Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Molecule most rapidly depleted after neuronal injury

A



Phosphocreatine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
    
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Failure to establish HR by 10 minutes results in ___

A

death or severe permanent disability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Best predictor of intrauterine hypoxia

A

Metabolic acidosis on cord gas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Best predictor of long-term outcome in asphyxia

A

Requirement for tube feeding at two weeks of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Minimal neuronal injury

A

Minimal ATP reduction followed by recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Moderate neuronal injury

A

Biphasic depletion

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Severe neuronal injury

A

Energy failure with predominant necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

 Cerebral blood flow autoregulation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CO2 and cerebral blood flow

A

Increased CO2 -> increased CBF (dilates blood vessels)

Decreased CO2 -> decreased CBS (constriction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Arterial 02 content and cerebral blood flow

A

Increased O2 -> decreased CBF

Decreased O2 -> increased CBF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Glucose and cerebral blood flow

A

Increased glucose -> decreased CBF

Decreased glucose -> increased CBF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Calcium and cerebral blood flow

A

Increased calcium -> decreased CBF

Decreased calcium -> increased CBF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Prostaglandins and cerebral blood flow

A

Increased prostaglandins -> increased CBF

Decreased prostaglandins -> decreased CBF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

CBF ___ with postnatal age

A

Increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Normal intracranial pressure

A

30-70 mmH2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of increased intracranial pressure

A 
Major intracranial hemorrhages
Post hemorrhagic hydrocephalus
Seizures
Pneumothorax
Tracheal suctioning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Germinal matrix

A

Site of neuronal precursors between 10-20 weeks gestation

3rd trimester becomes site of glial precursors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

When does germinal matrix involute

A

By 36 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Intravascular factors and IVH

A

Increase or decrease in CBF
Fluctuating CBF
Platelet and coagulation problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Extravascular factors and IVH

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cerebral autoregulation

A

Maintain stable cerebral blood flow in face of altering perfusion pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

When does cerebral autoregulation fail?

A

High PCO2 (>70)

After hypoxia/ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Mechanism of brain injury in IVH

A 
Hypoxic ischemic injury
Distraction of germinal matrix/glial precursors
Periventricular hemorrhagic infarct
PVL
PHH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

IVH presentation: saltatory syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When does 90% of IVH occur?

A

First three days of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

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

A

10%

Grade II worse than no hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Percentage of neonates with grade 3 IVH with developmental abnormalities?

A

35-40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Percentage of neonates with grade 4 IVH with developmental abnormalities?

A

80-90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Causes of IVH in term neonates

A

Trauma and hypoxic events 50%

25% with no identifiable cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Location of IVH in term neonates

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Symptoms of IVH in term neonates

A

Irritability, stupor, apnea, seizures

Seizures are focal or multifocal and present in 65%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

HIE symptoms 12-24 hrs.

A 
Variable change in level of alertness
Typically when we see seizures start
Apneic spells
Jitteriness
Weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

HIE symptoms 24-72 hrs.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

HIE symptoms >72 hours

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Long-term outcomes with parasagittal injury

A

Vascular watershed areas
Spastic quadriparesis
Intellectual deficits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Long-term outcomes with selective neuronal necrosis

A 
Cognitive deficits
Spastic quadriparesis
Choreoathetosis
Dystonia
Seizure disorder
Ataxia
Bulbar and pseudobulbar palsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Periventricular leukomalacia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

PVL is associated with injury to which cells?

A

Oligodendrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Subdural hematoma

A

Due to tears and bridging veins

Can be due to traumatic delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Four categories of cerebellar hemorrhage

A

Primary
Venus infarction
Extension of IVH
Subarachnoid hemorrhage into cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Caput succedaneum

A

Molding of head

Crosses suture lines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Cephalohematoma

A

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


How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Diffuse neuronal injury

A

Insult is very severe and very prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Cerebral cortex (nuclear) neuronal injury

A

Insult is moderate to severe and prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Deep nuclear/brainstem neuronal injury

A

Insult is severe and abrupt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Ventral induction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

127
Q

Do all hypotonic infants have weakness?

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?

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions