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Neurology I- VI Flashcards

1
Q

Anencephaly
Encephalocele
myelomeningocele
Arnold-chiari malformation
Myeloschisis

These conditions have problem with what neural developmental process?

A

Primary neurulation (dorsal induction)
3-4 weeks

FYI: myeloschisis is a flat neural tube defect without a layer of skin covering the opening in the spine. (the spinal cord and the surrounding nerve tissue are also exposed to the amniotic fluid. similar risks and symptoms as myelomeningocele)

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2
Q

what does each of the following Prefix/Suffix mean?
An- or a -
encephalo-
myelo-
meingo -
holo -
- cele -
pros -

A

An- or a - : “not”, “without”
encephalo- : “brain”
myelo- : “spinal cord”
meningo - : “membrane” , “meinges, coverings of the brain and spinal cord”
holo - : “entire”, “complete” (i.e. no cleavage)
- cele : “hernia”, “swelling”
pros - : “before”, “forward”

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3
Q

tethered cord, lipoma, teratoma spinal cysts, myelocystocele, meningocele-lipomeningocele

These conditions have problem with what neural developmental process?

A

Secondary neurulation (dorsal induction)
4-7 weeks

These are are spinal cord and lower sacral segment

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4
Q

aprosencephaly
holoprosencepahly
Midline development defect:
agenesis of corpus callosum,
agenesis or absence of septum pellucidum,
septo-optic dysplasia

These conditions have problem with what neural developmental process?

A

Prosencephalic development (ventral induction)

(ventral induction)

2-3 months

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5
Q

Micrencephaly
Macrencephaly

These conditions have problem with what neural developmental process?

A

Neural and glial proliferation

3-4 months

Micrencephaly: abnormal smallness and underdevelopment of brain
Macrencephaly: hypertrophy of the brain

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6
Q

Schizencephaly
Lissencephaly
Pachygyria
Polymicrogyria

These conditions have problem with what neural developmental process?

A

Neuronal migration
3-5 months

Schizencephaly: abnormal clefs of the brain
Lissencephaly: underdevelopment of gyri, smooth brain
Pachygyria: broad, abnormally large gyri, lead to less sulci
Polymicrogyria: numerous small convolutions

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7
Q

Mental deficiency, Trisomy 21, Fragile X, Autism, Angelman, Prematurity

has issue in what neural development process.

A

Neuronal organization

(axonal outgrowth and proliferation, dendritic and synapse, synaptic rearrangements

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8
Q

what is the last pathway to myelinate

A

association bundle (prefrontal cortex with temporal and parital lobe): complete at 32 yrs of age.

myelination normally happens birth to years.

Corticospinal tract myelinate 38 wk GA to 2 year.

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9
Q

Anecephaly is due to failure of __ closure. (It happens within __day of gestation)
Encephalocele is due to failure of __ closure.
Myelomeningocele is due to failure of ___ closure

A

Anecephaly - anterior tube closure (within 26 days)
Encephalocele - rostral neural tube closure
Myelomeningocele - posterior neural tube closure

All are Primary neurulation defect

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10
Q

How are Anecephaly and Aprosencephaly different?

A

Anecephaly: primary neurulation defect. failure of anterior tube closure. Degeneration of forebrain (no skull, scalp, large amount of brain tissue).
female > male
hispanic women, increase risk with maternal hyperthermia, maternal folate, copper, zinc defieincy.
^ recurrent risk 2-6%.
association with other abnormalities

Aprosencephaly: abnormal development in prosencephalic stage in formation. There is abscence of telencephalon and diencephalon with porencephalic remnant. minimal brain volume. Has intact skull, hair, and dermal coverings.
cyclopia or no eye. associated external genitalia and limb abnormalities.
autosomal recessive

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11
Q

For anecephaly, during prenatal testing, what level is elevated in maternal serum

A

maternal alpha-fetoprotein.

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12
Q

Encephalocele is associated with what syndrome?
Does encephalocele has a genetic cause?

A

Meckel-Gruber syndrome.

Genetic cause of encephalocele is suggested. risk higher in families with history of NTD.

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13
Q

Maternal alpha-fetoprotein level in encephalocele is __ ? (higher, lower, norrmal)

A

normal

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14
Q

where is the most common location of defect in encaphlocele? which locations has better prognosis.

A

Occipital more common
Frontal has better prognosis

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15
Q

what is cranial meningocele?

A

a type of encephalocele but does not have CNS tissue protruding through the lesion.

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16
Q

Difference between Meningocele and Myelomeningocele?

A

Meningocele: defect in spinal canal, meninges herniate through the defect.
Myelomeningocele: spinal cord, meninges herniat through the defect.

