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Unit 17 > CP > Flashcards

CP Flashcards

1
Q

describe defining characteristics of CP

A

group of permanent disorders

disorders of movement and posture

non-progressive injury to the brain

can have progressive secondary MSK issues

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2
Q

true or false: any child w/ a brain injury before 3 years can go on to develop CP

A

true

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3
Q

Motor disorders of CP are often accompanied by what other things?

A

perception

sensation

congnition

communication

behavior

epilepsy

2ndary MSK problems

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4
Q

what are the two main things CP is classified by?

A

neuropathic: type of muscle tone
anatomic: distribution of limb involvement

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5
Q

How do CMFCS levels change as the child grows?

A

they normally do not! once a child is at a certain level you can prognosticate they’ll be at this level their entire life

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6
Q

Describe GMFCS levels

A

I: walks w/o limitations

II: walk w/limitations

III: walks using hand held mobility device

IV: self mobility w/limitations, may use power mobility but control it themselves

V: completely dependent, transported in manual WC

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7
Q

True or false: CP is a relatively uncommon diagnosis?

A

false!

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8
Q

in diplegia what is more effected? Upper or LE?

A

LE&raquo_space;»UE

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9
Q

what is the most common kind of CP

A

spastic diplegia

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10
Q

what is more common, isolated CP or CP and co-occuring developmental disabilities?

A

a combination of CP and Developmental disabilities

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11
Q

true or false, many times we know the specific cause of CP

A

false! but we know a lot about what sets the stage/risk factors

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12
Q

are genes a predisposing risk factor for CP?

A

YES! 14% found to have genetic mutation.

but more research needed to be done

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13
Q

what are two major risk factors for developing CP in preterm babies?

A

structural and functional immaturity of blood vessels

physiologic immaturity of cerebral vasculature: no autoregulation!

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14
Q

Explain preterm arterial system an the risk associated with it

A

arteries grow inward from cerebral cortex towards the germinal matrix (sparsely supplied so its at high risk of ischemia)

terminal branches of arteries are small, fragile and prone to hemorrhage

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15
Q

Explain the preterm venous system and the risk associated with it

A

big terminal vein, if there is a hemorrhage from the end branches of the arteries this can clog up the veins and cause ischemia or a hemorrhage of the vein itself

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16
Q

what do full term babies have that preterm infants do not have in terms of blood flow?

A

they have less auto regulation of cerebral blood flow leading to increased risk of underflow/overflow. if there is a change in systemic vitals, this is going to change blood flow in the brain

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17
Q

other than blood flow, what is another system in preterm that makes them vulnerable to CP?

A

(if you said oligodendrocytes you’re also right)

CV system susceptibility: ineffective heart due to not being totally developed

fluctuations in BP and systemic oxygenation

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18
Q

other than blood and CV system what is another system at risk in preterm infants?

A

oligodendrocyte development: responsible for myelination.

If there is ischemia injury to these cells then there is a risk for disruption of future myelination of white matter

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19
Q

what is arterial ischemic injury to arterial end-zones?

A

PVL: perventricular keukomalacia

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20
Q

what does PVL affect

A

immature white matter

necrosis to all celll types and axonal pathways (including oligodendrocytes)

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21
Q

is PVL normally bilateral or unilateral?

A

bilateral

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22
Q

what lobes does PVL normally affect

A

frontal and parietal bilaterally

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23
Q

other than PVL what is the other main injury seen in preterm babies?

A

IVH: intraventricular hemorrhage

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24
Q

Grade I-IV of IVH

A

I: bleed into germinal matrix

II: bleed into lateral ventricles w/no hydrocephalus

III: bleed into lateral ventricles w/hydrocephalus

IV: PVHI - periventricular hemorrhagic infarction

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25
Q

is PVHI normally unilateral or bilateral?

A

unilateral

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26
Q

obstructed drainage in the terminal vein causing large area’s of ischemia is normally what?

A

PVHI a complication of IVH

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27
Q

other than PVHI what is another complication of IVH

A

posthemorrhagic hydrocephalus

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28
Q

blood obstructs the CSF pathway, get ventricular distension, and compression/ischemia of white matter all describe what?

A

posthemorrhagic hydrocephalus

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29
Q

what symptom are you likely to see in a child who had IVH

A

hemiparesis: bc its normally unilateral in nature

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30
Q

what kind of injury in a preterm infant is likely to form a germinal matrix hemorrhage?

