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Neuro Rehab 1 > Neural Tube Defects & Spina Bifida > Flashcards

Neural Tube Defects & Spina Bifida Flashcards

1
Q

what is a neural tube defect

A

most commonly-occurring complex congenital birth defect associated w long-term survival

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2
Q

what development is occurring at an embryonic level

A

mass cell division & early differentiation
- ectoderm
- mesoderm
- endoderm

beginnings of heart, CNS, MS system formation

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3
Q

what does the ectoderm develop into

A

NERVOUS SYSTEM**
skin
teeth

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4
Q

what does the mesoderm develop into

A

blood vessels
ms
bone

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5
Q

what does the endoderm develop into

A

GI
GU
non-ms portion of pulm system (ie lungs)
urinary tract

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6
Q

what is the process of ectoderm development into the nervous system

A

ectoderm ->
neural plate (formed day 18)

** neural tube > CNS
- brain
- SC

** neural crest > PNS
- CNs
- spinal n.
- autonomic n.
- ganglia

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7
Q

when does the neural ectoderm close

A

26-28days after fertilization

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8
Q

what are the 2 processes after the ectoderm closes

A

neurulation (cranial)
canalization (caudal)

starts @C1 and proceeds cephalad and caudal directions simultaneously

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9
Q

what are the 2 theories behind path of NTD and what is the flaw

A
  1. failure of closure
  2. rupture of previously closed neural tube

flaw: neither adequately explains all deficits

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10
Q

what are the assumed causes of NTD

A

genetic vulnerability and/or environmental trigger (ie teratogens, nutritional deficiencies)

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11
Q

what is spinal dysraphism

A

general term to describe congenital abnormalities that include defects of vertebra, SC, or nerve roots

  • many types of NTD/dysraphisms
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12
Q

what is spina bifida occulta

A

non-fusion vertebral arches
no neural problems
- no change to underlying neural tissues

not visible, it is hidden

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13
Q

where is spina bifida occulta most common

A

in lumbo and sacral regions

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14
Q

what may be the only evidence of spina bifida occulta

A

darkened area or pigmentation of skin

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15
Q

what is spina bifida cystica

A

non-fusion vertebral arches
neural damage

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16
Q

what are 2 types of spina bifida cystica

A

meningocele
myelomeningocele

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17
Q

what is meningocele

A

cystic sac w meninges & CSF

SC stays w/i canal but may have abnormalities

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18
Q

what are clinical signs of meningocele

A

none
- or may have (varied)

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19
Q

what is myelomeningocele

A

cystic sac like meningocele, but SC and meninges in sac
- could be open

neural tissue - abnormalities

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20
Q

what are the results of myelomeningocele

A

varying sensory and motor impairment @ level of lesion and below

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21
Q

what is an interchangeable term for meningomyelocele

A

myelodysplasia

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22
Q

what is the risk w open myelomeningocele

A

additional damage d/t exposure to amniotic fluid
- high risk for infection and meningitis

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23
Q

what ethnicity is the incidence of spina bifida the highest

A

hispanic

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24
Q

what are risk factors for spina bifida (8)

A
  1. previous NTD-affected pregnancy
  2. maternal insulin-dependent diabetes
  3. seizure meds
  4. medically diagnosed obesity
  5. maternal hyperthermia
  6. low folic acid levels
  7. lower SES
  8. agent orange
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25
Q

what is a key preventative measure

A

folic acid
- 400mcg/day preconception up to 3mo of pregnancy
- 4000mcg/day if prior NTD

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26
Q

what do folic acid supplements modify the risk of

A

modifies inc risk for NTDs for pregnant persons w periconceptual fever

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27
Q

what are 2 clinical presentations of NTDs

A
  1. absent sensory/motor below level of lesion (B)
  2. loss of neural bowel and bladder control
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28
Q

what type of NTDs is absent sensory and motor really common in

A

myelomeningocele

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29
Q

what are the implications for sensory loss

A

skin safety and skin care
- teach for inspection

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30
Q

why is ICC important for someone w a loss of neural bowel and bladder control

A

allows bladder to fully empty and dec risk of infection

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31
Q

for people w a loss of neural bowel and bladder control, what are common intervention/management plans

