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Neonatal Neurology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Neuronal cell differentiation

A

the process during which young, immature (unspecialized) cells take on individual characteristics and reach their mature (specialized) form and function

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2
Q

Baby’s brain is fully developed by…

A

Baby brains are fully developed by 9 mo

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3
Q

Neuronal cell death (apoptosis)

A

a type of cell death in which a series of molecular steps in a cell lead to its death

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4
Q

5 months after conception

A

baby’s lobes are fully developed ready for differentiation

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5
Q

Synaptogenesis

A

a process involving the formation of a neurotransmitter release site in the presynaptic neuron and a receptive field at the postsynaptic partners, and the precise alignment of pre- and post-synaptic specializations.

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6
Q

infant viability

A

in the 3rd trimester

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7
Q

Extracorporeal Membrane Oxygenation

A

blood is pumped outside of your body to a heart-lung machine that removes carbon dioxide and sends oxygen-filled blood back to tissues in the body

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8
Q

Synaptic refinement

A

he reorganization of synapses and connections without significant change in their number or strength

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9
Q

A newborns preference for mutual, rather than unilateral, gaze shows…

A

that babies are designed for reciprocity(communication between child and parent)

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10
Q

Neurulation

A

the folding process in vertebrate embryos, which includes the transformation of the neural plate into the neural tube

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11
Q

What part of development takes the longest time?

A

Development of the Brain

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12
Q

40 days after conception

A

spinal develops(when?)

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13
Q

Dr. Coubey’s Premature Baby Shows

A

obtained six incubators in 1896 in France to demonstrate the new technology for saving infants. To add drama, six preterm infants from Virchow’s maternity unit in Berlin were brought and exhibited inside the incubators at the 1896 Berlin Exposition

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14
Q

35 days after conception

A

the pituitary gland forms

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15
Q

25 days after conception

A

the forebrain, hindbrain, and the midbrain develop

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16
Q

Attempts to stimulate and revive apparently dead newborns include:

A

beating, shaking,yelling, fumigating, and dipping in ice-cold water(shocking)

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17
Q

50 days after conception

A

the cerebral hemispheres form

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18
Q

US ranks 30th in world infant mortality (why?)

A
  • more teen births
  • more obese moms
  • more unplanned pregnancies
  • US count all births as live births
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19
Q

100 days after conception

A

development of the cerebellum, pons, midbrain, and medulla take place along with cell migration

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20
Q

Historical attempts at resuscitation of newborns

A
  • beating
  • shaking
    -yelling
  • fumigating
  • dipping in ice-cold water
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21
Q

consequences of prematurity

A

Underdeveloped infants lead to illness and disability
ex. cerebral palsy

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22
Q

A newborn’s preference for mutual, rather than unilateral, gaze shows…

A

that babies are designed for reciprocity(communication between child and parent)

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23
Q

Extracorporeal Membrane Oxygenation

A

blood is pumped outside of your body to a heart-lung machine that removes carbon dioxide and sends oxygen-filled blood back to tissues in the body

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24
Q

Function and responsibility of the NICU

A

to care for ill preterm and term infants born in the hospital

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25
Q

Dr. Couney’s Premature Baby shows

A

obtained six incubators in 1896 in France to demonstrate the new technology for saving infants.

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26
Q

Reasons why the US ranks 30th in world infant mortality(tied with Slovakia)

A
  1. more teen births
  2. more obese moms
  3. more unplanned pregnancies (40%)
  4. the US counts all births as live births
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27
Q

NICU

A

department in charge of the care of ill preterm and term infants born in that hospital

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28
Q

Autism (synaptogenesis problem)

A

cause by the over population of neuroconnections

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29
Q

Synaptogenesis

A

the creation of synapses between neurons in the nervous system

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30
Q

Apoptosis

A

programmed cell death

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31
Q

Astrocytoma

A

a tumor that begins in the CNS in a star shaped cell that supports nerve cells

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32
Q

double band cortex

A

a disorder in neuronal migration that usually present with seizures and intellectual impairment (almost exclusive in females)

