CP Flashcards
How is CP diagnosed?
Not one thing diagnoses:
- dx through imaging - MRI; lesion doesn’t necessarily correlate with degree of disability, amt of damaged wh matter does; US to dx bleeds
- formalized testing
- clinical assessement/ observation - doesn’t meat motor milestones, exhibits abnormal m tone, or qualitative diff in movement
Where is the damage for spastic, athetoid, ataxic an hypotonic CP?
- Spastic = motor cortex or wh matter projections to and from cortical sensorimotor areas
- athetoid = BG (intermittent m tension and involuntary movement patters)
- ataxic = cerebellar (instability of movement)
- hypotonic = unknown where lesion is (diminished resting tone and decr ability to generate m force)
What are key predictors that decrease life span in a child with CP?
- Decreased mobility
2. poor feeding
When is most of the motor potential achieved for GMFCS level 1? level 5?
1 - 90% motor potential achieved by 5
5 - motor potential achieved by 3
- motor potential = basic developmental skills, postural control
How can you prognose walking capability in children with CP?
- Persistence of Primitive Reflexes (Bleck) - greater persistence = bad
- Type of CP - hemi = high prob, quad = low prob
- Sitting without support (Molnar and Gordon) and pulling to stand by 2 years of age
- Creeping on hands and knees and rate of acquisition of motor milestones before 30 mo.
- Independent transfer of sitting to standing and standing to sitting in young children = strength as predictor (biggest factor)
CP characterized by:
- Early lack of physiological flexion
- Weak postural muscles
- As child fights gravity, extremities demonstrate increased mm tone
- Transitional vertebrae become hypermobile; the rest become hypomobile
- Inappropriate sequencing and coactivation of synergists and antagonists
Spastic
- reduced reciprocal inhibition of antagonist motoneuron pools by Ia affarents, decreased presynaptic inhibition of Ia afferents, decreased nonreciprocal inhibition by Ib afferents; Reciprocal inhibition is reduced
- Decreased force production may be due to Mechanical changes in the muscle rather than to increased stretch reflex from spasticity
CP characterized by:
- Hypotonic early
- Not capable of midrange control**
- Movement can trigger pathological reflexes and/or synergies
- Asymmetrical
- Visual disorganization severe
- Extensor tone is dominant-although total flexion is not unusual
- Reduced risk of contractures
Athetoid
- midrange control - can get on POE, but can’t reach; can walk but can’t reach and bend knee in static standing
CP characterized by:
- Not often a problem from birth
- Usually problems with gait and upright control
Ataxic
- more of a problem when upright
CP characterized by:
- Undiagnosed degenerative disorder
- Precursor to athetosis
- Not uncommon to see hypotonic trunk in spastic, athetoid, and ataxic types
hypotonic
- usually mixed with outer CP types
What are primary impairments in CP?
- Changes in muscle tone - Hyperactive Reflexes
- Impaired Postural stability
- Impaired Motor Coordination
- Insufficient Force Production (both primary and secondary)
What are secondary impairments in CP?
- Decreased ROM - Joints commonly at risk for contracture*; Shoulder adductors, elbow, wrist, and finger flexors, hip flexors and adductors, knee flexors, ankle PF’s
- Decreased Force Production - Poor selective control of muscle activity; UMN lesion makes it difficult to fire a single m and enough m units in that m (No significant correlation between spasticity and weakness)
- Poor muscle regulation in anticipation of postural changes and movement
- Difficulty learning unique movements due it inability to produce isolated motor movements
When do secondary impairments begin to present?
as young as 18-30 months
What are some of the potential Clinical Manifestations of these secondary impairments?
Orthopedic malignment
- torsion, hip subluxation, scoliosis, calcaneovalgus, equinovarus, windswept hips, pelvic obliquities
During an eval, what parts of a child’s history is especially improtant to include in children with CP?
- Parents concerns
- Prenatal, Birth, and Post Natal history
- US or MRI imaging
- Medications
- PMH including hospitalizations and surgeries
What should you ask about in regards to nutrition?
What, how, and how much intake
- make referral recommendations SLP:
- is the child able to manage secretions?
- speech/ lang/ cog
What should you observe for posture?
- How is the infant/child held? and/or in what device are they positioned
- Resting and Active?
What should you observe for voluntary movements?
- Normal/Abnormal patterns of movement?
2. Does effort to move result in increased tone?
What should you observe for mobility?
- Primary means of mobility.. Or are they held or carried the entire time
- Independent or assist
- Assistive Device?
What should you assess for the musculoskeletal part of the examination?
- ROM - R1/R2 and capsular tightness
- Strength - extremities, core, movement isolation, m testing (?); need voluntary isolated control
- Special tests - Ryder’s, femoral and tibial torsion, foot angle, etc.
What should you assess for the neuromotor part of the examination?
- M tone - m ash worth scale; activities that result in more/ less tone
- Primitive reflexes and how they interfere - ATNR, Moro, and Startle most important
- Development of postural rxns - Supine, prone, sitting, 4 point, standing; Righting/Equilibrium; Protective**
- Sensory - Sensation, vestibular, proprioception