Clinical Features and Management of Cerebral Palsy

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CHAPTER 225 Clinical Features and Management of Cerebral Palsy

Janice E. Brunstrom-Hernandez, Ann Tilton

Cerebral palsy (CP) is “a group of disorders affecting the development of movement and posture, causing activity limitation, that are attributed to non progressive disturbances that occurred in the developing fetal or infant brain. The motor disorders of cerebral palsy are often accompanied by disturbances of sensation, cognition, communication, perception and/or behavioral and/or by a seizure disorder.”1

The estimated prevalence of CP is 1.5 to 3.0 per 1000 live births worldwide, with differences among countries, racial/ethnic groups, and socioeconomic classes.2,3 In most cases the cause of CP is not well defined, and it may vary with the subtype; prematurity and low birth weight are major risk factors for CP, especially bilateral spastic CP associated with periventricular white matter injury. Although birth asphyxia is uncommon, it is associated with the dyskinetic CP subtypes.3 Multiple genetic and metabolic factors may predispose infants to an increased risk for brain injury and CP.4

Diagnosis and Classification

Children with CP have a delay in motor development and abnormal motor findings on examination. Evaluation begins with a detailed history and physical and neurological examination, including careful documentation of prenatal, perinatal, and neonatal events and risk factors, developmental milestones, family history, general medical history, and a detailed survey to look for associated impairments (e.g., seizures, language disturbance, vision and hearing loss, nutritional difficulties). All CP patients should undergo magnetic resonance imaging, which may help reveal the underlying brain injury,5 although neither imaging nor laboratory tests can prove the diagnosis. An atypical history, clinical features, or imaging findings should trigger further evaluation, especially if there is any history of developmental regression or loss of skills.3,6 Disorders that masquerade as CP include familial spastic paraparesis and dopa-responsive dystonia. Some patients, including those with typical risk factors for CP (twin gestation, prematurity, periventricular leukomalacia) have “CP plus” and are found to have a coexisting metabolic disorder (e.g., mitochondrial encephalomyopathy).

There is currently no universally accepted classification system for CP, but since the mid-1900s, CP has most commonly been classified into “spastic” or “dyskinetic” subtypes based on the predominant type of tone abnormalities or movement disorders, or both, present. Spastic CP is the most common and is further divided into spastic diplegia (legs more than the arms), spastic quadriplegia (arms equal to or more than the legs), and spastic hemiplegia (involvement of one side of the body). Dyskinetic CP is divided into dystonic and choreoathetoid forms. A small subset of patients may be classified as ataxic. However, there is great disparity among practitioners regarding the use of these terms, such that a given patient may be classified differently by different clinicians.7 This is a major weakness in the field, and correcting it is a priority for furthering research and treatment.

In 2000, the Surveillance for Cerebral Palsy in Europe group adopted a standardized system for database and registry purposes that is used throughout Europe and Australia. Patients are classified as “spastic bilateral” or “spastic unilateral.” Individuals with variable tone are classified as “dyskinetic” and then further classified as dystonic or choreoathetoid/hyperkinetic. Those with hypotonia and ataxia are classified as “ataxic.” Some patients are nonclassifiable. Additionally, clinically useful functional scales for both gross motor function (Gross Motor Function Classification Scale [GMFCS],8 Functional Mobility Scale9) and fine motor/hand function (Manual Ability Classification Scale,10 Bimanual Function Measure11) are now available to allow improved description of motor function in patients with CP. A Communication Function Classification System is currently being validated (M. J. Cooley Hidecker, personal communication).

The clinical description of a patient with CP should include a detailed account of the movement disorder and tone abnormalities (e.g., spasticity, dystonia, athetosis, chorea, myoclonus), the presence of abnormally persistent primitive reflexes (startle, asymmetric tonic neck reflex) and absence of protective reflexes (parachute), assessment of muscle strength when possible (although a patient’s inability to isolate specific muscle groups may limit such assessment), topography of the movement disorder (limbs and body parts involved and how they are affected), motor function (including use of the aforementioned scales), and secondary musculoskeletal impairments (osteopenia, fracture, scoliosis, hip dysplasia, muscle contractures, bony deformities) that may further compromise mobility and quality of life. Most patients have multiple impairments. Dissecting out and treating, as possible, the various abnormalities will have the biggest impact on future motor outcome.

