neurological dysfunction

8/13/2019 Neurological Dysfunction

1/121

Neurological Dysfunction


2/121

OverviewNeurological Assessment

Anatomic and Physiologic Changes

Increased Intracranial Pressure

Meningitis

Reye Syndrome

Febrile Seizures

Hydrocephalus

Acute Head Injury

Seizure Disorder

Meningomyelocele


3/121


4/121

Neurological Assessment/History

It all begins with the history...


5/121


Prenatal Factors:

Maternal Age

Maternal Health

Adequacy of Prenatal Care

Exposure to Teratogens

Family Support

Resources during Pregnanacy


6/121


Perinatal Factors

position of fetus

progression of labor

premature ROM/fever

anesthesia/medicationsplacental function

monitoring abnormalities


7/121


Postnatal Factors

APGAR scoresmeconium

hypoxia (ABGs)

assisted ventilationhyperbilirubinemia

infections

seizures


8/121


Childhood Problems

Growth Parameters

Illnesses/Operations

Immunizations

Exposure to Illness

Injuries

Seizures


9/121

Assess individual

trend on curve

Height, Weight, Head

Circumference ismonitored

Be alert to growth

deceleration


10/121


Developmental HistoryAge milestones achieved

School performance

Need for early intervention

Plateau or regression


11/121


Family History

sudden death/cardiac problems

genetic conditions/mitochondrial conditions

frequent miscarriages

hypotonia

cerebral palsy

epilepsy

mental retardation

developmental delay

s stemic roblems


12/121

Neurological Assessment/Physical Exam

Observation is the cornerstone of the pediatric exam!


13/121

Neurological Assessment/Physical Exam

Do not require the patient to sit on table or bedunless appropriate

Examine from least painful/intrusive to most

Allow parent to hold the child

Make a game out of the examination

Use familiar toys or objects

Look for symmetry


14/121

Neurological Assessment

General Exam

Note head shape, symmetry, and size

Measure occipitofrontal circumference (OFC)Note general appearance of spine

Note overall tone and symmetry of extremities

Note general appearance and behaviorNote socialization skills and interpersonal interaction

Note interaction with caregiver


15/121

Head Circumference


16/121

Fontanelle Assessment

Assess for overriding,nonmobile sutures

AF = closes 14-18 months

PF = closes 6-8weeks

Fontanelles bulge withcrying and activity


17/121

Components of the

Neurological ExaminationMental State

Cranial NervesMotor

Sensory

Cerebellar

Reflexes


18/121

Mental State: Attention

Note level of infant alertnessNote ability to engage child

Adolescent: ask to spell house

forward and backward


19/121

Mental State: Orientation

Infant: assess quality of awake time, ease of arousal

ability to calm

As child develops can begin to assess orientation aroundage 3-4

Full orientation assessment begins at ages 7-8

The adolescent should respond to all components of the

orientation exam


20/121

Mental State:

Speech and LanguageInfant: note cry (shrill, lusty, weak, silent)1-3 months: Ooh, ah sounds

5-7months: single syllables (dada, baba) babbling12-18 months: 3 words

17-24 months: combines words

By age 2: 50 words18-24 months: begins to learn body parts

**Language is closely related to speech, if a childhas language difficulty suspect hearing loss!!!


21/121

Mental State: Memory

As the child learns memory is constantly in play

Assess fund of knowledge, recognition of objects,evaluate school performance

If note developmental delay where memory ability isin question, refer for neurophsychological testing


22/121

Cranial Nerves: I

OlfactoryRarely tested in children; testing same as adult


23/121

Cranial Nerves: IIOptic Nerve


24/121

Cranial Nerves: II

Optic NerveNote infants ability to fix on face and objects

Binocular vision attempted at 3 monthsElevated disc margins and 20/20 vision by age 2 years

Observe the toddler interacting with the environment

Age 7-8 can begin to use Snellen eye chart


25/121

Cranial Nerves: II

Optic Nerve


26/121

Cranial Nerves:

III, IV, VITested together because they control eye movementIII: Oculomotor:

pupil constriction, holds eye open, movement superiorly,inferiorly, and medially

IV: Trochlear:

moves eye down and outVI: Abducens:

lateral gaze


27/121

Cranial Nerves:

III, IV, VINystagmus:

normal to 3 monthsStrabismus:

may be normal up to 6months

Test Visual Fields:

use brightly coloredtoy


28/121

Cranial Nerves: V

Trigeminal Nerve


29/121

Cranial Nerves: V

Trigeminal NerveInfant: assess ability to suck

Child: assess strength of chewing/biting

Adolescent: clench jaw

Sensation throughout face is assessed in all agegroups


30/121

Cranial Nerves: VII

Facial

Note symmetry of face

Note ability to move face

Strength of eye closure

Have child make funny faceswith you


31/121

Cranial Nerves: VIIFacial

What is this?


