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Peds Rotation > 3 Peds Neurology > Flashcards

3 Peds Neurology Flashcards

1
Q

____% of kids 18 or younger experience some sort of developmental delay

A

18%

Common concern presenting to primary care, with many etiologies

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2
Q

What is important to ascertain when investigating a potential developmental delay?

A

You want to see a TREND over time, not a single out-of-range measurement/milestone

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3
Q

Non-progressive central motor impairment secondary to fetal or infantile brain injury

A

Cerebral Palsy

Incidence: 2 per 1,000 births

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4
Q

Possible etiologies of cerebral palsy

A 
Hypoxia***
Trauma
Premature birth
Infections
Toxins
Structural abnormalities
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5
Q

What are the different subtypes of cerebral palsy?

A

SPASTIC - most common (70-80%)
Muscles appear stiff and tight, arises from MOTOR CORTEX damage

ATAXIC (6%)
Characterized by the shaky movements; affects balance and sense of positioning in space; arises from CEREBELLUM damage

DYSKINETIC (6%)
Involuntary movements, arises from BASAL GANGLIA damage

Can have a combo, sometimes not noticed until 18-24 months

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6
Q

SSx of Cerebral Palsy

A 
Abnormal tone and/or posture
RETAINED PRIMITIVE REFLEXES
Not reaching milestones 
Excessive irritability
Poor feeding, drooling
Poor visual attention
Difficult to hold, cuddle
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7
Q

What are some retained primitive reflexes common in cerebral palsy

A

ATNR (Asymmetric tonic neck reflex - the fencer’s pose) - baby turns head to extended arm; usually gone by 4-6 months

Moro Reflex - baby stretching out his arms with a startle on suddenly being released for an instant

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8
Q

Management of Cerebral Palsy

A

EARLY RECOGNITION, REFERRAL, AND INTERVENTION

Parental support and counseling

Symptomatic management
• OT, PT, bracing
• Anti-spasmodic
• Botulism toxin

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9
Q

Nervous system malformations are present in ____% of infants who die <1 year

A

40%

Type of malformation dependent on what gestational period the insult occurs

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10
Q

Etiologies of congenital malformations of CNS

A 
Infections 
Toxins
Genetic
Metabolic
Vascular
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11
Q

Cerebellum tonsils displaced causally below the forsaken magnum

A

Chiari Type I

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12
Q

Can be associated with syringomyelia (fluid filled cyst within spinal cord)

A

Chiari Type I

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13
Q

Symptoms of this CNS malformation often don’t present until teen or adult years

A

Chiari Type I

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14
Q

Loss of abdominal reflex

Neurological Sx assoc with syringomyelia

Cape-like numbness

A

Chiari Type I

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15
Q

What’s the other name for Chiari Type II?

A

Arnold-Chiari malformation

It’s a Type I + myelomeningocele

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16
Q

CNS malformation usually detected prenatally or at birth

A

Chiari Type II

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17
Q

Hydrocephalus

Dysphagia

UE weakness

Apneic spells and aspiration

A

Chiari Type II

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18
Q

What are the three types of Spinal Dysraphism?

A

Spina Bifida Occulta (most mild)

Meningocele

Myelomeningocele (most severe)

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19
Q

Incomplete closure of the spinal canal, usually on the lower back but can be anywhere

A

Spina Bifida Occulta

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20
Q

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

A

Spina Bifida Occulta

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21
Q

Outpouching of the spinal fluid and meninges through a vertebral cleft

A

Meningocele

Mild problems associated with the sac protrusion

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22
Q

Spinal cord and/or nerves protrude from the vertebral cleft

A

Myelomeningocele

Most severe form of spina bifida

Weakness, loss of bladder and/or bowel control, hydrocephalus, and inability to walk result

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23
Q

Spinal Dysraphisms can occur anywhere along the spine but _________ is most common

A

Lumbar spine

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24
Q

What are some common etiologies of spina bifida

A

Genetics

LOW FOLATE***

Medications during pregnancy (esp anti seizure meds)

Poorly managed diabetes

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25
Q

Early recognition of spina bifida is possible by…

A

U/S

Alpha-feto protein markers

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26
Q

Best way to prevent Spina Bifida

A

Prenatal vitamins including folic acid 3 months prior to conception

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27
Q

Increased volume of CSF causing ventricular dilation and increased intracranial pressure

A

Hydrocephalus

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28
Q

What are the two types of hydrocephalus?