Associated Impairments

Although the hallmark of CP is the motor disorder, nearly all children with CP have one or more associated impairments that may impede their functional abilities, health, and overall quality of life; they often prove more detrimental than the motor disability. Associated neurological impairments (e.g., vision, hearing, and sensory deficits, epilepsy) can be attributed to brain/nervous system injury that extends beyond the motor system. Other impairments (e.g., musculoskeletal deformities, contractures, fractures, pain) may be secondary to spasticity, other movement disorders, and immobility. Several health impairments in children with CP may have a neurogenic component and can also be further exacerbated by the impaired mobility (e.g., bladder dysfunction, disorders of intestinal motility, sleep disorders). Every child with CP deserves a systematic and detailed survey to identify associated impairments because appropriate treatment can be life changing.

Neurological Impairments

Sensation

Visual disorders are common in children with CP but are often missed or inaccurately diagnosed.12 Over half of children with spastic CP and no obvious visual deficit will nonetheless have visual perception disorders.13 The severity of the visual deficit tends to correlate with the severity of CP involvement and is increased with a history of prematurity, severity of periventricular leukomalacia, and the presence of dyskinetic CP.12,14

Children with multiple visual impairments are often misdiagnosed as having untreatable “cortical visual impairment,” which leads to devastating consequences on communication, learning, social interactions, and quality of life. True cortical visual impairment affects approximately 16% of patients.12 Detailed assessment may be required to untangle the various contributors to the visual impairment but may lead to dramatic improvement in vision through surgery (e.g., strabismus correction, lens replacement, laser treatment) and corrective lenses.

Hearing impairments occur in approximately 7% of children with CP but are likely to be missed, especially in nonverbal children.

Even children with the mildest spastic CP are likely to have deficits in tactile and proprioceptive sensation,15 and their severity may correlate with the severity of the motor dysfunction.16

Communication

Communication difficulties are present in nearly 60% of all patients with CP, including up to 90% of children with quadriplegic or dyskinetic CP, or both.17

Epilepsy

Approximately a third of all children with CP have epilepsy. The prevalence varies with the subtype of CP, from 16% in children with diplegic CP to 50% in those with quadriplegic CP.17 The prognosis depends on the subtype of CP, brain imaging abnormality, and cognitive ability. Children with CP and epilepsy are much less likely to achieve freedom from seizures with or without antiepileptic drugs, and they are more likely to require polytherapy.18

Cognition/Behavior

Median intelligence quotient (IQ) scores are lower in children with CP, with 40% to 65% having an estimated IQ of less than 70. Detailed neuropsychological testing should be performed before a child starts school. Accurate assessment is difficult if not impossible in many children because of their multiple other impairments. Thus, low estimates of intellect should be interpreted cautiously. Children with severe CP and limited or absent communication skills often have spared nonverbal reasoning abilities. Conversely, nonverbal learning disorders may be missed in a child with superior verbal skills.19

Health Impairments

Impaired motor function leads to significant health problems. Children with severe mobility impairments tend to be less healthy and spend more time in bed and more days in the hospital, are more likely to be malnourished, and are often taking more medications than their nondisabled peers.20,21 Additionally, risk for fracture, hip dislocation, and scoliosis is elevated in nonambulatory patients with CP.22–24

Gastrointestinal

Moderate gastrointestinal symptoms occur in up to 90% of children with CP, including one or more of the following: drooling, swallowing problems (30% to 60%), regular vomiting (30%), gastroesophageal reflux disease, and delayed gastric emptying (70%).25–28 Even mild feeding dysfunction is significant and associated with lower body weight and reduced body fat stores.

Renal

Approximately two thirds of patients with CP have symptoms of voiding dysfunction, including difficulty voiding and daytime urinary incontinence. The prevalence of significant pathology (increased detrusor muscle contraction, reduced detrusor muscle compliance, reduced bladder capacity, inability to relax the external urethral sphincter, and high postvoid residuals) may be as high as 97%29–33 and can increase the risk for progressive decline in upper urinary tract function and renal disease.34,35 Urinary tract infections are also common in children with CP29,36 and can lead to scarring and chronic renal insufficiency.37

Improving Mobility and Motor Function (“I Want to Walk”): How Do We Help Them?