A

cerebellar injury

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31
Q

if there is an inflammatory injury in a preterm baby, what is at risk?

A

cytokines released which are toxic to oligodendrocytes

circulation and predispose to ischemia

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32
Q

characteristics of PVL

A

arterial endzone injury

bilateral

Frontal: cognition often spared, trunk and UE

Parietal: cognition, vision affected

Generally LE&raquo_space;UE involvement

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33
Q

characteristics of PVHI

A

terminal vein hemorrhage

unilateral

massive

severe impairment

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34
Q

2 characteristics of cerebellar injry

A

hypotonia

ataxia

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35
Q

Does posthemorrhagic hydrocephalus tend to affect lower or upper extermities more?

A

LE>UE

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36
Q

name three common non-motor symptoms of preterm infant brain injury

A

cognitive and learning deficits (often seen with bilateral injury)

epilepsy

language/behavioral challenges with cerebellar lesions

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37
Q

Is spastic diplegia associated with IVH or PVL?

A

PVL: white matter disease

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38
Q

oligodendrocytes being more mature in full term infants can lead to what issue?

A

developing neurons in grey matter have incredibly high glucose and oxygen demand. This leads other areas of the brain susceptible to ischemia bc the blood is shunted to the areas that need the blood most

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39
Q

in a full term infant, the areas most vulnerable to ischemia are areas supplied by what three things?

A

MCA, PCA, ACA

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40
Q

Cerebrovascular injuries can come in three flavors for full term babies what are they?

A

global hypoxia

ischemic infarct/stroke

hemorrhage

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41
Q

Blood diverts from where to where in the event of global hypoxia/ischemia?

what areas are supplied?

A

from organs to the brain

areas supplied are those most in need: BG, thalamus, brainstem, sensorimotor cortex

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42
Q

match the following global hypoxia to their sx

prolonged/incomplete

brief/incomplete

brief/complete

no deficits

injury to area with the greatest demand, no organ damage

parasagittal watershed and white matter injury, end organ damage

A

prolonged/incomplete: parasagittal watershed and white matter injury; end organ failure (blood diverted to grey matter)

brief/complete: injury to grey matter areas with most demand; no organ damage

brief/incomplete: no deficits

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43
Q

Name the three kind of strokes in full term infants?

A

AIS: arterial ischemic stroke

CVST: cerebral venous sinovenous thrombosis

ICH: intracranial hemorrhage

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44
Q

small amount of clotting in the venous system gernally causing what kind of stroke?

A

CVST: cerebral venous sinovenous thrombosis

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45
Q

Aneurysm, AVM, damage or fragile blood vessels generally cause what kind of stroke in full term babies?

A

ICH: intracranial hemorrhage

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46
Q

Cardiac disease, arteriopathy, intravascular, blood abnormalities, trauma/clotting at birth are all what?

A

potential causes of stroke

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47
Q

Describe an artery dissection

A

fragment of the inner layer breaks off, can have pooling, clotting or aneurysm due to pressure build up

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48
Q

most common kind of AVM is found where?

what is it?

what is the most common presenting symtpom?

A

vein of Galen malformation

there is no capillary bed because the vein is just one giant ball, blood is flowing too fast

blood pressure regulation issues!

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49
Q

Vein of Galen malformation presenting symptom

A

inability to regulate blood pressure

they cannot coordinate suck, swallow, breath

surgical intervention needed

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50
Q

generally speaking you have a good idea how a child with CP will present based on imaging and diagnosis?

A

nope! You can line up different babies with the same initial injury and look totally different! We’re not sure why.

but its still good to think about what a typical presentation based on hx and MRI would be and figure out why the child you’re looking at might look different from that.

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51
Q

CP is a non-progressive disorder of _____ and/or ______

A

movement and posture

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52
Q

Is CP diagnosis looking for UMN or LMN issue?

A

UMN; remember its the brain!

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53
Q

Cp is a diagnosis of what?

A

exclusion! rule out other diagnoses

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54
Q

is prevalence of CP increasing or decreasing

A

increasing due to an increase in NICU survivors

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55
Q

true of false perinatal hypoxia is the majority of CP

A

false! its the minority of cases, its common we don’t really know the cause many times.