A

Obstructive - due to blockage

Non-obstructive - impaired absorption or (rarely) overproduction

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29
Q

Etiologies of Hydrocephalus

A 
CNS malformations
Infection
Intraventricular hemorrhage
Genetic defects
Trauma
CNS tumors
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30
Q

SSx of hydrocephalus

A 
(Can be asymptomatic)
Bradycardia, HTN, altered respiratory rate
HA, N/V, behavior changes
Papilledema
Macrocephaly
Spasticity
Diplopia 
Spinal abnormalities
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31
Q

How is hydrocephalus diagnosed?

A

Newborns/infants: U/S

Older infants/children - MRI or CT

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32
Q

Treatment for hydrocephalus

A

Refer to neurosurgeon

Shunt

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33
Q

What is the definition of Microcephaly

A

Head circumference ≥2 standard deviations below average or <5th percentile

Can be primary (congenital) or secondary (postnatal)

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34
Q

Lack of brain development or abnormal development due to timing of insult

A

Primary microcephaly

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35
Q

Injury or insult to a previously normal brain

A

Secondary (postnatal) microcephaly

36
Q

If microcephaly is symptomatic, what might you see?

A

Delayed milestones

Seizures or spasticity

Fontanelle may close early and sutures may be prominent

37
Q

What is the definition of Macrocephaly?

A

Head circumference ≥2 standard deviation above average or >95th percentile

Can be due to increase in size of any components of cranium (brain, CSF, blood, or bone)

38
Q

Rapid growth —> macrocephaly is suggestive of…

A

Increased intracranial pressure

39
Q

Catch-up growth macrocephaly is typically seen in…

A

Premature infants (neurologically intact)

40
Q

Normal growth rate macrocephaly is usually the result of …

A

Familial macrocephaly or megaloencephaly

41
Q

How are micro- and macrocephaly managed?

A

Neurology referral

Labs/imaging

Treat underlying cause

42
Q

Inheritance pattern for Neurofibromatosis (NF1)

A

Autosomal dominant

43
Q

What neurological abnormalities are associated with neurofibromatosis?

A

Macrocephaly, seizures, cognitive defects

44
Q

Clinical manifestations of NF1

A

Cafe-au-lait macules (appear 1st year)

Axillary and/or inguinal freckling (3-5 years)

Lisch nodules

Optic gloom a

Neurofibromas

45
Q

Most common types of primary headache

A

Migraine and tension

46
Q

Most common secondary headache

A

Acute Febrile Illness

47
Q

Migraine or Tension H/A:

Focal, unilateral or bilateral

A

Migraine

48
Q

Migraine or Tension H/A:

Diffuse, frontal or temporal

A

Tension

49
Q

Migraine or Tension H/A:

Duration = 2-72 hours

A

Migraine

50
Q

Migraine or Tension H/A:

Duration = 30 min - 7 days

A

Tension

51
Q

Migraine or Tension H/A:

Moderate to severe intensity, pulsatile/throbbing

A

Migraine

52
Q

Migraine or Tension H/A:

Mild to moderate intensity, constant pressure/non-throbbing

A

Tension

53
Q

Migraine or Tension H/A:

Aggravated with activity or reduced activity

A

Migraine

54
Q

Migraine or Tension H/A:

Not aggravated with activity

A

Tension

55
Q

When to worry about a headache

A

Abnormal neurologic or visual exam

Severe upon awakening or awaken in the middle of the night

Daily symptoms with progressive worsening

Accompanied with vomiting

Acute onset with previous history

Increased with coughing or bending

56
Q

Idiopathic intracranial hypertension without mass or hydrocephalus, typically seen in obese teenage girls

A

Pseudotumor cerebri

57
Q

SSx of Pseudotumor Cerebri

A 
HA***
Papilledema***
Visual symptoms
Visual field loss, visual acuity loss
Pulsatile tinnitus
58
Q

How is pseudotumor cerebri diagnosed?