Improving a child’s ability to move is a major goal for most parents (and children). Children enjoy moving! The secondary consequences of immobility are high. Most children with CP have inadequate physical fitness, which further contributes to their poor health, pain, and secondary impairments.38

Physical and Occupational Therapy

Physical and occupational therapy occurs in many different settings, including traditional (home, school, private clinic) and nontraditional (e.g., therapeutic horseback riding39,40 and adapted sports). The therapist has a pivotal role as a teacher to help patients master new motor skills and teach parents (and older patients) exercises (stretching, strengthening, balance) and adaptive techniques (assistive technology for activities of daily living, access to computers or communication devices) that they can integrate into their daily life.

A variety of new tools are available to the physical therapist, such as electrical stimulation, which may have a positive effect on range of motion,41–43 and treadmill training with partial body weight support, which may be beneficial for a moderately severely impaired child (GMFCS III or IV).44 Ankle-foot orthoses are commonly prescribed for children who have a dynamic equinus abnormality, may be more effective in younger children,45 and can improve their ability to perform sit-to-stand transitions.46 The most effective type and “dose” or frequency of physical therapy remains controversial. Recent studies suggest that intermittent bursts of intense therapy for a few weeks with several weeks off between sessions may be as effective as continuous therapy 1 to 2 times per week.47

In the upper extremity, constraint-induced therapy and forced use have re-emerged as a useful tool. In clinical trials, restraint of the child’s better functioning hand/upper limb in combination with occupational therapy improves function in the affected limb (new motor skills and increased dexterity) for at least 6 months.48–52 Repeat courses of treatment lead to additional improvement.53 Botulinum neurotoxin (BoNT) combined with occupational therapy is another effective strategy.54 Recent, exciting advances include the use of robotics to improve upper extremity function.55

Therapy programs along with overall management of a child’s hypertonia and mobility impairments must be goal-driven and tailored specifically to each child’s needs (Table 225-1). For example, children with spasticity need regular stretching of spastic muscles to optimize range of motion and prevent contractures. Strengthening exercises to reverse disuse atrophy may improve gait and do not worsen the spasticity.56–59 Conversely, in children with generalized dystonia and hyperkinetic CP who are constantly moving or contracting their muscles, both stretching and strengthening may prove impractical if not impossible.

TABLE 225-1 Therapeutic Approach to Patients with Cerebral Palsy Based on Distribution and Severity*

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Management of Hypertonia and Spasticity in Children with Cerebral Palsy

Hypertonia is defined as abnormally increased resistance to externally imposed movement about a joint. The Task Force on Childhood Motor Disorders recently developed a consensus definition of spasticity as “hypertonia in which one or both of the following signs are present: (1) resistance to externally imposed movement increases with increasing speed of stretch and varies with the direction of joint movement, and/or (2) resistance to externally imposed movement rises rapidly above a threshold speed or joint angle.”60

Tone reduction may be considered if the hypertonia/spasticity interferes with function, cosmesis, comfort, or care. However, spasticity and hypertonia rarely exist as isolated impairments in children with CP, and many children also have associated weakness (trunk, neck, limbs) and loss of selective motor control. Systemic medications to alleviate hypertonia in the extremities may worsen head and trunk control in patients with quadriplegia or moderate to severe diplegia. Some patients with severe lower extremity hypertonia effectively use their tone to “stand up” on otherwise weak limbs and may lose their ability to participate in transfers after treatment. Thus, a comprehensive team approach that includes physicians, allied health therapists, and the family and patient leads to the best outcome. Treatment goals should be continuously re-examined and revised in accordance with the entire picture, including clinical, home, and school factors.

Oral Medications

Oral medications are often considered the first line of intervention for spasticity despite the fact that none have been approved by the Food and Drug Administration (FDA) or even adequately tested in children. Most studies documenting efficacy were conducted many years ago with less than adequate study designs and no functional measures. Data from more recent trials in adults cannot be directly extrapolated to children. Oral medications are prescribed for patients with widespread spasticity and for those with only mild hypertonia. Although these medications are attractive because of the ease of use, this benefit is often outweighed by side effects, especially sedation.