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33
Q

consequences of premature birth

A

abnormal development of the posterior fossa, some lesions may be overlooked or missed, diagnosis could be delayed due to subtle or silent early postnatal clinical features

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34
Q

Autism (synaptogenesis problem)

A

cause by the over population of neuroconnections

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35
Q

cell migration

A

the direct movement of a single cell or group of cells in response to chemical and/or mechanical signal

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36
Q

Six stages of CNS development

A

Neurogenesis, migration, differentiation, synaptogenesis, neuronal cell death, synaptic refinement

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37
Q

The shortest and most intense stages in development…

A

Neurogenesis and Migration

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38
Q

Central Nervous System (CNS) Develops…

A

Central Nervous System (CNS) Develops…

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39
Q

Neurogenesis

A

mitosis produces neurons and glial cells in the area next to the central canal

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40
Q

migration

A

Neuronal cell migration

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41
Q

Microcephaly

A

condition where a baby’s head is smaller than expected

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42
Q

neurogenesis

A

the process by which new neurons are formed in the brain

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43
Q

Differentiation

A

final stage in development of neurons where neurons develop according to the need of their system by creating connections with other cells, ect.

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44
Q

Sarnat Stage 1 (mild encephalopathy)

A

✓ Hyperalert
✓Normal muscle tone, active suck, strong Moro, normal grasp, normal doll’s-eye reflex ✓Increased tendon reflexes
✓Hyper-responsiveness to stimulation
✓Dilation of pupils, reactive
✓Usually lasts <24 hours

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45
Q

Sarnat Stage 2 (moderate encephalopathy)

A

✓Hypotonia and lethargy
✓Increased tendon reflexes
✓Diminished brainstem reflexes - weak suck, incomplete Moro reflex, varying respiration ✓Possible clinical seizures

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46
Q

Recovery to Stage 1

A

✓No further seizure activity
✓Transient jitteriness
✓Improvement in level of consciousness

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47
Q

Sarnat Stage 3 (severe encephalopathy)

A

another name: acute phase

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48
Q

Sarnat Stage 3 (severe encephalopathy)

A

✓Apnea/bradycardia; mechanical ventilation needed
✓Brainstem: Pupils unequal; variable reactivity & poor light reflex
✓Level of consciousness deteriorates to coma ✓Seizures in first 12 hours: multifocal clonic seizures

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49
Q

Sarnat Stage 3 (severe encephalopathy): deterioration

A

✓Occurs within 24 to 72 hours
✓Severely affected infants worsen, then death maybe

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50
Q

ways of intervention to delay neuronal death

A

Therapeutic hypothermia

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51
Q

Therapeutic hypothermia

A

cooling to 33 degrees celsius is the only neuroprotective treatment in HIE term infants

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52
Q

Treatment of ischemic brain injury aims:

A
  • Slow release of excitatory neurotransmitters
  • Decrease caspase-3 activation and apoptosis
  • Reduce oxygen free-radicals
  • Block inflammatory mediators and inhibit apoptotic pathways
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53
Q

When hypothermia is started

A

by 6 hours of birth and continued for 72 hours

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54
Q

Why is hypothermia used?

A

Cooling reduces death or major neurodevelopmental disabilities in neonates with moderate to severe HIE

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55
Q

32-year-old woman whose first baby was delivered via CS attempted vaginal birth this pregnancy. During labor, she had sudden severe abdominal pain, became hypotensive, and fetal heart rate was undetectable. Emergent CS is performed and baby is brought to the resuscitaire
Initial exam reveals an unresponsive floppy infant with no respiratory effort and heart rate of 80 bpm. Apgar scores are 1, 4, and 7 at 1, 5 and 10 minutes
Weight 3720 gms (>90%), T 96.5o , HR 190 bpm, BP 37/23 mmHg (low)
Pale and poorly perfused. On ventilator with periodic respiration effort
Level of consciousness: poor eye opening to stimulation, no sustained alertness Movements and Tone: minimal spontaneous activity, hypotonia Brainstem/Autonomic Function: pupils constricted but reactive, no suck, no gag Reflexes: incomplete Moro, no DTRs

Dx?

