neurological assessment and disorders
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Neurological Assessment and Disorders. Fetal Brain Development. The brain is one of the earliest organs formed during embryonic development Week 3 - beginning development of the brain, spinal cord, and heart - PowerPoint PPT PresentationTRANSCRIPT
Neurological Neurological AssessmentAssessment
andandDisordersDisorders
Fetal Brain DevelopmentFetal Brain Development The brain is one of the earliest organs formed during
embryonic development Week 3 - beginning development of the brain, spinal
cord, and heart Weeks 4 to 5 - formation of tissue that develops into
the vertebra and some other bones At 7weeks the medulla, pons, and midbrain is
formed By 9 wks, the fetus will display spontaneous mvmt 10 wks – begins to breathe 13 wks - sucking motions are made with the mouth 20 wks – responses to sound
NutritionNutrition Certain nutrients have a important roles in brain
development; some have greater impact than others Protein, fats, iron, zinc, iodine, vitamins A, B6
&K, folate Any nutrient deficit effect is dependent on
timing, doseand duration
Timing in terms of brain development process Timing in terms of prevalence of nutrient deficit in
population Little evidence currently for enhancement of brain
development in typically developing humans
Anatomy and Physiology of Anatomy and Physiology of the Brainthe Brain
Brain anatomy Composed of 2 major areas
Cerebellum Cerebrum
Anatomy and Physiology of Anatomy and Physiology of the Brainthe Brain
Cerebellum Promotes intregrative muscle function Maintains balance Enables smooth, purposeful movements
Anatomy and Physiology of Anatomy and Physiology of the Brainthe Brain
Cerebrum Central hemispheres with 4 lobes
Parietial Frontal Occipital Temporal
Corpus Callosum – fiber bundles connecting the cerebral hemispheres
Cerebral Cortex The ‘mind’, intellect Grey matter Third ventricle Thalamus (integrates sensory input) Hypothalamas (regulates body tempature)
Anatomy and Physiology of Anatomy and Physiology of the Neurological Systemthe Neurological System
Brain Anatomy Brain stem
Relays input and output signals between the higher brain and the spinal cord.
It has three main components The medulla, which controls areas of the abdomen,
thorax, neck, throat, and mouth, and is part of cranial nerves VIII, IX, X, XI, and XII
The pons, which carries information between the brainstem and cerebellum
The midbrain, which is involved in eye movements
Glucose Glucose Glucose metabolism
The neonatal brain is glucose dependent and the serum glucose provides the brain with a glucose pool.
The body preferentiallypreferentially pumps glucose against the gradient to the brain and cerebral metabolism is influenced by the availability of glucose and oxygen.
Anything that causes inadequate cerebral perfusion will compromise the glucose and oxygen supply to the brain.
Anaerobic metabolism causes lactic acid build-up and produces significantly smaller amounts of energy.
The premature infant has minimal-to-no glucogen stores and a less efficient glucose uptake mechanism.
Physiology of the Physiology of the Neurological SystemNeurological System
Cerebral blood flow Affected by pH, K, hypoxemia,
osmolarity,and Ca The brain will increase blood flow to spare
itself inadequate supply of oxygen and electrolytes.
Low pH, hypoxia, hyperkalemia, and increased osmolarity will cause an increase in cerebral blood flow.
Increased Ca ion causes a decrease in cerebral blood flow.
