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Peds Exam 2 > Peds Neurology > Flashcards

Peds Neurology Flashcards

1
Q

PE for neuro

A 
vitals
head circumference, fontanelles
general
skin, eyes, ears, extremities, midline
dev. exam
mental state
CN
motor
reflexes
sensory
station & gait
cerebellar
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2
Q

Cerebral palsy

A

motor impairment secondary to fetal or infantile brain injury

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3
Q

Etiologies of cerebral palsy

A 
hypoxia
trauma
premature birth
infections
toxins
structural abnormalities
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4
Q

Subtypes of cerebral palsy

A

spastic - most common
ataxic
dyskinetic
mixed

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5
Q

S/sx of cerebral palsy

A 
abnormal tone and/or posture
retained reflexes
NOT REACHING MILESTONES (sit by 8 mos, walk by 18 mos)
excessive irritability
poor feeding, drooling
poor visual attention
difficult to hold, cuddle
ASYM. TONIC NECK REFLEX (ATNR)
MORO REFLEX  - retained after 4 mo
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6
Q

Managment of cerebral palsy

A

early recognition and referral
parental support

symptomatic: OT, PT, bracing
anti-spasmodics
botulism toxin

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7
Q

Etiologies of congenital malformations

A 
infection
toxin
genetic
metabolic
vascular
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8
Q

Prognosis of congenital malformation

A

present in 40% of infants who die <1 YO

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9
Q

Chiari Type 1

A

cerebellar tonsils displaced caudally BELOW the foramen magnum

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10
Q

Chiari type 1 can be associated w/

A

syringomyelia = fluid filled cyst w/ in spinal cord

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11
Q

Sx of chiari type 1

A

appear as teen/adult
loss of abdominal reflex
neuro sx associated w/ syringomyelia –> h/a worse w/ increase pressure (sneeze, cough, valsalva)

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12
Q

Chiari type II (arnold-Chiari malformation)

A

type 1 + myelomeningocele

usually detected prenatally or at birth

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13
Q

S/sx of chiari type 2

A

HYDROCEPHALUS (CSF build up in head)
dysphagia
UE weakness
apneic spells and aspiration

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14
Q

Spina bifida occulta

A

incomplete closure of spinal canal (closed type)
no or mild signs

hair patch, dimple, dark spot, swelling on back at the site of the gap in the spine

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15
Q

Open types of spina bifida

A

meningocele

myelomeningocele

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16
Q

Meningocele

A

outpouching of spinal fluid and meninges through vertebral clef

mild problems w/ sac protrusion

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17
Q

Myelomeningocele

A

most severe form

spinal cord &/or nerves protrude from vertebral cleft

weakness, loss of bladder and/or bowel control, hydrocephalus, inability to walk
learning problems

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18
Q

Etiology of spina bifida

A

genetics
LOW FOLATE
medications during pregnancy
poorly managed DM

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19
Q

Management of spina bifida

A

early recognition (US, AFP)
prevention
neurosurgeon refer: surgery, shunt

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20
Q

Hydrocephalus

A

increased volume of CSF – causing ventricular dilation and increased ICP

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21
Q

types of hydrocephalus

A

obstructive - blocakge

non-obstructive - impaired absorption or rarely overproduction

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22
Q

Etiologies of hydrocephalus

A 
CNS malformation
infection
Intraventricular hemorrhage
genetic defects
trauma
tumor
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23
Q

S/sx of hydrocephalus

A 
asymptomatic
bradycardia, HTN, altered RR
h/a, n/v, behavior changes
papilledema
macrocephaly
spasticity
diplopia (compression of cranial nerves)
spinal abnormalities
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24
Q

Dx of hydrocephalus in newborns/infant

A

US

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25
Q

Dx of hydrocephalus in infants/children

A

MRI or CT

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26
Q

Management of hydrocephalus

A

refer to neurosurgeon

shunt (to periotneal space)

