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Summer Disciplines 3 > Peds neuro > Flashcards

Peds neuro Flashcards

1
Q

What is static

A

Sx seen in the first few months, does not change over time

congenital abnormality or brain injury ex: cerebral palsy

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2
Q

What is progressive

A

degenerative disease or neoplasm

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3
Q

What is intermittent

A

epileptic or migraine syndromes

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4
Q

What is saltatory

A

bursts of Sx followed by partial recovery

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5
Q

On neuro PE note

A
  • hair, skin, teeth, nails (brain and skin have same embryonic origin)
  • head circumference
  • fontanelles (some bulging with crying or vomiting is normal. but stay bulged with high ICP or infection)
  • eyes, ears
  • hands, feet: single simian crease in down’s syndrome, polydactyly abnormal
  • midline defect (hair tuft, lipoma, dimpling): can indicate spina bifida
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6
Q

What is the cut off point for micro and macrocephaly

A

2-3 SD above or below normal

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7
Q

What patterns can mean different things in head circumference

A

accelerated growth: hydrocephalus
decelerated growth: degenerative neurologic disorder
abnormal shape: craniosynostosis (premature closure)

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8
Q

How do you test the cranial nerves

A 
I: smell 
II: pupil light reflex, visual acuity 
III, IV, VI: EOM 
V: suck, swallow, light touch 
VII: observe face at rest, crying, blinking 
VIII: hearing 
IX, X: gag reflex, sucking, salivation 
XI: posture, spontaneous movement 
XII: tongue movement
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9
Q

When do fontanelles close

A

Posterior: 2 months
Anterolateral: 3 months
Posterior lateral: 1 year
Anterior: 2 years

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10
Q

What are the primitive reflexes

A 
Moro 
Grasp
Rooting
Foot placing 
Tonic neck (fencing ninja) 
-Most disappear by 4-6 months old 
Asymmetry= focal brain or PNS lesions
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11
Q

Where do upper motor neurons originate

A

in motor region of cerebral cortex or brainstem, and they terminate at brainstem and spinal cord

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12
Q

Upper motor neurons cause

A 
spastic paralysis 
increased tone 
increased DTR (babinski) 
minimal muscle atrophy/strength loss 
No fasciculations 
sensory disturbance
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13
Q

Lower motor neurons originate

A

in brainstem and spinal cord and terminate at skeletal muscle fibers

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14
Q

Lower motor neurons cause

A 
flaccid paralysis 
decreased tone 
absent DTR 
profound muscle atrophy 
fasciculations present 
sensory disturbances
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15
Q

How do you assess strength in infants vs Toddlers

A

infant: symmetry of movement when held supine
toddler: reach high, run, walk, hop, climb

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16
Q

How do UMN and LMN lesions present with strength

A

UMN: stiffness
LMN: weakness

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17
Q

How do you assess tone

A

infant: passive (resistance to stretch) and active (posture adopted when put in a specific position) movement

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18
Q

How do UMN and LMN lesions present with tone

A

UMN: (slide 12)
LMN: decreased passive tone

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19
Q

How does gait evolve

A

it narrows until age 6 then normalizes

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20
Q

How can you check cerebellar function

A

finger to nose
heel to shin
heel toe walking
exchange objects

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21
Q

What is normal babinski in kids

A

neonate: variable

older kids: toes down is normal after 18 months

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22
Q

How do you check sensory function

A

infant (harder): light touch vs pinprick. simulate by withdrawing limb
Older: proprioception, vibration, graphesthesia, stereognosis, 2 point discrimination

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23
Q

Red flags for kid headache are

A

pt < 5 y/o
new explosive onset and worsening HS in prev. healthy kid
worst HA of life
unexplained fever
nighttime or warly morning awakening
HA w/ vomiting or worse w/ straining
postural HA (worse w/ lying or standing)
neurocutaneous stigma (cafe au lait spots, hypopigmented macules, etc)

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24
Q

Explain acute vs acute recurrent HA

A

acute: single episode, no Hx. MC 2/2 febrile illness
AR: pattern of episodes separated by pain free intervals. typical migraine and tension HA pattern