Physiology of the Physiology of the Neurological SystemNeurological System
Autoregulation Maintains a steady-state of cerebral blood flow
despite systemic blood pressure changes. Limited or impaired autoregulation exists in
premature or sick newborns. Without autoregulation systemic blood pressure
regulates cerebral perfusion. Hypotension will lead to ischemia, which
damages blood vessels, and surrounding tissues. When adequate blood supply resumes,
hemorrhage can occur into the ischemic areas. Hypertension without autoregulation will
increase cerebral flow rupturing blood vessels leading to hemorrhage
Neurological AssessmentNeurological Assessment
Determination of state, posture, and evaluation of
movements
ReflexesReflexes Assessment is based
on gestational age Reflexes
Root Suck (begins at
~32wks, intact by ~36wks)
Moro Tonic neck Grasp (very strong in
premmies) Babinski Hand- Mouth Others
The presence or absence of these reflexes are indicative of: Gestational age Neurological
abnormalities Progression of care
Neurological AssessmentNeurological Assessment
State Deep sleep, drowsy, quiet-alert, active, crying,
or active with stimulation Posture
Posture is determined by gestational age The more premature infant has extended, open
posture, reflecting diminished tone. The more term infant has flexed posture, reflecting
adequate tone Abnormal posture includes hyperextension,
asymmetry, and flaccidity.
Neurological AssessmentNeurological Assessment Evaluation of movements
Should be symmetrical with smooth, coordinated quality. Note if jittery or tremulous, or if seizure activity is present.
Respiratory activity is observed for any signs of distress or apnea.
Cranial nerve function assessment. Corneal reflex indicates intact cranial nerves V and
VII. An absent corneal reflex with tonic neck reflex present is associated with severe brain damage
Blink reflex requires intact cranial nerves III and VII. Tongue movement, suck, swallow, gag, and cry are regulated by cranial nerves IX, X, XII
Muscle tone: Evaluate head lag, ventral suspension, clonus and recoil from extension. Check symmetry and briskness vs. flaccidity
SeizuresSeizures
SeizuresSeizures
Result from excessive simultaneous electrical discharge or depolarization of neurons; can have many different causes. Metabolic: Due to ischemia, hypoxemia,
hypoglycemia, hypo- or hypernatremia, hypocalcemia, and hypomagnesemia.
Structural: Due to IVH, intrapartum trauma or hypoxic ischemic encephalopathy.
Intracerebral meningitis. Withdrawal from maternal drug use
IncidenceIncidence
Incidence of neonatal seizures in term vs preterm infants 1.5-3.0 per 1000 live term births 50-150 per 1000 live preterm births
Incidence as a function of birth weight 57.5 per l000 in infants < 1500 grams 2.8 per 1000 in infants 2500 to 3999 grams
IncidenceIncidence
Precise frequency is difficult to delineate Most of neonatal seizures we know is
based on clinical observation EEG monitoring with video recorder or
direct inspection showed Some clinical seizures do not have EEG
correlation Some electrographic seizures are not
accompanied by clinical seizures
HistoryHistory Family history may suggest genetic syndrome
Many of these syndromes are benign In the absence of other etiologies, family history
of seizures may suggest good prognosis Pregnancy history is important
Search for history that supports TORCH infections, history of fetal distress, preeclampsia or maternal infections
Apgar scores offer some guidance Low Apgar score without the need for
resuscitation and subsequent neonatal intensive care is unlikely to be associated with neonatal seizures
What are the causes of neonatal seizures ?What are the causes of neonatal seizures ?