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17
Q

What maternal medications and what maternal medical conditions increase risk of NTD?

A

valprroate
carbamazepine

maternal diabetes

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18
Q

NTD might need VP shunt due to risk of hydrocephalus

A
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19
Q

level of lesions, segmental innervation, reflex present and ambulation potential

A

Do we need to know? (page 6)

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20
Q

What are the difference and similarities between Arnold-Chiari malformation and Dandy-Walker Malformation?

Name/describe two types of Arnold-chiari malformation.
What other CNS conditions are Dandy-Walker highly associated with?

A

Arnold-Chiari Malformation:
- primary neurulation defect.
- caudal displacement of cerebellar tonsils below foramen magnum.
*Type I: most common. caudal displacement of cerebellar tonsils below foramen magnum. 4th ventricle and brainstem in normal position.
associate with syringomyelai, hydromelia, skeletal anoamlies.
*Type II: in infants. more extensive elongation and caudal displacement of cerebrella tonsils, 4th ventricles, choroid plexus and brainstem, into the cervical spinal canal.
associated with hydrocephalus, myelomeingocele.

Dandy-Walker Malformation:
- occurring very early in neurological developmental phase.
- AGNESIS / Hypoplasia of the cerebellar vermis, cystic dilation of the 4th ventricle, enlargement of the posterior fossa.
- associated with hydrocephalus, risk of motor and cognitive delays.

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21
Q

holoprosencephaly’s epidemiology and association

A

increase risk in IDM. familiar reoccurences described.
30-50% w/ chromosomal anomalies (T13)
50% w/ extracranial abnormalities.

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21
Q

Holoprosencephaly happens in __ stage of neurodevelopment? It’s the primary defect in __?

A

prosencephalic stage
defect in cleavage.

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21
Q

4 types of holoprosencephaly

A

middle interhemispherice varient (MIHV)
Lobar
Semilobar
Alobar

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22
Q

Agenesis of Corpus Calllsum happens in __ stage of neurodevelopment? It’s the primary defect in __?
cause/inference

A

prosencephalic stage
defect in mideline development

some x-linked dominant and some autosomal recessive.
Fetal infection earlier in pregnancy or intrauterine alcohol exposure.

