Hypertonia: abnormally increased resistance to externally imposed movement about a joint. It may be caused by spasticity, dystonia, rigidity, or a combination of features
Spasticity: a velocity-dependent resistance of a muscle to stretch. One or both of the following signs may be present:
1. Resistance to externally imposed movement increases with increasing speed of the 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
Dystonia: a movement disorder in which involuntarily sustained or intermittent muscle contractions cause twisting and repetitive movements, abnormal postures, or both
Rigidity: hypertonia in which all of the following are true:
1. The resistance to externally imposed joint movement is present at a very low speed, and does not exhibit a speed or angle threshold
2. Simultaneous co-contraction of agonists and antagonists may occur, and this is reflected in an immediate resistance to a reversal of the direction of movement about a joint
3. The limb does not tend to return toward a particular fixed posture or extreme joint angle
4. Voluntary activity in distant muscle groups does not lead to involuntary movements about the rigid joints, although rigidity may worsen
Chorea: an ongoing random-appearing sequence of one or more discrete involuntary movements or movement fragments
Athetosis: a slow, continuous, involuntary writhing movement that prevents maintenance of a stable posture
Myoclonus: a sequence of repeated, often nonrhythmic, brief shock-like jerks due to sudden involuntary contraction or relaxation of one or more muscles
Tremor: a rhythmic back-and-forth or oscillating involuntary movement about a joint axis
Tics: repeated, individually recognizable, intermittent movements or movement fragments that are almost briefly suppressible and are usually associated with an awareness of an urge to perform the movement
Stereotypies: repetitive, simple movements that can be voluntarily suppressed
According to these definitions, childhood disorders can be divided into three major categories: hypertonic disorders, hyperkinetic disorders, and negative signs. Hypertonic disorders include spasticity, dystonia, and rigidity. Hyperkinetic disorders encompass chorea, dystonia, athetosis, myoclonus, tremor, stereotypies, and tics. Negative signs consist of weakness, reduced selective motor control, ataxia, apraxia, and developmental dyspraxia, although these are not discussed here [2].
In adult MDs, it is frequently helpful to divide disorders into primary and secondary disorders, although there is no consistent definition of these terms. Many authors refer to disorders as primary if there is only a single dominant symptom, and the underlying cause is presumably genetic or an identified gene. However, the existence of a single symptom in childhood MDs is probably the exception rather than the rule [2].
As this is a book that deals with rehabilitation of MDs, we discuss the disorders that are of interest in pediatrics: cerebral palsy and dystonia.
Cerebral Palsy
The term “cerebral palsy” constitutes a useful socio-medical framework for certain motor disabled children with special needs. However, it does not describe a single disease entity but rather a collection of disorders with different etiologies [6].
Cerebral palsy (CP) is defined as “a group of disorders of 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” [7]. Virtually all such disturbances occur during or before early infancy. Although tone and postural abnormalities may become more pronounced during early childhood, qualitative evolution is uncommon. The full extent of motor disability may not be evident until the age of 3 or 4 years [8]. Intellectual, sensory, and behavioral difficulties may accompany CP, and are especially common in patients with spastic quadriplegia and severe motor disability [9].
Children with CP often exhibit mental retardation (52 %), hearing impairment (12 %), and speech and language disorders (38 %) [10], in addition to congenital anomalies [11]. Epilepsy occurs in 34–94 % of children with CP, depending on the study population. Although neurological impairment beyond the motor involvement frequently occurs, the diagnosis of CP rests upon the presence of motor disability alone [8].
Cerebral palsy occurs in 1.2–3.6 children per 1,000 live births [8]. Numerous CP registries exist throughout the world, and population prevalence rates from four continents have remained consistent over several decades [12]. Prematurity is the single most important risk factor for CP. The risk of CP in very low birth weight infants is as high as 4–10 %, whereas the risk in term infants is only 1–0,1% live births [13].
Attempts at classification of CP have been multiple and no system has been completely satisfactory. An etiological classification is not useful because similar etiological factors can produce different topology and extent of lesions and thus different clinical features. The use of neuroimaging, and its role in the understanding of CP pathogenesis, has dramatically increased over the last 20 years. It plays an increasing role in the diagnosis of CP, and a classification according to imaging results could be considered. However, neuroimaging, and especially magnetic resonance imaging (MRI), is not consistently available in all countries; thus, comparison among countries and across time periods would be difficult, especially as normal MRI does not rule out the diagnosis of CP [6].