Cause Frequency
Hypoxic-ischemic encephalopathyIntracranial hemorrhageCerebral infarctionCerebral malformationsMeningitis/septicemiaMetabolic Hypoglycemia Hypocalcemia, hypomagnesemia Hypo/Hypernatremia Inborn errors of metabolism Pyridoxine deficiency Kernicterus HyperammonemiaMaternal drug withdrawalIdiopathicBenign idiopathic neonatal seizuresNeonatal epileptic syndromesCongenital infectionsUnintentional injection of local anesthetic during laborMaternal vitamin D deficiency
30-53%7-17%6-17%3-17%2-14%
0.1-1.5%4-22%
3-4%
1%
4%2%1%
Clinical PresentationClinical Presentation
May be subtle tonic, multifocal, focal clonic, or myoclonic seizure activity
Subtle SeizuresSubtle Seizures Selected Major Manifestations
Ocular phenomena Tonic horizontal deviation of eyes with or without
jerking of eyes Sustained eye opening with ocular fixation
Oral-buccal-lingual movements Chewing, sucking, lip smacking
Limb movements Cycling, swimming, rowing
Autonomic phenomena Increase in blood pressure, brady/tachycardia
Apneic spells
Clonic SeizuresClonic Seizures
Usually involve one limb or one side of the body jerking rhythmically at 1-4 times per second
Focal Clonic Seizures Well localized clonic jerking Infant usually not unconscious
Multifocal Clonic Seizures Involves several parts of the body in
migrating fashion (non-ordered fashion) Simultaneous or in sequence
Focal and Multifocal Focal and Multifocal MyoclonicMyoclonic
Focal and Multifocal Myoclonic Seizures Well localized, single, multiple, migrating jerks
usually of limbs Usually not accompanied by EEG seizure
discharges Rare in neonates
Focal Typically involve flexor muscle of upper extremity Uncommon
Multifocal Asynchronous twitching of several parts of the
body Characteristic in full term infants with hypoxic
ischemic encephalopathy (HIE).
Tonic SeizuresTonic Seizures Characteristic of infants < 2500 gms and
seen with severe IVH Focal Tonic Seizures
Sustained posturing of limb Asymmetrical posturing of trunk and neck
Generalized Tonic Seizures Tonic extension of upper and lower limbs
(mimics decerebrate posturing) Tonic flexion of upper limbs and extension of
lower limbs (mimics decorticate posturing) Most are not accompanied by EEG seizure
discharges (only 30% have EEG correlates)
SeizuresSeizures Patient Care:
Positively identify movement as seizure activity by trying to stop movement with gentle passive flexion of the affected extremity
If the movement stops, it was not seizure activityIf the movement stops, it was not seizure activity Check lab work; electrolytes, glucose, ABG,
and septic work up. Administer Phenobarbital or Valium as
ordered. Monitor oxygenation and vital signs. During a
seizure, an infant’s blood pressure will rise, O2 saturation will drop, and CO2 will increase
Document carefully. Educate and support the family.
Jitteriness vs SeizureJitteriness vs SeizureClinical Feature Jitteriness Seizure
Abnormality of gaze or -- + eye movementMovements stimulus + --
sensitivePredominant movement Tremor
Clonic jerkingMovements cease with passive
flexion + --Autonomic changes -- +
Volpe JJ. Neonatal seizures. In: Neurology of the Newborn 1995
TreatmentTreatment Ensure adequate ventilation and perfusion If with hypoglycemia
Glucose 10% 2 ml/kg IV If without hypoglycemia
Anticonvulsant therapy (Phenobarbital) Etiology-Specific (as indicated)
Hypocalcemia (calcium gluconate 5% 4 ml/kg IV) Hypomagnesemia (MgSO4 50% 0.2 ml/kg IV) Pyridoxine deficiency (pyridoxine 50-100 mg IV) Meningitis (Ampicillin/Cefotaxime
Neurological DisordersNeurological Disorders
Microencephaly OFC is < 10% for gestational age It is caused by a neuronal proliferation
defect and occurs between 2 and 4 months gestation
The most severe cases occur in earlier gestation
Outcome is dependent on severity and may be associated with developmental delays
Neurological DisordersNeurological Disorders Anencephaly - absence of
neural tube closure exposing neural tissue Occurs as a malfunction in the
first state of neurological development,dorsal induction.
Infants lack brain above the brainstem and partial absence of skull bones with absent cerebrum.
May or may not lack cerebellum, brainstem and spinal cord.
Infants do not usually survive beyond the neonatal period.
Care includes comfort measures for the infant, and family support.
Encourage the family to see the infant and obtain genetic counseling for the family.
Neurological DisordersNeurological Disorders Hydrocephaly
Congenital hydrocephalus is excess cerebral spinal fluid (CSF) in the ventricles of the brain.