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23
What is septum pellucidum? Abesecence of septum pellucidum is associated with what?
double thin vertical membrane separating the anterior horns of the left and right lateral ventricles (cavum septum pellucidum is the potential space in between the two double membranes) learning disabilities, vision problems, seizures, behavioral issues, septo-optic dysplasia
24
Diagnosis of septo-optic dysplasia criteria
2 out of 3 features: optic nerve hypoplasia pituitary gland dysfunction absence of septum pellucidum
25
Name the three main cerebral arteries and the area of they supply
Anterior Cerebral Artery: from internal carotid supply medial, frontal, parietal lobes, AND caudate Middle: from internal carotid supply lateral hemispheres Posterior: from basilar artery, which from vertebral artery supply midbrain, occipital lobes and inferior temporal lobes
26
cerebral perfusion pressure (CPP) equation CPP = ?
CPP = MAP - ICP ICP: intracranial cerebral pressure MAP: mean arterial pressure If given BP and not MAP, remember: MAP = 2/3 DBP + 1/3 SBP
27
autoregulation with blood pressure change: describe the curve in premature infant and curve in normal state what's x-axis and what's y-axis
x-axis: BP y-axis: cerebral blood autoregulation: with increase BP, cerebral blood flow can remain stable for a period of time. no regulation: BP and cerebral flow are directly correlated.
28
PaO2 and PaCO2 impact on CBF (cerebral blood flow)
Increased PaCO2 increases CBF (cerebral blood flow) Decrease PO2 increases CBF.
29
name factors that increase CBF
^ PaCO2, decrease PaO2 ^ BP in asphyxiated infant/ premature infant dopamine decrease hemoglobin (Hgb) concentration increase proportion of fetal hemoglobin hypoglycemia seizures.
30
name all cranial sutures (4 total)
metopic, coronal sagittal lambdoidal
31
Types of Craniosynostosis (and what suture was closed)
Scaphocephaly or Dolichocephaly (sagittal suture closure) most common male > female small or absent anterior fontanel more benign, less likely to associate with other lesions, brain growth normal. surgery for cosmetic Frontal plagiocephaly (unilateral coronal suture) female > male ^ developmental delay associated w/ **Crouzon and Apert syndrome** surgery to improve neurological sequelae Brachycephaly (b/l coronal suture) **Carpenter syndrome** Trigonocephaly (metopic suture) male > female associated for hypotelorism surgery for cosmetic Occipital plagiocephaly (unilateral lamboid suture) not common Multiple suture involvement combine above skull shapes. increased risk of ^ ICP, ^ mental deficiency. surgery soon.
32
common syndromes and causes of cranyosynostosis
crouzon, apert, carpenter, idiopahtic hypercalcemia, rickets, hypophosphatemia
33
syndromes associated with Microcephaly (decrease HC > 2-3 standard deviation below mean)
chromosomal: T 12, 18, 21 deleition 13q CHARGE Meckel-Gruber syndrome Smith-Lemli-Opitz syndrome Intrauterine or postnatal infection (CMV, Zika) IUDE (alcohol. isotretinoin) prenatal radiation exposure maternal phenylketonuria and phenylketonuria (Meckel-Gruber syndrome: autosomal recessive, lethal malformation Triad of occipital encephalocele, bilateral polycystic kidneys and post axial polydactyly.)
34
syndromes associated with Macrocephaly (^ HC > 3 SD above mean, without hydrocephalus or cranial mass)
Benign family macrocephaly ( 50%, AD, m > f, normal developmental outcome) Beckwith-Wiedemann syndrome Neurofibromatosis Soto syndrome Fragile X syndrome Achondroplasia Aqueductal stenosis
35
what is Mobius syndrome
b/l facial paresis due to hypoplasia of cranial nerve nuclei expressionless face no treatment.
36
when is clonus normal and when is it not normal
5-10 beats normal in newborn abnormal if present > 3 months of age.
37
When does Palmer reflex appear and when does it disappear? Persistent palmer reflex means what?
appear by 26 weeks (one of the earliest), establish by 32 weeks. disappear in 2-4 month asymmetric = peripheral injury (root, plexus, or nerve) persistance = athetoid cerebral palsy non-habituating = cerebral injury
38
sucking relex appears by what age ? and establish by what age?
28 weeks 32-34 weeks (when start to learn to feed)
39
Moro reflex appear at what age and disappear at what age if not symmetric, what does it indicate ? if non-habituating, what does it indicate?
appear at 30-34 week. disappear by 2-4 month. if asymmetric, peripheral injury. if non-habituating, + cerebral injury
40
name three reflexes that appeared earliest (26 - 28 weeks)
Palmer (26 wk) Plantar (26 wk) Sucking (28 wk)
41
name three reflexes disappearing around 2 - 4 m.
Palmer (2-4 m) Crossed extensor (2 m) Moro (2-4 m) Placing and Stepping (2-3 m)
42
describe CSF fluid path:
CSF made in lateral ventricles by choroid plexus (0.37 ml/min) > intraventricular foramen of Munro > 3rd ventricle > cerebral aqueduct of Sylvius > 4th ventricle > lateral foramens of Kuschka and Magendie > subarachonoid space > brainstem, cerebellum, spinal cord.
43
what does choroid plexus do
secreting or absorbing CSF
44
choroid plexus cysts: what are they and what is their clinical significance
neuroepithelial folds filled with CSF and debris detect at 11 wk and disappear by 26 week. normalin 0.5% small percentage infant has T18
45
What at CSF fluid made off
99% water, Na major cation remade very 5-7 days. 10-30ml in preterm infant 40 ml in term infant
46
in EEG, when does "delta brushes" in central region appear and when does it disappear?
Delta brushes Appear: 29-30wk Disappear: 36-37 wk from central region, 38-40 wk from occipital region.
47
in EEG, when does activity become continous?
31-33 weeks (also first synchrony during active sleep around 31-33 weeks)
48
in EEG, when does EEG changes with **external stimuli**?
34-35 weeks
49
EEG Pattern: **Central positive sharp waves**
characteristic pattern in preterm infants with PVL
49
EEG Pattern: **Hypsarrhythmia**
infantile myoclonic spasms (after 2 months age)
50
EEG Pattern: Background depression
occurs after **generalize insults** (i.e. HIE, meningitis, encephalitis, metabolic disorder) - if unilateral: one-sided cerebral lesion caused by ischemia, hemorrhage, or abnormal development - persistence of background dpression > poor prognostic sign
51
EEG Pattern: Burst Suppression
intermediate stage between depression and electrocerebral silence no EEG response to external stimuli poor prognosis
52
Electrocerebral silence
persistence > 72 hr indicates cerebral cortical death not always have brainstem death if brainstem activity, survived pt in persistent vegetative state.
53
Periodic discharges on EEG
Preterm infants: associated with various insults in prematurity Term infants: associated with infarction in the MCA area
54
Multifocal sharp waves
high voltage for long periods
55
what is aEEG?
filtered or compressed EEG using 1-2 channels Used in NICU to evaluate infants with suspected HIE.
56
Describe continuous aEEG patten vs. discontinuous aEEG pattern (preterm infant)
Continuous: normal, term infant. smooth, cyclic "fuzzy caterpillar". Amplitudes: 10-25 mcV Discontinuous: preterm. Amp ~ 5-10 mCV. no cyclic.
57
Seizures: aEEG pattern
"arches", "saw tooth" increases in min and max amplitude, periods of decreases amplitutde.
58
what is MRI/DWI and what can it detect?
MRI w/ diffusion weighted images. Measures random Brrownian motion of water molecules earlier identification of ischemic stroke.
59
what is CT scan superior to MRI for?
detecting intracranial calcifcation CT can detect bleeding/fluid in subdurral, subarachnoid space and in the posterior fossa.
60
what are causes of Obstructive hydrocephalous (name 6)
1. PHH (most common) 2. Aqueductal stenosis 3. Agenesis of corpus callosum 4. Dandy-Walker malformation 5. Congenital hydrocephalus 6. Mass
61
Aqueductal stenosis: pathogenesis etiologies
congenital obstruction of the aqueduct (duct connecting 3rd and 4th ventricles) -> 3rd land lateral ventricular dilation Etiologies: 1. possible unrecognized viral illness (mumps, rubella, parainfluenza) 2. associated with Arnold-Chiari malformation 3. x-linked recessive: adducted thumbs, agenesis of corpus callosum, mental deficiency 4. autosomal recessive (nonfamilial) w/ associated VACTERL.
62
Congenital hydrocephalus Timing of disease: Etiology: management:
onset in utero, presentation in the first days after birth. Etiology: Dandy-walker (5-10%), teratogenesis (radiation exposure), intrauterine infection (toxo, CMV), maternal malnutrition, genetic factors, tumor, IVH, vein of Galen) VP shunt.
63
in HIE, when does seizure occur? how do they respond to anti-convulsant treatment
12-24 hours. resolved by 5-7 days does not respond well to anti-convulsant treatment
64
what are three phases in HIE
latent (1-6 hr) -> hypoperrfusion secondary (6-24hr to days) -> hyperperfusion Tertiary (weeks to years) -> normalisation
65
Meckel Syndrome - defect and triad?
Defect with cilia Triad: Encephaloceles Multicystic kidneys Polydactyly (fingers or toes)
66
Chemical conjunctivitis - onset and characteristics?
Onset: within 24 hours after exposure Characteristics: Following prophylaxis Decreased incidence because less usage of 1% silver nitrate for prophylaxis Negative culture Spontaneously resolves within 48 hours
67
Bacterial conjunctivitis - onset and characteristics?
Onset: 24-48 hours of age (can be later in life) Characteristics: Staph aureus (most frequent organism, golden crust around eyelids), also secondary to Group B Streptococcus, Haemophilis influenzae (dacrocystitis), Strep pneumonia (dacrocystitis), Pseudomonas aeruginosa
68
Gonoccal conjunctivitis - onset and characteristics?
Onset: 2 to 5 days of life aka gonococcal ophthalmia neonatorum Characteristics: Abrupt onset of extremely copious, purulent bilateral discharge Medical emergency because can progress to involve cornea and ulceration/perforation if untreated Treat with 3rd generation cephalosporin Can prevent with prophylaxis (0.5% erythromycin most common, ideal if applied < 1 hour of age, decreases incidence of gonorrheal conjunctivitis from 10 to 0.5%)
69
Chlamydial conjunctivitis - onset and characteristics?
Onset: 5-14 days of life (can be earlier if premature rupture of membranes) Characteristics: ~ 8/1,000 births Most common cause of coniunctivitis in 1st month of life In ~1/2 of infants with colonized mothers Typically bilateral Initially watery discharge that becomes purulent Often associated with chlamydia pneumonia Diagnose by Giemsa-stain of conjunctival scrapings Treat with oral erythromycin x 14 days (20% require second course)
70
Herpes simplex conjunctivitis - onset and characteristics?
Onset: Broad range (4 days to 3 weeks of age) Characteristics: Most frequent viral etiology May also have keratitis, chorioretinitis, retinal dysplasia Assess for systemic herpes and herpes encephalitis
71
T12-L 2, thoracolumbar, Reflex. Ambulation potential?
None Full braces, long term ambulation unlikely
72
L3-L4 Reflex present. Ambulation potential
Knee jerk May ambulate with braces and crutches
73
L5 - S1 Reflex. Ambulation potential?
Ankle jerk present Ambulate with or without short braces
74
S2-S4, Reflex. Ambulation potential?
Anal wink present Ambulation without braces

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