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PTA - Neuro Peds > Neuro Peds - 02 - Cerebral Palsy > Flashcards

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.
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2
Q

Name the two greatest risk factors for CP

A
  1. Prematurity (gestational age less than 37 weeks)

2. Low birth weight (typical is 7.7 lb)

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3
Q

What is the most common type of abnormal tone seen in children with CP?

A

spasticity

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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.
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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
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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

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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.
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8
Q

What type of orthosis is most commonly used by children with CP who ambulate?

A

ankle-foot orthosis (AFO)

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9
Q

At what age should a child with CP begin to take some responsibility for her therapy program?

A

school-age

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10
Q

What medications are used to manage spasticity in children with CP?

A

diazepam
baclofen - oral or pump
dantrolene
botox injection

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11
Q

What are the expected life outcomes that should be used as guide for goal setting for children with disabilities?

A
  1. Have a safe, stable home in which to live now and in the future
  2. Have access to a variety of places within a community
  3. Engage in meaningful activities
  4. Have a social network of personally meaningful relationships
  5. Be safe and healthy
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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
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13
Q

When is CP typically diagnosed?

A

at 8 to 12 months (not at birth)

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14
Q

What is the most prevalent form of CP?

A

spastic diplegia

which is not what the book says

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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
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16
Q

what is the percentage breakdown of prenatal, perinatal and postnatal causes (etiology)?

A
  • Prenatal causes = 70%
  • Perinatal causes = 20%
  • Postnatal causes = 10%
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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
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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
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19
Q

What is APGAR?

A 
Activity - muscle tone
Pulse
Grimace - reflex irritability
Appearance - skin color
Respiration
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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

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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
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22
Q

what is the survival rate of babies born between 24-28 weeks?

A

74%

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23
Q

out of the 25% of impaired preemies, what is the rate of CP?

A

11%

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24
Q

The preemie is 60% more likely to have CP if he weighs what at birth?

A

less than 3.5 lb

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25
Q

how is Cerebral Palsy diagnosed?

A

based on:

  • neurological status
  • muscle function
  • primitive reflexes
  • posture
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26
Q

fill in the blank:
diagnosis is missed at ___ month
overdiagnosed at ___ month
correctly diagnosed at ___ month

A

missed - 1
over - 4
correct - 8

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27
Q

what are some signs that would indicate a diagnosis of CP?

A
  • 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
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28
Q

what are some general problems associated with CP?

A
  • Seizure disorders
  • Mental retardation
  • Behavior disorders
  • Learning disabilities
  • Speech-language disorders
  • Strabismus
  • Nystagmus
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29
Q

name the 4 topographical components of CP classification by Topography and Muscle Function

A
  • 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
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30
Q

name the 5 muscle function components of CP classification by Topography and Muscle Function

A
  • 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
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31
Q

what is the difference between Spasticity and Hypertonicity?

A

both are hypertone.

spasticity is velocity dependent.

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32
Q

describe the CP classification based on Gross Motor Function (GMFCS)

A 
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
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33
Q

define pathophysiology

A

the functional changes associated with or resulting from disease or injury

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34
Q

what are some functional changes associated with Spastic Cerebral Palsy?

A
  • 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
Q

What is the most common cause of Spastic CP?

A

PVL

  • leaky ventricles which damage tracts
  • such as corticospinal
  • one side leaky = hemiplegia
  • both sides leaky = diplegia or quadriplegia
36
Q

Remember the circle of willis!

A

middle cerebral artery is the one over the corticospinal tract

37
Q

What Impairments will you see in Spastic Cerebral Palsy?

A

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
Q

what is on the long list of impairment for spastic CP?

A 
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
Q

what are some of the associated impairments for Spastic CP?

A

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
Q

what are some functional limitations due to Spastic CP?

A 
Mobility - moving between classrooms
Play
Social interaction
Communication
Self care
Leisure
School
Transportation
41
Q

what is the posture and movement of the head and neck in Spastic CP?

A 
Asymmetric extension of C spine
Upward visual gaze
Tongue retraction
Jaw extension
Shoulder complex elevation (IR) – to stabilize
42
Q

what is the posture and movement of the UE in Spastic CP?

A 
Elbow flexion
Forearm pronation 
Wrist flexion
Wrist ulnar deviation
Finger flexion
Thumb flexion and adduction
43
Q

what is the posture and position of the low back in prone and supine in Spastic Quadriplegic/Diplegic CP?

A

lumbar extension
hip flexion - anterior tilt of pelvis
abs stretched out

decreased ability to move

44
Q

what is the posture and position in sitting for Spastic Quadriplegic/Diplegic CP?

A

lumbar flexion

LE flexion, adduction, IR

45
Q

what would help the sitting posture for Spastic Quadriplegic/Diplegic CP?

A

get the knee flexed
get the hips flexed to 90
get the feet on the floor

then work on core strength, for example

46
Q

what is the standing posture for Spastic Quadriplegic/Diplegic CP?

