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becky: neuro MSK > LECTURE 9: PEDIATRICS > Flashcards

LECTURE 9: PEDIATRICS Flashcards

1
Q

NS first appears at about ___ of gestation

A

21 days (before pt knows she is pregnant)

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2
Q

neural tube closure occurs at ___ days, from ___ to _____

A

23-25 days, anterior to posterior

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3
Q

neural tube (spinal cord and brain) starts at

A

21 days (closure)
24 days: fused

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4
Q

telencephalon forms

A

cerebral hemispheres

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5
Q

diencephalon

A

thalamus, GP, hypothalamus

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6
Q

mesencephalon becomes

A

midbrain

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7
Q

metencephalon forms

A

pons, cerebellum

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8
Q

myelencephalon

A

medulla

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9
Q

dysraphism etiology

A

unknown mainly
but prevention: folate!
risk factors; low SES (maternal nutritional status, prenatal care, teratogens (alcohol, retinoic acid, valproic acid)

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10
Q

seizure meds could cause

A

DYSRAPHISM
chemo meds (folate metabolism)

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11
Q

diagnosis of dysraphism

A

ultrasound
alpha-fetal protein

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12
Q

prevention of dysraphism

A

FOLATE

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13
Q

zika causes

A

ancephaly

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14
Q

dysraphism is a disorder of

A

neural tube closure (anterior neuropore open: cranial dysraphism: brain coming out with skull defect)

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15
Q

what is spinal dysraphism?

A

spina bifida (vertebral abnormality)

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16
Q

3 types of spina bifida

A

myelomeningocele: SC and meninges through defect
meningocele: dura and arachnoid herniation
occulta: vertebral arch defect only, 10% of pop (tuft of hair)

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17
Q

spina bifida occulta is usually

A

asymptomatic
skin abnormalities maybe over defect
L5-S1

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18
Q

myelomeningocele

A

B AND B DYSFUNCTION
SC stuff
often associated hydrocephalus
*Sx helps with infection risk (high risk of meningitis) but neuro deficits remain
*risk for tethered cord syndrome

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19
Q

Tethered Cord

A

when patient grows, spinal cord is stuck
LMN dysfunction (cauda equina)
*prevention of mvmt of conus medullaris
most common is unilateral one leg LMN

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20
Q

arnold-chiari malformation

A

(descended cerebellar tonsils-incidental tonsillar herniation)
less than 5 mm is not a problem, often not symptomatic

21
Q

type I AC malformation

A

cerebellar tonsils displaced > 6mm

22
Q

type II AC

A

associated myelomeningocele (syrinx in spinal cord)

23
Q

type III AC malformation

A

associated encephalocele

24
Q

what are symptoms of arnold chiari malformation?

A

hydrocephalus (poor prog) or later with cerebellar, medullary, cranial nerve signs (or headache)

25
how to treat arnold chiari malformation
close myelomeningocele, VP shunt for hydrocephalus posterior fossa decompression
26
dandy walker malformation is what
cerebellar vermis abnormality, large cyst in posterior fossa *common hydrocephalus *spastic diplegia *mental retardation
27
developmental delay is defined as
less than 70% developmental quotient global delay: 2 or more domains
28
what could mimic regression?
1. misperception of attained milestone 2. seizures 3. spasticitiy 4. movement disorders 5. hydrocephalus
29
What is down syndrome?
multi-organ disorder (congenital chromosomal abnormality of 3 copies of 21)
30
neurocutaneous disorders
skin manifestations of neurological disorders phakomatoses
31
red flags
fisting past 3 months rolling before 3 months, not rolling after 7 MORO after 6 months ATNR after 7 months not sitting after 9 months not talking after 2 years echolalia after 3 yrs stutter after 4 yrs HANDEDNESS BELOW 12 MONTHS OR ROLLING BEFORE 3 MONTHS = WEAKNESS
32
important features of down syndrome
trisomy 21 *short, stubby digits *small pelvis *AA instability of c-spine *hypotonia *intellectual disability *SEIZURES *cardiac and GI defects
33
important features of fragile x syndrome
most common chromosomal cause of intellect. disability low IQ, ADHD, seizures low mm tone and hyperextended
34
what does TORCHS stand for
toxoplasmosis other (zika) rubella cytomegalovirus herpes simplex, HIV syphilis (infection causes of delay)
35
what is CP?
group of permanent disorders of mvmt/posture cause activity limit non-progressive disturbances in fetal/infant brain
36
what can cause CP
hypoxia (10%) toxins metabolic disturbances infections TORCHS genetic, traumatic, vascular
37
what is most common type of CP?
spastic (85-90%) *others include dyskinetic, ataxic, mixed
38
spastic hemiplegia, diplegia, quadriplegia
hemiplegia: arms (MCA) diplegia: scissoring, adductor spasm quadriplegia: seizures, intellectual disability, MOST SEVERE
39
dyskinetic CP
Basal ganglia lesion can't walk chorea, athetosis, dystonia
40
what is the rarest form of CP?
ataxia CP *cerebellum *truncal/gait ataxia *not responsive to drugs/PT
41
2 types of neurocutaneous disorders
neurofibromatosis tuberous sclerosis
42
2 types of neurofibromatosis
NF1: PNS (cafe au lait, neurofibromas, PNS, optic glioma) NF2: CNS (acoustic neuromas, meningioma, gliomas) *scoliosis, hypotonia, poor coordination *hearing, vision, language, epilepsy *ADHD *pain *hypertension *cancers
43
what is tuberous sclerosis?
ADominant NS, skin, bones, retina, kidney calcifications on brain and into ventricles *skin macules, retina hemartomas, CNS (mental retardation and seizures)
44
adrenoleukodystrophy
x-link recessive boys, 8 normal, then vision loss, dementia, seizures, spastic gait, behavior changes *adrenal failure (high VLCFA)
45
metachromatic leukodystrophy
lacking arylsulfatase A enzyme A recessive *degen of Central and peripheral meylin *gait, mental deterioration, seizures
46
duchenne's MD
3-5: DF, hip flex/ext weak, hyperlordotic and toe walking calf pseudohypertrophy *wheelchair by 9-12 years (20: respiratory weakness lead to death or ventilator)
47
Becker MD
toe walking pseudohypertrophy less severe, normal IQ, rhabdo, heart probs, quad weak, cramps *ambulatory until 30 ish *dystrophin levels in mm!
48
spinal mm atrophy levels 0-4
LOSS OF SMN1 protein, LMN looks like ALS type 0: prenatal, die before 6 mo type 1: never sit (before 6 mo, die before 2 years) type 2: never stand (6-12 mo, die around 25) type 3: never run (after 1 yr, normal life) type 4: adult prox leg weakness

becky: neuro MSK (14 decks)

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