A

HIE (diagnosis)

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56
Q

Good news: immature brain is more resistant to HI than brain of a term neonate, due to the immature brain’s:

A

✓ Lower cerebral metabolic rate
✓ Lower cerebral O2 demand
✓ Lower sensitivity to neurotransmitters with potential neurotoxicity ✓ Greater plasticity

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57
Q

OTOH: premature birth

A

✓ Any injury disrupts areas of active neural development
✓ Glucose uptake mechanisms are underdeveloped
✓ Autoregulation of increased cerebral blood flow is immature

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58
Q

A 2-month-old infant is brought to ER by her mother who fears her daughter had a stroke. An hour ago, she was breastfeeding when she began to repeatedly kick her right foot in the air. After 2 minutes, her right arm and leg ‘went limp’. The infant has returned to baseline.
She was born at 40 weeks’ gestation after an uncomplicated pregnancy, with no postnatal complications or recent illnesses
The infant now has normal vital signs and is a well-appearing, playful infant who shows no weakness.
dx?

A

seizure(dx)

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59
Q

Seizure

A

Stereotypic spell of abnormal neurologic function (behavior, motor, and/or autonomic function)

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60
Q

Seizures are…

A

✓More likely than in older patients
✓Behavioral expression is different
✓They reflect rapid ontogeny of ion channel expression
✓Long-term development consequences are worse
✓Need different drug treatment than adults

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61
Q

Neonatal seizures- unusual presentations

A

Electrographic seizures
Clinical seizures * Subtle
* Tonic
* Clonic
* Myoclonic

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62
Q

Case
Term girl born to a 28-year-old mother. Labor and delivery were notable for tight nuchal cord. She was delivered vaginally. Apgar scores were 7 (-1 tone, -2 color) and 9 (-1 color) at 1 and 5 minutes. The infant had no respiratory distress and fed well overnight. Early on 2nd DOL, she had a 1-minute bilateral clonic seizure.
* She is taken to nursery, where her rapid glucose is 60mg%. An IV is started and phenobarbital is given. She is transferred to NICU, where she has a second seizure, starting in the right arm.
* Exam: VS T36.8, P140, R60, BP 90/50, birth weight 3300g. Length and head circumference are 50th percentile. She is sleepy. There is mildly decreased generalized tone. DTRs are 1-2+ and symmetric.
* A second dose of phenobarbital is given, and no further seizures are noted.
* Serum electrolytes and glucose are normal. CBC is remarkable for hematocrit 36%
(anemic), normal WBC, normal platelet count. Lumbar puncture shows normal CSF.
* Brain MRI scan shows increased signal in left hippocampus.
Dx?

A

seizures dx

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63
Q

Electrographic seizures

A

Abnormal electrocortical activity - EEG
✓No behavioral change
✓Cannot be provoked by tactile
stimulation
✓Cannot be suppressed by restraint of infant

Hypersynchronous discharge of a critical mass of neurons

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64
Q

Neonatal seizures (Etiology)

A

❖85% - Most neonatal seizures are acute provoked seizures Hypoxic-ischemic encephalopathy
Structural brain injuries, especially stroke Transient glucose and electrolyte abnormalities CNS infections
❖15% - Genetic epilepsy syndromes Channelopathies
Brain malformations IEMs

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65
Q

Subtle seizures

A

✓ More in preterm than in term infants
✓ Gaze deviation (term)
✓ Blinking, fixed stare (preterm)
✓ Repetitive mouth/tongue movements
✓ Pedaling/posturing of limbs

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66
Q

Tonic seizures (Clinical Seizure Classification)

A
  • Primarily in preterm infants with ICH
  • Focal or generalized
  • Sustained extension of limbs (decerebrate posturing)
  • Sustained flexion of upper/extension of lower limbs (decorticate posturing)
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67
Q

