Cerebral palsy cp
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Cerebral Palsy (CP). Disorders characterized by early onset and impaired movement and posture. It is a non-progressive disease. Incidence. 1.9-2.3 in every 1000 live births  in prevalence since the 1960’s due largely to the improved survival of VLBW infants. Etiology.

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Cerebral Palsy (CP)

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Cerebral palsy cp

Cerebral Palsy (CP)

Disorders characterized by early onset and impaired movement and posture. It is a non-progressive disease.


Incidence

Incidence

  • 1.9-2.3 in every 1000 live births

  •  in prevalence since the 1960’s due largely to the improved survival of VLBW infants.


Etiology

Etiology

  • 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.


Pathophysiology

Pathophysiology

  • 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.


Clinical classification of cp see box 40 2 in wong p 1693 9 th ed

Clinical Classification of CP(see box 40-2 in Wong, p.1693 9th ed.)


Clinical classification of cp cont

Clinical Classification of CP(cont)


Clinical classification of cp con t

Clinical Classification of CP (con’t)


Clinical manifestations box 40 4 wong p 1695 9 th ed possible signs

Clinical Manifestations ( Box 40-4, Wong, p. 1695 9th ed.—Possible Signs)

  • 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


Clinical manifestations box 40 4 wong p 1695 9 th ed possible signs1

Clinical Manifestations (Box 40-4, Wong, p. 1695 9th ed. —Possible signs)

  • Alterations of Muscle Tone—

    •  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 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.


Clinical manifestations box 40 4 wong p 1695 9 th ed possible signs2

Clinical Manifestations (Box 40-4, Wong, p. 1695 9th ed. —Possible signs)

  • 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


Diagnostic evaluation

Diagnostic Evaluation

  • 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.


Therapeutic management general concepts box 40 5 p 1696 9 th ed therapeutic interventions for cp

Therapeutic Management: General Concepts Box 40-5 p. 1696 9th ed.Therapeutic Interventions for CP

  • Broad aims:

    • Establish locomotion, communication, and self-help

    • Gain optimum appearance & integration of motor functions

    • Correct associated defects as effectively as possible

    • Provide educational opportunities adapted to the needs and capabilities of the individual child

    • Promote socialization experiences with other affected and unaffected children.


What is done

What is done—

  • 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.


What is done cont d

What is done—(cont-d)

  • 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.


Therapeutic management therapies education recreation

Therapeutic Management: Therapies, Education, Recreation

  • Physical Therapy—one of the most commonly used conservative txmodalites. 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


Nursing care see care plan pp 1702 1703 in 9 th ed

Nursing Care (see Care Plan pp.1702-1703 in 9th ed.)

  • 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://www.ucpa.org/search.cfm

  • Support hospitalized child—

    • the nurse’s actions should convey acceptance, affection, and friendliness and promote a feeling of trust and dependability.


Muscular dystrophy

Muscular Dystrophy

Gradual degeneration occurs in muscle fibers progressive weakness and symmetric wasting away of skeletal muscle


3 types of dystrophy table 40 2 p 1725 9 th ed

3 Types of DystrophyTable 40-2; p. 1725 9th ed.

  • 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

      • Website Part 2 with newest multidisciplinary guidelines from MDA—12-09


Limb girdle

Limb-Girdle

  • Onset after 8 y/o

  • Weakness of proximal muscles of pelvic and shoulder girdle

  • Slow progression 

    • Incapacitated 20 years after onset

    • OR slight disability


Facioscapulohumeral lansouzy dejerine

Facioscapulohumeral(Lansouzy-Dejerine)

  • Early adolescence

  • Symptoms

    • Lack of facial mobility

    • Can’t raise arms over head

    • Shoulders slope forward

  • VERY SLOW PROGRESSION


General dx tests

General Dx Tests

  • Serum Creatinine Phosphokinase (CPK)

  • Electromyography (EMG)

  • Muscle Biopsy


General trx

General Trx

  • Supportive

    • Physical Therapy

    • Orthopedic Trx (casting, bracing, surgery) to minimize deformities and maintain ability to perform ADL’s


Duchenne

Duchenne

  • Most severe + most common type

  • X-linked recessive

    • Inherited MOTHER carrier/Son Symptoms

  • Genetic mutation—ABSENT skeletal muscle protein


Cerebral palsy cp

S/S

  • Muscle weakness by 3 y/o

  • Hx delayed motor development

  • Abnormal Gait, Waddling

  • Falls Frequently

  • Marked Lordosis when standing

  • Gower’s Sign


Cerebral palsy cp

S/S

  • Enlarged calves, upper arms, thighs  fatty infiltration of muscle  pseudohypertrophic

  • Contractures

  • 12 y/o = unable to walk

  • Weakened respiratory muscles

  • Death


Complications

Complications

  • Contracture Deformities

  • Atrophy

  • Trx

    • PROM & AROM

    • Casting/Bracing

    • Rigid Corset

    • Frequent Rest

  • PT 3 hrs of ambulaton/day


Complications1

Complications

  • 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


Cardiac complications

Cardiac Complications

  • D/T Weakening of Cardiac Muscle

  • Treatment

    • Digoxin

    • Diuretics e.g furosemide


Diagnosis

Diagnosis

  • 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


Diagnosis1

Diagnosis

  • Muscle Biopsy

    • Degeneration of muscle fibers

    • Fatty deposits

    • Fibrosis

  • EMG

    • Diminished duration and amplitude of existing motor unit potentials


Nursing care

Nursing Care

  • 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


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