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25
Q

What is the most concerning peds HA pattern

A

chronic progressive- may be increased ICP

DDx think pseudotumor, brain tumor, hydrocephalus, chronic meningitis, abscess. etc. (BAD shit)

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26
Q

What is a chronic non-progressive HA pattern

A

> 4 months or >15x month

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27
Q

What are worsening HA signs and symptoms

A

most severe on awakening, wake in middle of night
Severely exacerbated by coughing or bending
acute onset
present daily w/ progression
associated vomiting
focal neuro Sx
aggravated by valsalva

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28
Q

What imaging should you get for a headache and when

A

MRI! but you have to sedate peds..

Get if abnormal neuro exam, or concern for space occupying lesion

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29
Q

Typical peds migraine Sx are

A

frontal, bitemporal, or unilateral throbbing for 2-72 hours (usually unilateral after puberty)
Sx relieved by sleep
+/- aura 15-30 min prior
Sensory and motor Sx rare

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30
Q

Some migraine triggers include

A 
diet 
menses
stress 
increased exercise, sleep, routines 
-Eliminate triggers by keeping HA diary!
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31
Q

Acute migraine Tx is

A

NSAIDs, APAP, triptans (>12 y/o), antiemetics (compazine-benadryl-toradol)

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32
Q

migraine prophylaxis is

A

<6: cyproheptadine
>6: propranolol, amitryptaline, topiramate
non-pharm: B12 25-400mcg

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33
Q

prognosis of migraines

A

good- can improve with time

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34
Q

What is pseudotumor cerebri (idiopathic, intracranial HTN)

A

d/o w/ Sx of high ICP (HA, papilledema, vision loss)
Elevated ICP with normal CSF and no other cause of IC HTN on neuroimaging
MC in females of childbearing age, but can happen <11 y/o
Obesity is a RF
Tetracycline, steroids, and retinol also linked

35
Q

What are Sx of pseudotumor

A 
HA 
transient visual obscurations 
IC noises )pulsatile) 
Photopsia 
back pain 
retrobulbar pain 
diplopia
sustained visual loss
36
Q

In order to diagnose pseudotumor, the following must be present

A 
Papilledema OR CN6 palsy 
Normal neuro exam other than papilledema and CN abn
Normal neuroimaging 
Normal CSF composition 
Elevated LP opening pressure
37
Q

What MUST you do before an LP

A

imaging! increased ICP may cause cerebral herniation when LP is preformed if it is obstructed by a mass

38
Q

Major morbidity with pseudotumor is

A

loss of vision!

but persistent HA are a major source of disability

39
Q

How do you treat pseudotumor

A

Sometimes LP resolves Sx
weight loss if obese
Acetazolamide, Topiramate
Surgery (optic nerve sheath fenestration, optho eval, CSF shunt when all else fails)

40
Q

What is cerebral palsy

A

heterogenous group of conditions involving permanent, nonprogressive central motor dysfunction
Muscle tone, posture, and movement ffected
2/2 abnormalities in developing fetal or infantile brain, brain injury or malformation before birth or during/after delivery
(affects person’s ability to move and maintain posture)

41
Q

Prenatal causes of cerebeal palsy are

A 
prematurity 
IUGR
IU infection 
anteartum hemorrhage 
severe placental pathology 
multiple pregnancy 
hypoxic brain injury 
stroke 
cerebral dysgenesis
42
Q

Postnatal causes of cerebral palsy are

A 
stroke 
kernicterus (high bilirubin) 
trauma 
near drowning 
toxins 
hypoxic brain injury
43
Q

MC developmental delays are

A

not sitting by 8 months
not walking by 18 months
early asymmetry of hand function (hand preference) before 1 y/o

44
Q

4 major classifications of cerebral palsy are

A

Spastic (MC): UMN syndrome
Dyskinetic (decreased spontaneous movement) / Athetoid (slow, smooth writhing of distal muscles)
Ataxic (rare): wide gait, slow jerking movements, affects fine coordination, language and motor skills delayed, ataxia improves with time
Atonic: severe hypotonia, cerebral dysgenesis, microcephaly, intellectual disability

