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Neo Board Review MAP > Neurology > Flashcards

Neurology Flashcards

1
Q

Hearing loss severity

A 
Mild: 26-40 db
Moderate: 40-55 db
Moderate-severe: 55-70 db
Severe: 70-90 db
Profound: >90 db
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2
Q

Molecule most rapidly depleted after neuronal injury

A



Phosphocreatine

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3
Q

Necrosis (Asphyxia)

A
  1. Hypoxia/glucose deprivation disrupt cellular hemostasis and ATP depletion
  2. Loss of Na/K-ATPase -> membrane depolarization, influx of Na, Ca, H2O (cell swelling)
  3. Excess extracellular glutamate increases Ca entry into cells
  4. Activation of phospholipases, xanthine oxidase, nNOS
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4
Q

Apoptosis (HIE)

A

Programmed cell death
1. Cytochrome C released from mitochondria activates caspase 8 & 9
2. Cell death by activation of caspases and endonucleases
3. Blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, DNA fragmentation
Therapeutic hypothermia can prevent this

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5
Q

Oxidative stress (HIE)

A
  1. Reperfusion phase yields 02 radicals, NO
  2. Radicals react with proteins, lipids, DNA producing oxidative damage
  3. Lack of scavengers (glutathione, SOD, catalase, cholesterol)
    
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6
Q

Failure to establish HR by 10 minutes results in ___

A

death or severe permanent disability

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7
Q

Best predictor of intrauterine hypoxia

A

Metabolic acidosis on cord gas

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8
Q

Best predictor of long-term outcome in asphyxia

A

Requirement for tube feeding at two weeks of age

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9
Q

Long-term complications of kernicterus

A 
TEAM (it takes a team to treat these babies)
Teeth (dental enamel hypoplasia)
Eye (upward gaze palsy)
Auditory (aud neuropathy)
Movement (athetoid CP)
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10
Q

Minimal neuronal injury

A

Minimal ATP reduction followed by recovery

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11
Q

Moderate neuronal injury

A

Biphasic depletion

Apoptosis

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12
Q

Severe neuronal injury

A

Energy failure with predominant necrosis

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13
Q

 Cerebral blood flow autoregulation

A

With decreasing gestational age, mean arterial pressure values approach the lower limits

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14
Q

CO2 and cerebral blood flow

A

Increased CO2 -> increased CBF (dilates blood vessels)

Decreased CO2 -> decreased CBS (constriction)

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15
Q

Arterial 02 content and cerebral blood flow

A

Increased O2 -> decreased CBF

Decreased O2 -> increased CBF

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16
Q

Glucose and cerebral blood flow

A

Increased glucose -> decreased CBF

Decreased glucose -> increased CBF

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17
Q

Calcium and cerebral blood flow

A

Increased calcium -> decreased CBF

Decreased calcium -> increased CBF

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18
Q

Prostaglandins and cerebral blood flow

A

Increased prostaglandins -> increased CBF

Decreased prostaglandins -> decreased CBF

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19
Q

CBF ___ with postnatal age

A

Increases

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20
Q

Normal intracranial pressure

A

30-70 mmH2O

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21
Q

Causes of increased intracranial pressure

A 
Major intracranial hemorrhages
Post hemorrhagic hydrocephalus
Seizures
Pneumothorax
Tracheal suctioning
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22
Q

Germinal matrix

A

Site of neuronal precursors between 10-20 weeks gestation

3rd trimester becomes site of glial precursors

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23
Q

When does germinal matrix involute

A

By 36 weeks

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24
Q

Intravascular factors and IVH

A

Increase or decrease in CBF
Fluctuating CBF
Platelet and coagulation problems

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25
Q

Extravascular factors and IVH

A

Deficient vascular support (decreased astrocytes)
Fibrinolytic activity
Postnatal decrease in tissue pressure

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26
Q

Cerebral autoregulation

A

Maintain stable cerebral blood flow in face of altering perfusion pressure

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27
Q

When does cerebral autoregulation fail?