Baclofen

Baclofen is a γ-aminobutyric acid type B receptor (GABAB) agonist that is well recognized to be efficacious for spasticity of spinal cord origin in adults. There are limited studies in childhood addressing the use of oral baclofen and even fewer double-blind, placebo-controlled studies. Milla and Jackson showed in a double-blind crossover trial that baclofen reduces spasticity and allows more passive and active movements than placebo does.61 However, in a separate trial, there was no effect measured by the Pediatric Evaluation of Disability Inventory or the Modified Tardieu Scale. On the Goal Attainment Scale there was some functional improvement.62

Reports of side effects with baclofen use are varied. Confusion and sedation are a concern, although this tends to improve with use. The initial dose is traditionally 2.5 mg/day and is gradually increased up to a maximum of 20 to 60 mg/day.63 As with most medications, baclofen must be weaned slowly to avoid a withdrawal syndrome, which includes increased spasticity, mental confusion, and possibly seizures.64

Tizanidine

Tizanidine is a centrally acting α2-adrenergic agonist that reduces tonic stretch reflexes by presynaptic inhibition. Only one English-language trial of tizanidine in children has been published, and it showed that tizanidine was superior to oral baclofen as an adjunct to BoNT-A in patients with gastrocnemius spasticity, as measured by the Gross Motor Function Measure and caregiver questionnaire.65 Sedation and frequent dosing have been reported as limiting factors in adults, although in patients who have difficulty with sleep initiation, the sedative quality can actually be an advantage.

Diazepam

Diazepam is a benzodiazepine that acts by facilitating the postsynaptic action of GABA. Studies from the 1960s indicate its capacity to reduce spasticity. More recently, Mathew and colleagues compared diazepam with placebo in 180 children and demonstrated its ability to reduce muscle overactivity.66 A comparison of diazepam and dantrolene showed that both agents were equally effective and that a combination of the two was superior to either alone.67 The usual dosage of diazepam is 0.12 to 0.8 mg/kg up to the adult maximum. This dosage is divided into three to four doses across the day. Sedation is a known side effect of the benzodiazepines. Thus, use as a sleep aid may also be an added advantage.

Dantrolene Sodium

Dantrolene inhibits release of calcium from the sarcoplasmic reticulum. In two double-blind, crossover studies, spasticity was reported to be reduced67,68; however, in another placebo-controlled study, the reduction in spasticity could not be verified.69 The side effect profile is also a limiting factor. Diffuse weakness and sedation despite the peripheral mode of action have been noted. Moreover, hepatotoxicity is a concern for adults and thus considered a risk factor for children as well.

Focal Spasticity

Botulinum Toxin

BoNT, a chemodenervant that is produced by Clostridium botulinum and injected into muscle, prevents the release of acetylcholine and causes nerve terminal atrophy (e.g., gastrocsoleus injection to improve heel cord range). There are seven naturally occurring serotypes, all of which are proteolytic enzymes that target acetylcholine vesicle fusion at the neuromuscular junction. Loss of acetylcholine release causes muscle weakness. Serotype A is commercially available in several forms, including Botox, Dysport, and Xeomin. Serotype B is marketed as Myobloc in the United States and as Neurobloc elsewhere. The serotypes differ in their molecular targets, and even within a serotype, individual products differ in unit potency, side effect profile, duration of action, and immunogenic potential. Because of these differences, there are no simple dose conversion ratios among the various marketed products. When discussing dosing, it is critical that the commercial brand be specified. When it is not specified in the literature, it is not appropriate to assume that a particular brand is being used.

All forms of BoNT have come under recent review by the FDA after postmarketing reports that its effects may spread to produce symptoms distant from the injection site. Symptoms include generalized muscle weakness, vision difficulties, ptosis, swallowing difficulties, urinary incontinence, and respiratory compromise. These symptoms have been reported hours to weeks after injections and in some cases have been life-threatening or associated with patient death. The risk is probably greatest in children treated for spasticity because of the relatively large doses used and the presence of comorbid conditions.

Overall, BoNT-A has a good safety profile and appears to be effective in the management of focal spasticity in both the upper and lower extremities in patients who have CP. To date, only a few open trials using BoNT-B in this population have been published. BoNT-B has a tendency to cause more autonomic side effects than BoNT-A, and this must be taken into consideration with its use.