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56
Q

TORCHS is what?

A

an acryonym for the list of infections that lead to prenatal risk factors for CP in fetus’s

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57
Q

name a couple prenatal risk factors for CP

A

exposure to toxins

TORCHS: infections

genetics

drug or alcohol use

Rhesus incompatibility

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58
Q

true or false: there is a correlation between low birth weight and CP

A

true! <1,500 grams 9% have CP

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59
Q

two major risk factors of perinatal CP

A

PVL

IVH

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60
Q

major risk factor for postnatal CP

A

stroke, hypoxia (cardiac arrest, near drowning, respiratory failure), infection

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61
Q

what does the diagnosis of CP tell you about what the child will look like?

A

it doesn’t really tell you anything

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62
Q

What are the two ways CP is classified?

A

neuropathic: type of muscle tone
anatomic: distribution of limb involvement

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63
Q

what is athetoid movement

A

slow, involuntary, convoluted, writhing movements

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64
Q

what are the two caveats of GMFCS classification

A

useful for >6 years old

its all self initiated movement

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65
Q

what kind of involvement do most patients have with CP

A

mixed with one region predominating (cortica/pyramidal, BG, or cerebellum)

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66
Q

CST involvement normally leads to what kind of sx

A

spasticity

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67
Q

cerebellum involvement normally leads to what kind of sx

A

ataxia

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68
Q

BG involvement normally leads to what kind of symptoms

A

everything other than spasticity and ataxia; athetosis, chorea, chreoathetosis, ballismus, dystonia

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69
Q

loss of supraspinal inhibition creates what?

A

spasticity

70
Q

talk about the cascade of spasticity

A

spasticity –> no stretch in the muscles during normal play –> contractures –> abnormal skeletal forces –> bony deformity

71
Q

are there other concerns than MSK for kids with CP

A

DUH

CNS, gastrointestinal(speech, swallowing), genitourinary (bladder, reflux)

72
Q

what is the principle of surgery for these kids

A

problem oriented! if the problem is the hip subluxing then we’re going to do surgery to prevent subluxation.

set realistic goals!
Pt priorities!

73
Q

compare and contrast dynamic and static contracture

A

dynamic: due to spasticity
static: actual contracture of the. muscle so no matter what you won’t get full ROM

74
Q

These are the four top priorities for CP patients, put them in order from most to least important

ADL’s
Communication
Walking
Mobility

A

Communication

ADL’s

Mobility

Walking

75
Q

Loss of selective motor control, abnormal balance and spasticity are three common primary problems of CP (BRAIN RELATED). What are the three options for medical treatment for spasticity

A

drugs

botox

neurosurgery: dorsal rhizotomy, thrathecal baclofen

76
Q

Diazepam, tizanidine and baclofen are all used for what purpose?

A

decrease tone/spasticity BUT can lead to sedation, hypotonia and parents don’t like it necessarily

77
Q

mechanism for botox?

A

irreversibly blocks ACH release by nerves at motor end points

BUT more motor end points grow so it is reversible chemical denervation!!!!

78
Q

how long does botox last?

A

4-6 months

79
Q

What are the two characteristics for a pt selected for botox?

A

dynamic muscle contracture

<4 muscles involved

80
Q

these are all goals of what medical intervention?

delay surgical intervention
facilitate stretching
adjunct to PT and casting
stimulates surgery

A

botox

81
Q

what does a phenol/alcohol nerve block do?

A

similar to botox, destorys motor end points

last longer

more painful

82
Q

what medical intervention decreases stimulation from muscles spindles through getting rid of a section of afferent rootlets?

A

doral rhizotomy

83
Q

what intervention prevents the need for orthopaedic surgery in about 50% of people.

A

dorsal rhizotomy

84
Q

This is the selection criteria for what intervention

pure spasticity 
no fixed contracture 
good selective motor control 
4-8 yrs old 
good congition to coooperate with rehab
A

dorsal rhizotomy

85
Q

This is the selection criteria for what intervention

3-8 yr old spastic diplegic
former preemie
Low body weight
pure spasticity

A

selective dorsal rhizotomy (SDR)

86
Q

what are the results of dorsal rhizotomy

A

PERMANENT decrease in spasticity

supraspinal effects (UE function, bladder function, speec, swallowing)

87
Q

Complications of dorsal rhizotomy include

A

sensory loss and dysethesias (abnormal sense), weakness, neurologic bladder

88
Q

what intervention gives you local delivery of meds ot the SC?

