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Neonatal Pathophysiology > Neurology of the Newborn > Flashcards

Neurology of the Newborn Flashcards

1
Q

What are the 3 layers of cells in early embryologic development?

A

endoderm, mesoderm and ectoderm

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2
Q

What will the endoderm form?

A

the epithelium

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3
Q

What will the mesoderm form?

A

muscle and connective tissue

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4
Q

What will the ectoderm form?

A

skin and the nervous system

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5
Q

How does the CNS initially appear?

A

the ectoderm thickens and flattens to form the neural plate; one of the first systems to develop

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6
Q

When does the neural plate appear in embryologic development?

A

at the beginning of the 3rd week of life

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7
Q

How does the neural groove form?

A

the lateral edges of the neural plate elevate to form the neural folds, and subsequently creating a neural groove

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8
Q

What does fusion of the neural folds create?

A

the neural tube

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9
Q

When does the formation of the neural fold occur in embryologic development?

A

beginning of the 4th week of life; fusion occurs at the level of the 4th cervical vertebrae

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10
Q

In what direction does neural tube fusion occur?

A

proceeds from cephalad and caudal directions

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11
Q

What are neuropores?

A

fusion delayed at the cranial and caudal ends leaves openings at either pole

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12
Q

What do the neuropores create?

A

open communication between neutral tube and the amniotic cavity

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13
Q

When is the cranial neuropore expected to close?

A

on day 25 after conception

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14
Q

When is the caudal neuropore expected to close?

A

on day 27 or 2-3days after

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15
Q

What is the physiologic cause of a neural tube defect?

A

failure of the neural tube to close between 25-28 days after conception

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16
Q

What diagnosis accounts for most the CNS congenital anomalies?

A

NTD

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17
Q

How prevalent are NTD in the US?

A

second most common congenital anomaly (after CHD)

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18
Q

What are the risk factors for NTDs?

A

1) folic acid deficiency
2) maternal diabetes (poor glycemic control in the first trimester is a high risk factor)
3) Maternal exposure to certain medications (anticonvulsants and folic acid antagonists)
4) previous infants with NTDs

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19
Q

If a family had a child with a NTD, what is their risk for subsequent pregnancies?

A

with 1 child with a NTD, the risk is 2-4%; if > 1 child with a NTD, the risk is > 10%

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20
Q

What medications are associated with an increased risk for NTDs?

A

phenytoin, phenobarb, carbamazepine and trimetoprima

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21
Q

What is the greatest measure of NTD prevention?

A

folic acid supplementation before conception (1-3mo) and during the first month of pregnancy can prevent up to 70% of NTD cases.

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22
Q

What is the recommended doseage of folic acid?

A

0.4mg for normal women; mother’s at increased risk should take 4mg throughout their pregnancy

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23
Q

What are the different forms of NTDs?

A

1) Anencephaly
2) Encephalocele
3) Myelomeningocele

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24
Q

What is Anencephaly?

A

the most severe form of NTD, not compatable with life.

failure of the cephalic end of the neural tube to close and results in degredation of the forebrain

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25
Q

What is the extent of structural damage with an Anencephaly diagnosis?

A

absence of scalp, skull and brain tissue, may be able to visualize the brain stem, exposed hemorrhagic fibrotic tissue; may have brain stem sparing

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26
Q

How is Anencephaly diagnosed?

A

will have elevated maternal alpha fetoprotein; US 14-15 weeks GA

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27
Q

What is the rate of spontaneous abortion in infants with Anencephaly?

A

65%; most families elect to abort child

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28
Q

Why do infants with Anencephaly typically continue on into post term maturation?

A

pituitary and adrenal functions are important in triggering labor; these structures are typically underdeveloped and labor may subsequently occur spontaneously

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29
Q

What is the survival expectancy of infants with Anencephaly?

A

75% will be stillborn, other infants typically die within a few hours, days or a few weeks

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30
Q

What is the clinical presentation of infants with Anencephaly?