Clonic seizures (Clinical Seizure Classification)

A

✓Primarily in term
✓Focal or multifocal
✓Clonic limb movements (may migrate)
✓Consciousness may be preserved

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68
Q

Myoclonic seizures

A

✓ Rare, usually bad
✓ Focal, multifocal or generalized
✓ Single jerks of extremities (upper > lower)

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69
Q

Myoclonic movements

A

rapid, isolated jerks that can be generalized, multifocal, or focal in a trunk or limb distribution

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70
Q

Prognosis of Neonatal Seizures (term)

A

Mortality and morbidity
Normal= 60%
Dead= 20%

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71
Q

Prognosis of Neonatal Seizures (<2500g)

A

normal= 35%
dead= 40%

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72
Q

Prognosis of Neonatal Seizures (<1500g)

A

normal=20%
dead=60%

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73
Q

Two ways to predict the outcome of neonatal seizures

A

✓ EEG
✓ Underlying neurological disease

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74
Q

Prognosis of neonatal seizures in relation to EEG
(EEG Background Normal)

A

normal = </= 10%

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75
Q

Prognosis of neonatal seizures in relation to EEG
(EEG Background Moderate abnormal)

A

~50 Voltage asymmetry, severe immaturity

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76
Q

Prognosis of neonatal seizures in relation to EEG
EEG Background (Neurologic Sequelae)

A

90 Discontinuity

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77
Q

Neonatal Seizures and Outcome by Cause(poor=0-10)

A

Cause=
Brain malformations(% Normal Development = 0

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78
Q

Neonatal Seizures and Outcome by Cause(Good=100)

A

hypocalcemia 100
Benign familial neonatal seizures ~100

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79
Q

Neonatal Seizures and Outcome by Cause(fair=50)

A

50% normal development

Hypoglycemia
Bacterial meningitis
Hypoxia-ischemia

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80
Q

Neonatal seizures (prognosis)

A

best if the cause is transient, or has a genetic cause with otherwise normal metabolism and brain formation

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81
Q

newborn brain is biased toward excitation (why?)

A

NMDA/AMPA receptors are transiently overexpressed in developing cortex; coincides with increased seizure susceptibility

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82
Q

In an immature brain…

A

NMDA receptor makeup is developmentally regulated
predominant NR2 subunit is NR2B - (longer current decay time than NR2A subunit on mature neurons)
NR2C, NR2D, and NR3A subunits are increased - reduces magnesium sensitivity and thus increases excitability

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83
Q

In immature forebrain…

A

GABA receptor activation causes depolarization rather than hyperpolarization
KCC2 is virtually absent in first months of life, whereas Cl- importer NKCC1 is overexpressed

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84
Q

In immature forebrain…

A

Cl- equilibrium potential is positive to the
resting membrane potential
Activation of GABAA receptors results in Cl- efflux
and depolarization

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85
Q

In immature forebrain…

A

Glutamate is overactive and GABA is excitatory until about 6 weeks of life

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86
Q

An otherwise normal-term boy started having seizures at age 3 days. He had 4–8 seizures per 24 hours, which started with tonic limb posturing with apnea for ~10s followed by vocalizations, eye-rolling, chewing, and asymmetric jerks of the limbs
All relevant tests including interictal EEG were normal
Recommended treatment with valproate was vigorously rejected by the grandmother, the dominant member of the family, who herself, her father, and two of her 4 children had similar neonatal seizures without consequence in their successful lives
He had seizures up to age of 6 weeks but was normal in between seizures. On follow-up at age 2 years, he is a normal child
‘Granny was right again’ the family admitted
Dx?