A

High PCO2 (>70)

After hypoxia/ischemia

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28
Q

Mechanism of brain injury in IVH

A 
Hypoxic ischemic injury
Distraction of germinal matrix/glial precursors
Periventricular hemorrhagic infarct
PVL
PHH
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29
Q

IVH presentation: catastrophic syndrome

A

Deterioration in minutes to hours
Coma, respiratory abnormalities, generalized seizures, pupils fixed to light
Dropping hematocrit, bulging fontanelle, hypotension, metabolic acidosis

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30
Q

IVH presentation: saltatory syndrome

A

More subtle
Alteration in consciousness, hypotonia, respiratory problems
Evolves over several hours to days

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31
Q

IVH presentation: clinically silent

A

25-50% infants with IVH may fail to display a distinct constellation of signs indicative of the lesion

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32
Q

Why is grade 4 IVH different?

A

Venous infarction - pressure from IVH impedes blood through venous system -> hypoperfusion and infarction

Blood in ventricle releases vasoactive compounds with the same conclusion

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33
Q

When does 90% of IVH occur?

A

First three days of life

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34
Q

Percentage of neonates with grade 1/2 IVH with developmental abnormalities

A

10%

Grade II worse than no hemorrhage

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35
Q

Percentage of neonates with grade 3 IVH with developmental abnormalities?

A

35-40%

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36
Q

Percentage of neonates with grade 4 IVH with developmental abnormalities?

A

80-90%

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37
Q

Causes of IVH in term neonates

A

Trauma and hypoxic events 50%

25% with no identifiable cause

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38
Q

Location of IVH in term neonates

A

Early - bleeding from choroid plexus or subependymal germinal matrix
Late - thalamus

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39
Q

Symptoms of IVH in term neonates

A

Irritability, stupor, apnea, seizures

Seizures are focal or multifocal and present in 65%

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40
Q

HIE symptoms birth to 12 hours

A 
Decreased consciousness
Ventilatory disturbances
Intact pupillary responses
Intact oculomotor responses (dolls eyes)
Hypotonia
Can see seizures
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41
Q

HIE symptoms 12-24 hrs.

A 
Variable change in level of alertness
Typically when we see seizures start
Apneic spells
Jitteriness
Weakness
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42
Q

HIE symptoms 24-72 hrs.

A

Stupor or coma
Respiratory arrest
Brainstem ocular motor and pupillary disturbances
Can have catastrophic deterioration

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43
Q

HIE symptoms >72 hours

A

Persistent yet diminishing stupor
Disturbed sucking, swallowing, gag, tongue movements
Hypotonia
Weakness

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44
Q

How does therapeutic hypothermia help HIE?

A 
Inhibition of apoptosis
Reduction in cerebral metabolism
Decreased leukotriene production
Preservation of endogenous antioxidants
Decreased intracellular acidosis
Reduction in glutamate release
Prevention of brain edema
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45
Q

Long-term outcomes with parasagittal injury

A

Vascular watershed areas
Spastic quadriparesis
Intellectual deficits

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46
Q

Long-term outcomes with selective neuronal necrosis

A 
Cognitive deficits
Spastic quadriparesis
Choreoathetosis
Dystonia
Seizure disorder
Ataxia
Bulbar and pseudobulbar palsy
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47
Q

Long-term outcomes with basal ganglia injury

A

Onset of dystonia at 13 years (avg)
50% have history of normal neurological development
Intellect is normal in 80%
Progression of dystonia continues for a mean of 7years

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48
Q

Periventricular leukomalacia

A

Necrosis of white matter and a characteristic distribution with less severe injury peripherally

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49
Q

PVL is associated with injury to which cells?

A

Oligodendrocytes

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50
Q

Subdural hematoma

A

Due to tears and bridging veins

Can be due to traumatic delivery

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51
Q

Four categories of cerebellar hemorrhage

A

Primary
Venus infarction
Extension of IVH
Subarachnoid hemorrhage into cerebellum

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52
Q

Caput succedaneum

A

Molding of head

Crosses suture lines

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53
Q

Cephalohematoma

A

Subperiosteal bleeding
Limited by suture lines
Underlying linear skull fracture detected 10-25% of time


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54
Q

Subgaleal hemorrhage

A

Beneath aponeurosis covering scalp
Can spread beneath entire scalp and dissect into subQ tissue of the neck
Firm fluctuant mass, increases in size after birth