Well in excess of 100 studies involving BoNT-A in children with CP have been published, the majority of which were positive, with spasticity significantly reduced even at 3 months after injection.70 Functional improvements after BoNT injection have been demonstrated in the lower71–73 and upper53 extremities. BoNT has also been used to reduce pain.74

Dosing recommendations for BoNT-A as Botox have been developed over time by consensus.75 Dosing must be individualized and is based on multiple parameters, including the child’s weight, muscle bulk, degree of spasticity, and previous response to therapy, if any. The lowest effective dose should be used, and an injection interval of at least 3 months is recommended to minimize the risk for antibody formation. Most children tolerate the injections because of the very short time frame required to complete them. Some children may need a topical anesthetic or light sedation.

Adverse effects of BoNT injections are usually mild and transient. There is pain at the time of injection, and a mild flu-like syndrome has been reported. Excessive weakness has also been reported, as has migration of medication, as mentioned earlier.76,77

Serial Casting

Serial casting of the ankle is an effective treatment of ankle equinus and, when combined with BoNT injections, produces results superior to those of BoNT alone.78 It has been recommended that casting should follow injections by 2 to 4 weeks to make use of the peak effect of the toxin.79

Phenol and Alcohol

Phenol and alcohol cause axonal degeneration and are used by some clinicians to target larger lower extremity muscles (e.g., obturator nerve injection to improve adductor range). Phenol and ethyl alcohol have not been rigorously tested in children. Use of these agents often requires sedation or anesthesia because of the duration of the procedure and discomfort. Adverse effects include pain or paresthesias, or both, if a mixed motor and sensory nerve is targeted; the effects may be long lasting.

Multisegmental and Generalized Spasticity

Selective Dorsal Rhizotomy

Selective dorsal rhizotomy (SDR) has been used to treat moderate to severe lower extremity spasticity since the 1980s (see Chapter 227).80–83 A patient who is selected for SDR is typically ambulatory or nearly ambulatory (GMFCS II to III, sometimes GMFCS I) and between 4 and 7 years of age, has spared cognitive skills and is motivated to walk, has some degree of preserved selective motor control in the lower extremities, has adequate strength, and exhibits minimal if any dystonia. Additionally, it is critical that the family commit to a rigorous daily physical therapy program for 6 to 12 months.

Intrathecal Baclofen

Intrathecal baclofen is a technique in which a very low dose of baclofen is delivered into the intrathecal space by way of a catheter attached to a programmable, implantable pump (see Chapter 226).84,85 The dose is less than 1% of that delivered orally because of the direct delivery system to the central nervous system; such delivery reduces the principal side effect of sedation. Intrathecal baclofen is generally a consideration in children who have multisegmental or generalized spasticity/hypertonia, particularly those in whom lower extremity spasticity is a major component. Upper extremity spasticity can also be treated, particularly when the catheter tip is placed at the high thoracic or even cervical level.

Orthopedic Surgery

Despite aggressive therapies and management of spasticity/hypertonia, many children with spastic CP eventually require orthopedic surgery to treat secondary deformities (muscle contractures, hip dysplasia, bony deformities).86 Correction of hip subluxation typically involves adductor tenotomies, femoral osteotomy, or acetabular repair (or any combination of these procedures). An equinovarus foot is the most common deformity in CP and can become fixed and refractory to bracing, casting, or BoNT. Surgical treatments include tendon- or muscle-lengthening procedures, or both, to restore heel cord range. In children with severe varus posturing of the foot (as can be seen in focal spasticity or mixed spastic-dystonic disorders), split-tendon transfers may be of some benefit. Progressive hamstring contractures can occur after growth spurts, and hamstring tenotomies are commonly performed in adolescent patients with CP. Osteotomies to derotate the femur or tibia may be needed to correct rotational deformities when internal or external foot progression impedes gait or these deformities place undue strain on the knee.

Dystonia and Mixed Movement Disorders in Cerebral Palsy

The motor dysfunction in children with CP is not simply attributable to spasticity or corticospinal tract dysfunction but instead is due to disruption of the complex integration of multiple areas of the brain, including the cortex, cerebellum, basal ganglia, brainstem, and other areas. As a result, a child with CP may manifest other kinds of hypertonia and movement disorders.

It is becoming increasingly apparent that mixed movement disorders are more the norm than the exception in patients with CP and that isolated “pure” spasticity or dystonia is relatively uncommon. The severity and predominance of the primary component of the mixed movement disorder have a direct impact on the success of treatment. Movement disorders such as dystonia and choreoathetosis are much less responsive than spasticity to the traditional measures described earlier (physical therapy, oral medications, BoNT, surgical interventions).

