Transcript Slide 1
Disorders characterized by early
onset and impaired movement and
posture. It is a non-progressive
disease.
1.9-2.3
in every 1000 live births
in prevalence since the 1960’s due largely
to the improved survival of VLBW infants.
Greatest
prevalence is seen in prematurely
delivered infants.
Formerly
thought to be R/T perinatal birth
asphyxia, but now it is known that CP more
commonly results from existing prenatal
brain abnormalities.
24%
of cases have no identifiable cause.
Difficult
to determine exactly
ANOXIA
is most significant factor to cause
pathologic brain damage. This is often 2ndary
to other etiology.
The
area of the lesion in the brain mostly
determines the subsequent pathology.
•May involve one or both
sides.
•Hypertonicity with poor
control of posture, balance, &
•usually caused by hypoxic coordinated motion
infarction in the area
•Impairment of fine and gross
adjacent to the lateral
motor skill
ventricles.
•Active attempts at motion
•Upper motor neuron type increase abnormal postures
of muscular weakness.
and overflow of movement to
•See Box 40-3 (p.1693) for other parts of the body
Types of Spastic Cerebral
Palsy
Spastic:
MOST COMMON
Dyskinetic/
athetoid—
•Athetosis— slow, wormlike writhing
movements that usually involve the
extremities, trunk neck, facial muscles,
and tongue
•Abnormal involuntary
•Involvement of the pharyngeal,
movement
laryngeal, and oral muscles causes
drooling and dysarthria (imperfect speech
•Caused by kernicterus & articulation)
hemolytic disease of the
•Involuntary movements may take on
newborn which leads to
choreoid (involuntary, irregular, jerking
pigment deposits in the
movements) and dystonic (disordered
basal ganglia & some
muscle tone) manifestations that increase
cranial nerve nuclei.
in intensity with emotional stress and
around adolescence.
Ataxic
•Wide-based gait
•Rapid, repetitive movements
performed poorly
•Disintegration of movements of the
upper of the upper extremities when
the child reaches for objects
Mixed Type/
dystonic
•Combination of spasticity and
athetosis
Delayed
gross motor development—
universal manifestation of CP
Especially significant if other developmental
behaviors e.g. speech & personal social are normal
Abnormal
motor performance—
Early sign is preferential unilateral hand use
that may be apparent at ~6months of age.
May stand or walk on toes
Alterations
or resistance to passive movements is a sign of
abnormal muscle tone.
Child may exhibit opisthotonic postures and stiffness
on handling, dressing, or diapering.
Abnormal
of Muscle Tone—
Postures—
From an early age, a child lying in a prone position
will maintain the hips higher than the trunk with the
legs and arms flexed or drawn under the body.
Spasticity may be mild or severe.
Reflex abnormalities—
Persistence of primitive infantile reflexes is one of the
earliest clues to CP.
Associated Disabilities and problems—
Intellectual impairment—possible, but 70% are WNL
ADHD—poor attention span, marked distractibility,
hyperactive behavior,and defects of integration
Seizures—most common in postnatal acquired hemiplegia
Drooling, feeding and speech needs, risk of aspiration &
possible inadequate gas exchange.
Orthopedic complications
Constipation
Dental caries, malocclusion, gingivitis
Nystagmus, amblyopia & hearing loss
Neurologic
Examination & History are the
primary modalities for diagnosis
Recognizing
etiologic factors that put the
infant at risk is critical in the assessment and
diagnostic process.
Broad aims:
1. Establish locomotion, communication, and selfhelp
2. Gain optimum appearance & integration of
motor functions
3. Correct associated defects as effectively as
possible
4. Provide educational opportunities adapted to
the needs and capabilities of the individual child
5. Promote socialization experiences with other
affected and unaffected children.
Mobilizing devices—braces, crutches, wheelchairs,
walkers
Surgery—when spasticity causes further deformities
Medication—drugs to spasticity are often NOT
helpful in CP. Antianxiety meds may help child with
athetosis.Skeletal muscle relaxants e.g. baclofen,
methocarbamol (Robaxim), or dantrolene
(Dantrium) & Valium may help short-term for older
children & adolescents. Antiepileptic meds, e.g.
phenobarbital & phenytoin are used routinely for
children with seizures & CP.