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55
Q

Diffuse neuronal injury

A

Insult is very severe and very prolonged

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56
Q

Cerebral cortex (nuclear) neuronal injury

A

Insult is moderate to severe and prolonged

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57
Q

Deep nuclear/brainstem neuronal injury

A

Insult is severe and abrupt

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58
Q

Ventral induction

A

5-6th week of gestation
Closure of neural tube -> procephalon/mesencephalon/
rhombencephalon
Associated with cleavage defects

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59
Q

Examples of ventral induction defects (brain)

A

Holoprosencephaly
Septo-optic dysplasia
Agenesis of the corpus callosum

60
Q

Neuroepithelial cell proliferation/migration

A

7-20th week of gestation

Migration from inside brain to outside of brain

61
Q

Examples of neuronal proliferation defects

A

Microcephaly

Megalencephaly

62
Q

Examples of neuronal migration defects

A 
Lissencephaly
Polymicrogyria
Schizencephaly
Cortical dysplasia
Periventricular heterotopia
63
Q

Cortical organizations/connectivity

A

20th week
Cortical organization
Synaptic formations
T21, Fragile X, Rhett, Angelman syndrome, autism

64
Q

Holoprosencephaly

A

Failure of cleavage of the two sides of the brain
Lobar (some cleavage anterior and posterior)
Semilobar (cleavage only posterior)
Alobar (no cleavage)


65
Q

Genetics of Holoprosencephaly

A

Mutations in:
Sonic hedgehog gene
Fibroblast growth factor
Bone morphogenetic protein

66
Q

What syndromes is holoprosencephaly associated with?

A

Trisomy 13

Smith-Lemli-Opitz Syndrome

67
Q

Septo-optic dysplasia

A

Septum pellucidum
Hypoplasia CN2
Pituitary insufficiency

68
Q

Genes associated with Septo-optic dysplasia

A

HESX1
SOX2
SOX3
OXT2

69
Q

Aprosencephaly

A

Failure of cleavage of prosencephalon -> no diencephalon

Have midbrain and brainstem still

70
Q

Genetics of agenesis of the corpus callosum

A

Frameshift mutation DCC Netrin 1 Receptor gene

71
Q

Symptoms of agenesis of the corpus callosum

A

Autism
Stereotypies
Antisocial

72
Q

Primary Microcephaly

A
  • Microcephaly with normal to thin cortex, simple gyri
  • Microlissencephaly (thick cortex)
  • Microcephaly with polymicrogyria
    Over 25 genes found
73
Q

Secondary microcephaly

A

More common

Infection, hypoxia, alcohol, radiation

74
Q

Primary Megalencephaly

A

Too much proliferation, not enough pruning
Associated with autism
Distinguish from macrocephaly
Phosphatidylinositol-3-kinase (PI3K/AKT)

75
Q

Secondary Megalencephaly

A

Deposition into white matter

Seen with Canavan and Alexander syndromes

76
Q

Hemimegalencephaly

A

One hemisphere is larger than the other - usually epileptogenic
Seen with linear sebaceous syndrome, tuberous sclerosis, neurofibromatosis

77
Q

Type 1 lissencephaly

A

Classical lissencephaly
Thick cortex with agyria or pachygyria
Tangential and radial migration disorder
LIS1, DCX, RELN, ARX, 14-3-3e

78
Q

Type 2 lissencephaly

A

Cobblestone lissencephaly
Loss of convolutions
TUBA1A, GPR56

79
Q

Polymicrogyria

A

Two types in spectrum: abnormal four layer cortex and disorganized cortex

Due to persistence of reelin expression in Cajal-Ritzius cells
Associated with 22q11.2, Aicardi syndrome, Oculocerebrocutaneous syndrome, Sturge-Weber, Warburg micro

80
Q

Schizencephaly etiology

A

Genetic, migrational, and environmental factors

Possible ischemic episode in 7-8th week of gestation

81
Q

Type 2 schizencephaly

A

Open lip

Connecting the ventricle and meningeal surface, lined with polymicrogyria and separated lips

82
Q

Type 1 Schizencephaly

A

Closed lip

Gray matter lined cleft with lips in contact

83
Q

Cortical dysplasia

A

As cells migrate out a trail is left

Won’t see as a neonate, need myelin to see on imaging

84
Q

Periventricular heterotopia

A 
Bumpy appearance of ventricles
Nodules due to cells failing to migrate
Can have seizures
Filimin A (FLNA Xq28)
ADP ribosylation factor quinine nucleotide exchange (ARFGEF2)

85
Q

When does myelination occur?