A

Severe Myoclonic Epilepsy of Infancy

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87
Q

Severe Myoclonic Epilepsy of Infancy

A

A SCN1A channelopathy
Begins during first year of life with myoclonic seizures Development arrests
Partial and generalized seizures also occur

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88
Q

Pyridoxine-dependent seizure- Clinical seizure

A

Clinical seizure - eye deviation to right and asymmetric clonic movements of extremities, associated with widely distributed high voltage electrographic seizures

89
Q

Pyridoxine-dependent seizure- Clinical seizure (lasts)

A

Five minutes after the patient received 100mg pyridoxine by IV infusion. EEG shows normal background.

90
Q

Cranial sonography is best for…

A

high-risk and unstable premature infants (US type)

91
Q

Cranial sonography is best for high-risk and unstable premature infants (why?)

A

Rapid evaluation of infants in NICU without need for sedation and with no risk
A good imaging modality due to its portability, lower cost, speed, with no radiation

92
Q

Cranial sonography is best for…(dx?)

A

Most useful for
✓intracranial hemorrhage
✓ hydrocephalus
✓periventricular leukomalacia (PVL)

93
Q

Triplets are born at 24 weeks gestation to a G1P0 mother for premature labor. Triplet C dies on DOL3 of lung prematurity. Triplets A and B are stable until DOL4 when they become suddenly hypertensive and anemic. Stat head ultrasounds are done. Dx?

A

PVL

94
Q

Grade I IVH

A

Germinal matrix hemorrhage with no or minimal IVH (bilateral germinal matrix hemorrhage)

95
Q

Grade II IVH

A

IVH (10–50% of the ventricular area without hydrocephalus)

96
Q

Grade III IVH

A

IVH (>50% of the ventricular area) with hydrocephalus)

97
Q

Grade IV IVH

A

Periventricular hemorrhage

98
Q

HUS grading levels

A

Normal
Grade 1
Grade 2
Cystic PVL

99
Q

Normal HUS grading

A

echogenicity of periventricular white matter (PVWM) (brightness of PVWM is same as choroid plexus)

100
Q

Grade 1(HUS)

A

slightly increased echogenicity of PVWM, the affected region as bright as the choroid plexus)

101
Q

Grade 2(HUS)

A

very increased echogenicity of PVWM, the affected region obviously brighter than the choroid plexus

102
Q

Cystic PVL(HUS)

A

holes in the PVWM

103
Q

PVL grade 1

A

areas of increased periventricular echogenicity without any cyst formation

104
Q

PVL grade 2

A

the echogenicity has resolved into small periventricular cysts

105
Q

Cerebral edema

A

Gray-white matter blurring

106
Q

Neonatal EEG 24-26 wks

A

hypersynchronous/discontinuous (EEG)

107
Q

Neonatal EEG 29-30 weeks

A

synchronous/ discontinuous (EEG)

108
Q

Neonatal EEG 40 weeks

A

Dysynchronuous/ continuous (EEG)

109
Q

Synchronicity is achieved(when)

A

eeg is reactive and synchronous by 32 weeks

110
Q

discontinuity is…(eeg)

A

common early, but by term should only be in quiet sleep

111
Q

Neonates’ states of consciousness

A

Awake, active sleep, and quiet sleep

112
Q

In neonatal eeg(by term)

A

awake and active sleep look similar

113
Q

In neonates’ quiet sleep is marked by…

A

marked by attenuated periods in prematurity, after which it evolves to slow wave sleep

114
Q

Concern for epileptic activity

A

discharges that are extremely frequent, persistently in one area, or become rhythmic

115
Q

Neonatal seizures (evolve)

A

evolve just like adult seizures, but are usually focal rather than generalized

116
Q

normal 40.5 weeks PMA

A

the tracing is continuous with multiple admixed frequencies, and of moderate amplitude
- chaotic appearing wavelengths are normal for neonates when awake

117
Q

Quiet sleep

A

trace alternant in quiet sleep starts around 34 weeks PMA and gradually evolves into slow-wave sleep

118
Q

trace alternant

A

characterized by quiet periods of voltage over 25 μV, alternating with bursts of 100- to 200-μV amplitude

119
Q

Active sleep

A

in a normal 41 week PMA neonate the continuous tracing with a mixture of frequencies, as well as lateral eye movements

120
Q

How can a neonatal EEG be abnormal?