A

Neuro eval —> MRI to exclude secondary causes, LP

Ophthalmologic eval

59
Q

What will an LP show in pseudotumor cerebri?

A

Elevated opening pressure

60
Q

Treatment of pseudotumor cerebri is focused on …

A

Managing symptoms and preserving vision

DOC - ACETAZOLAMIDE to reduce rate of CSF production

Topiramate to help control HA and reduce weight

Furosemide to reduce fluid and pressure

Weight loss

Shunting of fluid

Optic nerve fenestrations

61
Q

Sudden, transient disturbance of brain function manifested by involuntary sensory, motor, autonomic symptoms with or without loss of consciousness

A

Seizure

62
Q

What is the definition of epilepsy?

A

≥ 2 seizures occurring more than 24 hours apart

Types:
Focal (partial) - with or without impaired awareness
Generalized
Unknown
Unclassified
63
Q

Sudden impairment of consciousness w/o loss of tone, provoked by hyperventilation and presumed to be genetic

A

Absence Seizures

Presents between age 4-10 and most often spontaneously remits by puberty

Arrest in activity generally lasts 9-10 sec and may occur 10x/day

64
Q

1st line medication for absence seizures

A

Ethosuximide

65
Q

Convulsion w/ temp > 38˚C (100.4˚F) in a child age 6 months to 5 years

A

Febrile seizure

Often associated with viral infection, genetic predisposition

66
Q

Most common type of febrile seizure, lasting <15 min

A

Simple febrile seizure

67
Q

How are complex febrile seizures defined?

A

Focal, last >15 min or occur >1/24 hours

68
Q

How do you manage a febrile seizure

A

Generally self-limiting

If >5 min, give IV benzodiazepines

69
Q

Acute immune-mediated polyneuropathy preceded by illness (most commonly campylobacter)

A

Guillian-Barre Syndrome

70
Q

Most common cause of acute flaccid paralysis in health infants/children

A

Guillian-Barre Syndrome

71
Q

ASCENDING symmetric weakness, neuropathic pain, gait instability/refusal to walk, and absent reflexes

A

Guillian-Barre Syndrome

72
Q

What is the primary diagnostic tool for Guillian-Barre syndrome?

A

Electrodiagnostic studies (EMG)

Can also do CSF analysis or Spinal MRI

73
Q

Treatment of Guillian-Barre Syndrome

A

Hospitalization and close monitoring

Treatment with IVIG or plasma exchange

74
Q

Honey and home canning are no-nos because of …

A

Risk of ingesting clostridium botulinum spores —> botulism

75
Q

90% of infants with botulism are _______

A

<6 months old

76
Q

DESCENDING weakness

Constipation, poor feeding

Hypotonia, loss of DTRs

Irritable and lethargic

A

Botulism

77
Q

How is botulism diagnosed?

A

Stool sample

EMG

78
Q

How is botulism treated?

A

Hospitalization and close monitoring

Botulism immune globulin (BIG-IV or BabyBIG)

79
Q

Inheritance pattern for Duchenne Muscular Dystrophy

A

X-linked recessive

Defect is in genes responsible for muscle function —> elevated muscle enzymes

80
Q

What is the outlook for kids with DMD?

A

Wheelchair bound by age 13 and mortality by 18-20 years

81
Q

Progressive weakness, proximally before distally, LE before UE

A

Duchenne Muscular Dystrophy

82
Q

What is Gower’s sign?

A

Using hands to push up from floor (DMD)

83
Q

Conditions associated with DMD?

A

DCM

Orthopedic complications (ie scoliosis)

Cognitive impairment

84
Q

Diagnosis of Duchenne Muscular DystrophY

A

Elevated muscle enzymes - CK ≥10-20x normal

Genetic testing

85
Q

Treatment for DMD

A

GLUCOCORTICOIDS

86
Q

How is Becker Muscular Dystrophy different from DMD?

A

Symptom onset later

Muscle involvement not as severe

CK elevated ≥5x

Cardiomyopathy may be more predominant

Peds Rotation (13 decks)

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