A clinical, phenomenological classification, therefore, is more useful than etiological or pathological ones. From a clinical viewpoint, CP is usually classified into neurologically defined subtypes: spastic, dyskinetic, and ataxic. The spastic types can in turn be subdivided according to the topography of involvement into spastic hemiplegia, spastic diplegia, and spastic quadriplegia [6].
Spastic forms of CP account for the majority (85–90 %) of cases, around one third being unilateral and two thirds bilateral; dyskinetic forms occur in around 7 % and ataxic forms in around 4 % of cases [14].
Spastic Cerebral Palsy
Spastic CP is divided into unilateral forms (hemiplegia , hemiparesis) and bilateral spastic CP. Bilateral forms in turn are divided into “leg-dominated” forms, also termed diplegia or diparesis, in which involvement of the lower limbs is dominant, and “arm-dominated” forms or quadriplegia/tetraplegia or paresis, where the upper limbs are predominantly affected or all four limbs are approximately equally involved. These forms are further subdivided into mild, moderate, and severe types, taking into account the functional severity [6].
Spastic Diplegia
The most common type of bilateral spastic CP is spastic diplegia, defined as a type in which the lower limbs are much more severely affected than the arms. Involvement of the upper limbs is constant, however, even though it may be very mild and detectable only by careful examination. Preterm infants are particularly prone to spastic diplegia. Approximately 80 % of preterm infants who manifest motor abnormalities have spastic diplegia [15]. In recent years, the survival of very small preterm infants has resulted in a larger group of more severely neurologically impaired survivors [16].
The pathology of diplegia is related to periventricular lesions, which are the predominant type of brain damage in preterm babies. Intraventricular hemorrhage, especially when followed by ventricular dilatation, is a possible cause of diplegia. Periventricular leukomalacia is the most common lesion responsible for spastic diplegia [6]. This is easily understandable, as the involved areas are located along the external angle of the lateral ventricles, thus damaging the fibers from the internal aspect of the hemisphere, which includes the motor fibers to the lower limbs (Fig. 9.1). The location of leukomalacia along the posterior part of the lateral ventricles, interrupting the optic radiations, is responsible for visual impairment [17].
Fig. 9.1
Periventricular leukomalacia in a child with spastic diplegia. Axial fluid attenuation inversion recovery (FLAIR) images showing ventriculomegaly with irregular margins of bodies and trigones of the lateral ventricles, loss of periventricular white matter with increased signal, and thinning of the corpus callosum
Some infants with spastic diplegia manifest ataxia after further maturation. These infants have a great increase in tone of the leg muscles and accompanying difficulties in coordination and strength. Impairment may be asymmetric. When a small child is held in the vertical position by the examiner and the plantar surfaces of the feet are bounced lightly on the examining table, adduction of the legs (scissoring) and obligatory extension (extensor thrust) are seen. The feet are also kept in an equinovarus posture. Further examination reveals weakness of dorsiflexion of the feet. In older children, this same spasticity causes them to toe-walk. As expected, signs of upper motor unit involvement are easily demonstrable in the legs (e.g., hyperactive deep tendon reflexes, bilateral ankle clonus, extensor toe signs). Striking spasticity of the hip muscles may lead to subluxation of the femur and associated acetabular pathological conditions and further restriction of motion [8]. After a variable period, usually 18 months to 2 years in children with moderate involvement, spasticity is increasingly accompanied by contractures that maintain the hips and knees in flexion, and the feet in an equinovarus position.
Spastic Quadriplegia
Spastic quadriplegia is the most severe type of CP. The condition is characterized by bilateral spasticity predominating in the upper limbs with involvement of the bulbar muscles, almost always in association with severe mental retardation and microcephaly. Quadriplegia, also termed tetraplegia, bilateral hemiplegia or four-limbed dominated CP, is less common than diplegia. Although it accounts for only 5 % of all cases of CP, it represents a significant problem, as affected children are totally dependent and pose the most difficult problems with regard to care, feeding, and prevention of deformities [6].
There is a high incidence of brain malformations in this group, and destructive processes of pre- or perinatal origin such as multicystic encephalomalacia or CNS infections are common (Fig. 9.2). The predominance of term children is confirmed in many series [14, 18, 19].
