Occurs within the first month of life
neural tube is formed
closure of the neural to gives rise to the central nervous system, including the cranial nerves
this evolution results in the formation of the skull and vertebrae
in accuracy resultant anencephal
Primary neurulation
Peak development is in the second and third months of gestation
influences the formation of the face, forebrain, corpus callosum, optic nerves, thalamus and hypothalamus, and the cerebral hemispheres
disturbances can cause holoproencephaly, midline and mi
Prosencephalic development
Occurs between three and four months
toxins inherited diseases can significantly alter the number of neurons
chemical and environmental substances can reduce the number of neurons
Proliferation of the neurons
Can occur as early as two months
by six months neurons have migrated to the final permanent place
migration is critical for the development of cerebral cortex and deeper nuclear structures
Neuron migration
Primary neurulation: 3 to 4 weeks of gestation
Prosenphalic development: 2 to 3 months gestation
Neuronal proliferation: 3 to 4 months gestation
neuronal migration: 3 to 5 months gestation
organization: five months of gestation to years postnatal
myelinat
Major events in brain development and peak times of occurrence
Promotes integrative muscle function
maintains balance
enable smooth purposeful movements
Cerebellum
Contains four lobes: frontal, parietal, occipital common and temporal
frontal lobes make up the command center concerned with decision-making
parietal lobes are responsible for hearing understanding speech and forming integrated sense of self
occipital lo
Cerebrum
Fiber bundles connecting the cerebral hemispheres
Corpus callosum
Encompasses the mind and intellect
gray matter
Cerebral cortex
Integrate sensory input
Thalamus
Regulates body temperature
Hypothalamus
Relays input and output signals between higher brain centers and the spinal cord
three main components:
Medull Oblongata -a implicated within cranial nerves eight, nine, 10, 11, and 12. Controls areas of the abdomen and thorax throat and mouth.
Pons: carr
Brainstem
Cerebral metabolism is influenced by availability of glucose and oxygen
glucose is transported from the blood to the brain by a glucose transporter founding capillaries
serum glucose provides the brain with a glucose pool
neonatal brain is glucose depende
Glucose metabolism in the brain
Cerebral blood flow is affected by pH, potassium, hypoxemia, osmolarity, and calcium ion concentrations.
The brain increases blood flow to spare itself inadequacies
as pH decreases cerebral blood flow increases
as potassium levels increased cerebral blood
Cerebral blood flow
Cerebral blood flow over a broad range of perfusion pressures
cerebral blood flow increases with advancing gestational age and metabolic demands
normal or Terrier blood pressure in the preterm neonate is thought to be near or at the lower auto regulatory
auto-regulation of cerebral blood flow
Ischemia damages blood vessels and surrounding elements supporting blood vessels
blood flow to cerebral white matter restored only after reperfusion of other brain regions once adequate blood supply resumes, hemorrhage can occur into ischemic areas.
Hyper
Hypotension leads to ischemia
Preterm infants: open extended reflecting reflecting diminishing tone
term infants: flex position reflecting adequate tone
Abnormal findings are: hyperextension, asymmetry, flacidity
Neurologic assessment: posture
Consider meningitis, drug withdrawal, neurologic abnormalities
Neurologic assessment:High-pitched cry
Consider vocal cord damage or paralysis
Neurologic assessment:Strider
Six or more lesions of greater than 1.5 cm; may indicate neurofibromatosis.
Neurologic assessment: Caf� au lait spots
Consider Stern Weber syndrome
Neurologic assessment: port wine facial hemangioma
Checks goal size, shape, symmetry, here worlds, fontanelle's, and sutures
measure OFC
examine phase for abnormalities in structure
examine spine intact, opening, masses
assess cranial nerve function
assess muscle tone
assess reflexes
Physical examination the neurologic system
Consider clavicular or humoral fracture or brachial nerve plexus
Abnormal moro reflex
Risk factors talk to be due to a combination of genetic and environmental influences
risk appears to be with low socioeconomic status and history of affected siblings
more common in whites
common in females
Anencephaly
Failure of anterior neural to closure
malfunction of the first stage of neurologic development
most commonly involves the forebrain and variable amounts of upper brainstem
partial absence of skull bones, with absent cerebrum and with or without missing ce
Pathophysiology of anencephaly
Expose nerve tissue with little definable structure
anomalous skull has brought like appearance
amniotic fluid reveals high levels of alpha fetal protein late in first trimester
Clinical presentation of anencephaly
Provide comfort measures
genetic counseling
support the grieving process
encourage the family to see their baby because of imaginary impressions may be worse than reality
maintain delicate balance between benefit and harm
Patient care management of anencephaly
Occipital frontal circumference greater than two standard deviations below the mean for age and gender
small brain implies neurologic impairment
Microcephaly
Maternal
Viral inflections including toxoplasmosis syphilis rubella CMv and herpes
exposure to radiation
diabetes
prescription and street drugs in first trimester
genetic autosomal recessive autosomal dominant X linked
malnutrition
Fetal:
perinatal insult
Risk factors for microcephaly
Clinical presentation of microcephaly
Small head small head, backward sloping of the four head, small cranial volume
neurologic deficits rarely evident at birth
Patient care management are microcephaly
Record accurate OFC, length, weight
note percentiles an alert physician to abnormalities
document clearly any deviations from normal
obtain test as ordered
ensure families informed
obtained genetics and infectious disease consultations
Hydrocephalus
Excess cerebrospinal fluid in the ventricles of the brain due to decrease in reabsorption or overproduction
CSF is produced from the brain parenchyma, cerebral ventricles, areas along the spinal cord, and the choroid plexus (70% is from the choroid plexus
Pathophysiology of hydrocephalus
Excessive CSF production is rare
inadequate CSF absorption secondary to abnormal circulation
excess CSF secondary to outflow obstruction
Risk factors for congenital hydrocephalus
Aqueduct stenosis
dandy-Walker cyst
myelomeningocele
congenital masses and tumors
congenital infection: toxoplasmosis, CMV
Clinical presentation of hydrocephalus
Large head
wide sutures
bulging fontanelle
Increasing OFC
Patient care for hydrocephalus
Intrauterine diagnosis/more options
perform thorough physical exam for other anomalies
obtain neurosurgery and genetics consult
consider possible need for reservoir placement
decreased stimulation
position had carefully water pillow beds diminish skin bre
Signs of infection or blocked shot
Irritability, vomiting, increased head size, lethargy, changes in feeding patterns, bulging fontanelle
post-hemorrhagic hydrocephalus
Progressive dilation of the ventricles after IVH
acute: rapidly appears within days of initial IVH; probably occurs secondary to malabsorption of CSF secondary to a blood clot
Subacute: inhibition of CSF flow; blood from IVH
Clinical presentation of post-hemorrhagic hydrocephalus
Insidious following mild ventricular dilation
may be profound following severe ventricular dilation
rapid increase in head size
episodic apnea and bradycardia
lethargy
increased ICP
tense bulging interior fontanelle
cranial suture separating
ocular moveme
Patient care management of post hemorrhagic Hydrocephalus
Daily OFC
serial cranial ultrasound
neuro consult
serial lumbar punctures
Lasix
observed for signs of increasing ICP
support family
Myelomeningocele
a congenital defect of the central nervous system in which a sac containing part of the spinal cord and its meninges protrude through a gap in the vertebral column
Arnold - Chiari malformations
Hindbrain malformation with or without aqueduct built atresia
although most always present with Meylomeningocele
hydrocephalus present in 70%
common futures include reflux and aspiration, laryngeal stridor, central hypoventilation
Clinical presentation of myelomeningocele
The majority of cases occur in the lumbar in lumbosacral regions
herniated sack, sealed or leaking, protrudes from the back
defects include vascular network surrounding abnormal neural tissue
most lesions have incomplete scan coverage
Patient care management for myelomeningocele
Examined lesion
culture specimen if sack is open
rap lesion with sterile gauze moistened with warm sterile saline
immediate consultation with neurosurgery and urology
perform thorough physical exam to assess level of injury
encourage open discussion among
Encephaolcele
Neural herniation
may or may not contain brain
risk factors may be environmental or genetic or multifactorial
presents with protruding midline skin covered sack from head or base of neck
majority of sacks occur in the occipital region
Cephalohematoma
Does not extend across the suture lines
usually unilateral
Clinical presentation of cephalohematoma
Enlarges during the first few days after birth
feels firm
does not transilluminate
Patient care for cephalohematoma
Provide supportive care to the family
watch for hyperbilirubinemia
if sudden enlargement occurs question infection
educate family
A bony calcified ring may develop; usually disappears within six months
usually takes two weeks to three months to resolve
es
Caput succedaneum
Hemorrhagic the Dema Crossing cranial suture lines
commonly seen after vaginal birth
evident at birth
does not grew in size after birth
new treatment is given to educate and counsel the family
subgaleal hemorrhage
Hemorrhage beneath the scalp into loose connective tissue below
possible entry of blood into the subcutaneous tissue of the neck
hematoma may cross suture lines if insufficient quantities to lead to exsangunation of the infant
Usually associated with diff
Clinical presentation of subgaleal hemorrhage
History of fetal distress noted in 50% of cases
often fluctuate mass scalp
may increase in size
hypotonia, pallor, or lethargy, seizures
falling hematocrit
Patient management far subgaleal hemorrhage
Rapid diagnosis and blood replacement is key to management blood transfusions observed for hyperbilirubinemia
Brachial nerve plexus injury
Caused by excessive stretching of the brachial plexus during delivery
Erb palsy risk factors include multiples, prolonged labor, LGA, shoulder dystocia
Erb palsy
Affected arm is abducted and internally rotated
elbows extended with warm pronation and wrist flexion (waiters tip position)
asymmetric Moro reflex
Klumpke paralysis
Swelling in shoulder and supraclavicular fossa, clavicle may be broken
involves intrinsic muscles of the hand, with a clawl-and malformation
no grasp ineffective hand
Management of brachial nerve plexus
Obtain euro consult
primary goal to avoid contractures of the joints, passive range of motion, exercise the arm, physical therapy consult
Subdural hemorrhageSubdural hemorrhage
Due to laceration of the major veins and silences, usually associated with tear of the dura overlying the cerebral hemispheres
occurs both in term and preterm infants
occurs with or without laceration of the dura
Pathophysiology of subdural hemorrhage
C excessive vertical molding and frontal occipital elongation, for oblique expansion of the head results in stretching venous sinuses are stretched with possible rupture of the vein of Galen
Clinical presentation of subdural hemorrhage
Decreased LOC
seizure activity
asymmetry of motor function
often minimal to no clinical symptoms for first 24 hours due to slowly enlarging hematoma
O'Day to go three signs of increasing ICP
Signs of brainstem disturbance
Dilated, poorly reactive pupil on the same side as hemorrhage
respiratory abnormalities,
dolls as reflect
poor prognosis mortality 45%
Subarachnoid hemorrhage
And intracranial hemorrhage into the CSF filled space between the arachnoid and pial membranes
Intraventricular hemorrhage
Occurs once germinal matrix hemorrhage extends into lateral ventricles
risk factors include prematurity increasing arterial blood pressure internal general anesthesia low five-minute Apgar asphyxia and many others
Great one IVH
Often localized at the foramen of Monro
Great 2 IVH
Partial filling of lateral ventricles without that ventricular dilation
Great three IVH
Intraventricular hemorrhage with ventricular dilation
Grade 4 IVH
Involvement or extension of blood into the cerebral tissue itself
Morbidity of IVH
Correlation between severity or extent of involvement in subsequent impairment is not absolute
Clinical presentation of IVH
Sudden deterioration
oxygen desaturation
bradycardia
metabolic acidosis
significant decrease in hematocrit the
hypotonia
shock
hyperglycemia
tense anterior fontanelle
seizure activity
apnea
decreased LOC
When is the optimal time to screen for IVH?
7 to 10 days of age because 90% of all hemorrhages have occurred.
If test is normal no need to recheck
if test is positive for IVH repeat testing two weeks
serial cranial ultrasound
Patient care management for IVH
Prevent preterm birth provide efficient expedient intubation
minimal stimulation
avoid wide swings in arterial and venous pressure
avoid over ventilation
educate and support parents
Seizures
Symptom of neurologic dysfunction not a disease
Seizures result from excessive simultaneous electrical discharge of neurons
Risk factors for seizures
Decreased production of ATP
ischemia
hypoxia
hypoglycemia
hyponatremia or hypernatremia
hypocalcemia hypomanic knees anemia
inborn errors of metabolism IVH
hypoxic ischemic encephalopathy
group beta strep E. coli and listeria
withdrawal from maternal drug
Clinical presentation seizures
Subtle seizures Most frequently neonates, often unrecognized.
Presentation varies:1 horizontal deviation of the eyes. 2 peddling movements. 3 Rollings, stepping movements. 4 blanking or fluttering of eyes. 5 new nonnutritive sucking. 6 smacking of lips. 7
Physical exam procedures
Rule out jitteriness
characterized by trembling hands and feet
no involvement of eye movements
stopped by gentle, passive flexion of extremityThat
patient care management or seizures
Determine underlying etiology
necessitate
diagnostic studies
phenobarbital loading dose 20 mg per kilogram slow IV push for 10 to 15 minutes; make this dose 3 mg per kilograms per day beginning 12 to 24 hours after loading dose; therapeutic range 15 to 30
Periventricular Luke of Malaysia
Ischemic, necrotic periventricular white matter
principally ischemic lesion of arterial origin
multi- cystic encephalon Malaysia with or without secondary hemorrhage into ischemic area
Pathophysiology of Pvl
Systemic hypertension severe enough to impair cerebral blood flow
occurrence of focal cerebral infarction in cerebral ischemia
major systemic hypertension
episodes of apnea bradycardia
Clinical presentation of PVL
Acute phase hypertension and lethargy
6 to 10 weeks later: irritable hypertonic increase flexion of arms, frequent tremors and startles, abnormal Moro
Meningitis
Infection of the CNS
early onset infection from pathogens in vaginal flora GBS and E. coli
late onset from environmental microbes found in nursery
Risk factors for meningitis
Maternal infection
prolonged rupture of membranes
prematurity insert text
Clinical presentation of meningitis: congenital viral infection
Preterm delivery
low birth weight
blueberry muffin rash
inflammation
microcephaly
Clinical presentation of early onset bacterial meningitis
Shock in the first 24 hours
respiratory distress
hypertension
apnea
seizures
temperature instability
jaundice
Clinical presentation of late onset bacterial meningitis
Nonspecific symptoms
lethargy
feeding intolerance
irritability
posturing
temperature instability
apnea
nuchal rigidity
Patient care for meningitis
Initial antibiotic therapy: ampicillin or penicillin G
ampicillin and cefotaxime recommended for aminoglycoside resistant organisms
treatment 7 to 10 days for sepsis without focus minimum of 21 days for gram-negative meningitis
GBS = ampicillin are penici