Dystonia is defined as a movement disorder in which involuntary sustained or intermittent muscle contractions cause twisting and repetitive movements, abnormal postures, or both.60 Dystonia is often due to basal ganglia injury.

Dystonia may not be evident early in a patient’s life (before the age of 3 or 4 years) and may then evolve and progress over time.87–89 Patients may manifest significant dystonia at 12 or 13 years of age. This has obvious implications when considering that earlier interventions such as SDR might have been performed earlier in life. The development of unrecognized dystonia may lead to the erroneous conclusion that SDR had failed.

BoNT is an effective therapy for focal dystonia, as well as spasticity, and the indications for its use frequently coincide. There are limitations to its application in patients with multisegmental or generalized dystonia because of dosage restrictions and difficulty accessing deep muscles.

Dystonia can severely interfere with a patient’s daily function, and treatment choices are limited. Oral medications are often used but have been of controversial efficacy. Diazepam in particular has been tried in children with this movement disorder, but its clinical efficacy in ameliorating athetosis indicates that generalized relaxation is a major component of its action.90 A recent open-label, multicenter, clinical trial of trihexyphenidyl in children with CP showed some evidence of efficacy in the upper extremity 15 weeks after starting treatment, but not at 9 weeks. Children with hyperkinetic-dystonic movement disorders appeared to worsen during trihexyphenidyl therapy but returned to baseline after tapering from the medication.91 An additional pilot study of 14 children with generalized dystonia treated with trihexyphenidyl revealed improvement in both the Goal Attainment Scale and Canadian Occupational Performance Measure but not in the primary outcome measure, the Barry-Albright Dystonia Score.92 Side effects were frequent in both studies.

Levodopa/carbidopa has been used clinically because of its known action on other movement disorders, but clinical trials in children with CP are lacking. Levetiracetam has recently been reported to be helpful in managing paroxysmal kinesigenic choreoathetosis93 and may improve balance and fine motor skills in children with choreoathetosis.94–96

Tetrabenazine, a monoamine-depleting medication, has been used for multiple hyperkinetic movement disorders for more than 30 years. It has recently been approved in the United States for use in Huntington’s disease. Its use in patients with CP and associated hyperkinetic movement disorders has been anecdotal.97,98

Oral baclofen has been used for hyperkinetic movement disorders with minimal success by clinical report. Several studies have reported improvement of generalized secondary dystonia with intrathecal baclofen: improved comfort and ease of care in 85% and functional improvement in approximately 33%.99 Interesting clinical data have come from an open-label study of 10 patients with either severe secondary generalized or heredodegenerative dystonia and the use of intraventricular baclofen for dystonia.100 Eight of the 10 patients responded to the infusion with significant improvement as measured by the Barry-Albright Dystonia Score. The medication is hypothesized to act at the cortical level.

Bilateral pallidal deep brain stimulation has also gained interest in the care of children and adults with CP and associated dystonia after its successful use for many cases of idiopathic and secondary dystonia of other causes.101,102 In a prospective pilot multicenter study of 13 adult patients with dystonic-choreoathetoid CP, improvements were seen in the Burke-Fahn-Marsden dystonia rating scale, as well as measures of functional disability, pain, and mental health–related quality of life at 1 year. The posterolateroventral region of the globus pallidus pars interna was deemed the optimal target.102

Conclusion

The highest standard of care for children with CP requires a team of experts working together who understand the importance of a “leave-no-stone-unturned” approach to systematically identify and treat the motor disorders, other neurological disorders, and myriad associated impairments affecting these children. There is a great dichotomy in the treatment and prognosis of children with different functional levels and CP subtypes. Ambulatory children with mild spastic CP have more options from which to choose and are likely to do well.103 Treatment options for children with severe motor impairment and complicated mixed movement disorders are much fewer and less effective, and these children are at higher risk for medical complications and poor health. The neurosurgeon has the capacity to make a powerful impact on the lives of these children. Procedures such as SDR and intrathecal baclofen in the right clinical setting can change the life of a child for the better. Yet there is much more work to be done to develop neurosurgical techniques that will reach even the most severely disabled children who are currently “locked in” their uncooperative bodies waiting for their chance at full participation and optimal quality of life.

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