CSF is produced from the parenchyma, cerebral ventricles, areas along the spinal cord, and the choroids plexus
Excessive CSF production, inadequate CSF absorption, or obstruction in the outflow tract can all result in hydrocephalus
Infants have a large head, separated sutures, full and tense fontanelles, increasing OFC, sunset eyes (signifies brain tissue damage) and visible scalp veins
Neurological Disorders - Neurological Disorders - HydroencephalyHydroencephaly
Patient care Neurosurgery and
genetic consults Placement of VP shunt,
subgaleal shunt or reservoir
Careful positioning of the head using cushions to prevent skin break down
Normalize care as much as possible
Review shunt placement and care with parents
Post shunt placement Watch for signs of
infection or blocked shunt, such as irritability, vomiting, increased head circumference, lethargy.
Monitor for a change in feeding pattern.
Assess for full or bulging fontanelles.
Keep infant’s head off of the shunt site
Neurological DisordersNeurological Disorders Post-hemorrhagic hydrocephalus
The progressive dilatation of the ventricles following intraventricular hemorrhage (IVH).
Caused by periventricular white matter injury in the area of the germinal matrix.
Can be acute or chronic. Acute rapidly appears within days of the initial
bleed occurring secondary to malabsorption of CSF due to a clot in the ventricles.
Chronic is from inhibition of CSF flow or from blood from an ICH or pus from infection. The infants have a rapid increase in OFC, apnea, lethargy, increased intracranial pressure, and tense fontanelle, or may be asymptomatic. As progression occurs the signs of an acute bleed may become evident.
Neurological Disorders – Neurological Disorders – Post Hemorrhagic Post Hemorrhagic
HydrocephalusHydrocephalus Patient care:
Daily OFC. Serial head ultrasound. Neurosurgery consult Serial LP if indicated to
decrease ICP or medications to decrease CSF production, such as Lasix or Diamox. Infant may need a ventroperitoneal shunt placed if hydrocephalus does not resolve.
Observe for signs of increased intracranial pressure and hydrocephalus
Neurological DisordersNeurological Disorders Myelomeningocele
A neural tube defect that is a protrusion of the meninges lying directly under the skin, the internal surface of the spinal cord and or the nerve roots
It results from an error in dorsal induction The majority of cases occur in the thoracolumbar,
lumbar and lumbosacral regions. There may be a herniated sac protruding from
the back; it can be sealed or leaking It is usually associated with hydrocephalus or
Arnold-Chiari malformation, which involves some common features like reflux and aspiration, laryngeal stridor, central hypoventilation and apnea
MyelomeningoceleMyelomeningocele Pt CarePt Care
Examine and measure defect, note location and appearance.
Culture lesion of sac if open. Wrap the lesion with sterile gauze moistened with
warm NS. Keep the infant in a prone position; place drape over
the buttocks below the lesion to avoid contamination. Consult a neurosurgeon for surgical closure of defect
and a urologist to rule out neurogenic bladder Follow developed protocol
MyelomeningoceleMyelomeningocele
Most infants will have no significant mental retardation with varying degrees of paralysis of lower extremities. Lesions below S-1: Children will learn to
walk unaided. Lesions between L-4 and L-5: Children
will be able to walk with crutches. Lesions above L-2: Children are usually
wheel chair dependent.
EncephaloceleEncephalocele
A neuronal herniation that may or may not contain meninges or brain parenchyma
Presents as a skin-covered sac protruding from the head or base of the neck
The majority occur in the occipital region
EncephaloceleEncephalocele Patient care
Close physical examination Neurosurgeon consult Diagnostic studies such as CT scan and HUS Treat any seizure activity Educate and support the family
Outcome is dependent on brain involvement. May have motor deficits Impaired intellectual function May be complicated with hydrocephalus
CraniosynostosisCraniosynostosis Patient care
Close physical examination.