Fig. 9.2
Multicystic encephalomalacia in a child with spastic quadriplegia. Axial T1-weighted images showing numerous loculated, lacy pseudocysts within the white matter and cortex
Opisthotonic posturing may be evident in early infancy and may persist throughout the first year of life. Movement of the head often initiates forced extension of the arms and legs, resulting in a position similar to that in decerebrate rigidity. Accompanying supranuclear bulbar palsy, the result of bilateral corticobulbar tract impairment, may produce difficulties with swallowing and articulation. The incoordination of the oropharyngeal muscles may predispose the patient to recurrent pneumonia during the first years of life [8].
Neurological examination demonstrates marked spasticity and accompanying signs of corticospinal tract involvement, including hyperactive deep tendon reflexes, ankle clonus, and extensor toe signs. Weakness of dorsiflexion of the feet, associated with equinovarus deformities, is common. Marked spasticity of the hip muscles may lead to subluxation of the femur and associated acetabular pathological conditions. Flexion contractures of the wrists and elbows of various degrees and spasticity of the arm muscles are readily apparent [8].
The severe forms often have some dystonic features that affect the hands, face, and even trunk, so that differentiation from dystonic CP is not always clear-cut. The borderline between tetraplegia and dystonic CP may be difficult to draw, and the term spastic–dyskinetic CP reflects the possible interaction of dystonic and spastic features (Fig. 9.3).
Fig. 9.3
Selective gray matter lesions in a child with mixed cerebral palsy (CP). Axial FLAIR images showing (a) basal ganglia and (b) perirolandic lesions. This child suffered a severe perinatal hypoxic–ischemic injury
The incidence of auditory, visual, motor, and learning disability is much higher in children with spastic quadriplegia than in children with spastic hemiplegia, spastic diplegia, or ataxic CP [9].
Spastic Hemiplegia
Although children may manifest obvious hemiplegia in the second year of life, specific difficulties may not be observed during the first 3–5 months of life. After a perinatal stroke, an infant may be neurologically normal until the development of pathological handedness at approximately 4–6 months of age. For unexplained reasons, the left hemisphere (right side of the body) is affected in two-thirds of patients, and perinatal stroke is more common on the left than on the right [20].
Spastic hemiplegia is the most common form of CP found in term-born children; around one quarter to one third of patients are born preterm [21]. The prevalence of unilateral spastic CP, or hemiplegia/hemiparesis, is reported in the European survey to be about 0.6 per 1,000 live births [14].
Neonatal stroke, which encompasses ischemic perinatal infarction and sinovenous thrombosis occurring in the perinatal period (before the age of 7 days) or the neonatal period (before 28 days of age), is a particularly important cause of CP [20]. Ischemic perinatal stroke may be responsible for 28–50 % of all cases of hemiplegic CP in term infants [22]. Obvious prenatal factors (e.g., brain malformations) were present in 7.6 % of a cohort in one series [23], but the proportion is higher in others [24]. Obvious perinatal factors, mainly intracerebral hemorrhage, were found in 4.5 % of term and 8.1 % of preterm infants, and postnatal factors in 10.7 % of cases (Fig. 9.4). Etiology remained unspecified in one third to one quarter of cases, even though abnormal prenatal events were much more frequent in patients than in control infants [6].
Fig. 9.4
Perinatal ischemic stroke in a child with hemiplegic CP. (a) Diffusion-weighted image and (b) axial T1-weighted image showing hyperintensity in the middle cerebral artery territory (M2)
During the examination, the child exhibits impaired gross and fine motor coordination, has difficulty moving the hand quickly, and is frequently unable to grasp small items with a pincer grasp. The obligate (palmar) grasp reflex, which is usually absent by the age of 6 months and frequently rudimentary after the age of 4 months, may remain obligate. Weakness of the wrist and forearm is often associated with a limited range of motion of supination. The range of elbow extension may be restricted. Attempts at reaching for objects may be accompanied by athetotic posturing with flexion of the wrist and hyperextension of the fingers (avoidance reaction). Facial involvement is unusual [8].