A

intrathecal baclofen

89
Q

what are indications for intrathecal baclofen

A

spasticity interfering w/ function or ease of care

ambulatory pts where rhizotomy is contraindicated

90
Q

what are the four main times that PT’s are used for CP patients

A

early intervention: <3

post-op

targeted intervention: coming back after a couple months out for a tune up

Primary care: 3-4 times a week coordinating a lot of care

91
Q

Serial casting how many weeks per cast for how many weeks

A

casts every 1-2 weeks for 6-8 weeks

92
Q

true or false, for these patients orthotics commonly come above their knees?

A

false! they’re very heavy and hard to donn and doff

93
Q

Role of orthopedic surgery is to restore anatomy and maximize biomechanical function through changing _____ and ______

A

ROM and alignment

94
Q

the focus is on what for sugical intervention in PG

A

FUNCTION!

95
Q

true or false: for CP surgery they are trying to address one thing at ta time?

A

false! address all components at once (lever arm, soft tissue, bony deformity)

96
Q

what is the deal with goal setting as far as surgery goes

A

make it realistic! for someone who is GCMS 5 you’re not doing surgery so they can walk again, you’re doing it so they can be comfortable in their WC

97
Q

primary, secondary or tertiary problems are being addressed with orthopedic treatment

A

teritary for sure, maybe secondary

98
Q

what is the primary, secondary problem here

contracture and spasticity

A

spasticity = primary (from the brain and decrease in descending inhibition)

secondary = contracture causing bony deformity and muscle shortening and LEVER ARM DYSFUNCTION

99
Q

is lever arm dysfunction talking about greater or lesser moment arms?

A

smaller moment arms where in normal individuals there are larger ones AS WELL AS lever arms existing which shouldn’t exist (such as a large transverse plane lever arm on the foot)

100
Q

what happens in the pre-op evaluation?

A 
functional level
strength
ROM
observational gait analysis 
x-rays of involved body part 
problems list
maybe even instrumented motion analysis
101
Q

true or false: dynamic and static soft tissue contractures are treated with muscle tendon lengthening surgeries.

A

true!

102
Q

what do you need to think about as far as PT for someone who has undergone a muscle tendon lengthening procedure?

A

weakens the muscle!

103
Q

what intervention change the pull of overactive muscles in order to substitute for weaker muscles?

A

tendon transfer: done for “muscles out of phase?” or ones that are creating deformity

104
Q

cutting and realigning bones to correct a deformity

common in the hip and knee is what kind of surgical intervention

A

osteotomy

105
Q

what is a surgical stabilizing procedure commonly done in the spine and the foot

A

fusion

106
Q

what is the montra for CP surgery?

A

address as much as you can at once

107
Q

if someone has femoral torsion which way is it commonly rotated

A

commonly femoral ANTEVERSION

108
Q

intramuscular psoas lengthening would be done for what deformity?

A

hip flexion deformity

109
Q

where do you lengthen for a psoas procedure

A

“at the brim” not at the insertion which is the lesser trochanter

110
Q

what procedure is described

  • pt in prone
  • tibia is straight up and down
  • guidewire from head of femoral neck to to head
A

Derotational osteotomy: guidewire is defining torsion:

111
Q

what is normal femoral anteversion in degrees?

A

20-25

once you get the person to this normal anteverison you put plates and screws in to hold it here

112
Q

who are you doing the following procedures in

  • psoas lengthening
  • derotational osteotomy
  • rec femoris transfer
  • medial hamstring lengthening
  • tibial derotational osteotomy
  • recession technique (for equinus)
  • lateral column lengthening
  • triple arthrodesis
  • intramuscular tib posteiror, gastroc lengthening or split tendon transfer

etc. etc.

A

ambulatory individuals!

113
Q

hamstring contracture and torsional deformity cause cause what problem

A

excessive knee flexion in stance phase

114
Q

spastic rec fem can cause what?

A

impaired clearance during swing: it should be relaxed but its straightening.

115
Q

rec fem transfer what do they make the rec fem?

A

they cut it and make it a knee flexor rather than an extender

116
Q

for ambulatory pts which hamstrings are you lengthening?

A

medial ones (tendinosus, membranosus, gracilis)

117
Q

after medial hamstring lengthening how long do they have a knee immobilizer on/

A

7-10 days and go to PT

118
Q

if tibial torsion is > than what degree, will they do a fibular osteotomy for?

A

> 25 degrees

119
Q

ankle equinus is what?

A

stuck in PF

120
Q

what do you want to avoid in procedures for equinus?

why?

A

Z/achilles lengthening

soleus is essential for stance support and power generation: you really really don’t want to overstretch it its super hard to come back from!

121
Q

what is the major thought behind all the surgical techniques done for equinus?

A

leave the muscle intact, just cut the fascia, its hard to overlengthen by accident this way

122
Q

what is this the postop follow up for?

short leg ast 4-6 weeks
WBAT vs. NWB
MAFO

A

gastroc soleus recession

123
Q

equinovalgus is most common in what kind of CP.

what is equinovalgus?

A

diplegia.

“bad flat foot”

Makes them wt. bear medially on their foot

equinovalgus = rear foot valgus/eversion.

forefoot ABD’s

124
Q

what is the major issue being equinovalgus?

A

tight achilles or gastroc soleus complex so they focus on lengthening it!

bracing –> surgery

125
Q

other than gastroc lengthening what kind of surgery is done for equinovalgus?

A

calcaneal osteotomy, lengthens the lateral foot and pushes the forefoot back to midline (it drifts into ABD due to valgus of forefoot)

126
Q

what are the two common deformities for equinovalgus?

A

rear foot valgus

forefoot varus

127
Q

you would do a medial cuneiform osteotomy or talonavicular arthrodesis for what deformity?

A

equinovalgus where the forefoot goes ABD

128
Q

when is a triple arthordesis indicated?

A

severe equinovalgus (forefoot is way over so they have to do a fusion)

pt is very limited or non ambulatory

129
Q

flexible equinovarus is what

A

foot is supinated

130
Q

intramuscular

tib posterior lengthening would be indicated in what deformity?

A

flexible equinovarus

as well as gastroc lengthening

and split tendon tarnsfer

131
Q

a split tendon transfer for flexible equinovarus changes

tib posterior to ______

tib anterior to ______

A

tib posterior to PERONEUS BREVIS

tib anterior to CUBOID

132
Q

posterior tib tendon transfers to where

A

half the tendon stays at its insertion of the navicular, half goes to the lateral side to the peroneals!

Creating a Y out of the muscle: half still wants to invert and half wants to evert

133
Q

what is this the post op for

WBAT 6 weeks
MAFO 6-12 months

A

posterior tib tendon transfer

134
Q

Fixed equinovarus what are you thinking the surgical intervention is going to involve?

A

some kind of fusion/osteotomy

135
Q

loss of what couple in crouched gait?

A

PF and knee extension

136
Q

posterior capsule, knee flexion and hip flexion contracture are common in what gait?

A

crouched

137
Q

quad insufficiency and patella alta are common issues in what deviation?

A

crouched gait

138
Q

what are these the options for intervention for?

Serial casting
Hamstring lengthening
“Guided growth” with Plate or staples
Hamstring lengthening + posterior capsulotomy
Distal femoral extension osteotomy and patellar ligament advancement

A

crouched gait

139
Q

crouched is what kind of gait

A

non sustainable!! they end up in WC

140
Q

explain what guided growth is and what its used for

A

used for crouched gait “hamstring lengthening”

plates go in the anterior femur to stop growth, while posterior is left to grow so they straighten out

141
Q

what is distal femoral extension osteotomy used for?

what is it?

A

crouched gait

cut the distal femur and tilt it up: allows for the same ROM just more of an arc of motion in the extension direction.

142
Q

what do you need to do in conjunction to the distal femoral extension osteotomy?

A

patellar ligament advancement to make sure it has the correct length tension to allow for knee extension which is the overall goal anyway.

