Neuro Peds - 02 - Cerebral Palsy Flashcards
1
Q
Why may the clinical manifestations of CP appear to worsen with age even though the pathologic features are static?
A
- Movement demands will increase as the child ages.
- Since the child’s motor abilities are impaired, they will not be able to keep up with the demands.
- Thus, the clinical manifestations will appear to be worsening.
2
Q
Name the two greatest risk factors for CP
A
- Prematurity (gestational age less than 37 weeks)
2. Low birth weight (typical is 7.7 lb)
3
Q
What is the most common type of abnormal tone seen in children with CP?
A
spasticity
4
Q
How may abnormal tonic reflexes interfere with acquisition of movement in a child with CP?
A
- Lack of development of motor control results in retention of reflexes, with the result that the reflexes become obligatory.
- When the reflex is obligatory, it dominates the child’s posture, leading to increased tone, which in turn leads to delayed acquisition of movement.
5
Q
What is the focus of physical therapy intervention for a child with Spastic CP?
A
Mobility, as there is high tendency to develop contractures
- Mobility in all postures
- Transitions between postures
- Active trunk rotation
- Dissociation of body segments
- Isolated joint movements
6
Q
What is the focus of physical therapy intervention for a child with Athetoid CP?
A
- Stability in weight bearing
- Use of developmental postures for trunk or extremity support
7
Q
What is the role of the PTA when working with a preschool-age child with CP?
A
Working to implement certain aspects of the plan created by the PT.
- facilitating postural reactions to improve head and trunk control
- teaching transitions between positions such as sit to stand
- stretching, strengthening and endurance exercises to promote function
- practice of daily self-care skills.
8
Q
What type of orthosis is most commonly used by children with CP who ambulate?
A
ankle-foot orthosis (AFO)
9
Q
At what age should a child with CP begin to take some responsibility for her therapy program?
A
school-age
10
Q
What medications are used to manage spasticity in children with CP?
A
diazepam
baclofen - oral or pump
dantrolene
botox injection
11
Q
What are the expected life outcomes that should be used as guide for goal setting for children with disabilities?
A
- Have a safe, stable home in which to live now and in the future
- Have access to a variety of places within a community
- Engage in meaningful activities
- Have a social network of personally meaningful relationships
- Be safe and healthy
12
Q
What is Cerebral Palsy?
A
- a disorder of movement and posture due to a defect or lesion of the immature brain (6 mos or younger)
- persistent - no cure
- non-progressive - only looks worse as child ages and has to work harder for same movement
13
Q
When is CP typically diagnosed?
A
at 8 to 12 months (not at birth)
14
Q
What is the most prevalent form of CP?
A
spastic diplegia
which is not what the book says
15
Q
what are the statistics of incidence and prevalence?
A
- About 2-3 per 1000 live births
- Prevalence consistent over time
- Increase survival in VLBW = increase CP
- Increase in spastic diplegia
- 764,000 children and adults in US manifest one or more symptoms of CP
- 8,000 – 10,000 babies and infants diagnosed with CP each year
- 1,200 – 1,500 preschool aged children are recognized to have CP each year
16
Q
what is the percentage breakdown of prenatal, perinatal and postnatal causes (etiology)?
A
- Prenatal causes = 70%
- Perinatal causes = 20%
- Postnatal causes = 10%
17
Q
what are some Prenatal Risk Factors for CP?
A
- Maternal infection (rubella, CMV)
- Rh or other blood incompatibility factors
- Toxemia in the mother
- Factors that interfere with intrauterine growth (malnutrition, drug and alcohol exposures ,etc)
- Trauma (from and amnio or physical trauma)
- Gestational Diabetes
- Placenta Abnormalities - previa, detachment
18
Q
what are some Perinatal Risk Factors for CP?
A
- Trauma that induces early labor
- Fetal hypoxia or anoxia in perinatal period
- High levels of jaundice shortly after birth
- Low APGARs
- Low birth weight
- Gestational Age - premature
- Prolonged labor - taxing on mom and baby
- Rupture of blood vessels
- Placenta previa/ detachment
- Breech birth - more tendency to have cord wrapped
- Compression of the brain - forceps
19
Q
What is APGAR?
A
Activity - muscle tone Pulse Grimace - reflex irritability Appearance - skin color Respiration
20
Q
How is the APGAR scored?
A
Activity - absent 0, UE/LE flexed 1, active movement 2
Pulse - absent 0, < 100bpm 1, > 100bpm 2
Grimace - flaccid 0, some UE/LE flexion 1, active motion 2
Appearance - blue/pale 0, body pink UE/LE blue 1, all pink 2
Respiration - absent 0, slow, irregular 1, vigorous cry 2
severely depressed 0-3
moderately depressed 4-6
excellent condition 7-10
21
Q
what are some Postnatal Risk Factors?