A

prophylactics for infection
bowel programs

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32
Q

what does (B) absent sensory and motor below level of lesion look like

A

may be asymmetrical
may skip levels
may be incomplete/complete

flaccid paralysis unless incomplete -> mix of spasticity & volitional control

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33
Q

what does a loss of neural bowel and bladder control look like

A

neurogenic w sacral plexus involvement
- neurological control of bladder & sphincters are impaired or absent

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34
Q

what is a red or yellow flag w NTD

A

new presence of or change in spasticity may be indicative of progressive neurologic dysfunction

35
Q

what is the PT implication w the possibility of skip lesions in NTDs

A

PT must test motor function
- left/rest sides
- all myotomes
- all dermatomes

exam must include tests of spasticity and DTRs

36
Q

what are skip lesions

A

innervation is intact or partially intact below areas w little to no innervation

37
Q

what are systems w common complications (3)

A

CNS
msk
multisystem

38
Q

what are common CNS complications (3)

A
  1. hydrocephalus
  2. arnold chiari malformation
  3. progressive neurological dysfunction
    - tethered cord syndrome
    - hydromyelia
39
Q

what are 2 examples of multisystem complications

A

latex allergy
obesity

40
Q

what is hydrocephalus

A

abnormal accumulation of CSF in ventricles d/t obstruction
- interrupting CSF circulation

41
Q

what are sx of hydrocephalus

A

“sunsetting” of eyes
bulging fontanelle in young infant
VS instability

42
Q

what is the treatment for hydrocephalus

A

shunt
- ventriculo-peritoneal (VP)**
—– most common
- ventriculo-atrial (VA)
- ventriculo-pleural

43
Q

what are reasons for shunt dysfunction

A

infection
disconnected tubing
tubing needs to be repaired

44
Q

what are general early warning s/sx of shunt dysfunction (7)

A

dec activity level
dec school performance
incontinence
visual disturbances
neuro sx (sz, spasticity, arousal, HA)
infection signs (fever, malaise)
speech

45
Q

what is arnold chiari II malformation (ACMII)

A

cerebellar hypoplasia
- caudal displacement of cerebellum and medulla thru foramen magnum

severity varies

46
Q

what are sx of ACMII (7)

A

stridor
apnea
GE reflux
paralysis of vocal cords
swallowing problems
aspiration (may need tracheostomy)

47
Q

what is ACMII associated with

A

hydrocephalus

48
Q

what is the path of ACMII that is creating the sx seen

A

impacts the CNs
- think ab bulbar and brainstem functioning and CN compression

49
Q

what are treatment options for ACMII

A

manage sx
cervical laminectomy - relieve pressure on SC

50
Q

what are 3 signs of progressive neurologic dysfunction

A
  1. changes in spasticity, strength, sensation, pain
  2. scoliosis development/worsening
  3. change in bowel/bladder sphincter control
51
Q

what are 3 causes for progressive neurologic dysfunction

A
  1. tethered cord syndrome
  2. severe intervertebral disk herniation into spinal canal
  3. hydromyelia
52
Q

what is tethered cord syndrome

A

scarring to SC to overlying dura or skin leading to traction on neural structures

53
Q

what sx are seen as a result of tethered cord syndrome and why

A

progressive neurologic changes seen w growth spurts

metabolic changes and ischemia can result from stretching of neural tissues

54
Q

what is hydromyelia

A

UE weakness, changes in spasticity d/t altered communication w higher motor centers