A

✓Asymmetric – left and right sides look different
✓Seizing – a focal rhythmic wave
✓Flat - flat
✓(Dysmature) - normal for a younger infant

121
Q

Asymmetric

A

left and right sides look different

122
Q

Seizing

A

a focal rhythmic wave

123
Q

Flat

A

flat

124
Q

(Dysmature)

A

normal for a younger infant

125
Q

formal testing is seldom needed(why?)

A

information can usually be gleaned from talking to parents and watching, handling, and listening to the baby carefully throughout the exam

126
Q

Testing during the first few days after delivery

A

newborns may be neurologically labile

127
Q

when testing a baby(consider what?)

A

gestational and postnatal age(considered when?)

128
Q

Neonates’ first movement occurs…

A

movement occurs @ 2 months gestation (development of brainstem)

129
Q

Neonates’ first movements

A

hiccup, breath, swallow, startle, partial movement

130
Q

28 week mental status

A

needs gentle rousing to awaken

131
Q

28 week cranial nerves

A

pupils: blinks to light
hearing: pauses, no orientation to sound
suck + swallow: weak suck, no synchrony with swallow

132
Q

28 week motor function

A

minimally flexed

133
Q

28 week reflexes

A

MORO: weak, incomplete, hand opening
ATNR:
Palmer grasp: present, but weak

134
Q

32 week mental status

A

opens eyes spontaneously, sleep-wake cycle is apparent

135
Q

32 week cranial nerves

A

consistent pupillary reflex, suck is strong with better synchrony with swallow

136
Q

32 week motor

A

flexed hips and knees

137
Q

32 week reflexes

A

MORO: complete extension and abduction

138
Q

34 week cranial nerves

A

fix and follow (ability to focus and follow an object with eyes)

139
Q

34 week motor

A

increased flexion at hips and knees

140
Q

34 week palmar grasp

A

grasp is stronger

141
Q

40 week mental status

A

at 36 weeks alertness increases and cries when awake

142
Q

40 week cranial nerves

A

head and eyes turn to sound
coordinated suck and swallow at 37 weeks

143
Q

40 week motor

A

flexed in all extremeties

144
Q

40 week MORO

A

full MORO with ant. flexion

145
Q

40 week ATNR

A

Appears at 35 wks

146
Q

40 week palmar grasp

A

strong grasp, able to be lifted out of bed

147
Q

Red flag mental status

A

irritable infant or lethargic infant

148
Q

Red flag cranial nerves

A
  • no response to auditory stimulus
  • chomp suck; clamps down on pacifier but no suck indicating bulbar dysfunction
149
Q

chomp suck indicates…

A

bulbar dysfunction

150
Q

Red flag motor

A

-hypotonia
- hypertonia
- 28 wk infant with jerky movement
- full-term infant with writhing movements

151
Q

Red flag pallmar grasp

A
  • asymmetry
  • if obligatory or sustained, suggest pyramidal or extrapyramidal motor abnormality
  • fixed obligate grasp (suggest B hemisphere dysfunction)
152
Q

Term baby posture

A

when prone, the knees are often tucked under the abdomen, fists clenched, thumbs intermittently curl, when the head is midline, limbs are roughly symmetric, like boxers

153
Q

32 week baby posture

A

infant lies in froglike position while supine. Legs are slightly flexed at hips and knees, but arms are extended and hypotonic

154
Q

infant spontaneous motor activity

A

normal infants move their limbs in alternating fashion (like boxers)

many babies are jittery:
some are jittery only when crying and some are jittery in several behavioral states, but excessive jitter is abnormal

155
Q

Arousal

A

Healthy-term infants move between behavioral states, mostly in quiet or active sleep; quiet or active

156
Q

Visual tracking

A

Newborns should follow at least 90 degrees with their eyes
Mostly saccadic movement

157
Q

Primitive reflexes

A

rooting, sucking, moro, traction, ATNR(asymmetric tonic neck reflex)