A
- Brain infections - viral meningitis, cephalitis
- CVA - kinks and curls in vessels
- Intraventricular hemorrhage - aneurysm
- Tumors - may develop up to 6th month
- Hypoxia/anoxia (near drowning/strangulation)
- Head trauma (abuse, falls, motor vehicles)
- Seizures
- PVL- periventricular leukomalacia - most common cause for spastic diplegia
22
Q
what is the survival rate of babies born between 24-28 weeks?
A
74%
23
Q
out of the 25% of impaired preemies, what is the rate of CP?
A
11%
24
Q
The preemie is 60% more likely to have CP if he weighs what at birth?
A
less than 3.5 lb
25
how is Cerebral Palsy diagnosed?
based on:
- neurological status
- muscle function
- primitive reflexes
- posture
26
fill in the blank:
diagnosis is missed at ___ month
overdiagnosed at ___ month
correctly diagnosed at ___ month
missed - 1
over - 4
correct - 8
27
what are some signs that would indicate a diagnosis of CP?
- Tonal abnormalities
- Primary reflexes - persist or absent
- No emergent reactions (righting, protective, equilibrium)
- Asymmetry - synergy
- Functional and behavioral characteristics - no creeping or transitions between positions
- Delayed milestones - missing spontaneous movement
28
what are some general problems associated with CP?
- Seizure disorders
- Mental retardation
- Behavior disorders
- Learning disabilities
- Speech-language disorders
- Strabismus
- Nystagmus
29
name the 4 topographical components of CP classification by Topography and Muscle Function
- Spastic – increase tone when try to move (velocity dependent hypertonicity)
- Athetoid/dystonia – fluctuation between low tone and high tone
- Ataxia – tremors with purposeful movement, can’t maintain static position
- Hypotonic – floppy
30
name the 5 muscle function components of CP classification by Topography and Muscle Function
- Monoplegia – only one extremity, rare
- Hemiplegia – one side
- Paraplegia – LE, not typical to see this
- Quadriplegia – all four extremities, UE worse than LE
- Diplegia – all four, LE worse than UE
31
what is the difference between Spasticity and Hypertonicity?
both are hypertone.
| spasticity is velocity dependent.
32
describe the CP classification based on Gross Motor Function (GMFCS)
```
Gross Motor Function Classification Scale
GMFCS E&R (expanded and revised, includes 12-18)
Severity rated on 5 point scale
- level 1 is high function
- level 5 is low function
Functional abilities: sitting, walking, and wheeled mobility
Age Dependent:
- Before 2nd birthday
- 2-4 years of age
- 4-6 years of age
- 6-12 years of age
- 12 – 18 years of age
```
33
define pathophysiology
the functional changes associated with or resulting from disease or injury
34
what are some functional changes associated with Spastic Cerebral Palsy?
- Corticospinal tracts (pyramidal) _________________
- Cerebral hypoxia – common cause. Brain did not get some oxygen
- Global involvement of CNS
- Diffuse cortical atrophy
- Multiple cystic lesions in white matter: PVL
- Hydrocephalus (chicken/egg scenario)
- Seizure activity and cognitive impairments
35
What is the most common cause of Spastic CP?
PVL
- leaky ventricles which damage tracts
- such as corticospinal
- one side leaky = hemiplegia
- both sides leaky = diplegia or quadriplegia
36
Remember the circle of willis!
middle cerebral artery is the one over the corticospinal tract
37
What Impairments will you see in Spastic Cerebral Palsy?
Spasticity in extremities
Increased tone in upper AND lower extremities
Decreased tone in trunk
Can’t grade contractions – miscommunication between brain and extremities
Problem with reciprocal inhibition – opposing muscle groups fighting each other. Comes into play with righting reaction or trying to walk.
Difficulty initiating movement – signal from brain is delayed, increased or decreased tone play a part
Can’t sustain trunk muscles
Decreased eccentric control – due to posture and tone
Increased type 1 and 2 muscles fibers. Not even enough mm fibers to recruit to carry out task
38
what is on the long list of impairment for spastic CP?
```
Use mm synergy for function
Decreased ROM
Decreased strength
Decreased body awareness
Decreased tactile discrimination
Visual limitations
Decreased automatic postural reactions
Decreased velocity
Decreased variety of movements
```
39
what are some of the associated impairments for Spastic CP?
Cognitive delays
Hearing deficits
Seizures - check their chart
Oral motor - muscles, asymm head posture
Musculoskeletal - contractures, scoliosis, hip sublux
Cardiopulmonary - shallow breathing, barrel chest
Digestion/elimination - a result of not moving a lot
Skin condition - ulcer, breakdown in position and orthotics
40
what are some functional limitations due to Spastic CP?
```
Mobility - moving between classrooms
Play
Social interaction
Communication
Self care
Leisure
School
Transportation
```
41
what is the posture and movement of the head and neck in Spastic CP?
```
Asymmetric extension of C spine
Upward visual gaze
Tongue retraction
Jaw extension
Shoulder complex elevation (IR) – to stabilize
```
42
what is the posture and movement of the UE in Spastic CP?
```
Elbow flexion
Forearm pronation
Wrist flexion
Wrist ulnar deviation
Finger flexion
Thumb flexion and adduction
```
43
what is the posture and position of the low back in prone and supine in Spastic Quadriplegic/Diplegic CP?
lumbar extension
hip flexion - anterior tilt of pelvis
abs stretched out
decreased ability to move
44
what is the posture and position in sitting for Spastic Quadriplegic/Diplegic CP?
lumbar flexion
| LE flexion, adduction, IR
45
what would help the sitting posture for Spastic Quadriplegic/Diplegic CP?
get the knee flexed
get the hips flexed to 90
get the feet on the floor
then work on core strength, for example
46
what is the standing posture for Spastic Quadriplegic/Diplegic CP?
upper lumbar spine is at end range extension
| hips are flexed - anterior tilt of pelvis
47
what is the likely gait pattern for Spastic Quadriplegic/Diplegic CP?
Crouched
- scissoring - adducted, IR
- lurching to clear foot - weak abductor
48
why might rear-wheel walking be preferred for Spastic Quadriplegic/Diplegic CP?
facilitate upright position
| better access to things
49
what is the pathophysiology of Spastic Hemiplegic CP?
Unilateral presentation
Maldevelopment in CNS
Middle cerebral artery damage - hemorrhage, but not anuerysm
Subdural or intradural bleeding = PVL
50
what is the posture of the spine in Spastic Hemiplegic CP?
Asymmetric extension of C spine - head lateral flex to affected side
T spine asymmetric, mild increased flexion
Lateral flexion of the spine
similar as Di- or Quad-
51
what is the UE posture and position in Spastic Hemiplegic CP?
```
Elevated shoulder complex
Elbow flexion
Forearm pronation
Wrist flexion
Ulnar deviation
```
52
what is the lumbar and pelvis postutre in Spastic Hemiplegic CP?
Pelvis elevated, pulled back, shortened
| Lumbar spine extreme extension - no active spinal rotation, inhibits use of abs for lower trunk stabilization
53
what are the sitting postures for Spastic Hemiplegic CP?
Collapsed into involved side
or
Elevate involved pelvis to bear weight on non-involved side
54
what needs to happen for equal weight-bearing in seated position for Spastic Hemiplegic CP?
Elongation of the affected side spine
guide into position
maybe put some bubble wrap under that butt
55
what are the three standing and walking postures for Spastic Hemiplegic CP?
1. Stiff: hip flexion; adduction; IR; knee flexion; plantar flexion; ankle inversion; supination with WB
2. Less hip flexion and IR; knee hyperextension with WB and plantar flexion; ankle inversion; supination with WB
3. Slight hip ER; mobile knee (flexion and extension phases); slight plantar flexion; and pronation with WB
56
what is the pathophysiology for Athetoid CP?
Damage to basal ganglia and thalamus
| Secondary to prenatal hypoxia; asphyxia; or severe jaundice
57
what are the impairments of Athetoid CP
- Over fluctuation and under fluctuations between co activations and no activation
- Hard to initiate and terminate move
- Variations due to fluctuations – shoulder and hip instability, muscle misfire
- Huge variations in grading ant and ag
- Disorganized movement - flailing
- Extension synergy does help for walking – limit how many people with this CP actually walk
- Extreme oral – use jaw and eyes to stabilize – messes up oral motor – hard to eat – hard to speak – may not talk at all – communication device
- Oral speech impair and respiratory speech impair – not enough air to talk
- Respiratory – exercise ability decreased
58
what are the sensory and perceptual impairments of Athetoid CP?
Nystagmus - worse than for spastic
Decreased ocular pursuits - because using eyes to stabilize
Upward visual gaze - because using eyes to stabilize
More intact motor execution skills - but fluctuating tone means can't perceive
Kinesthetic awareness better for those who are hypertonic - hypo have poor awareness
59
what helps the sensory and perceptual impairments for Athetoid CP?
clasp hands - avoid flailing arms for balance and safety
deep pressure touch preferred over light touch
lower, calmer voice - avoid startle response, which could cause TMJ and cervical issues
60
describe the musculoskeletal impairments of Athetoid CP
```
TMJ deformity
C-spine instability
Shoulder joint instability
Elbow hyperextension
Finger, thumb IP hyperextension
Anterior hip capsule and ligament over lengthening
Plantar flexor and ankle invertors over lengthening
Anterior hip dislocation
```
61
what is the posture and movement of Athetoid CP?