45
Q

Treatment goals of cerebral palsy are

A 
improve social and emotional development 
communication 
education 
nutrition 
mobility 
maximal independence in ADL
46
Q

What is spina bifida

A

neural tube disorder where caudal tube closes defectively in early gestation (by week 4)
Can be just a defect of L5-S1 vertebral arch, or more serious like exposure of meninges and spinal cord

47
Q

What are the subtypes of spina bifida

A
  • meningomyelocele: meninges and spinal cord are exposed, total paralysis, loss of bowel/bladder control, chiari II malformation
  • meningocele: spinal canal and meninges exposed but underlying spinal cord intact
  • occulta: skin intact w/ underlying bone and spinal canal defects. +/- sinus tract, dimple, or tuft of hair, +/- neuro deficits
48
Q

How can you prevent spina bifida

A

Folic Acid supplementation in pre-pregnancy and during pregnancy

49
Q

How can you diagnose spina bifida

A

routine screen AFP at 16-18 weeks in mom, and US at 12-14 and 18-20 wks

50
Q

How do you manage spina bifida

A

surgical closure
VP shunt
adjust support (self cath, dealing w/ cognitive disabilities, atc.)

51
Q

What are chiari malformations

A

heterogenous group of disorders w/ anatomic anomalies of cerebellum, brainstem, and craniocervical junction w/ DOWNward displacement of cerebellum into spinal canal

52
Q

What are the types of chiari malformations

A

1: down displacement of medulla
2: hydrocephalus, kink in medulla, myelomeningocele
3: herniation of cerebellum below foramen magnum
4: not compatable w/ life- cerebellar hypoplasia

53
Q

How do chiari malformations create hydrocephalus

A

the malformation obstructs the outflow of CSF

54
Q

What is hydrocephalus

A

increased volume of CSF w/ progressive ventricular dilation

congenital or acquired (tumor, meningitis, infx, hemorrhage, cyst, TBI, idiopathic)

55
Q

Difference between communicating and non-communicating hydrocephalus

A

C: CSF circulates through ventricular system and into subarachnoid space w/o obstruction
NC: obstruction blocks flow of CSF w/in the ventricular system or from ventricular system into subarachnoid space

56
Q

What Sx indicate obstruction of CSF (increased ICP)

A

HA, vomiting, AMS, visual changes, Ocular nerve palsy (CN6)*, FND
infant: vomiting, lethargy, irritable, bulging fontanelle, poor feeding, macrocephaly, excessive head growth (more non-specific)

57
Q

How do you treat hydrocephalus

A

Temp: loop diuretic, acetazolamide
Long: remove obstructive lesion, VP shunt*

58
Q

What are spinal muscular atrophy disorders

A

Degeneration of anterior horn cells in the spinal cord and motor nuclei in the lower brainstem= progressive muscle weakness and atrophy
Autosomal recessive dz 2/2 mutation in SMN gene on chromosome 5q13

59
Q

What are the subtypes of SMA

A

0: prenatal onset, hypotonia and areflexia at birth
1 (Hoffman disease): worst, mild weak at birth, respiratory failure by 1 y/o
2: weakness and decreased DTR by 2 y/o
3: weakness in adolescence
4

60
Q

Always suspect SMA in infants

A

with unexplained weakness or hypotonia
progressive proximal weakness
decreased spontaneous movement
floppiness (loss of head and leg control)
decreased facial expression and drooling
-usually by 6 mo - 6 y/o

61
Q

SMA kids have normal

A

mental status
social and language skills
sensation

62
Q

How do you diagnose SMA

A

EMG, muscle biopsy, DNA testing

homozygous deletion of exon 7 of SMN1 confirms Dx

63
Q

How do you treat SMA

A

No Tx

Sx therapy improves flexibility, prevents infection, maintains social language and intellectual stimulation