158
Q

rooting(primitive reflex)

A

reflex helps your baby find and latch onto a bottle or your breast to begin feeding

159
Q

Neonatal neurologic red flag signals

A

✓ Persistent irritability
✓ Difficulty in feeding
✓ Persistently deviated head and/or eyes
✓ Persistently asymmetric posture and movements
✓ Persistent adducted thumbs in a fisted hand
✓ Opisthotonos
✓ Persistent posture of flexed arms and extended legs
✓ Apathy and immobility ✓ Floppiness (hypotonia) ✓ Convulsions
✓ Abnormal cry
✓ Setting-sun sign, vomiting, rapid increase in head circumference

160
Q

Neonatal neurologic exam alarm signals

A

Persistent:
Asymmetric posture/movements
Limb abduction
Adducted thumb in a fisted hand
Hypotonia
Opisthotonos

161
Q

Opisthotonos

A

a condition in which a person holds their body in an abnormal position. The person is usually rigid and arches their back, with their head thrown backward

162
Q

Neonatal neurologic alarm signals (hydrocephalus )

A

Setting-sun sign, vomiting, rapid increase in head circumference

163
Q

Brain development takes the _______ time

A

takes the longest time

164
Q

CNS develops _________ gestation (and then some)

A

develops throughout gestation

165
Q

The shortest and most intense stages are …

A

Neurogenesis and Migration (which stages?)

166
Q

1st stages of brain development

A

Neurogenesis

167
Q

Neurogenesis

A

mitosis produces neurons and glial cells in the area next to the central canal

168
Q

Error in neurogenesis (proliferation)

A

microcephaly (what stage of development)

169
Q

microcephaly (definition)

A

a condition where a baby’s head is much smaller than expected.

170
Q

2nd stage of band development

A

cell migration

171
Q

cell migration (definition)

A

the directed movement of a single cell or a group of cells in response to chemical and/or mechanical signals

172
Q

Double band cortex (what stage of development)

A

Error in cell migration

173
Q

double band cortex (definition)

A

a rare neuronal migration disorder, classically present with seizures and intellectual impairment and is seen almost exclusively in females

174
Q

3rd stage of brain development

A

Differentiation

175
Q

Neuronal/ cell differentiation

A

a given population of neurons gives rise to subpopulations that are specific to the various parts of the nervous system

176
Q

Error in differentiation

A

Astrocytoma (error in what step)

177
Q

Astrocytoma

A

a type of cancer that can form in the brain or spinal cord in the star-shaped cell

178
Q

Error in synaptogenesis

A

Autism (error in what?)

179
Q

Synaptogenesis

A

the formation of synapses between neurons in the nervous system

180
Q

Autism

A

A serious developmental disorder that impairs the ability to communicate and interact.

181
Q

4th stage of brain development

A

synaptogenesis (what step?)

182
Q

5th stage of brain development

A

Neuronal cell death (what stage?)

183
Q

Apoptosis

A

neuronal cell death

184
Q

Fragile X syndrome

A

error in neuronal cell death

185
Q

Stage 6 of brain development

A

Synaptic refinement (what step?)

186
Q

Synaptic refinement (allows for?)

A
  • Make new friends; keep some of the old friends
  • Lifelong
  • Activity-dependent
  • Allows learning
187
Q

Error in synaptic refinement

A

Autism, ADHD, Dyslexia, ect…( error in what?)

