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PEDS 2- clinical disciplines > Neuro > Flashcards

Neuro Flashcards

1
Q

Which neuro abnormalities are seen in pts w/ static sxs?

A

congenital abnormalities or brain injury (think cerebral palsy)

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2
Q

Which neuro abnormalities are seen in pts w/ progressive sxs?

A

degenerative disease or neoplasn

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3
Q

Which neuro abnormalities are seen in pts with intermittent sxs?

A

epileptic or migraine syndromes

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4
Q

Which neuro abnormalities are seen in pts with saltatory sxs?

A

bursts of sxs followed by partial recovery

-vascular, demyelinating d/o

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5
Q

What PE findings may indicate spine bifida?

A

Midline defects:

tufts of hair, lipomas, dimpling

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6
Q

Accelerating pattern of head circumference may indicate? decelerating pattern?

A

hydrocephalus

degenerative neurologic disorder

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7
Q

How can you assess CN II?

A

pupillary light reflex, visual acuity

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8
Q

How can you assess CN III, IV, VI?

A

following objects, fixating, oculocephalic reflex, EOMs

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9
Q

How can you assess CN V?

A

sucking/swallowing, light touch

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10
Q

How can you assess CN VII?

A

observe fast at rest, crying/blinking

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11
Q

How can you assess CN VIII?

A

hearing

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12
Q

How can you assess CN IX, X?

A

gag reflex, sucking, salivation

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13
Q

How can you assess CN XI?

A

posture, spontaneous movement

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14
Q

How can you asses CN XII?

A

tongue movement

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15
Q

What are some primitive reflexes? When do most of them disappear?

A

Moro, grasp, rooting, foot placing, tonic neck

4-6 months

asymmetry indicates focal brain or PNS lesions

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16
Q

s/s seen w/ upper motor neurons

A

Spastic paralysis, Increased tone

Increased DTRs/+Babinski (in older children, normal in infants); usually with clonus

Minimal muscle atrophy/strength loss

Fasciculations absent

May have sensory disturbances

STIFFNESS, INCREASED PASSIVE TONE

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17
Q

s/s seen w/ lower motor neurons?

A

Flaccid paralysis

Decreased tone

Absent DTRs

Profound muscle Atrophy

Fasciculations present

May have sensory
disturbances

WEAKNESS, DECREASED PASSIVE TONE

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18
Q

What are some red flags for children w/ headaches?

A

headache in child <5y/o

new (“explosive onset”) & worsening HA in a previously healthy child

worst HA of life

unexplained fever

night time or early morning awakening HA

HA w/ vomiting

HA worse w/ straining

postural HA

neurocutaneous stigmata

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19
Q

What is the most concerning headache pattern in children?

A

chronic progressive
>4 months or >15x/month

usually increased ICP

possible psych factors

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20
Q

When should you order imaging in child presenting w/ HA?

A

Abnormal neurologic exam

Concern for space occupying lesion

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21
Q

Typical pediatric sxs for migraines?

A

Frontal, bitemporal or unilateral throbbing for 2-72 hrs (Unilateral sxs usually after puberty)

sxs relived by sleep

+/- visual aura

N/V, abdominal pain, phono/photophobia

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22
Q

Tx for migraines?

A

eliminate triggers: HA diary

acute: NSAIDs, APAP, triptans, antiemetics

Prophylaxis:
<6: Cyproheptadine
>6: Propranolol, Amitriptyline, Topiramate

Non pharm: B12

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23
Q

What is Pseudotumor Cerebri - Idiopathic intracranial hypertension (IIH)

A

elevated ICP w/ norm cerebrospinal fluid composition, and no other cause of intracranial hypertension

s/s: HA, papilledema, vision loss, intracranial noises, photopsia

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24
Q

Epidemiology of pseudotumor cerebri?

A

MC in females of childbearing age; does occur in peds- usually adolescents (11 years +)

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25
Q

MC risk factor for pseudotumor cerebri?

A

obesity

assoc. meds: tetracycline, steroids, retinol

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26
Q

Dx criteria for pseudotumor cerebri?

A

each of the following:
Papilledema OR VI (abducens) nerve palsy (unilateral or bilateral)

Normal neuro exam, except for papilledema and CN abn

Neuroimaging: norm brain parenchyma w/o evidence of hydrocephalus, mass, structural lesion, or meningeal enhancement

Normal CSF composition

Elevated LP opening pressure

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27
Q

When should you check imaging in pt with concern for pseudotumor cerebri?

A

Imaging BEFORE lumbar puncture

Increased ICP may cause cerebral herniation when LP is performed if obstructive hydrocephalus or mass

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28
Q

What is the main complication of pseudotumor cerebri?

A

vision loss

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29
Q

Tx for pseudotumor cerebri?

A

sometimes sxs resolve after diagnostic LP

wt loss for obese pts

Meds: (decreases the volume & pressure of CSF w/in the CNS):
Acetazolamide
Topiramate

Surgery

  • optho eval critical
  • CSF shunt when all else fails

decrease salt intake

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30
Q

What is cerebral palsy?