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27
Q

Microcephaly is considered

A

head circumference >2 SD BELOW mean or <5th percentile

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28
Q

types of microcephaly

A

primary (congenital) - lack of brain dev or abnormal dev due to timing of insult

secondary (postnatal) - injury or insult to previously normal brain

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29
Q

Etiology of microcephaly

A 
genetic
prenatal/perinatal injury
CRANIOSYNOSTOSIS
postnatal injury
metabolic
toxins
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30
Q

S/sx of microcephaly

A

delayed milestones
seizures or spasticity
fontanelle may close early and suture may be prominent

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31
Q

Macrocephaly is considered

A

head circumference >2 SD above mean or >95 percentile

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32
Q

Cause of macrocephaly

A

increase in size of any components of cranium (brain, CSF, blood or bone)

rapid growth: increased ICP
catch up growth: premature infants, neurologically intact
normal growth rate: familial macrocephaly or megaloencephaly

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33
Q

management of micro and macrocephaly

A

Neuro referral - labs and imaging

treat underlying cause

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34
Q

NF1 etiology

A

auto dominant

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35
Q

Clinical manifestation of NF1

A 
neuro abnormalities: macrocephaly, seizures, cognitive deficit
Cafe-au-lait spots (1st yr)
axillary/inguinal freckles (3-5 yrs)
lisch nodules
optic glioma
neurofibromas
36
Q

Management of NF1

A

consult neuro, genetics, optho

37
Q

PE for headaches

A 
general
vitals
head circumference
growth chart
HEENT
skin
Neuro exam
38
Q

Types of headaches

A

primary - migrane and tension

secondary- acute febrile illness

39
Q

Migraine

A

location- FOCAL, unilateral or bilateral
Duration 2-72 hrs
Character- mod/severe intensity, PULSATILE/THROBBING

worse w/ activity or reduced activity

40
Q

Tension h/a

A

location: DIFFUSE, frontal or temporal
duration: 30 min - 7days
character: mild/mod, constant PRESSURE/NON-THROBBING

not aggravated w/ activity

41
Q

Worse w/ acivity

A

migraine

42
Q

throbbing/pulsatile

A

migraine

43
Q

diffuse

A

tension

44
Q

management of h/a

A

track and avoid triggers

ibuprofen, tylenol, biofeedback, relaxation therapy

45
Q

when to worry about h/a

A
  • abnormal neuro or visual exam
  • severe upon awakening or awaken in middle of night
  • daily sx w/ progressive worsening
  • vomiting
  • acute onset w/o previous hx
  • increased w/ coughing or bending
46
Q

Pseudotumor cerebri: what is it?

A

idiopathic intracranial HTN; increase ICP w/o mass or hydrocephalo

47
Q

Pseudotumor cerebri typically seen in

A

obese teenage girls

48
Q

S/sx of pseudotumor cerebri

A 
HA*
Papilledema* - hallmark
visual sx
visual field loss, acuity loss
Pulsatile tinnitus*
49
Q

Papilledema seen in

A

hydrocephalus

pseudotumor cerebri

50
Q

Dx of pseudotumor

A 
(mainly diagnosis of exclusion)
neuro eval
MRI - r/o other cause
LP - elevated opening pressure
Optho eval
51
Q

Management of pseduo tumor

A 
Acetazolamide* - reduces CSF production
Topiramate - helps HA and reduce weight
Furosemide- reduces fluid, reduced pressure
weight loss
shunting of fluid
optic nerve fenestrations
52
Q

main tx for pseudo

A

acetazolamide

53
Q

Seizure

A

sudden, transient disturbance of brain function manifested by involuntary sensory, motor, autonomic sx w/ or w/o LOC

54
Q

Epilepsy

A

> 2 seizures occuring more than 24 hours apart

55
Q

Types of seizures:

A

focal (partial): w/ or w/o awareness
generalized
unknown
unclassified

56
Q

Absence seizure sx

A

sudden impairment of consciousness w/o loss of tone (blank stare)
provoked by hyperventilation
genetic cause
presents b/w age 4-10 and remits after puberty

ARREST IN ACTIVITY, lasting 9-10 seconday, may occur 10x/day

57
Q

Age of absence seizures go away

A

pubery

58
Q

absence seizures start

A

4-10 YO

59
Q

Dx of absence seizures

A

Hx PE, EEG

Hyperventilation test

60
Q

Management of absence seizures

A

neuro refer

neurocognitigve testing

61
Q

Pharm tx for absence seizures

A

Ethosuximide (anticonvulsant)

62
Q

Tx for pseudotumor

A

Acetazolamide*
Furosemide
Topiramate

63
Q

Febrile seizure features

A

convulsion w/ temp >38 C

age 6 mo - 5 yo
often associated w/ virus (roseola)
+ genetic predisposition

64
Q

age for febrile seizures

A

6 mo - 5 YO

65
Q

Types of febrile seizures

A

simple: most common, <15 min (no inc risk for more)
Complex: focal, last >15 min or occur >1/24 hours (inc risk for more)

66
Q

Dx of febrile seizure

A

hx and PE
CNS infection - LP or neuro image
EEG - only if at risk for future epilepsy

67
Q

Management of febrile seizures

A

self-limiting

Sx >5 min – IV benzodiazepines

68
Q

Tx for febrile seizure

A

IV benzodiazepines (> 5 min seizures)

69
Q

Guillian-Barre syndrome

A

acute immune-mediate polyneuropathy; preceded by illness (campylobacter)

70
Q

Most common caue of acute flaccid paralysis in healthy infant/child

A

guillian-barre

71
Q

main cause of guillian-barre

A

campylobacter infection

72
Q

S/sx of guillian barre

A

ASCENDING symmetric weaknes
neuropathic pain
gait instability or refusal to walk
absent reflexes

73
Q

Dx of guillian-barre

A

EMG
CSF analysis - increased protein w/ normal WBC
Spinal . MRI w/ and w/o contrast – enhance spinal nerve roots & cauda equina

74
Q

Managment of guillian-barre

A

hospitilize and close monitor

IVIG or plasma exchange

75
Q

Botulism is usually caused by

A

consuming honey or home canning

76
Q

What does the botulinum toxin do

A

bind Ach receptors

77
Q

Age of infants w/ botulism

A

90% are <6 mos

78
Q

S/sx of Botulism

A

DESCENDING weakness
constipation, poor feeding
HYPOTONIA, loss of DTRs
irritable, lethargic

79
Q

Dx for botulism

A

stool sample

EMG

80
Q

Management of botulism

A

hospitilize and close monitor

botulism immune globulin (BIG-IV or BabyBIG)

81
Q

Education on botulism

A

don’t feed babies <1Yo honey

82
Q

Duchenne Muscular Dystrophy (DMD) cause

A

X-linked recessive
defect in dystrophin gene

elevated muscle enzymes (CK, ALT, AST)
more severe sx and earlier onset –> age 2-3
wheelchair bound by age 13 and mortality by 18-20

83
Q

Sx of DMD

A

progressive weakness (proximal –> distal, LE –> UE)
GOWER’S SIGN - use hands to get off floor
PSEUDOHYPERTROPHY of calves
growth delay (short)
cognitive impairment

84
Q

Associated conditions w/ DMD

A

cardiomyopathy (dilated ventricle)
ortho complications (scoliosis)
cognitive impairment

85
Q

Dx for DMD

A

elevated muscle enzymes (CK >10-20 x)

Genetic testing

86
Q

Management of DMD

A

Glucocorticoids (keeps sx worsening slower)

87
Q

Becker Muscular Dystrophy (BMD)

A

later onset than DMD
less severe than DMD
CK (>5 x)
cardiomyopathy more predominant*

Peds Exam 2 (3 decks)

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