188
Q

Neuronal proliferation/ migration (glutamate)

A

main excitatory neurotransmitter glutamate is involved in promoting and/or inhibiting the proliferation, survival, migration, and differentiation of NPCs (neuropathic progenitor cells) acting via ionotropic or metabotropic receptors

189
Q

GABA Neurons

A

inhibit the production of glutamate

190
Q

primary microcephaly (genetic)

A

babies are born with a small brain, which grows but always is small – a disorder of neuronal proliferation, resulting in fewer neurons

191
Q

Secondary microcephaly (acquired)

A

from injury during rapid brain growth Environmental insults: prenatal irradiation, drugs, congenital
infections (Zika, cytomegalovirus, toxoplasmosis, HSV) In utero ischemia is a common cause

192
Q

Megalencephaly - large brains

A

Neuroepithelial overproliferation, or insufficient apoptosis → too many cells in the brain

193
Q

Megalencephaly (Familial)

A

individuals have normal or near-normal intelligence

194
Q

megalencephaly individuals syndromes…

A

Syndromes include cerebral gigantism, fragile-X syndrome, autism, and neurocutaneous disorders

195
Q

Hemimegalencephaly

A

enlargement of 1⁄2 the cerebrum. Primary symptom is refractory epilepsy, but also MR and hemiparesis

196
Q

Hemimegalencephaly (FYI)

A

can occur alone or with neurocutaneous disorders: linear sebaceous nevus, hypomelanosis of Ito, neurofibromatosis

197
Q

Hemispherectomy is most effective for…

A

most effective for medically refractory epilepsy

198
Q

Neuronal Migration and Cortical Lamination (Neocortical migrating)

A
  • have 2 main trajectories
  • Most neurons migrate radially, along radial glial guides, from germ zone to cortical plate aka. (over the hill)
    Some neurons migrate tangentially through prospective white matter from the ganglia eminences. Most will be GABA interneurons aka. (through the woods)
199
Q

ganglia eminences

A

a transitory structure in the development of the nervous system that guides cell and axon migration. It is present in the embryonic and fetal stages of neural development and found between the thalamus and caudate nucleus.

200
Q

Neuronal Proliferation Step 1

A

Overproduction of neuroblasts in all parts of the neural tube is followed by apoptosis of redundant neurons

201
Q

Neuronal Proliferation Step 2

A

Neuroblast migration to cerebral cortex is complete by 16 weeks

202
Q

Neuronal Proliferation Step 3

A

Neocortex is composed of vertical units (neuronal columns)

203
Q

Neuronal Proliferation Step 5

A

Glutamate neurons of neocortex are generated in ventricular (VZ) and subventricular (SVZ) zones of lateral ventricles

204
Q

Neuronal Proliferation Step 6

A

GABAergic neurons of neocortex are generated in the ganglionic eminences

205
Q

diffuse lissencephaly (caused by)

A

Incomplete migration in the cortex causes

206
Q

pachygyria

A

Focal lissencephaly

207
Q

Mistimed arrest of neurons migrating along radial glia to cortex:

A

Periventricular nodular heterotopia

208
Q

Periventricular nodular heterotopia

A

Failure of neurons to leave the ventricular zone

209
Q

Subcortical laminar heterotopia

A

Failure of a subgroup of neurons to complete migration, while others finish their migration

210
Q

Overmigration of neurons

A

migration of neurons beyond their intended cortical site

211
Q

Lissencephaly

A

smooth brain - without gyri Pachygyria describes an area of broad and flat gyri, shallow sulci, and fewer foldings of the cortex

212
Q

Lissencephaly (Affected infants)

A

Affected infants fail to thrive, microcephaly, mental retardation, severe epilepsy

213
Q

Periventricular nodular heterotopia (Nodules)

A

grey matter located along both lateral ventricles: total failure of migration of a few mitotic neurons

214
Q

Subcortical laminar heterotopia

A
  • One population of neurons forms relatively normal cortex
  • A second population arrests during migration - leading to a band of neurons beneath the cortex
215
Q

micropolygyria

A

excessive cortical folding

216
Q

ectopias

A

clusters of extra cells

217
Q

BNFC – benign neonatal familial convulsions

A
  • Focal seizures begin in the first week
  • Are due to mutant K+ channel
  • Usually resolves in a few weeks

These infants have low seizure thresholds compared with children

218
Q

Neurotransmitter receptors mature

A

Some change their function (what?)

219
Q

GABA changes from…

A

changes from excitatory to inhibitory about the time of birth

Neonatal Neurology (2 decks)

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