55
Q

what is the intervention for hydromyelia

A

might put another shunt in
- this time a spinal shunt

56
Q

what are complications related to CNS dysfunction

A
  1. perceptual motor deficits
  2. communication issues
  3. developmental delays
  4. vision (ie strabismus, nystagmus)
57
Q

how do communication issues related to CNS complications present

A

early in language development
better expressive than receptive

58
Q

what is strabismus

A

problem of control of extraocular eye ms
- eyes do not align w each other when focused on a target
- what is initially received is blurry and confusing

59
Q

what can cause strabismu

A

multiple etiologies
- ex: CN damage

60
Q

what happens if strabismus is untreated

A

one eye will become more dominant than the other

61
Q

what is nystagmus

A

involuntary, uncontrolled repetitive eye movement
- seen in infancy or acquired

62
Q

what are causes of nystagmus

A

vestibular main one
- others too

63
Q

can nystagmus resolve on its oqn

A

yes - but depends on severity

64
Q

what nystagmus is the most common

A

horizontal pendular nystagmus

65
Q

what can inc nystagmus sx

A

when one eye is occluded (dec vision)

66
Q

what is the role of MSK complications like deformities

A

primary or secondary impairments

67
Q

what are 5 factors of MSK complications

A
  1. ms imbalance
  2. progressive neurological dysfunction
  3. intrauterine positioning
  4. anomalies
  5. deformities after fx
68
Q

what are 4 MSK complications seen at LE

A
  1. developmental dysplasia of hip
  2. tibial torsion
  3. genu varus/valgus
  4. club feet/foot
69
Q

what is a consideration when treating someone w LE MSK complications

A

might not correct bc of neg impact on prolonged immobilization
- depends on pt

70
Q

what MSK complications are seen at the spine

A

scoliosis
lumbar kyphosis

71
Q

what MSK complications are seen at UE and why

A

overuse syndrome(s)
- depending on motor level, may rely heavily on UE for amb and other functions

72
Q

what are 4 complications seen at a multisystem level

A

osteoporosis & osteoporotic fx
skin breakdown
latex allergies
obesity (multifactorial)

73
Q

what is the PT implication for managing someone w osteoporosis & osteoporotic fx

A

careful w handling
- short lever arms

74
Q

what are 3 medical management interventions

A

prenatal testing: screening & dx
management of neonate
general care guidelines

75
Q

what are 2 screening tools for prenatal

A

alphafetoprotein (AFP)
US

76
Q

what is alphafetoprotein (AFP) and how is it used in prenatal testing

A

AFP produced by fetal liver, which will go up and travel thru mother’s blood stream
- maternal AFP measured

screening tool
taken b/w 16-18wks (retest prn)

77
Q

how is US used in prenatal testing

A

screen/dx tool
screens for abnormalities

78
Q

how is amniocentesis used in prenatal testing

A

dx tool

check acetylcholinesterase (more accurate than AFP)
- also check for chromosomal abnormalities

79
Q

what are medical treatment options if NTD detected prenatally

A

can treat intra-uterinely or after birth

80
Q

how is NTD treated intra-uterinely

A

intra uterine closure of defect
- fix baby and pop back in
- would rather do closer to gestation (20-26wks gestation)

81
Q

how does intra uterine closure of NTD impact the infant vs mother

A

infant - reduced complications
- improved function

mother - inc risk of preterm delivery
- thinning of uterus @surgical site

82
Q

how is detected NTD treated after birth

A

deliver via C-section (esp if open skin lesion)
- reduces damage to defect

immediate sterile care of lesion
- great risk once exposed to area

surgical closure w/i 24-72hrs
shunt placement prn

83
Q

what is the goal of SBA care guidelines

A

EBP guidelines to treat and care for individuals not just conditions associated w SB

84
Q

what are the 3 key concepts of SBA care guidelines

A

care coordination
- pt/family centered care w//i medical home

care co-management - team based care in community

considerations
- language
- level of acculturation
- cultural constructs of care

Neuro Rehab 1 (27 decks)

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