A

heterogeneous group of conditions involving permanent nonprogressive central motor dysfunction that affect muscle tone, posture, and movement

results from brain injury or malformation (before birth, during or after delivery)

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31
Q

Prenatal causes of cerebral palsy?

A

Prematurity

IU growth restriction

IU infection

Antepartum hemorrhage

Severe placental pathology

Multiple pregnancy

Hypoxic brain injury

Stroke

Cerebral dysgenesis

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32
Q

Postnatal causes of cerebral palsy?

A 
Stroke
Kernicterus
Trauma
Near-drowning
Toxins
Hypoxic brain injury
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33
Q

What are the MC delayed motor milestones in children w/ CP?

A

Not sitting by 8 mo

Not walking by 18mo

Early asymmetry of hand function (hand preference) before 1yr

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34
Q

What are the 4 major classification of CP?

A

spastic (MC)

athetoid/dyskinetic

Ataxic (extremely rare)

Atonic

35
Q

Describe spastic CP

A

features of an upper motor neuron syndrome

36
Q

Describe athetoid/dyskinetic CP

A

Athetoid: slow, smooth, writhing movements that involve distal muscles

Dyskinetic: decreased spontaneous movement, hypotonia, and suppressed primitive reflexes

37
Q

Describe ataxic CP

A

wide-based gait, intention tremor, slow, jerking movements

affects fine coordinated movements of the UE

motor milestones & language skills are usually delayed

ataxia may improve w/ time

38
Q

Describe Atonic CP

A

Severe hypotonia,
never stand or walk.

may have cerebral
Dysgenesis,
microcephaly,
profound intellectual disability

39
Q

CP tx goals?

A

Social and emotional development

Communication

Education

Nutrition

Mobility

Maximal independence in ADLs

40
Q

What is spina bifida?

A

Neural tube disorder (NTD)= defective closure of the caudal neural tube early in gestation (about week 4)
-spina bifida is MC

41
Q

What are the subtypes of spina bifida?

A

Meningomyelocele-most serious!

Meningocele

Spina bifida occulta

42
Q

Describe a meningomyelocele

A

Meninges and spinal cord exposed

total paralysis, loss of B/B control

accompanying Chiari II malformation*

43
Q

Describe a meningocele

A

Spinal canal and meninges are exposed, underlying spinal cord is intact

44
Q

Describe spina bifida occulta

A

Skin intact but underlying defects in bone and spinal canal present

May see sinus tract, dimple or tuft of hair. May have neuro deficits

45
Q

Prevention of spina bifida?

A

FOLIC ACID supplementation- pre-preg & during preg

46
Q

Dx of spina bifida

A

Routine screening w/ alpha-fetoprotein (AFP) level (16-18 w) in maternal serum & US (12-14 w & 18-20 w)

47
Q

management of spina bifida?

A

Surgical closure

VP shunt

Adjunct supportive therapies etc.
Cognitive disabilities, self-catheterization, etc.

px varies

48
Q

What is a chiari malformation?

A

heterogeneous group of disorders:
anatomic anomalies of the cerebellum, brainstem, and craniocervical junction, w/ downward displacement of the cerebellum, either alone or together with the lower medulla, into the spinal canal

49
Q

What are the types of chiari malformations?

A

Chiari 1: downward displacement of medulla and cerebral tonsils, syringomyelia

Chiari 2 (Arnold-chiari malformation)

Chiari 3

Chiari 4: hypoplasia/aplasia of the cerebellum w/ spina bifida NOT COMPATIBLE W/ LIFE

50
Q

Chiari malformations cause…

A

malformation obstructs the outflow of cerebral spinal fluid (CSF) through the posterior fossa –>

HYDROCEPHALUS

51
Q

Almost all pts w/ a myelomeningocele have…

A

chiari II malformation

and most have assoc. hydrocephalus

52
Q

What is hydrocephalus?

A

Increased volume of CSF w/ progressive ventricular dilation

Slowly evolving accumulation of CSF over weeks to months

can be congenital or acquired

53
Q

What is communicating hydrocephalus?

A

CSF circulates through the ventricular system & into the subarachnoid space w/o obstruction

54
Q

What is non-communicating hydrocephalus?

A

an obstruction blocks the flow of CSF w/in the ventricular system or blocks CSF from going from the ventricular system into the subarachnoid space

55
Q

Presentation of hydrocephalus?

A

Sx related to ventricular distention and increased ICP
obstruction of CSF flow

HA, vomiting, AMS, visual changes, ocular nerve palsies, and focal neuro findings

Infants: nonspecific –> vomiting, lethargy, irritability, bulging fontanelle, poor feeding, etc.

56
Q

PE findings seen in pt with hydrocephalus?

A

VS- bradycardia, HTN, altered respiration (think brainstem)

Increased head circumference, bulging anterior fontanelle, abn skull contour, CN dysfunction, papilledema.

57
Q

Tx for hydrocephalus?