A

unconscious with varying degrees of brain stem function

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31
Q

What are the management strategies typically recommended for infants with Anencephaly?

A

comfort care, genetic consultation and maybe organ donation

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32
Q

Why are infants with Anencephaly not typically good organ donor candidates?

A

infants may not meet criteria for brain death until they deteriorated and their solid organs have been damaged

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33
Q

How does encephalocele occur?

A

failure of complete closure of anterior neural tube

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34
Q

What is an encephalocele?

A

herniation of meninges with or without brain tissue through a skull defect

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35
Q

Where do encephaloceles occur?

A

75% occipital; 90% midline; can also occur in the frontal, parietal or nasopharyngeal regions

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36
Q

What is the expected result of an encepholocele on the maternal alpha-fetoprotein level?

A

normal levels; lesion is covered by skin; only elevated in 3% of cases

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37
Q

How should an encephalocele be managed?

A

detailed maternal and family history, genetics consultation, surgery consultation (involved prior to delivery if known) and examination for associated anomalies

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38
Q

What is the percentage of comorbid anomalies associated with an encepholocele?

A

60%

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39
Q

What is the prognosis with an encephalocele?

A

depends on size, involved brain tissue and additional associated anomalies

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40
Q

What is the most common NTD?

A

spina bifida

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41
Q

What is the physiologic mechanism that causes spina bifida?

A

failure of the caudal neuropore to close

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42
Q

What are the three types of spina bifida?

A

1) spina bifida occulta
2) meningocele
3) myelomeningocele

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43
Q

What percentage of the population has spina bifida?

A

10-20%; most people are dx incidentally from a spinal xray

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44
Q

what is spina bifida occulta?

A

Spina bifida occulta is the mildest type of spina bifida. It is sometimes called “hidden” spina bifida. With it, there is a small gap in the spine, but no opening or sac on the back. The spinal cord and the nerves usually are normal. Usually doesn’t cause disabilities.

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45
Q

How does skin present with at the site of a spina bifida occulta lesion?

A

may be normal, hair tuft, skin dimple, hemangioma, lipoma or birth mark

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46
Q

What is a meningocele?

A

only involves the meninges bulging through the defect in the spinal column

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47
Q

What is a myelomeningocele?

A

herniation of meninges and nerve tissue through a defect in the spinal column

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48
Q

Where do myelomeningoceles most commonly present?

A

lumbo-sacral (75%)

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49
Q

What is the expect degree of paralysis with a myelomeningocele diagnosis?

A

depends on the level of the defect

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50
Q

What conditions are typically comorbid with a myelomeningocele?

A

Chiari malformation (90%) and hydrocephalus (84%)

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51
Q

How is a myelomeningocele diagnosed prenatally?

A

elevated AFP and US at 14-16 weeks GA

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52
Q

What considerations should be observed for the management of a myelomeningocele in the DR?

A

keep the area sterile; use non latex gloves (minimize the risk of latex sensitization); prevent heat loss, decrease pressure by maintaining infant in lateral or prone position; keep site moist

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53
Q

How should a myelomeningocele be managed?

A

look for other anomalies, HUS (hydrocephalus) and renal US (structural anomalies), multidisciplinary team, surgical repair, support family, genetics, treatment of hydrocephalus

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54
Q

When should fetal surgery occur for primary closure of a myelomeningocele in utero?

A

between 18-25 weeks

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55
Q

What are the results of primary closure in utero of a myelomeningocele?

A

1) reduced the risk of death and need for shunt placement during the first yr of life
2) improvement in a composite score for mental development and motor fx at 30 months of age

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56
Q

What is the prognosis of infants born with a myelomeningocele?

A

14% will not survive past 5 years; mortality of 35% in infants with brain stem dysfunction

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57
Q

Describe the ventricular system of the brain.

A

2 lateral ventricles that have a frontal and occiptal horn, the lateral ventricles open to the 3rd ventricle by the foramen of monroe. the 3rd ventricle is midlined and opens into the fourth ventricle through the acqueduct of Sylvius. The 4th ventricle will open into the subarachnoid space through the foramen of Luschke and magendie

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58
Q

What is the typical volume of CSF in term newborns?

A

50mL

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59
Q

What is the range of normal pressure within a newborn’s ventricular system?

A

8-10cm H2O

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60
Q

What is the rate of CSF production in a term neonate?

A

500 mL/day

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61
Q

Where is CSF produced?

A

by the choroid plexus which is present all of the ventricular system except the frontal and occipital horn of the lateral ventricles and the acqueduct system

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62
Q

How is CSF reabsorbed?

A

CSF will be absorbed with the arachnoid villi and enter the dural venous sinuses and returns to the vascular and lymphatic systems

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63
Q

What can cause anomalies in CSF flow?

A

) an imbalance to CSF inflow or outflow

2) obstruction to flow
3) barriers to reabsorption
4) inadequate production

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64
Q

What is hydrocephalus?

A

excessive accumulation of CSF either due to over production or failure of reabsorption

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65
Q

What are the 2 types of hydrocephalus?

A

communicating and non-communicating; either type can be congenital or acquired; other forms include hydrocephalus ex-vacuo and normal pressure hydrocephalus (affecting adults)

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66
Q

What is hydrocephalus ex-vacuo?

A

damage to the brain caused by traumatic stroke or injury

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67
Q

What is the clinical presentation of hydrocephalus?

A
  • rapid increase in OFC, bulging AF, separated sutures
  • apnea and bradycardia
  • lethargy
  • abnormal eye movement (restricted upward gaze)
68
Q

What are possible etiologies of non-communicating hydrocephalus?

A

1) post-hemorrhagic (most common- especially in preterm)
2) aqueduct stenosis (1/3 of cases); caused by viral infx (torch), autosomal recessive, x-linked defects
3) dandy walker (5-10%)

69
Q

What are possible etiologies of communicating hydrocephalus?

A

1) IVH
2) Arnold Chiari malformation
3) Lissencephaly
4) encephalocele
5) leptomeningeal inflammation
6) choroid plexus papilloma (overproduction)

70
Q

What is an Arnold-Chiari Malformation?

A

structural anomaly of the hind brain affecting the stx relationship of the cerebllum, the brain stem, the upper cervical and the posterior cranial fossa; resulting herniation of the cerebellar vermis through the foramen of magna

71
Q

What is type I Arnold- Chiari Malformation?

A

caudal displacement of cerebellar tonsil

72
Q

What is type II Arnold- Chiari Malformation?

A

elongation and displacement of cerebellar tonsils, 4th ventricle and medulla; also may p/w a lumbo-sacral myelomeningocele; collectively leading to hydrocephalus

73
Q

What is type III Arnold- Chiari Malformation?

A

displacement of cerebellum and lower brainstem in sac; may p/w occipital encephalocele; may also lead to hydrocephalus

74
Q

What features make up dandy walker?

A

a congenital malformation of the cerebellum

1) cystic dilation of the 4th ventricle
2) cerebellar vermis hypoplasia or aplasia
3) hydrocephalus (75%)

75
Q

How is hydrocephalus managed?

A

detailed history, evaluation for other anomalies, genetics evaluation, TORCH titer, urine CMV, fundal exam for chorio, MRI/CT and VP shunt if indicated

76
Q

What is microcephaly?

A

OFC < 3rd percentile for sex and GA; or 2 stnd deviations below the mean for sex and GA

77
Q

Why might an OFC on admission be unreliable?

A

OFC in the first 2-3d may ∆ because of molding, a caput or a cephalohematoma; OFC measurements should be serial

78
Q

When can microcephaly present?

A

may be present at birth or it may develop in the first few years of life

79
Q

What is primary microcephaly?

A

brain is small and never formed properly; usually an effect of a genetic or chromosomal anomaly

80
Q

What is secondary microcephaly?

A

brain was forming normally but a disease process impaired growth; will have a normal OFC at birth followed by a failure to grow

81
Q

What are possible etiologies of primary microcephaly?

A

1) genetic & chromosomal disorders- majority
2) defective neurulation
3) encephalocele
4) agenesis of the corpus callosum
5) holoprosencephaly
6) defective cellular migration

82
Q

What are possible etiologies of secondary microcephaly?

A

1) infections: TORCH- majority
2) teratogen exposure: ETOH, hydantoin, cocaine/stimulants
3) maternal PKU
4) metabolic disorders
5) vascular perinatal brain injuries, stroke
6) HIE
7) ICH

83
Q

What is the effect of cocaine and stimulants such as meth and amphetamines on the fetus?

A

potent vasoconstrictors

84
Q

What is the clinical presentation of primary microcephaly?

A

small head with backward sloping of the forehead; small OFC at birth

85
Q

What is the clinical presentation of secondary microcephaly?

A

perinatal brain damage does not cause a recognizeable decrease of OFC until 3-6 months of age

86
Q

What are the outcomes of microcephaly?

A

depends on the severity and cause; developmental delays

87
Q

When should evaluation of microcephaly begin?

A

when there is 1 OFC that fits the parameters or serial measurements that demonstrate a progressive decrease in head size

88
Q

How should microcephaly be managed?

A
  • thorough history
  • physical exam
  • signs of metabolic dz
  • maternal and fetal phenylalanine level
  • torch titer and urine CMV
  • neuroimaging
  • consultations: clinical genetics, peds neuro, radiology, early intervention programs
89
Q

What are the 4 most commonly presenting ICHs in the NI?

A

1) Subdural hemorrhage
2) Subarachnoid hemorrhage (most common in term)
3) Germinal matrix, intraventricular hemorrhage (most common in preterm)
4) Intraparenchymal hemorrhage

90
Q

What is the typical population of GMH/IVH?

A

premature infants; 15-20% PT <32 weeks GA

91
Q

When do GMH/IVH occur in postnatal life?

A

critical period in within first 72 hours; 90% of cases will occur within first 7 dol

92
Q

What are the primary etiologic factors for GMH/IVH?

A

varies with GA, birth asphyxia and birth trauma (and also in combination) are the primary causes

93
Q

What makes GMH/IVH unique to the PT babe?

A

subependymal germinal matrix- very vascularized region, blood vessels are fragile and lack of supporting structural elements- vulnerable to hemorrhage secondary to hypoxic ischemic event, metabolic and BP ∆.

94
Q

Why is the subependymal germinal matrix less of a threat to FT infants?

A

the SE germinal matrix will physiologically involute in the last trimester and is absent in term infants

95
Q

What are risk factors for GMH/IVH?

A
  • PREMATURITY
  • asphyxia
  • BP swings
  • respiratory distress
  • pneumothorax
  • Sz
  • hypercarbia
  • coagulopathies
  • hyperosmolar solutions (ex: NaHCO3)
96
Q

Why is hypercarbia a risk factor for IVH?

A

hypercarbia causes cerebral vasodilation and increases risk for bleeding

97
Q

What is the clinical presentation for GMH/IVH?

A
  • 50% of pts are asymptomatic
  • apnea spells
  • irritability/ lethargy
  • Sz
  • full AF
    in G3 and G4:
  • shock
  • anemia
  • metabolic acidosis
  • hyperglycemia
98
Q

What is a Grade I IVH?

A

subependymal germinal matrix hemorrhage only

99
Q

What is a Grade II IVH?

A

GMH with bleeding in normal sized ventricles

100
Q

What is a Grade III IVH?

A

GMH with bleeding into dilated ventricles

101
Q

What is a Grade IV IVH?

A

GMH with bleeding into dilated ventricles and involevement of adjacent brain parenchyma

102
Q

What is the prognosis of Grade 3 & 4 IVH?

A

poor neurodevelopment; high rates with periventricular hemorrhagic infarction and PVL: have mortality rate up to 50% and neurologic sequelae in up to 90%

103
Q

How is GMH/ IVH diagnosed?

A

with serial HUS

104
Q

What can be visualized with a HUS in the sagittal section?

A

looking at one ventricle at a time

105
Q

What can be visualized with a HUS in the coronal section?

A

ventricles on both sides and the septum

106
Q

How can GMH/IVH be prevented?

A
  • prevent PTL
  • in-utero transfer
  • antenatal steroids (protective)
  • prompt resuscitation
  • minimal handling of the infant
  • slow infusion of colloid and hyperosmolar solutions
  • avoid BP swings
107
Q

What supportive care should be offered to infants with known GMH/IVH?

A

correct anemia, acidosis, hyperglycemia, ventilation, resp support

108
Q

Why are f/u HUS and OFCs indicated for known GMH/IVH patients?

A

for prevention of hydrocephalus

109
Q

When might post-hemorrhagic ventricular dilation occur?

A

days to weeks after IVH; not all dilation will progress to hydrocephalus

110
Q

How does communicating hydrocephalus progress into post-hemorrhagic ventricular dilation?

A

impaired reabsorption of CSF

111
Q

How does non-communicating hydrocephalus progress into post-hemorrhagic ventricular dilation?

A

obstruction along CSF pathway by blood clot

112
Q

How is post-hemorrhagic ventricular dilation treated?

A

serial LPs when the baby is symptomatic and there are rapidly enlarging ventricles; tap will show increased protein and RBCs

113
Q

When is an external reservoir an indicated treatment for post-hemorrhagic ventricular dilation?

A

permits serial tapping and testing of CSF; when the infant is too small for surgery

114
Q

What is PVL?

A

white matter injury which is characterized by necrosis of white matter lateral to the ventricles

115
Q

What is the etiology of PVL?

A

results from inadequate cerebral perfusion at the periventricular watershed areas of deep penetrating arteries of the middle cerebral arteries leading to necrosis; direct result from hypotension and ischemia

116
Q

How common is PVL?

A

most common ischemic brain injury in PT babes; 3-5% of infants < 1500g

117
Q

What are the risk factors for PVL?

A
  • hypoxia, ischemia, acidosis
  • hypotension
  • hypocarbia
  • sepsis, Sz, meningitis, IVH, cardiorespiratory arrest or apnea
  • maternal chorioamnionitis
  • maternal cocaine or other stimulants
118
Q

What is the result of profound hypocarbia?

A

severe vasoconstriction

119
Q

What is the clinical presentation of PVL in the neonate?

A

asymptomatic in the neonatal period; first sign is on HUS of increased echodensities in the periventricular areas; f/u in 3-4 weeks may see cystic lesions

120
Q

What are the potential outcomes of PVL?

A

CP, developmental delay, visual impairments, auditory impairments

121
Q

What is a subdural hemorrhage?

A

least common ICH; rupture of draining veins and sinuses of the brain in the subdural space

122
Q

What is the cause of a subdural hemorrhage?

A

most commonly a result of birth trauma in the FT infant; small SDH may be fairly common in uncomplicated deliveries

123
Q

What are risk factors for SDH?

A
  • large fetal head (cephalic/pelvic disproportion)
  • rigid pelvic structures
  • non-vertex presentation; breech, face
  • rapid or prolonged labor or delivery
  • difficult instrumental delivery
124
Q

What is the typical presentation for a large vein SDH?

A

presents shortly after birth; evolves rapidly, signs of meningal irritation (nuchal rigidity, opisthotonus, coma, apnea), unreactive pupils, abnormal extraocular movements, anemia, hypovolemia and shock

125
Q

What is the typical presentation for a small vein SDH?

A

few signs for up to 1 weeks, neurologic signs or hydrocephalus appears when hematoma attains critical size, Sz (in 50%), irritability, mild disturbance in consciousness

126
Q

What is typically found in the labor history for an infant with a SDH?

A

difficult labor, instrument assisted delivery (forceps)

127
Q

what actions are indicated in the evaluation of a SDH?

A

No LP until after CT; small SDH- LP should be performed to r/o infx (meningitis)

128
Q

How should a SDH be managed?

A
  • evaluate for sepsis and bleeding diasthesis, supportive care, anticonvulsants, Large SDH: volume replacement, pressors, respiratory support, urgent CT for evidence of ICP, neurosurg consult (evacuation and managment; most infants don’t need surgery); monitor for hydrocephalus
129
Q

What is a chronic SD effusion?

A

develops over months, abnormally rapid head growth in the first weeks or months after birth

130
Q

what is the prognosis for SDH?

A

good prognosis in: non surgical SDH, no significant neurologic injury, successful prompt surgical evacuation, no parenchymal injury

131
Q

What is the pathophysiology for a subarachnoid hemorrhage?

A

rupture of bridging veins in the SA space; birth trauma; common in term infants

132
Q

What is the clinical presentation of an infant with a subarachnoid hemorrhage?

A

asymptomatic, anemia, sz, irritability, lethargy, characteristic presentation: infant appears well bw Sz

133
Q

How is a subarachnoid hemorrhage diagnosed?

A

CT scan or MRI, LP to r/o meningitis; will show RBCs

134
Q

What is the typical outcome for an infant with subarachnoid hemorrhage?

A

good; long-term sequelae uncommon, occasional hydrocephalus will develop in the event of a large bleed

135
Q

How are seizures unique in the neonatal population?

A

common, subtle, difficult to diagnosis, a/w possible risk of neurodevelopmental disability; sign of potential brain disorder; requires immediate investigation

136
Q

what should Sz in the neonate be considered?

A

the first sign of neurologic dysfunction; powerful predictors of long-term cognitive and developmental impairment

137
Q

What is the incidence of Sz in neonates?

A

1.5-3 per 1000 FT babes; 30-60 in 1000 PT babes (< 1500 g); 80% occur in the first week of life

138
Q

Why do many dz result in sz in the neonate?

A

because the brain has a transient overdevelopment of excitatory systems compared to the inhibitory systems

139
Q

What is the etiology of sz in the newborn?

A

most common: HIE (25-40%), stroke (15-25%) & ICH (10%); also: infx, metabolic disorders (Ca, Na, Glucose, inborn error), CNS malformations, NAS, & the rare benign familial neonatal sz

140
Q

What is characteristic of sz in the newborn?

A

not well-organized; can be focal, multifocal or generalized; lack of myelination and incomplete formation of dendrites and synapses in the brain will impede generalized sz

141
Q

What are silent sz?

A

electroclinical dissociation sz on EEG, but no clinical presentationl happens with severe brain damage or after starting anticonvulsant therapy

142
Q

What type of sz is the most common in the neonate?

A

subtle sz

143
Q

What is the clinical presentation of a subtle sz?

A
  • eye deviations, eyelid fluttering, staring
  • lip smacking, sucking, tongue thrusting, chewing
  • pedaling/ cycling, rowing movements
  • autonomic phenomena: tachycardia, apnea or BP fluctuations, sudden ∆ in skin color
144
Q

what are typical muscle actions indicative of clonic sz activity?

A

rhythmic biphasic with a fast contraction phase and a slower relaxation phase

145
Q

What is the presentation of focal clonic sz?

A

well localized rhythmic twitching of the face, upper and/or lower extremities on one side of the body; as seen with neonatal stroke

146
Q

What is the presentation of multifocal clonic sz?