A

First eight months of life

Caudal to rostral

86
Q

Stages of myelination

A

Posterior before anterior
Proximal before distal
Primary sensory before motor
Projection pathways before cerebral association pathways

87
Q

Do tone and movement develop first in the legs or the arms?

A

Legs first

88
Q

Tonic labyrinth reflex

A

Head forward -> legs up
Head back -> arms out
Appears in utero
Gone by 3 years

89
Q

Rooting/suck reflex

A

Appears at birth

Gone by three months

90
Q

Crossed adductor reflex

A

Appears at birth

Gone by 7-8 months

91
Q

Moro reflex

A

Appears at birth

Gone at 5-6 months

92
Q

Palmer grasp

A

Appears at birth

Gone at six months

93
Q

Plantar grasp

A

Appears at birth

Gone at 9-10 months

94
Q

Tonic neck reflex

A

Appears at birth

Gone by 5-6 months

95
Q

Galant reflex

A

Appears at birth

Gone by six months

96
Q

Cerebral palsy

A

Motor deficit that is not progressive

Can’t reach Milestones

97
Q

Which type of cerebral palsy is most common?

A

Spastic 85%

98
Q

Subtypes of cerebral palsy

A

Spastic
Dyskinetic
Ataxic-hypotonic (cerebellar)

99
Q

Types of spastic cerebral palsy

A 
Diplegic (both legs)
Hemiplegic (ipsilateral arm+leg)
Quadriplegic (all 4 limbs)
Monoplegic (1 limb, usually arm)
Triplegic (3 limbs, usually 2 legs + 1 arm)
100
Q

Types of dyskinetic cerebral palsy

A

Athetoid
Chorea
Dystonic

101
Q

Symptoms associated with cerebral palsy

A 
Developmental delay 50%
Visual defects
Hearing impairment
Speech and language delay
Feeding/swallowing difficulty
Seizures
102
Q

Most common cause of neonatal seizures

A

Vascular (HIE, stroke, hemorrhage)

103
Q

What kind of seizures appear at 24-72 hours of life?

A 
HIE
Hypoglycemia
Stroke
Drug withdrawal
IVH
Trauma
104
Q

What kind of seizures appear at 2-5 days of life?

A

Benign familial neonatal convulsions (fifth day fits)

Hypocalcemia

105
Q

What kind of seizures appear from 2-7 days of life?

A 
Once babies start feeding
Ohtahara
EME
Glucose transporter type 1 deficiency
Galactosemia
Aminoacidopathies
Nonketotic hyperglycinemia

106
Q

What kind of seizures appear from 4-7 days of life?

A

Benign idiopathic neonatal seizures

Migrating partial seizures of infancy

107
Q

Trace alternans on EEG

A 
36-40 weeks
Sleep cycle (Active -> quiet -> active)
108
Q

Trace discontinua on EEG

A

26-36 weeks

Long pauses between bursts (up to 1 minute)

109
Q

Neonatal seizures on EEG

A

Spike/wave pattern

110
Q

Burst suppression on EEG

A

High amplitude bursts over a short period

Long causes of low amplitude

111
Q

Discontinuous EEG

A

22-28 weeks

Left and right are not symmetric

112
Q

Symptoms of benign neonatal seizures

A 
5th day fits
90% occur days 4-6
Focal clonic seizures sometimes with apnea
Recur in a 24-48 hour span
Self resolve by six weeks of life
113
Q

Genetics of familial neonatal seizures

A

Autosomal dominant
KCNQ2 and KCNQ3
Family history of similar seizures

114
Q

Symptoms of familial neonatal seizures

A 
First few days to several weeks of life
Focal, multifocal, tonic, clonic
Resolved by five months to two years
Self-limiting
Can treat with oxcarbazepine
115
Q

Genetics of benign neonatal seizures

A

KCNQ2 mutation

116
Q

Symptoms of Ohtahara syndrome

A

Early infantile epileptic encephalopathy
In utero to postnatal
Tonic spasms with burst suppression on EEG
High risk for infantile spasms and refractory epilepsy