A

Temporary, symptomatic relief: loop diuretic, acetazolamide

Surg intervention: remove obstructive lesion, VP shunt

58
Q

Inheritance pattern for the common forms of SMA?

A

autosomal recessive

caused by biallelic deletion or mutations in the SMN1 gene on chromosome 5q13

59
Q

What are SMA disorders?

A

characterized by degeneration of the anterior horn cells in the spinal cord and motor nuclei in the lower brainstem, which results in progressive muscle weakness and atrophy

60
Q

When do most cases of SMA present?

A

in infancy

61
Q

What are the 5 subtypes of SMA?

A

SMA 0= prenatal onset, severe weakness, hypotonia and often reflexia at birth

SMA1: most devastating, present at birth, progress to respiratory failure by 1

SMA2: sxs begin later in life, weakness and decreased DTRs by 2

SMA3: weakness near adolescence

SMA4

62
Q

When should SMA be suspected?

A

for any infant with unexplained weakness or hypotonia

Presents with progressive proximal weakness , decreased spontaneous mvmt, “floppiness”

63
Q

Dx of SMA?

A

EMG, muscle Bx, DNA testing

homozygous deletion of exon 7 of SMN1 (confirms diagnosis)

64
Q

Tx of SMA?

A

No tx

Sx therapy to improve flexibility, prevent infections, maintain social, language and intellectual stimulation

65
Q

What is Guillain barre syndrome (acute idiopathic polyneuritis)

A

Acute immune-mediated polyneuropathy

Heterogenous syndrome, variant forms

66
Q

Presentation of GBS?

A

Usually presents as an acute paralyzing illness provoked by a preceding infection

Ascending weakness (symmetric)

Many have sensory sxs

Loss of DTRs early

May have autonomic nerve dysfunction

Children- refusal to walk and leg pain are MC presenting sxs

67
Q

Etiology of GBS?

A

Causes: Post-infectious

  • Resp or GI infection
  • Campylobacter jejuni MC
68
Q

Dx of GBS?

A

LP- Elevated CSF protein without increased WBC

Electromyography (EMG)

69
Q

Px of GBS?

A

85% of children have excellent recovery

May require ventilator support

Death from autonomic dysfunction, respiratory failure, complications (3-4%)
-PNA, PE, CV collapse

70
Q

Tx of GBS?

A

IVIG: combat invading organisms- lessen attack on NS

Plasmapheresis:
decrease severity and duration, removes Ab from circulation

71
Q

Transmission of duchenne muscular dystrophy (DMD)?

A

X-linked recessive- absence of dystrophin protein

Boys exhibit trait around age 3- rapidly worsens

usually 2-6 yrs

72
Q

Presentation of DMD?

A

Slower to develop motor milestones- walking/climbing stairs, walking on toes

Proximal muscles affected before distal; lower before upper

May have mild cognitive development, global developmental delay

73
Q

PE findings seen in DMD?

A

Calf hypertrophy and proximal leg/pelvic weakness

Waddling gait and inability to rise from ground easily

Gower’s sign

74
Q

Dx of DMD?

A

Muscle biopsy

Myopathic EMG

Serum CK levels

Genetic testing available for prenatal dx

75
Q

Tx of DMD?

A

sxs:
- Glucocorticoids
- new tx: gene therapy, creatine, aminoglycosides

close pulmonary & cardiac FU due to risk of cardiopulmonary failure in 2nd & 3rd decade of life

76
Q

Px of DMD?

A

Usually Wheel chair bound by 12 yo

Loss of UE mvmt by 16

Death due to PNA or CHF (in early 20s)

Average lifespan ~25

77
Q

What is neurofibromatosis type 1?

A

Multisystem disorder

Genetic disorder in which nerve tissue grows tumors that cause nerve/brain damage

78
Q

s/s of neurofibromatosis type 1?

A

criteria: need 2 or more

  • cognitive or psychomotor sxs MC
  • learning disabilities (40%)
  • cafe au lait spots >6
  • 2 or more neurofibromas
  • freckling or the axilla or inguinal regions
  • optic alimoa
  • 2 or more lisch nodes
  • distinctive bony lesions
  • 1st deg relative w/ NF type 1
79
Q

What are neurofibromas?

A

soft or firm pedunculated tumors that develop along a nerve

80
Q

Tx of NF type 1?

A

Surgical excision of tumors

Genetic counseling & screening (risk to sibs is 50%)

81
Q

Complications of NF type 1?

A

seizures, deafness, short stature, early puberty & HTN (<25%)

optic glioma ~15%

82
Q

What is NF type 2?

A

Dominantly inherited neoplasia syndrome- rare autosommal dominant disease

83
Q

Presentation of NF type 2?

A

Manifests as bilateral vestibular schwannomas (VIII nerve tumors)

vestibular schwannomas virtually never occur in NF type 1

other tumors of brain/spinal cord: meningiomas, other CN schwannomas, ependymomas

84
Q

Will see cafe au lait sports in NF type 2?

A

NO

PEDS 2- clinical disciplines (5 decks)

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