Neurosurgeon consult. Diagnostic studies such
as CT scan and HUS Treat any seizure activity. Educate and support the
family. Outcome is dependent
on brain involvement. May have motor deficits. Impaired intellectual
function. May be complicated with
hydrocephalus
Clinical presentation The infant presents
with suture lines that have a bony prominence, unmovable sutures, and abnormal cranial shape
Later signs include, increased ICP, increased irritability, and separation of other sutures
Diagnosis Skull x-rays or CT scan
CraniosynostosisCraniosynostosis
Patient care Thorough physical examination Neurosurgical consult Observe for signs of increased ICP, such
as irritability, lethargy, vomiting, and bulging fontanel
Support and educate the family Early surgical treatment recommended Good outcome with surgical correction
Birth InjuriesBirth Injuries
Any condition that affects the fetus adversely during the entire phase of labor and delivery
Patient care. Observe for bleeding, shock. Monitor blood pressure. Transfuse if needed. Observe for hyperbilirubinemia. Once
the infant has survived the acute phase recovery occurs in 2-3 weeks
CephalohematomaCephalohematoma
CephalohematomaCephalohematoma
A subperiosteal hemorrhage (bleeding between scalp and bone) resulting from a traumatic delivery
It is limited to the surface of the bone and does not cross suture lines
Resolution may take up to several months
CaputCaput
CaputCaput
A diffuse edema of the scalp, resulting from compression of local blood vessels
The edema crosses suture lines and disappears in a few days
Subgaleal HemorrhageSubgaleal Hemorrhage A hemorrhage beneath the scalp that can
enter the subcutaneous tissue of the neck Presents with acute blood loss after birth, is
often a moveable mass and may increase in size post-natally
Can actually bleed entire blood volume into injury
Patient care. Observe for bleeding, shock. Monitor blood pressure. Transfuse if needed. Observe for hyperbilirubinemia. Once the infant has
survived the acute phase recovery occurs in 2-3 weeks
InjuriesInjuries Skull fractures: Can be
linear or depressed secondary to excessive force with forceps and extreme molding. Linear fractures are
asymptomatic. Depressed fractures
present with a depressed surface of skull indented without craniotabies; does not cross suture lines and adjacent sutures are markedly separated
Patient care. Neurosurgical consult
and assess for neurological deficits.
Will usually resolve in a few weeks if lesion is less than 2 cm and patient is without neurological deficits.
Outcome of a linear fracture is good, depressed fracture outcome is dependent of cerebral injury
InjuriesInjuries Brachial nerve plexus
injuries Occurs from excessive
stretching of the brachial plexus during delivery.
Can involve part or entire arm depending on which nerves are affected.
Patient care. There is no treatment
except for passive range motion after swelling has decreased.
It may be necessary to immobilize the limb during the acute phase to decrease the pain.
Generally spontaneous recovery in the majority of cases by 3-4 months of life
InjuriesInjuries Phrenic nerve paralysis.
Caused by torn sheaths, edema, and hemorrhage of cranial nerves III, IV, and V
Results in diaphragmatic paralysis
Infant may have episodes of cyanosis, decreased breath sounds on the affected side, irregular labored breathing, and may have Erb’s palsy on the affected side
Patient care: Give oxygen and
ventilator support as needed.
Position with affected side down.
Educate parents
HemorrhagesHemorrhages Subdural hemorrhage
Caused by tears of cerebral veins or venous sinuses.
Occurs with or without laceration of the dura. Can be caused by CPD, abnormal labor duration,
vaginal breech delivery, malpresentation or assisted delivery.
Clinically are often normal but may have seizure activity on day 2 or 3 of life.
In more severe cases may be lethargic progressing to coma with dilated, poorly reactive pupils on the same side as the hemorrhage.
Infants with large tears and worsening condition have a poor outcome, but a high percentage of infants do well
Subdural HemorrhageSubdural Hemorrhage
HemorrhagesHemorrhages Subarachnoid hemorrhage
Bleeding in the subarachnoid space of venous origin.