Technical
aids—e.g. electromechanical toys
that use biofeedback; microcomputers
combined with voice synthesizers, or activated
with a head-stick, tongue,or other voluntary
muscle movement over which the child has
control.
Other Considerations—care of vision & hearing
deficits as well as dental care is essential early
on.
Physical
Therapy—one of the most commonly
used conservative tx modalites. Involves PT,
family, and nsg
Functional & Adaptive Training (Occupational
Therapy)—training in manual skills and ADL’s must
be started early
Speech Therapy—start early to prevent speech
problems.
Education—individualize to the needs of the child
Recreation—sports, physical fitness, & recreation
programs are encouraged for children with CP
Reinforce therapeutic plan/assist in Normalization
Address Health Maintenance needs
Watch for fatigue, nutritional needs, safety needs
Support family
Help them cope with the emotional aspects of the disorder
Make appropriate referrals to support groups e.g United
Cerebral Palsy Association.
http://cerebralpalsy.org/
Support hospitalized child—
the nurse’s actions should convey acceptance, affection,
and friendliness and promote a feeling of trust and
dependability.
Gradual degeneration occurs in muscle
fibers progressive weakness and
symmetric wasting away of skeletal muscle
Pseudohypertophic
(Duchenne)
X-linked Recessive
1-3 years of age
Lordosis, Waddling gait
Rapid progression—
Death 15-25 after onset
Website Part 1 with newest Guidelines from MDA—12/09
Part 2 with newest multidisciplinary guidelines from MDA—1209: Bushby, K., Finkel, R., Birnkrant, D. J., Case, L. E.,
Clemens, P. R., Cripe, L., & ... Constantin, C. (2010).
Diagnosis and management of Duchenne muscular dystrophy,
part 2: implementation of multidisciplinary care. Lancet
Neurology, 9(2), 177-189. doi:10.1016/S1474-4422(09)70271-6
Onset
after 8 y/o
Weakness of proximal muscles of pelvic and
shoulder girdle
Slow progression
Incapacitated 20 years after onset
OR slight disability
Early
adolescence
Symptoms
Lack of facial mobility
Can’t raise arms over head
Shoulders slope forward
VERY
SLOW PROGRESSION
Serum
Creatinine Phosphokinase (CPK)
Electromyography (EMG)
Muscle Biopsy
Supportive
Physical
Therapy
Orthopedic Trx (casting, bracing,
surgery) to minimize deformities and
maintain ability to perform ADL’s
Most
severe + most common type
X-linked recessive
Inherited MOTHER carrier/Son Symptoms
Genetic
protein
mutation—ABSENT skeletal muscle
Muscle
weakness by 3 y/o
Hx delayed motor development
Abnormal Gait, Waddling
Falls Frequently
Marked Lordosis when standing
Gower’s Sign
Enlarged
calves, upper arms, thighs
fatty infiltration of muscle
pseudohypertrophic
Contractures
12 y/o = unable to walk
Weakened respiratory muscles
Death
Contracture
Deformities
Atrophy
Trx
PROM & AROM
Casting/Bracing
Rigid Corset
Frequent Rest
PT
3 hrs of
ambulaton/day
Infections
d/t
decreased vital
capacity and atrophy
of resp muscles
Obesity
d/t
overfeeding and
decreased activity
Antibiotics
Resp.
Trx
Chest Physiotherapy
Diet
Recreation
as tol.
Maintain mobility as
long as possible
D/T
Weakening of
Cardiac Muscle
Treatment
Digoxin
Diuretics e.g
furosemide
Serum
Enzymes
Creatinine Phosphokinase
Aldoase
Glutamic-oxaloacetic transaminase (SGOT)
Very
high levels in 1st 2 years of life
Levels decrease as muscle deteriorates
WNL when severe wasting and disability
Muscle
Biopsy
Degeneration of muscle
fibers
Fatty deposits
Fibrosis
EMG
Diminished duration
and amplitude of
existing motor unit
potentials
Help
maintain independence
Continual evaluation of capabilities
Home Assessment
Set-up w/c assessible?, wide doors?, etc
Buying clothes
Respite
Care
Family Involvement
Genetic Counseling