117
Q

Genetics of Ohtahara syndrome

A

Genetic or cortical malformation

CDKL5, ARX, PLCB1, PNKP, SCN3A

118
Q

Early myoclonic epileptic encephalopathy

A

Myocalnic seizures with burst depression on EEG
Associated with inborn errors of metabolism
 High risk for infantile spasms

119
Q

KCNQ2 Encephalopathy

A 
Severe epileptic encephalopathy
Seizures, hypotonia, no visual response
Tonic seizures
Multifocal sharp -> burst suppression
Sodium channel medications
120
Q

Pyridoxine dependent epilepsy

A

Can’t make GABA

Treat with pyridoxine

121
Q

Phenobarbital

A

Hyperpolarizes cells

Cl channels kept open via GABA-A receptors

122
Q

Levetiracetam

A

SV2 release protein

Blocks release of glutamate

123
Q

Fosphenytoin

A

Sodium channel blocker

124
Q

What is hypotonia?

A

Appendicular: reduced resistance to passive ROM in joints
Axial: impaired ability to sustain postural control/antigravity movement

125
Q

What is weakness?

A

Reduction in the maximum power that can be generated

126
Q

Do all weak infants have hypotonia?

A

Yes

127
Q

Do all hypotonic infants have weakness?

A

No

128
Q

Hypotonic with normal strength and reflexes

A

Central hypotonia

129
Q

Hypotonic with weakness and areflexia

A

Peripheral hypotonia

130
Q

Examples of central hypotonia

A 
60-80%
HIE
Stroke
Fragile X
Prader Willi
Congenital syndromes
Metabolic disease
131
Q

Examples of peripheral hypotonia

A 
SMA
Congenital myotonic dystrophy
Congenital muscular dystrophy
Congenital myopathy
Congenital myasthenic syndrome
Pompe disease
Congenital neuropathy
Botulism
Brachial plexopathy
132
Q

Mental status in hypotonia

A

Central: abnormal (seizures, encephalopathy)
Peripheral: normal

133
Q

Cranial nerves in hypotonia

A

Central: localizing pattern
Peripheral: localizing pattern, extraocular muscle involvement, bulbar weakness

134
Q

Motor deficits in hypotonia

A

Central: upper motor signs

  • normal muscle bulk
  • spasticity
  • brisk reflexes
  • hemideficits
Peripheral: lower motor signs
- reduced muscle bulk
- hypotonia
- decreased reflexes
- weakness with different patterns

135
Q

Sensory deficits in hypotonia

A

Central: specific patterns

  • hemisensory loss
  • sensory level/sweat level

Peripheral: poor response diffusely

136
Q

Findings with anterior horn deficits

A 
Weakness
High arched palate
Bell shaped torso
Reduced muscle bulk
Absent reflexes
Fasciculations especially tongue

137
Q

Findings with neuropathy

A

Weakness
Absent reflexes
Rare fasciculations
Sensory deficits

138
Q

Findings with neuromuscular junction disorders

A

Weakness
Fatigability
Normal muscle bulk
Extraocular, bulbar, respiratory muscle involvement

139
Q

Findings with muscle disorders

A 
Weakness
Reduced muscle bulk
Pseudohypertrophy
Contractures
Proximal > distal most cases
Extraocular, bulbar, respiratory muscles involvement
140
Q

Transient neonatal myasthenia gravis

A

10% of women with MG
Circulating antibodies against fetal isoform of AchR
Transient, outcome is good if baby survives

141
Q

Congenital myasthenic syndrome

A

Rare
Fatigable weakness of eye movements, eyelids, swallowing, and proximal extremities since infancy
Albuterol and Pyridostigmine can help
Some worsened with Pyridostigmine

142
Q

Congenital myopathy

A

Core myopathy most common histopathologic type
Nemaline myopathy most common presenting in infancy
RYR1 most common genetic type
Often have normal CK

143
Q

What are people with RYR1 related myopathies at risk for?

A

Malignant hyperthermia

Occurs with exposure to certain anesthetics

144
Q

When does the germinal matrix start involuting?

A

32 weeks

145
Q

What do you worry about if you see thalamic hemorrhage on imaging?

A

Cerebral sinovenous thrombosis

146
Q

Syndromes associated with type 2 lissencephaly

A

Fukuyama type congenital muscular dystrophy
Muscle-Eye-Brain disease
Walker-Warburg syndrome

Neo Board Review MAP (18 decks)

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