Unable to predict, anticipate, or control the force and timing of mm activity in the limbs
Quick bursts of extension - especially with loud noises
Eyes follow or lead head movement - so no ocular pursuit
Jaw extension
Asymmetric jaw opening
Strong tongue retraction or tongue protrusion
62
what is the UE and spine posture of Athetoid CP?
```
Severe shoulder extension and IR
Limited UE WB
Strong elbow extension
Forearm pronation
Flexed thoracic spine
Extended and IR shoulders
```
63
before initiating movement on patient with Athetoid CP, what position shoulder and hip be in?
External Rotation at shoulder and hip
64
what is typical movement of patient who has Athetoid CP?
Use of ATNR - interferes midline, can't feed self
Very limited movement in prone - STNR dominate, no UE strength, can't quadruped, only bunny hop
More efficient supine scooting - on head - plagiocephaly or torticollis
Can move from Prone to W-sit without use of arms
65
what is typical low back and LE posture of patient who has Athetoid CP?
Thoracic spine rounded
No stability from abdominals
Strong hip extension with lumbar extension
66
what is the typical gait pattern of patient who has Athetoid CP?
```
T spine rounded
Arms clasped in front to prevent LOB
Hips and knees flexed slightly
Ankles dorsiflexed
Shuffle feet to progress forward
BOS wide
Lacks reciprocity
```
67
what is chance patient with Athetoid CP will be ambulatory?
< 10% actually walk.
better chance if clasp arms
68
what is typical cognitive level for patient who has Athetoid CP?
normal, above normal
69
what is the pathophysiology of Ataxic CP?
damage to the cerebellum
70
what are some cranial involvements of Ataxic CP?
dysmetria
dysarthria
intentional tremors
71
what must the patient with Ataxic CP rely heavily on to replace proprioception?
visual feedback
- so don't stand too close in front
- don't give them a toy to focus on
72
what are the impairments associated with Ataxic CP?
```
Hypotonia with decreased DTR
Difficulty initiating/terminating movement
-need external stimulus to initiate
Decreased sustained movement
Voluntary increase in CC
```
73
what is the deal with the impairments of Ataxic CP?
Motor component most normal
Deficits in sensory feedback - not properly interpreted
Difficulty scanning environment when moving - because using eyes to stabilize
Proprioceptive system impaired - because not properly interpreted
Tremors
Auditory processing delays
Difficulty with respiration
Speech impairments
fatigue easily
74
what is typical posture and movement in Ataxic CP?
drunken sailor walk
Use eyes and head for stability and movement
Elevated shoulder complex
Dec stability and control of lower trunk
Wide BOS, ER, abducted
Stiffen legs voluntarily - to hyperextend to maintain balance
75
when is Ataxic CP usually diagnosed?
later, when patient is trying to learn to walk
76
what is the pathophysiology of Hypotonic CP?
damage Cerebellar pathways
Enlarged ventricular system
Often lesion is unknown
77
what are the typical impairments of Hypotonic CP?
Depressed DTR - slow to react to pretty much everything
Impairment in motor neuron recruitment
Phasic bursts of movement
Decreased grading in terminating movement
Cannot generate or sustain co-contraction
Dec variety of movement
Wide BOS and low COM - because can't sustain postures - ready to fall
Primary visual impairments - strabisimus (more prominent - low tone = lazy eye), nystagmus
78
what are secondary impairments of Hypotonic CP?
Secondary visual impairments – causes by using eyes to stabilize head. Bad visual field
Decreased actile and proprioceptive input – not interacting with environment
Scoliosis - Spine instability
Hip sublux and dislocated - hip instability
shallow breathing - Can’t control diaphragm
79
what is typical head and neck control of Hypotonic CP?
Prone:
- Lengthening of C and T extensors
- Partial obstruction of airway
- Passive jaw opening
- Excessive drooling
Pull to sit:
- Lack of chin tuck
- No traction response from upper extremities
- way worse the lag we see in TD newborn
80
what is typical sitting posture of Hypotonic CP?
Head full extension - hanging out on bones
Shoulder complex elevated
Lock out UE
Upward visual gaze
Passive opening of jaw with tongue retraction
Posterior pelvic tilt and lumbar flexion - rest stomach on legs
Wide BOS
(see in Down Syndrome, too)
81
why is the typical sitting posture of Hypotonic CP the way it is?
uses less energy
since their muscles don't recruit well, they fatigue faster
any way to save energy is used
82
what is typical gait in Hypontonic CP?
wide BOS
mid arm guard
not really reciprocal
shoulders locked back
83
when will patient with Hypotonic CP learn to walk (such as it is)?
at 2-3 years old
84
what is cognitive level in Hypotonic CP?
typical.
| can be some delays.