May be due to prematurity, trauma, and hypoxia.
Clinically the infants range from normal, to having seizure activity on day 2 of life, and the infant looks healthy between seizures.
May have recurrent apnea and hydrocephalus.
Infants generally have a good outcome
Intracerebellar hemorrhage Occurs in the subependymal
region. Resulting from a primary bleed
or an extension of a hemorrhage into the cerebellum.
Is associated with RDS, perinatal asphyxia, and prematurity.
Contributing factors include: IVH with large volume of blood present, increased intracranial pressure, and incomplete myelination of the cerebellum.
Clinically the infant may present with apnea and bradycardia with decreasing Hct and bloody CSF
Subarachnoid Subarachnoid HemorrhageHemorrhage
Intracerebellar Intracerebellar hemorrhagehemorrhage
InsultsInsults
Hypoxic-Ischemic Encephalopathy (HIE) Occurs in term infants with a history of perinatal
asphyxia who exhibit clinical signs of acute brain injury.
Caused by hypoxemia and ischemia that follow asphyxia.
During asphyxia, cardiac output is redistributed, cerebral blood flow increases, and autoregulation is impaired or lost.
As asphyxia continues, cardiac output decreases causing decreased cerebral blood flow and ischemia, resulting in neurologic impairment
HIEHIE
HIEHIE Mild: Characterized by brief lethargy, jitteriness,
hyper-alert state, irritability, tachycardia, dilatation of pupils, decreased secretions, transient hypoglycemia, and EEG is WNL
Moderate: Lethargy, hypotonia, decreased spontaneous movement, jitteriness, and discrepant muscle strength between shoulders and pelvic region. The infant either improves or deteriorates in the 48-72 hours after birth
Severe: Infants progresses from obtund to stupor to comatose
Mechanical ventilation is required to sustain life. Symptoms include apnea, seizures, severe hypotonia, absent reflexes, reactive pupils, with deterioration 24-72 hours after birth
PVLPVL
Ischemic, necrotic periventricular white matter that can occur after severe IVH, inadequate cerebral perfusion or HIE in premature infants.
Clinical presentation: Weakness in lower extremities.
Outcome can include spastic quadriplegia, visual impairment, and lower limb weakness, but depends on location and severity.
PVLPVL
Cerebral PalsyCerebral Palsy Any one of a number of neurological disorders
that appear in infancy or early childhood and permanently affect body movement and muscle coordination but aren’t progressive
Not caused by problems in the muscles or nerves Caused by abnormalities inside the brain that
disrupt the brain’s ability to control movement and posture
Damage is a result of injury to the brain either before, during, or after birth. In either case, the damage is not repairable and the disabilities that result are permanent.
Cerebral PalsyCerebral Palsy Symptoms:
Lack of muscle coordination when performing voluntary movements (ataxia)
Stiff or tight muscles and exaggerated reflexes (spasticity)
Walking with one foot or leg dragging Walking on the toes, a crouched gait, or a “scissored”
gait Variations in muscle tone, either too stiff or too floppy Excessive drooling or difficulties swallowing or
speaking Shaking (tremor) or random involuntary movements Difficulty with precise motions, such as writing or
buttoning a shirt.
CystsCysts
Fluid- filled ‘holes’ or ‘voids’ where brain tissue should be
Can be located anywhere within brain Etiology is usually anoxia or structural
insult Rises from both in-utero and post-natal
insults Outcome based on location and extent of
cyst Ranges from benign to devastating
CystsCysts
Types:Types: ArachnoidArachnoid
Names based on locationNames based on location Dandy-WalkerDandy-Walker Ependymal Ependymal Rathke’s CleftRathke’s Cleft PorencephalicPorencephalic OthersOthershttp://www.thamburaj.com:80/cysts.htmhttp://www.thamburaj.com:80/cysts.htm
Ependymal CystEpendymal Cyst
Porencephalic CystPorencephalic Cyst