of sensitivity and specificity for predicting CP in the early months
**AIMS and NSMDA = better predictors when infants are older
Difficult to dx CP early on– important to differentiate from atypical motor trajectories that are indicative of CP and other situations such as recovery from a medical condition, including premature births
Dx should be performed by pediatric specialist to r/o other causes for similar clinical signs like brain tumor or metabolic disorders
important to follow-up to ensure nonprogressive nature
Recommend MRI of all children with CP
GMFCS
principal system for describing functional GM disability in children with CP
reliable 5 level age categorized system that places children with CP into categories of severity that represent clinically meaningful distinctions in motor function with particular emphasis on their usual performance in sitting, walking, and wheeled mobility
children younger than 2 y/o can be classified byt hey should be reclassified when they are older
GMFCS has shown strong correlations btwn classifications in the preschool years and those at 12 years and into adulthood
Manual Ability Classification System
tool for the hand and arm function similar to GMFCS
classifies the handling of objects in daily activities by children with CP and reflects typical performance rather than maximal capacity
Functional Mobility Scale
classifies mobility in children with CP on a 6-point ordinal scale according to the need for assistive mobility devices for moving distances of 5, 50, and 500 meters (distance reflect distances at home, school, and community)
reliable and valid classification tool
also used to detect change after surgery
Determinants of Prognosis or Outcome
walking ability varies by type of CP
Hemi and ataxic more likely to walk, dyskinetic and bilateral CP less like to walk
**cognitive functioning = best predictor of walking ability for all types of CP
Visual and hearing impairments and presence of epilepsy also correlated with walking abilities
**indep sitting by 24 months remains the best predictor of amb for 15 meters or more with or without AD by 8 y/o
If independent sitting is not achieve by age 3, there is very little chance of achieving functional independent walking
As age walking abilities decline in some individuals with CP
GMFM used to determine motor growth curves for children with CP
- children with CP reach 90% of motor potential by 3 y/o for severely impaired children (GMFCS level V) and by age 5 for GMFCS level I
- levels I-II do not demonstrated decline in GMFM scores
- mean scores for levels III-V peak at 7 y/o and then start to decline
Prognosis:
- -31% of adults with CP live indepedently
- positive prognostic factors for employment = mild physical involvement, good home support, education, vocational training, and good cognitive skills
Life Expectancy- associated with severity of motor, cognitive, and visual impairment
- 2 y/o child with severe CP has 40% chance of living to age 20
- mild CP 99% chance of living to 20
- people with CP have increased incidence of mortality due to external causes such as drowning or being struck by motor vehicles
ICF-CY and CP
International Classification of Functioning, Disability, and Health for Children and Youth
Important to consider ICF model when providing PT and support for children with CP and their families
Premature Birth and CP
contributes to 1/2 or fewer of cases
underlying brain pathology is white matter injury in sensorimotor pathways
prolonged rupture of membranes predisposes intrauterine infection
Increased reproductive technology can contribute to risk for CP as result for tendency for premature birth
Genetics and CP
can influence the risk of CP at a number of points along the causal pathway
risk factors include: premature birth, placental abruption, pre-eclampsia, chorioamnionitis and thrombophilias or presence of certain genotypes such as apoliprotein E
a form of hereditary spastic paresis has been identified