A

clonic movement that migrates from one extremity to another with a specific pattern

147
Q

What is the presentation of generalized clonic sz?

A

extremely rare in the newborn; also seen in benign familial neonatal sz

148
Q

what are typical muscle actions indicative of tonic sz activity?

A

sustained period of muscle contraction without repetitive features (posturing)

149
Q

What is the prognosis of tonic sz?

A

very poor; can be focal or generalized

150
Q

in what population are tonic sz most common?

A

PT infants with IVH or diffuse neurologic dysfx

151
Q

what are typical muscle actions indicative of myoclonic sz activity?

A

brief, spasmodic fast ctx and relaxation of the muscles of the trunk or one or more limbs, non-rhythmic; indicate diffuse brain dysfunction

152
Q

what are typical muscle actions indicative of focal myoclonic sz activity?

A

involves the flexor muscles of an upper extremitiy

153
Q

what are typical muscle actions indicative of multifocal myoclonic sz activity?

A

nonsynchronus with switching of several body parts

154
Q

what are typical muscle actions indicative of generalized myoclonic sz activity?

A

BL jerks of upper and sometimes lower extremities

155
Q

What is included in the differential diagnosis as seizure mimicks?

A
  • jitteriness
  • apnea
  • benign neonatal sleep myoclonus (dx of exclusion)
156
Q

What symptoms are indicative of sz activity?

A

1) rarely stimulus sensitive
2) not abolished by passive restraint
3) associated with autonomic ∆ or ocular phenomena

157
Q

What symptoms are indicative of jitteriness?

A

1) rapid, rhythmic, alternating movement of equal rate and amplitude
2) can be blocked by passive flexion or immobilization
3) not accompanied by ocular or autonomic phenomena
4) can be induced

158
Q

What is characteristic of benign neonatal sleep myoclonus?

A
  • repetitive myoclonic jerks
  • REM sleep
  • stop abruptly when the child is aroused
  • more in PT babes
  • occur from birth to 6 mos
  • not stimulus sensitive
  • normal EEG
159
Q

How are sz diagnosed?

A
  • difficult to dx
  • electroclinical dissociation (subclinical)
  • infx
  • treatable metabolic, genetic or symptomatic causes need to be identified
  • electrolyte disturbances
  • hypoglycemia
  • imaging: HUS, CT/MRI, EEG
160
Q

What is indicated in the acute management of sz?

A
  • ABC
  • est IV access
  • correct Ca, Mg, glucose
  • anticonvulsant medication
  • pyriodoxine dependency
  • folinic acid: refractory sz, folinic acid tril is warranted for 24-48h
161
Q

What is the first line anticonvulsant agent?

A

phenobarbital: loading dose of 20mg/kg (can be repeated up to 40mg/kg); maintenance 5mg/kg/d- need levels

162
Q

What is the second line anticonvulsant agent?

A

phenytoin (dilantin); combination of phenytoin and phenobarb can control sz in 85% of babes

163
Q

what medications are indicated for refractory sz?

A

benzodiazepine (lorazepam- ativan is preferred) and Levetiracetam (Keppra)

164
Q

Why is Keppra emerging as a promising drug in this population?

A

safety; no evidence of drug interaction, no evidence of neuroapoptosis and provides neuroprotection

165
Q

what is the prognosis for an infant with sz?

A

depends on etiology, severity and GA; survival 85%, adverse outcomes in 50%; DOES NOT NECESSARILY RESULT IN EPILEPSY

166
Q

What is indicative of a good prognosis with neonatal sz?

A

normal EEG tracings bw sz; clinical return to baseline bw sz

167
Q

What is indicative of a poor prognosis with neonatal

A 
PT < 32 weeks
IVH
Cerebral malformations
generalized tonic or myoclonic sz
associated anomalies

Neonatal Pathophysiology (17 decks)

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