A

upper lumbar spine is at end range extension

hips are flexed - anterior tilt of pelvis

47
Q

what is the likely gait pattern for Spastic Quadriplegic/Diplegic CP?

A

Crouched

  • scissoring - adducted, IR
  • lurching to clear foot - weak abductor
48
Q

why might rear-wheel walking be preferred for Spastic Quadriplegic/Diplegic CP?

A

facilitate upright position

better access to things

49
Q

what is the pathophysiology of Spastic Hemiplegic CP?

A

Unilateral presentation
Maldevelopment in CNS
Middle cerebral artery damage - hemorrhage, but not anuerysm
Subdural or intradural bleeding = PVL

50
Q

what is the posture of the spine in Spastic Hemiplegic CP?

A

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
Q

what is the UE posture and position in Spastic Hemiplegic CP?

A 
Elevated shoulder complex 
Elbow flexion
Forearm pronation
Wrist flexion
Ulnar deviation
52
Q

what is the lumbar and pelvis postutre in Spastic Hemiplegic CP?

A

Pelvis elevated, pulled back, shortened

Lumbar spine extreme extension - no active spinal rotation, inhibits use of abs for lower trunk stabilization

53
Q

what are the sitting postures for Spastic Hemiplegic CP?

A

Collapsed into involved side
or
Elevate involved pelvis to bear weight on non-involved side

54
Q

what needs to happen for equal weight-bearing in seated position for Spastic Hemiplegic CP?

A

Elongation of the affected side spine

guide into position
maybe put some bubble wrap under that butt

55
Q

what are the three standing and walking postures for Spastic Hemiplegic CP?

A
  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
Q

what is the pathophysiology for Athetoid CP?

A

Damage to basal ganglia and thalamus

Secondary to prenatal hypoxia; asphyxia; or severe jaundice

57
Q

what are the impairments of Athetoid CP

A
  • 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
Q

what are the sensory and perceptual impairments of Athetoid CP?

A

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
Q

what helps the sensory and perceptual impairments for Athetoid CP?

A

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
Q

describe the musculoskeletal impairments of Athetoid CP

A 
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
Q

what is the posture and movement of Athetoid CP?

A

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
Q

what is the UE and spine posture of Athetoid CP?

A 
Severe shoulder extension and IR
Limited UE WB
Strong elbow extension
Forearm pronation
Flexed thoracic spine
Extended and IR shoulders
63
Q

before initiating movement on patient with Athetoid CP, what position shoulder and hip be in?

A

External Rotation at shoulder and hip

64
Q

what is typical movement of patient who has Athetoid CP?

A

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
Q

what is typical low back and LE posture of patient who has Athetoid CP?

A

Thoracic spine rounded
No stability from abdominals
Strong hip extension with lumbar extension

66
Q

what is the typical gait pattern of patient who has Athetoid CP?

A 
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
Q

what is chance patient with Athetoid CP will be ambulatory?

A

< 10% actually walk.

better chance if clasp arms

68
Q

what is typical cognitive level for patient who has Athetoid CP?

A

normal, above normal

69
Q

what is the pathophysiology of Ataxic CP?

A

damage to the cerebellum

70
Q

what are some cranial involvements of Ataxic CP?

A

dysmetria
dysarthria
intentional tremors

71
Q

what must the patient with Ataxic CP rely heavily on to replace proprioception?

A

visual feedback

  • so don’t stand too close in front
  • don’t give them a toy to focus on
72
Q

what are the impairments associated with Ataxic CP?

A 
Hypotonia with decreased DTR
Difficulty initiating/terminating movement
-need external stimulus to initiate
Decreased sustained movement
Voluntary increase in CC
73
Q

what is the deal with the impairments of Ataxic CP?

A

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
Q

what is typical posture and movement in Ataxic CP?

A

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
Q

when is Ataxic CP usually diagnosed?

A

later, when patient is trying to learn to walk

76
Q

what is the pathophysiology of Hypotonic CP?

A

damage Cerebellar pathways
Enlarged ventricular system
Often lesion is unknown

77
Q

what are the typical impairments of Hypotonic CP?

A

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
Q

what are secondary impairments of Hypotonic CP?

A

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
Q

what is typical head and neck control of Hypotonic CP?

A

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
Q

what is typical sitting posture of Hypotonic CP?

A

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
Q

why is the typical sitting posture of Hypotonic CP the way it is?

A

uses less energy
since their muscles don’t recruit well, they fatigue faster
any way to save energy is used

82
Q

what is typical gait in Hypontonic CP?

A

wide BOS
mid arm guard
not really reciprocal
shoulders locked back

83
Q

when will patient with Hypotonic CP learn to walk (such as it is)?

A

at 2-3 years old

84
Q

what is cognitive level in Hypotonic CP?

A

typical.

can be some delays.

PTA - Neuro Peds (14 decks)

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