64
Q

What is Guillain Barre syndrome

A

acute immune mediated polyneuropathy; Acute paralyzing illness provoked by preceding infection
MC: Campylobacter jejuni
85% of kids have great recovery

65
Q

Sx of Guillain barre are

A

*Ascending weakness (symmetric)- feet dorsiflexed
Sensory Sx
loss of DTR
ANS dysfunction
Problems with respiration, talking, swallowing, B/B fxn
Kids refuse to walk and w/ leg pain

66
Q

How do you diagnose Guillain Barre

A

LP: elevated protein W/O high WBC

EMG

67
Q

Worrisome outcomes of Guillain barre are

A

death from ANS dysfunction, respiratory failure, and PNA/PE/CV collapse
Long term paresthesias, fatigue, and limb weakness

68
Q

How do you treat Guillain Barre

A

IVIG (combat invading organisms)

Plasmapheresis: decrease severity and duration, remove Ab from circulation

69
Q

What is DMD

A

X linked recessive d/o with absence of dystrophin protein
Sx by age 3 and rapidly worsen
slower to develop motor milestones (walking, climbing stairs)

70
Q

How does DMD present

A 
Proximal muscles affected first** LE before UE** 
Calf hypertrophy 
pelvic weakness 
waddling gait 
can't stand from ground easily 
**Gower's sign
71
Q

Early DMD manifestations (2-6 y/o) are

A 
Clumsy 
walking on toes 
waddling gait w/ excessive lumbar lordosis 
Gower's sign 
difficult to climb stairs
72
Q

How do you diagnose DMD

A

**Muscle biopsy: shows degeneration and regeneration, fiber size varies, inflammation, connective tissue proliferation,
**Myopathic EMG
Serum CK levels (high before Sx set in, peak at 2 y/o)
can do genetic testing

73
Q

How do you treat DMD

A

Glucocorticoids prolong independent ambulation by 2.5 years if started between 4-8 y/o
Gene therapy, creatine, aminoglycosides
Mainly supportive care
Close cardiac and pulm follow up 2/2 risk of failure in 20-30’s

74
Q

What is prognosis of DMD

A

Wheel chair by 12 y/o
Loss of UE movement by 16
Death from PNA or CHF in 20’s
Lifespan: 25 years

75
Q

What is neurofibromatosis

A

genetic d/o where nerve tissue grows tumors that cause nerve/brain __?
mutation in NF1 gene on chromosome 17q11.2

76
Q

To diagnose neurofibromatosis you need 2+ of the following

A
  • *Cognitive or psychomotor probles
  • learning disabilities
  • cafe au lait spots by 1 y/o
  • > 6 cafe au lait spots (5mm diameter prepubertal, 15mm in pubertal)
  • 2+ neurofibromas
  • Freckling of axillary or inguinal regions
  • Optic glioma
  • 2+ lisch nodules*
  • Distinct bony lesions
  • 1st degree relative with NF type 1
77
Q

Physical findings in neurofibromatosis are

A

care au lait spots
Neurofibromas in late teens (along a nerve)
Greater incidence of CNS tumors (astrocytoma, meningioma, Schwannoma)

78
Q

How can cognitive impairment present in neurofibromatosis

A

benign learning disability - mental retardation Seizures, macrocephaly, neuropathy

79
Q

How do you treat neurofibromatosis

A

Surgical excision of tumors

genetic counseling and screening (esp in siblings)

80
Q

Complications of neurofibromatosis are

A 
seizure 
deafness 
short stature 
early puberty 
HTN 
optic glioma
81
Q

What is NF type 2

A

dominantly inherited neoplasia syndrome (AD)

can appear in kids as loss of hearing

82
Q

How are T1 and T2 NF different

A

T1: has cafe au lait spots, no vestibular schwannomas
T2: Has bilateral vestibular schwannomas, no cafe au lait spots

83
Q

What other brain and spinal cord tumors are common

A

meningiomas
CN schwannomas
Ependymomas

Summer Disciplines 3 (9 decks)

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