143
Q

what are goals of surgeons for nonambulatory individuals

WC
Spine
hips
knees
feet
A

WC to maximize function
Spine

spine: straight enough to sit
hips: located, mobile, painless (Hip displacement can be super common - 2-75%)
knees: motion for sitting in good posture and transfers
feet: plantigrade

144
Q

with spastic quadriplegia what is the biggest issue with the hips

what is strong
what is not
what does this do to alignment and to surrounding muscles

A

ADD overcome ABD and the person ends up flexed and ADD position, this lever arms the hip right out of the acetabulum.. The femoral head presses on the ADD muscle bellies and this misshapes the femoral head as well as disrupts the shape of the muscle

145
Q

hips that are stable at ____ years remains table

A

18 years

146
Q

_____% of hip dislocation have pain

A

50% and a lot can’t communicate!

147
Q

true or false: you can expect hips with severe subluxation to progress to dislocation?

A

true!

148
Q

reasons to treat spastic hip

A

pain

ease of care

WC posture

pelvic obliquity and scoliosis

149
Q

Reimer’s migration index tells you the % of what?

A

femoral head outside of the acetabulum

150
Q

what is a normal Reimers migration index (how much of the femoral head is outside of the acetabulum

A

CP normal: <30%
Subluxation >30%
Dislocation >90%

151
Q

how many degrees of passive hip ABD is a red flag for spastic hip

A

< 45 degrees on either side

152
Q

what is this the treatment options for
early: soft tissue lengthening
bony changes: reconstruction
end stage: salvage

A

spastic hip

153
Q

if you are doing a STL (soft tissue lengthening) procedure for spastic hip, what would you be lengthening?

what assessment numbers would you look at?

A

ADD longus, gracilis, psoas

<8 years old
ABD <45
MI %: >30

THIS IS MODERATE

154
Q

if a child is older and has MP% of >40-60% what is the surgeon likely to do?

A

bony surgery on either the femur or the acetabulum to fix the shape of it because we know with spastic hip both get deformed

155
Q

femoral osteobomy for spastic hip are you tipping the femur into varus or valgus?

A

varus (remember its just the femur you’re talking about, you want it back in the socket)

normal anteversion is ~125 degrees

156
Q

explain acetabuloplasty simply

A

cut right above the cuff
cartilage inside is flexible
make a bone graft to put inside to shape the cuff

157
Q

true of false, scoliosis progresses with skeletal maturity?

A

true!

158
Q

True or false: 39-75% of individuals with spastic CP have scoliosis

A

true, idiot question

159
Q

small or progressive scoliotic curves what is done

A

observe

160
Q

true or false: bracing is the gold standard for scoliosis in CP

A

false! for idiopathic scoliosis it is! but kids with CP tend to not tolerate them well, and don’t stop the progression

161
Q

what are basically your two intervention options for scoliosis other than observing

A

surgery or brace (and bracing isn’t great for CP scoliosis)

162
Q

you want WC seat and back to be firm and squishy?

A

firm for support

163
Q

soft or hard spinal orthoses tolerated best?

A

soft!

164
Q

True or false: bracing in the CP population for scoliosis prevents progression

A

false! it slows the progression and may delay surgery

can improve sitting balance, function and ease of care

165
Q

if scoliotic curve is what degree do they consider surgery?

A

40-50 degrees

166
Q

what are the two ways they tend to do spinal surgery?

A

segmental instrumentation

fuse it to the pelvis in nonambulators

167
Q

true or false: complication rates for spine surgery are high?

A

true!

respiratory 
gastrointestinal 
skin wound
infection 
implant related 
pseudoarthrosis
168
Q

what kind of CP is this describing

abnormal tone
increases with activity but is constant  
squirming or writhing
disappears during sleep
kernicterus
non-ambulators
soft tissue surgery is unpredictable
A

athetoid CP

169
Q

true or false: CP encompasses a specturm of pathology?

A

true!

170
Q

just read it:
CP encompasses a spectrum of pathology
CNS lesion is static, musculoskeletal problems progress with growth
Priorities by adulthood are communication skills, ADL’s, and finally mobility
Treat each patient individually
Goal is to maximize function
Spasticity and it’s sequelae are amenable to treatment by neurosurgeons and orthopaedic surgeons but you’re not fixing the core problem (BRAIN)

A 
just read it: 
Orthopaedic treatment
Soft tissue and bony pathology
Hips, knees, ankles
Define problem list
Address all components at once
Have realistic goals
Adequate rehabilitation
Will still need orthotic support
Will still have problems with selectivity, balance, and  spasticity!

Unit 17 (9 decks)

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