Alterations in

Neurological, Mental
Health and Cognition
Functions
NR 322 Pediatric Nursing
Chamberlain College of Nursing
Week 2

Altered States of
Consciousness
Level of Consciousness
Increased Intracranial Pressure

Altered States of Consciousness

Level of consciousness
MOST CRITICAL CLINICAL INDEX OF NERVOUS
SYSTEM FUNCTION
Reflects status of BRAIN
Patterns of breathing
Reflects cerebral hemisphere/brain stem
function
Pupillary changes and eye movement
Reflects brain stem function
Motor responses
Reflects level, side &
severity of brain dysfunction

Nursing Assessment of Altered

Levels of Consciousness
Levels of consciousness (LOC)

most important indicator of

neurological dysfunction
Consciousnessreceptiveness to
stimuli
Alertnessarousal, ability to react
Cognitive power ability to
process data and respond

Neurological Assessment
Alertness arousal with touch, voice,

pain?
Cognition processes?
Posture and Movement MAE?
(moving all extremities) Purposeful?
Muscle tone mild, even resistance?
Homeostatic mechanisms Temp,
HR, RR, BP, U/O, digestion (vomit?)
Pain headache

Altered Levels of
Consciousness
Stages of altered LOC
1) Confusion inability to think rapidly,
impaired judgment or decision making
2) Disorientation to time, place, and
person; memory affected
3) Lethargy limited spontaneous
movement, sluggish speech. Will
arouse with moderate stimuli but
returns to sleep quickly

Altered Levels of
Consciousness
Obtunded reduced
arousal need loud voice or strong
touch, falls asleep often, yes/no ?s
OK; mentally dulled; out of it
5) Stupor- deep sleep; unresponsive;
arouses only to vigorous, repeated
stimulation; withdraws or grabs in
response to pain or stimulation.
6) Coma no motor or verbal
response to even deep pain
4)

Deterioration of LOC: A
Sequential Pattern
Awake and alert - responds appropriately
Slight disorientation to time, place, or

person
Restless, fussy, or irritable
Drowsy but responds to loud commands,
painful stimuli
Nonpurposeful response
Posturing
No response

Tool to Quantify LOC:

Pediatric Glasgow Coma Scale
Three part assessment
Eyes
Verbal response
Motor response
Score of 15: unaltered LOC
Score of 3: extremely

decreased LOC (worst possible

score on the scale)
9

Early Signs of Increasing ICP

Changes in LOC, irritability, restlessness
Headache, dizziness
Vomiting, possibly projectile
Blurred vision, double vision (diplopia)
HR, RR, BP or pulse pressure
Pupil reaction time ; unequal
Sunset eyes
Seizure activity
Kyle & Carman, Pediatric Nursing
Clinical guide, 2013

11

Additional Manifestations of
Increased ICP in Infants
Irritability, poor feeding
High pitched cry, difficult to soothe
Fontaneles: tense, bulging
Cranial sutures: separated
Eyes: setting-sun sign
Scalp veins: distended

12

Late Signs of Increasing ICP

Decreased LOC
Decreased motor and sensory

response to command
Alterations in pupil size and
reactivity; papilledema
Decerebrate or decorticate
posturing
Cheyne-Stokes respirations
Irregular respirations
Bradycardia

13

POSTURING

Decorticate

Decerebrate

15

Types of ICP Monitors

Intraventricular catheter
Subarachnoid screw or bolt
Epidural sensor
Anterior fontanelle

pressure monitor

18

Nursing Care for Child

with Increased ICP
Patient positioning
Avoid activities that may

increase ICP
Eliminate/minimize noise or
stimulation
Suctioning issues
Avoid overhydration
19

Seizure Disorders

Generalized Seizures
Partial Seizures
Febrile Seizures
Status Epilepticus

Epilepsy (Seizure disorder)

Seizures are triggered recurrently from

within the brain

Two or more unprovoked seizures
occur> 24 hours apart
Can be acquired or familial

Seizures: Incidence
Most common neurological

dysfunction in children
50% idiopathic
5% of children have at least one seizure
Occurs with wide variety of CNS
conditions
45,000 children develop epilepsy every
year, 30% by age 4 years old

Seizures: Patho
Caused by disruption of

electrical communication
among the brains neurons

Excessive uncontrolled discharge of neurons of

cerebral cortex that interferes with normal
function

Neurons recruit other neurons to fire

synchronously in adjacent and distant areas

May have aura or sensory experience
May occur without any clinical symptoms

Common Pediatric Seizure

Triggers
1. Changes in dark-light patterns

2.
3.
4.
5.

(camera flashes, headlights,

rotating fan blades,
reflections off snow or water)
Sudden loud noises
Extreme temperature changes
Dehydration
Fatigue
24

Clinical Manifestations:
Depends on the Type

Common Seizure Types

1.
2.
3.
4.
5.
6.
7.
8.
9.

Infantile spasms
Absence (formerly
petit mal)
Tonic-clonic (formerly
grand mal)
Myoclonic
Atonic
Febrile
Simple partial
Complex partial
Status epilepticus

General s & s

Change in LOC
Involuntary

movements
Posturing
Changes in perception
Changes in behavior
Changes in sensation
May be brief, selflimiting

Infantile Spasms

Uncommon type of generalized seizure

Incidence:

Usually seen between 3-12 months old, peak

incidence 4-8 months and usually stops by 2 years
old
Majority have some brain disorder before seizures
begin

Clinical Manifestations:

Sudden jerk followed by stiffening

Head flexed, arms extended, legs drawn up
Cry may precede or follow

Therapeutic Management: Steroids,

anticonvulsants

Absence Seizures
Sudden cessation of motor activity or
speech with a blank facial expression
or rhythmic twitching of the mouth
or blinking of the eyelids
Minimal

or no change in muscle tone

Almost always appear in childhood between
ages 5-12 years old

Sudden onset of up to 20+ events per day

No warning/no aura/no postictal
Duration < 30 seconds
May drop object, child rarely falls
No incontinence
27

Absence Seizures
Often unrecognized or mistaken

for:

Inattention/daydreaming
ADD/ADHD
School issues

Behavioral management

28

Tonic-Clonic Seizures:

Extremely common generalized seizure

Associated with an aura
Loss of consciousness occurs
Tonic-clonic movements
Cyanosis may be noted d/t apnea
Saliva may collect in mouth
May bite tongue
Loss of bladder

sphincter control
Postictal state

Myoclonic Seizures
Sudden, brief, massive contractions of

muscle group (whole body or 1 part)

May be single or repetitive
May or may not lose consciousness
Often occur with falling asleep
May be nonspecific symptom in many
CNS disorders
May be mistaken as exaggerated startle
reflex
32

Atonic Seizures
Sudden momentary loss of

muscle tone
Onset usually age 2-5 years old
May or may not have LOC changes
Sudden fall to ground, often on
face

Less severehead droops

forward several times
33

Febrile Seizures
Transient disorder of childhood
Affect approximately 3% of

children; 10% once dx epilepsy

Usually occur between ages 6 mos
and 3 yrs
Rare after age 5 years old
Two times more frequent in males
95%-98% of children with febrile
seizures will not have epilepsy or
neurologic damage
34

Febrile Seizures
Cause? unknown: linked to

immature CNS
Usually with temps >102F
Seizure occurs while temp is
rapidly increasing, not after
Seizure usually over by arrival
to ER (duration <5 minutes)
35

Partial Seizures (focal)

Limited functional area is involved

Simple Partial:

No loss of consciousness
No aura, <30 secs duration
No postictal state

Complex Partial:

Consciousness impaired
Aura often present
Up to 5 min duration
Automatisms
Post-seizure confusion present

Status Epilepticus
Seizure lasting >30 minutes or series

of seizures without regaining

consciousness between seizures
Can be life-threatening
Age of child, cause of seizure, duration of
status epilepticus influence prognosis

37

Diagnostics
Ascertain type of seizure

Health history, observation, risk factors

Physical Examination
Labs/diagnostic tests
Labs: glucose, lytes, calcium
Lumbar puncture
Skull xray, CT, MRI
EEG, Video EEG

38

Therapeutic Management
of Seizures
Anticonvulsants: Primary

mode of tx

Intractable seizures:
Surgery: if seizures
uncontrolled
Vagal nerve stimulator
(VNS)
Ketogenic diet

TABLE 536

Anticonvulsants Used to Treat Seizure Disorders

Nursing Care Management

for All Seizure Disorders
Obtain seizure history
Provide a thorough and accurate

description of the event.

Protect child from injury during seizures
Administer appropriate medications and
treatments
Lots of education of family members &
caregivers

Nursing Care:
Seizure Precautions
Pad side rails and other hard objects.
Raise side rails on the bed at all times when

child is in the bed.

Keep oxygen and suction at the bedside.
Provide supervision, especially during bathing,
ambulation, or other potentially hazardous
activities.
Encourage the use of a protective helmet
during activities.
Make sure child wears a medic alert bracelet.

Nursing Care:
During the seizure

Remain calm
Stay with the child until fully conscious
Protect from injury & remove hazards
Note time of onset, duration, details of seizure
Be ready with oxygen and suction
Move to flat surface, away from danger
Turn child to side, let saliva drain out
Support childs head to prevent head bang
DO NOT restrain child
DO NOT use tongue blades or insert any object into the
mouth (including fingers)
Loosen tight clothing & jewelry from around neck
Treat all injuries from fall
Document all details of the seizure

Interventions for
Status Epilepticus
Basic life support: ABCs
Administer anticonvulsants: crucial
Ensure safety
Establish intravenous access
Monitor vital signs and neurologic status
Blood glucose, electrolytes, blood gases

monitored
If hypoglycemic, administer glucose

Febrile Seizures
Management
Avoid

tepid bathsusually
ineffective
Vigorous use of antipyretics
Protect child from injury during
seizure
Call 911 if seizure >5 minutes
duration
Rectal diazepam
46

Infectious Diseases

Bacterial Meningitis
Viral Meningitis
Encephalitis
Reye Syndrome

Meningitis
Acute inflammation of the meninges

surrounding the brain and spinal cord caused

by a bacteria or a virus
Whos at Risk?
Children who are ill with an upper respiratory
infection such as sinus infections or ear infections
Children with head trauma/ post-lumbar
puncture/neurosurgical intervention/Congenital
structural abnormalities/ Foreign objects
Age factor (infants, adolescents, young adults 15
-24 years old)

Bacterial Meningitis:
Clinical Manifestations

Fever, chills, malaise, lethargy

Restless, lethargic, irritable, difficult to console
Changes in feeding pattern, vomiting, diarrhea
Headache, anterior fontanel bulging or flat
Nuchal rigidity (stiff neck), photophobia
Positive Brudzinskis sign flexion of neck causes neck pain and hips/knees flex
Positive Kernigs sign

flex hip and knee, then extend leg and note hamstring
pain!!

Seizures , Rash (Alert!! Meningococcal rash)

SIADH fluid overload or DI - dehydration

Bacterial Meningitis:
Diagnostics

LP is definitive diagnostic test.

Cerebrospinal fluid (CSF):

Increased WBCs
Increased Protein
Decreased Glucose
CBC:
Increased WBCs
Blood cultures:
Done to rule out sepsis. Positive in
cases of septicemia

Bacterial Meningitis:
Therapeutic Management
Isolation: Droplet precautions
Antimicrobial therapy

Started immediately after CSF

& blood cultures have been obtained.

Corticosteroids
Hydration and nutrition
Ventilation
Reduce ICP
Observe for/treat septic shock
Control seizures
Manage and reduce fever

57

Viral (Aseptic) Meningitis

Inflammatory response of meninges
Most common cause: Enterovirus
Child not as ill-appearing as child with

bacterial meningitis

Viral Meningitis:

Clinical Manifestations
Irritable or lethargic - general

malaise
Fever
Headache
Photophobia
Upper respiratory symptoms
Positive Kernig and Brudzinski signs indicate meningeal irritation
Seizures are rare

Viral Meningitis:

Therapeutic Management
Labs and cultures (blood, urine,

cerebrospinal fluid)
Intravenous antibiotics until cultures are
negative - treat as bacterial
meningitis until proven otherwise
Treatment of symptoms is supportive
Symptoms usually resolve in 3 to 10
days
Neurologic deficits are uncommon

Encephalitis
Acute inflammation of brain & sometimes

the meninges caused by infection

Highest incidence if < 1 year old
If survive, often have significant
neurological sequelae
Etiologies
Most common: Herpes viruses
Enterovirus, Epstein-Barr virus
Measles and varicella
Fungi, parasites

Encephalitis:

Clinical Manifestations
General Symptoms

Severe Symptoms

Malaise
Fever

High fever
Disorientation/

Headache/dizziness
Stiff neck

stupor/coma
Seizures
Spasticity
Ocular palsies
Paralysis

Nausea/vomiting
Ataxia
Speech difficulties

Encephalitis: Therapeutic &

Nursing Management
Pharmacological

Antibiotics if bacterial
Acyclovir if herpes virus
IVIG, corticosteroids, immune system modulators
if postinfectious encephalitis

Nursing Care focus: Supportive

Monitoring cardiopulmonary status

Preventing complications resulting from immobility
Reorienting the child when LOC improves
Teach family about childs condition

Reye Syndrome
Acute metabolic, non-inflammatory
encephalopathy of childhood with organ
involvement
Disrupts the process of changing ammonia to
urea hyperammonemia
Fatty degeneration of the liver, kidneys, brain
and myocardium
Whos at Risk?
Associated with viral illnesses
Strongly associated with the use of
salicylates (aspirin) to treat symptoms
of varicella or influenza infection

Reye Syndrome
Clinical Presentation
1. Encephalopathy
2. Increased ICP
3. Metabolic
dysfunction
4. Hepatic dysfunction
5. Renal damage
6. Fatty infiltration of
the viscera

Assessment Findings
1. Hypoxia
2. Seizures
3. Hypoglycemia
4. Coagulopathies
5. Electrolyte
Imbalances
6. Hyperthermia

Reye Syndrome:

Clinical Manifestations
Stage 1:
Vomiting,lethargy
Stage 2

Combative or stupor
Hyperactive reflexes

Stage 3:
Coma
Decorticated
Stage 4:

Coma
Decerebrated

Stage 5
Coma with Seizures
Loss of DTRs

Reye Syndrome
Therapeutic Management:
Corticosteroids
Barbiturates
Mannitol or hypertonic saline
Anticonvulsants
Vitamin K liver coagulopathy

Reye Syndrome:

Nursing Care Management

Priority: Monitor for changes in neurological

status, report immediately

Assess for GI bleeding, pancreatitis, liver failure
Provide IV hydration with glucose
Provide seizure precautions
Monitor respiratory status
Elevate HOB 30-45 degrees
Keep child calm and a quiet environment
Educate parents on need for long-term F/U

Headaches
Benign
Structural

Headaches- Stats
Up to 75% of children experience

headache by age 15 years old.

Migraines occur in 1% of children by

age 7 years and 5% by age 15 years.

Approx. 20% of children in U.S. have

chronic headaches.

Headaches:
Etiologies

BENIGN
Migraine: Vascular
Tension: Muscular

contraction
Inflammatory:
Sinusitis or dental
abscess

STRUCTURAL
Tumors
Hemorrhage
Increased ICP

MEDICATION OVERUSE
(Rebound)

Acetaminophen
NSAIDs
Decongestants
Ergotomines

Headaches:
Triggers

MIGRAINES
Stress
Food containing

nitrates, MSG,
caffeine, tyramine,
salt, yeast extracts,
aspartame (Equal)
Menses
Oral contraceptives
Fatigue
Hunger

TENSION
Stress associated with

school
Insecurity
Conflict in the family
Inadequate sleep

Structural Defects
Hydrocephalus
Neural Tube Defects: Spina
Bifida

Hydrocephalus
Increase in the amount of cerebrospinal fluid in
the ventricles and subarachnoid spaces. Results from
an imbalanced production or absorption of CSF. CSF
accumulates within the ventricular system and causes
the ventricles to enlarge and increases in ICP to
occur.
50% is idiopathic
Common disorders associated with hydrocephalus:
Neural tube defects
intraventricular hemorrhage IVH (prematurity)
Meningitis
Intrauterine viral infections
Lesions or malformations of the brain
Injury

Hydrocephalus:
Pathophysiology & Etiology
Non-communicating:
Most common type in children
Obstruction in ventricles blocks
outflow of CSF to subarachnoid space
CSF accumulates
Communicating:
Poor absorption of CSF
Often due to scars, IVH, or congenital
malformations of subarachnoid space

Hydrocephalus
(Note to instructor: Image available in

Electronic Image Collection)

77

78

Hydrocephalus:

Clinical Manifestations
In all ages, signs & symptoms of IICP
Positive Macewens sign
Infants Rapid increase in head
circumference, split sutures,
bulging fontanel

Older children HEADACHE!

Difficulty with balance and
coordination, loss of development,
Changes in personality

Hydrocephalus:

Diagnostics & Therapeutic Management

Diagnostics: Skull xray, CT & MRI

of head
Therapeutic Management:
Most

cases are treated with surgical

placement of an extracranial shunt
(Most often a ventriculoperitoneal
(VP) shunt)
Shunt revision surgery as child
grows

Ventriculoperitoneal
(VP) Shunt

VP Shunt
Complications
Infection

VS, temp
Poor fdg
Nauses/Vomiting
Malaise
Headache
Redness along
the tract

Malfunction
Vomiting
Drowsiness
Headache
83

Hydrocephalus
Nursing Management:

Keep head flat and midline (venous drainage)

Dont let baby lay on side of surgery
Educate s/sx of infection (fever, redness) and
IICP (seizure, lethargy, vomiting)
Monitor for complications

Neural Tube Defects

Congenital malformations that produce skull

and spinal column defects (failure to close)

usually at L5 or S1 level.
Cause? Folic Acid! Chemicals, genetics, Moms DM, Moms
meds: Valproic acid & Accutane (check AFP)

Types:
Anencephaly: No brain above the brainstem
Encephalocele: Protrusion of meningeal tissue or brain

through a defect in the skull

Meningocele: Protrusion of a meningeal sac filled with CSF
through a vertebral defect
Myelomeningocele: Protrusion of meningeal sac that contains
CSF, a portion of the spinal cord and nerves through a vertebral
defect

Spina Bifida Occulta:

Clinical Manifestations
Depression or dimple or tuft of hair over

spinal defect; possible sacral lipoma

May see port wine nevi or soft fatty deposits
at defect
Tethered cord
Abnormal

adhesion to body or fixed structure

Puts traction on the cord
Altered gait
Bowel/bladder problems
Foot deformities

Spina Bifida Cystica:

Myelomeningocele and
Meningocele

Myelomeningocele
Neural tube fails to close
May be anywhere along the spinal column
Lumbar and lumbosacral areas most common
May be diagnosed prenatally or at birth
Sac contains meninges, spinal fluid, and

nerves
Varying and serious degrees of neurologic
deficit
Clinically myelomeningocele term is used
interchangeably with phrase spina bifida

89

Spinal defects

90

Myelo/ Meningocele:
Clinical Manifestations
Sac like structure noted over spine
Often ulcerations or cyanotic area
Club foot
Knee contractures
Hydrocephalus seizure
Curvature of the spine
Neurologic dysfunction below defect
Bowel/bladder incontinence

Intact sac

Ruptured sac
92

Myelomeningocele:

Therapeutic Management
Surgical closure as soon as possible after birth

(within 48 hours)

Goal: Prevent infection and minimize further loss

of function

In utero fetal surgery

to repair defect
Life-long multidisciplinary
approach
Neurologist, neurosurgeon,
urologist, orthopedics, physical therapy,
rehabilitation, intense nursing care

Myelomeningocele:
Pre-op Nursing Care

Cover sac with sterile dressing (warm saline).

Avoid pressure on the sac.

Monitor for CSF leakage
Place infant in prone position
with knees slightly flexed
Keep lesion free of feces/urine
Keep in an isolette or warmer
Monitor for signs of infection
Feed with head turned to one side
Avoid latex products

Myelomeningocele:
Post-op Nursing Care

Monitor for wound healing

Monitor for signs of infection
Monitor for signs of hydrocephalus,

increased ICP
Place in prone or side-lying position
Measure head circumference daily
Assess intake and output
Keep diaper away from incision
site
Avoid latex products

Mylemeningocele: Nursing
Management Priorities
Prevent trauma and infection before and

after surgical repair of the defect

Promote urinary and bowel elimination
Neurogenic bladder is common
May need catheterization or surgery

Promote adequate nutrition

Prevent latex allergic reaction
Maintain skin integrity
Educate the child and family

Cerebral Palsy

Spastic
Dyskinetic
Ataxic
Mixed

Cerebral Palsy
Non-progressive, permanent, early onset motor disorder of
CNS resulting in alteration in movement and posture.
Results in activity limitations.
Etiology:
Intrauterine hypoxia/asphyxia
Intrapartum asphyxia
Preterm birth of LBW
Maternal infections rubella
Maternal drug use
Forceps, vacuum, trauma in

birth process
Kernicterus
Prolonged labor

CP: Clinical Manifestations

Classifications:
Spastic persistent primitive reflexes esp.
Babinski Hypertonicity- contractures scissor
gait= MOST COMMON CLINICAL TYPE

Dyskinetic

Athetoid chorea- involuntary, wormlike

movements of trunk, face and tongue
Dystonic drooling and imperfect speech + slow
twisting movement of trunk
Ataxic wide based gait, non spastic, cannot
reach for things or hold onto objects, disturbed
coordination, rapid repetitive movements
Mixed combination of spastic and athetosis

Possible Motor Signs of CP

Poor head control after age 3 mos
Stiff or rigid limbs
Arching back/pushing away
Floppy tone
Unable to sit without support at

age 8 mos
Clenched fists after age 3 mos

100

Cerebral Palsy:

Therapeutic Management
OVERALL FOCUS:
Assist the child to gain optimal
development and function within the
limits of the disease
TREATMENT IS:

Symptomatic
Preventative
Supportive

Cerebral Palsy:

Therapeutic Management
PHARMACOLOGIC MANAGEMENT:
Treat Spasticity:
Baclofen (Lioresal) po
Dantrolene sodium po
Diazepam po
Botulinum toxin injections
Continuous infusion of intrathecal
baclofen via implanted pump
SURGICAL MANAGEMENT
THERAPEUTIC MODALITIES:
Physical,

Speech, Occupational Therapy

Cerebral Palsy:

Nursing Management
Provide nursing care related to

therapeutic management modalities

Promote adequate nutrition
Maintain skin integrity
Promote physical mobility
Promote safety
Promote growth and development
Foster parental knowledge
Provide emotional support

Acceptance

Developmental and
Behavioral Disorders
Autistic Spectrum Disorders
Attention Deficit/hyperactivity
Disorder

Autistic Disorder
(Autism)
A developmental disorder characterized by
severely abnormal development of social
interaction and of verbal and nonverbal
communication skills which usually appears in
the first 3 years of life
Incidence:
Autism makes up 50% of the Autism Spectrum Disorders
2-15 times more common in males than females
1985:

0.4/1000 and in 2006: 6.6/1000

Affects 12-16% of children

Autism:

Etiology & Pathophysiology

Exact cause unknown
although biologically-based.
Possible Causes:
Biochemical

imbalances
Brain abnormalities
Genetic disorder of
pre/postnatal development
Immune responses to a virus
Toxic chemicals
No demonstrated relationship to
immunizations

Autism:

Warning Signs
Does not babble by 12 mos
Not pointing or using gestures

by 12 months
No single words by 16 mos
Does not use 2-word phrases
by 24 months
Losing language or social skills
at any age

Autism:

Clinical Manifestations
Inability to respond to change routine!
Echolalia repeating rhythm, rhyme, songs
Repetitive movements such as hand flapping or spinning
Stereotypy rigid, obsessive behavior
Inability to maintain eye contact, relate, refuses comforting
Indifference to touch or affection
Fascinated by spinning, light, sparkle, music
Self-injurious behaviors such as head banging, hand biting
Wont explore objects but will line them up, rituals
Restricted eating/touching certain colors, foods
Wide range of intellect Savant
May appear deaf
May make inappropriate noises

Autism:

Therapeutic Management
Goal: For child to reach optimal

functioning within the limitations of the

disorder
Individualized plans of care
Behavioral and communication therapies
important
Highly structured educational environments
Stimulants for hyperactivity
Antipsychotic medications for children with
repetitive and aggressive behaviors

Autism:

Nursing Management
Maintain

home routines as much as

possible
Set firm limits on behaviors
Provide safe environment
Stabilize environmental stimuli
Speak in short, direct sentences to
child
Provide anticipatory guidance
Assess parents need for respite care

ADD/ADHD
Attention Deficit Hyperactivity Disorder
is a variation in CNS processing
characterized by developmentally
inappropriate behaviors involving
inattention, impulsivity and hyperactivity
Incidence:
Males 4 x more than Females
25% - 1st degree relative

ADHD: Pathophysiology
Exact cause

unidentified
Possible deficit in
dopamine and
norepinephrine
Brain maturation delay,
as much as 3 years, on
imaging studies
Cortex especially
affected

ADHD: Risk Factors

Seizures and head trauma
High levels of lead or mercury exposure
Prenatal exposure to cigarette smoke or

alcohol
Prematurity, low birth weight
Genetic? Specific mechanism not yet
known. Genetic predisposition
Daily TV exposure from 1-3 years old
associated with attentional symptoms at
age 7

ADD/ADHD:
Clinical Manifestations
ADD - Difficulty concentrating; cannot

organize; loses things, forgets, failure to listen

when spoken to directly, forgets to finish
activity, feels different from others, isolated
ADHD: Frustration, labile moods, emotional
outbursts, peer rejection, poor school
performance, low self-esteem,
poor meta-cognitive abilities such as
poor organization
and poor time
management

Nursing Management:
ADD/ADHD
Administer stimulant medications
Minimize environmental distractions
Implement behavioral management

plans
Provide emotional support
Promote self-esteem

Cognitive Disorders
Down Syndrome
Fragile X
Fetal Alcohol Syndrome

Cognitive Impairment
Intelligence significantly below average,

existing with limitations in adaptive skills

Whos at Risk?
Prenatal Down Syndrome, fetal alcohol
syndrome, infections
Postnatal factors brain trauma, metabolism
Management:
Stimulation and activities
Positive self-esteem: ability not disability!
Head start < 3 y/o premie assessments
Disabilities Act (education for all, IEP)

Severity Scale
Mild IQ 50-70 (normal > 90)
Mental age 8-12 yrs, reads, writes,
basic math, vocational
Moderate - IQ 35-50 Mental age 37 yrs, trainable, sheltered work
Severe - IQ 20-35 Mental age 0-2
yrs, total care
Profound - <20, total care, infantile

Intellectual Disability:
General Concepts
Mild to severe
IQ is not as important as

functional assessment
Motor

movement
Language
Adaptive behavior

Achieve developmental milestones

slowly

Nursing Management of
Intellectual Disability
Early detection and screening

Developmental milestones
Denver II developmental screening test

Provide emotional support and information

Loss of perfect child

Support groups
Honest information

Maintain safe environment

Physical safety
Safety with strangers

Nursing Management of
Intellectual Disability
Promote adaptive functioning
Allow home routine during

hospitalization

Self-care routines
Medication schedules
Medication administration techniques
Interventions (suctioning, feeding, etc)

Down Syndrome
Trisomy 21, characterized by

intellectual disabilities in
varying degrees and multiple
associated defects
Life expectancy to ~60
y/o
Whos at Risk? 1:733
babies
Increasing with maternal
age
But 80% born to < 35 y/o

Down Syndrome:

Clinical Manifestations

Hypotonia
Simian crease on palm
Small stature
Epicanthal eye folds
Small, low set ears
Flat nose
Short, thick neck
Protruding tongue
Cognitive impairment- continuum

Common Co-existing Conditions:

Congenital heart disease
Respiratory infections d/t constant stuffy nose and
mouth breathing
Leukemia, Hearing loss, Thyroid disease, Strabismus

Fragile X Syndrome
Genetic anomaly on X chromosome
Protein necessary for normal brain

development is missing
Clinical manifestations
Long face with prominent jaw and large
ears
Strabismus
Aggressive behaviors
Intellectual Disability

Fetal Alcohol
Syndrome

Caused by effect of

alcohol on developing
fetus
Clinical manifestations
Failure to thrive
Flat midface with
low nasal bridge
Poor coordination
Poor impulse control
Low normal IQ to
Intellectual Disability