32/121


33/121

Cranial Nerves: VIII

VestibularcochlearInfants: use a bell or snap fingers behind ear

turns head to sound, startles to noise,

By 3 months: quiets to mothers voice

Toddler/child: speech delay may be a sign of hearing

impairment

School age and beyond: formal hearing screening


34/121

Cranial Nerves: IX, X

Glossopharyngeal, Vagus


35/121

Cranial Nerves: IX, X

Glossopharyngeal, VagusAssess ability to swallow, symmetry of uvula , speech


36/121

The posterior fossa surgical approach places the childat risk for IX and X cranial nerve damage


37/121

Cranial Nerves: XI

Spinal Accessory

Note stability of headposition

Ask child and adolescent to

shrug shoulders


38/121

Cranial Nerves: XII

HypoglossalMovement of tongue, observeat rest and have child stick

tongue out and move fromside to side

Note fasciculations (sign of

motor weakness)


39/121

Motor Exam

Note Tone and Strength

Assess Progression of Motor Milestones


40/121

Motor Milestones/Gross

Lifts head to chin, hands to midline: 2 months

Roll over: 2.5 - 5 months

Sit without support: 6 months

Crawl: 6-8 months

Pull to stand: 8-10 months

Walk: 11-15 months

Run: 14-19 months

Walks up steps: 15-22 months

Hop: 3-4 years


41/121

Motor Milestones/Fine

Neat pincer grasp: 9 months

Tower of 4 cubes: 15-20 months

Copy circle: 3 years

Draw a 3 part person: 3.5-4.5 years

Diagonal line: 7 years

Draws cross with same dimensions: 9 years

Draws 3 dimensional cube: 12 years


42/121

Sensory Exam

Pain is felt by all age groups and is subjective

Can begin to test vibration in the preschooler

Other sensory function can not be tested untilschool age years.

Assess for symmetry of sensation


43/121

Cerebellar Exam

Can not perform specific testing until age 3

Preschooler: unipedal hopping, stand on one footSchool Age: walk a straight line, heel to toe walking

Adolescent: finger to nose touch test, assess gait,rapid pronation and supination


44/121

Reflexes

All deep tendon reflexes are tested as in adults

Bicpes, brachioradialis, maxillary, patellar present at

birthAchilles present by 4 months

Triceps present by 6 weeks

May need to distract children to assess reflexes


45/121

Developmental Reflexes

Tongue Protrusion: present from birth

to 3 monthsAutomatic expulsion of solid object when

place in mouth


46/121


Moro:

Symmetric abduction andflexion of upper extremitieswhen allowed to fall back orwith loud noise

Present from birth to 6 months


47/121


Plantar Grasp

Place finger undertoes and infant graspsfinger with toes

Dissipates by 9months


48/121


Palmar Grasp

infant will grasp

object when placed inpalm

Present from birth to6 months


49/121


BabinskiPresent until 18 months

Indicates myelinization ofmotor tracts

Note: myelinization beginsat birth and is a process

that occurs over time


50/121

Increased Intracranial

Pressure


51/121

Increased Intracranial

PressureMonro Kellie Hypothesis:Brain: 80%

Blood: 10%

CSF: 10%

An increase or decrease in one

cranial content results in anequivalent replacement of theother

When the constant

relationship can not bemaintained intracranialpressure will rise


52/121

Etiology of IncreasedIntracranial Pressure

Mass:

Tumor, Hematoma

CSF Disturbances:

hydrocephalus, exposure to toxins ( ex. CMV),

congenital abnormalities, encephalopathy

Edema:cytotoxic, vasogenic, hypo-osmotic

Increased blood volume:

impaired venous outflow


53/121

Etiology of Increased

Intracranial PressureOther:

hypoxic injury, diffuse brain injury,

encephalopathies, infections


54/121


55/121

Clinical Manifestations

Infant:

tense, bulging fontanelle

separated cranial suturesMacewen sign (cracked pot sound)

high-pitched cry

irritability

feeding intolerance

seizures


56/121

Clinical Manifestations

Children:

headache

altered level of consciousnessvomiting (projectile)

visual changes

pupillary signsseizures

motor dysfunction


57/121

Late Signs

Depressed level of consciousness

unilateral/bilateral dilated pupils

sluggish or non-reactive pupils

respiratory abnormalities

decerebrate or decorticate posturing

Cushing Triad: hypertension, bradycardiawidened pulse pressure


58/121

Cerebral Perfusion Pressure

The goal of increased ICP management is to maintaincerebral perfusion pressure

CPP = MAP - ICP

Normal = 60 - 100 mm Hg

NOTE* All ICP interventions are customized to patient

response (examples given in class)


59/121

Medical Management

Maintain oxygenation

saturation at 100%

CO2 = 30-35

Control Ventilation


60/121


61/121

Medical Management

Glucocorticoidsused for focal edema as in tumor

Maintain normal blood sugar:

hypoglycemia increases secondary injury andworsens edema

hyperglycemia increases cerebral edema,

morbidity, and mortality

Surgery:

ICP monitor/CSF drainage

hemicraniotomy or lobectomy


62/121

Nursing Interventions

Positon head in neutral position to promote venous outflow

Elevate head of bed

Avoid extreme hip flexion

Avoid high peep on ventilator (increases intrathoracicpressure and thus, ICP)

Avoid noxious stimuli

Advocate for only the necessary invasive procedures

Maintain an ETT suctioning protocol that minimizes ICPelevation

Promote adequate sedation and pain control


63/121


Maintain normal to hypothermia

Every 1 degree of temperature elevation

increases cerebral metabolism by 5-10%AVOID SHIVERING

Use acetominophen aggressively

Control the environment (low lights,decrease sound, move patient to quiet area

of unit, direct staff and visitors tominimize noise)


64/121

Bacterial Meningitis

Acute inflammationof the meningessecondary to abacterial agent


65/121

Epidemiology

1993: 2 cases per 100,000 children


66/121

Etiology

3 pathogens account for > 80% of bacterial meningitis

Streptococcus pneumonia = pneumococcal meningitis

Neisseria meningitidis = meningococcal meningitis

Haemophilus influenzae = Hib meningitis


67/121

Symptomatology

Classic Triad: severe headache, fever, nuchal rigidity

Insidious nonspecific illness that starts with fever,malaise, irritability, and vomiting that progressesrapidly over 2-4 days

Notable petechial rash in 50% of meningococcal cases

Illness often becomes fulminating in < 24 hours and is

often associated with a poor outcome


68/121

Symptomatology

As the meningesbecome affected the

patient develops:

photophobia

nuchal rigidity

headache

increased ICP


69/121

Symptomatology/Infant


70/121

Symptomatology/ Kernigs Sign

Inability to extend knee with hip flexion


71/121

Symptomatology

Brudzinski Sign

When the patient is supine, passively flexing the

neck produces involuntary flexion of the kneesand hips


72/121

Management

Prevention through vaccination

Early identification and rapid treatment with

antibiotic therapyManagement of ICP

serial head circumference measurements in theinfant

Maintain fluid and nutrition status

Address skin integrity

Psychosocial support of patient and family


73/121

Aseptic Meningitis

Also called nonbacterial or viral meningitis

Most common type of meningitis75,000 cases per year are reported in the U.S.

Frequently underreported because of the mild natureof the disease

Peak in summer and fall


74/121

Etiology

enteroviruses

arboviruses

herpesviruses

85%-90% caused by enterovirus


75/121

Symptomatology

Usually milder than those of bacterialmeningitis and resemble influenza

duration of symptoms usually 1-2 weeksafter onset

headache, nuchal rigidity, photophobia,malaise, and nausea


76/121

Management

Provide supportive care

May give Acyclovir if HSV suspected

Patient education

Patient is expected to recover without neurologicalsequelae

If symptoms become severe the nursing care isconsistent with that of patients with bacterial

meningitis


77/121

Reye Syndrome

Toxic encephalopathy associated

with hepatic dysfunction

Potential associationwith aspirin therapyand influenza andvaricella


78/121

Symptomatology

Fever

Profoundly impaired consciousness

Disordered hepatic function

increased ammonia levels

Advances to coma and brainstem dysfunction

5 stages are correlated to the severity of illness

Definitive diagnosis is by liver biopsy


79/121

Management

Early diagnosis and aggressive therapy

Manage increased ICP

Do not use aspirin for fever management

Family education

Psychosocial support


80/121


81/121


82/121


83/121

SEIZURE CLASSIFICATION

SITE OF BRAIN

AFFECTED

DETERM INES

CLI NI CAL

EXPRESSI ON OF

THE SEI ZURE


84/121

PathophysiologyPathophysiologyEpileptogenesis originates from an imbalance between

cerebral excitation and inhibition. In a seizure, abnormal

neuronal pathways are established that lead to abnormal

electrical firing - Core Curriculum 2003

Three neurotransmitters involved in seizures:

1. Gamma-aminobutyric acid (GABA) 2. Glutamate

3. N-methyl-D-asparate (NMDA)

GABA = inhibition


85/121

facilitates activity of

chloride channels

making the cell

membrane more

negatively charged

opens potassium

channels leading to

post-synaptic inhibition

of impulse

closes calcium channels

which stabilizes the cell


86/121

Glutamate = Excitation

Most important excitatory

transmitter involved in

seizures

NMDA is a receptor subtype

which is implicated in

propagation of seizures


87/121


88/121


89/121

Medication Therapy

All anticonvulsants affect cognitive function

NEVER withdraw medication abruptly

Wean medication over a prolonged period

Be aware of blood level before administering the dose

Review side effect panel closely

Most anticonvulsants interact with other drugs

Provide detailed patient education


90/121


Assist with developing an individualized medicationadministration plan

Monitor drug levelsAssess for symptoms of drug toxicity

Patient safety

Initiate seizure precautionsFacilitate socialization with others

Dispel myths

F b il S i s


91/121

Febrile Seizures

Most common form of childhood seizures

Most common between ages of 6mos - 3 years

The fever usually exceeds 101.8 before the seizure

Usually occurs during the temperature rise

Lasts less than 5 minutes

95% will not develop epilepsy or have brain damage

Control by reducing the temperature with antipyreticsand tepid bath

Education and emotional support are the most important

intervention.


92/121

Acute Head Injury

Injuries are the leading cause of death in children over 1year of age

Estimated 300 per 100,000 children per year have atraumatic brain injury

The head of the infant and toddler is large and heavy in

relationship to other body parts making it most likely tobe injured

Male > Female


93/121


94/121

Types of Injury

Concussion

Contusion and Laceration

Fractures

Epidural Hemorrhage

Subdural Hemorrhage


95/121

Concussion

Most common injury

a traumatically

induced alteration ofconsciousness

LOC is not required

pathogenesisunclear;may be a resultof shearing forces


96/121

Contusion/Laceration

Visible bruising andtearing of cerebral tissue

Common in occipital,frontal, temporal lobes

symptoms may be

indistinguishable fromconcussion


97/121


98/121


99/121

Epidural Hemorrhage

blood accumulates between the dura and the skull

generally arterial

uncommon in children under 4 years of age

the classic clinical picture is rarely evident

the symptom free period can often last longer than

48 hours

symptoms: irritability, headache, vomiting


100/121

Subdural Hemorrhage

bleeding between dura and the cerebrum

10 times more common than epidural hematoma

peak incidence at 6months of age

develops more slowly

subdural and retinal hemorrhages = evaluation forShaken Baby Syndrome


101/121

FB Menu


102/121

FB Menu

Pearls of Head Injury Management


103/121

Pearls of Head Injury Management

a detailed history of the event is critical in diagnosisAssess ABC, LOC, pupils, seizures

crying for > 10 minutes after injury = serious injury

CT scan detects fracture and hematomamoderate concussion without LOC can be managed athome by checking child q 2 hours for 1-2 days

NPO, IVF, daily weights, manage painreview management of increased ICP

psychosocial support

consider mandatory abuse reporting


104/121

Myelomeningocele

Spina Bifida

derived from embryonic

neural tube

1996: 0.32/1000 live births

failure of neural tube closure

symptoms are related to thelevel and severity of thedefect

Preoperative Care


105/121

Preoperative Care

deliver via C-sectiongood neurological exam

strict aseptic technique to prevent infection

lay baby prone, ROMapply moist saline gauze dressing, change q 2 hours

prevent stool from soiling lesion with a stool flap

strict I and O (monitor urine output)Measure head circumference daily

Psychosocial support of parents

Surgical correction usually with first 24 hours


106/121

Postoperative Care

I. Potential for UTI and urinary retention

a. assess urine quantity, color, odor

b. strict I and O

c. straight cath (teach parents and staff)

d. administer antibiotics

e. document postvoid residuals


107/121

Postoperative Care

II. Potential for impaired skin integrity

a. Change diapers as soon as soiled

b. Keep perianal area clean and dry

c. Place child on pressure reducing surface

d. Massage healthy skin during cleansing


108/121

Postoperative Care

III. Potential for Latex Allergy

a. Reduce Latex exposure

b. Educate family and caregivers

c. Pretreatment with antihistamines and steroids

d. cross-reaction banana, avocado, kiwi, chestnute. incidence estimated 18% - 67%


109/121

Postoperative Care

IV. Potential for injury related to neuromuscularimpairment

a. bracing, PT, botox injections

b. tendon release, address scoliosis

c. ROM

d. maintain hips in slight abductione. maintain body alignment and good positioning


110/121

Hydrocephalus

Symptom of underlyingbrain disorder

caused by an imbalancein the production andabsorption of CSF

Congenitalhydrocephalus: 4/1000live births

E l


111/121

Etiology

Impaired absorption of CSF (communicating)

a. Congenital

b. Subarachnoid hemorrhagec. Infection

Obstruction to flow of CSF (noncommunicating)

a. Blockage at or above 4th ventricleb. Most common blockage in aqueduct of Sylvius

c. Tumor

l


112/121

Symptomotology

Infants:

large head circumference (plot on growth curve)

irritabilityextreme lethargy

dilated scalp veins

split sutures, tense or bulging fontanelleseizures

sunset eyes

l


113/121

Symptomotology

Toddler/Young Child

macrocephaly

poor appetite

failure to thrive

double vision/vision changes

loss of previous developmental ability

vomiting

seizures

l


114/121

Symptomotology

Adolescents

headache

vomiting

vision changes/double vision

decline in cognitive/school performance


115/121

Sh M


116/121

Shunt Management

Position on unoperated side immediately post-op

assess for signs of subdural hematoma

manage painstrict I and O

astute abdominal assessment

monitor incision siteprevent infection

routine postoperative care (IS, SCDs etc.,)

L T C id i


117/121

Long Term Considerations

Teach family signs of shunt malfunction and infection

provide reliable patient education/support group

materialsSeizure management (20-25% in first year of life)

encourage patient independence

address learning disabilitiesconsider motor deficits (75% occurrence)

consider ocular problems (25-30% occurrence)

Spinal Muscular Atrophy


118/121

Werdnig-Hoffman Disease

Autosomal recessive trait

progressive weakening ofskeletal muscles

degeneration of anteriorhorn cells of spinal cordand motor nuclei ofbrainstem

Age of onset variable;worse prognosis theearlier the onset

Cognitively normal

M t


119/121

Management

Promote skin integrity

Frequent suctioning, pulmonary toilet

Prevent feeding aspiration

Attend to potential for injury

Normal verbal, tactile, auditory stimulation

Promote social interaction

Intense family psychosocial support

M l D t h


120/121

Muscular Dystrophy

Largest single group of muscular diseases in children

All have a genetic origin

Gradual degeneration of muscle fibers

Progressive muscle wasting and weakness

Etiology unknown; appears to be related to a metabolicdisturbance independent of the nervous system

Most common form: Duchenne muscular dystrophy

M t


121/121

Management

Major emphasis is on assisting the child and family incoping with the progressive, incapacitating, and fatal

nature of the disease

Promote independence

Modify clothing

Education regarding assistive devices

Refer family to support resources

neurological dysfunction

Documents