Only 10 % of affected patients, including those with extensive hemiplegia, have homonymous hemianopia [25]. Children with hemiparesis may have a circumduction gait with a variable degree of abnormality. Most commonly, the child walks on the toes and swings the affected leg over a nearly semicircular arc during the course of each step. In contrast with the leg, the affected arm usually moves less than normal and does not participate in normal reciprocal motion during ambulation. An equinovarus positioning of the foot is seen; weakness and a lack of full range of motion of dorsiflexion are often present. Further evidence of upper motor neuron involvement on the hemiplegic side includes hyperreflexia of the deep tendon reflexes, ankle clonus, and extensor toe signs [8].
Although frequently overlooked, corticosensory impairment and hemineglect of the affected side are common. Examination for the integrity of stereognosis and graphesthesia usually reveals varying degrees of compromise [26].
Dyskinetic Cerebral Palsy
The prevalence of dyskinetic CP (dystonic and athetoid subtypes combined) is about 0.15 per 1,000 live births [14]. It is particularly reported in term-born children [21].
Dyskinetic CP is characterized by involuntary, uncontrolled, recurring, occasionally stereotyped movements, with persistence of predominant primitive reflex patterns and varying muscle [14]. The essential disability in dystonic–dyskinetic CP is an inability to organize and properly execute intended movements, to coordinate automatic movements and to maintain a posture. This results in major disability, all the more so as primitive motor patterns, such as the asymmetrical tonic neck reflex, are usually persistent and there is often some degree of associated spasticity [6].
In the dystonic subgroup, the motor disorder is characterized by sudden, abnormal shifts of general muscle tone, especially increases in muscle tone in trunk extensors induced by emotional stimuli and changes in the posture of neck muscles in intended acts or movements. These patients also have a tendency to repeatedly assume and retain distorted, twisted postures in the same stereotypical pattern [27]. As discussed above, severe bilateral spastic CP is very often characterized by additional dyskinetic—more specifically dystonic—features.
Choreoathetotic CP is characterized by large-amplitude, involuntary movements. Athetosis usually involves the distal limbs and results in slow, writhing, involuntary movements. Chorea may involve the face, limbs, and rarely the trunk. The combination of athetoid and choreiform movements results in a pattern of distal extremity movement, on-going hypertonia, and rotary writhing movements of the limbs. Tremor, myoclonus, and even some element of dystonia may also be evident. Pure dyskinetic MDs do not feature hyperreflexia with clonus or pyramidal signs, whereas in dyskinetic CP these spastic signs may be present [8].
Dyskinetic forms of CP constitute a rather well-defined group from the etiological point of view [27]. The incidence of perinatal factors is higher than in other types of CP, with 67 % of factors referable to the perinatal period, 21 % to the prenatal period , and a small proportion of postnatally acquired or untraceable cases. Hyperkinetic cases are seen both in term infants of normal birth weight who suffer severe asphyxia at birth and in small for gestational age infants with hypoxia [28]. Among hyperkinetic cases there is a very high proportion of preterm, appropriate for gestational age, infants, some with hyperbilirubinemia , often in combination with hypoxia (Fig. 9.5).
Fig. 9.5
Kernicterus in a child with dyskinetic CP. (a) Axial T2-weighted image shows bilateral pallidal hyperintensity (arrows) and (b) coronal T2-weighted image shows bilateral pallidal and subthalamic hyperintensity (arrowheads)
Ataxic Cerebral Palsy
Ataxic CP, called by some authors “nonprogressive congenital ataxia ” [29], occurred in 0.09 per 1,000 live births in a European series [14]. Nonprogressive ataxia is an obviously heterogeneous condition. Its pathogenic mechanisms are poorly known and its nosological interpretation is controversial. The term is used here to designate only those cases in which cerebellar symptoms and signs are clearly at the forefront.
Most cases of nonprogressive cerebellar ataxia are congenital, even though the clinical manifestations often do not become suggestive before 1 or 2 years of age, at the time when children normally begin to walk [6]. Prenatal factors play a dominant role in the etiology of nonprogressive cerebellar ataxia and genetic abnormalities are probably the main cause of this type of CP. Ataxia is discussed in Chap. 5.
Mixed Cerebral Palsy
Children with a combination of spastic and dyskinetic types are labeled as having a mixed type.
Management
The management of CP requires a comprehensive multidisciplinary team approach that can deal with the numerous psychological, behavioral, and physical needs of the child and family.
The goal of physical therapy is to help individuals develop coordination [30–32], build strength [33–37], improve balance [38–40], maintain flexibility [41–44], optimize physical functioning levels, and maximize independence [30, 32, 35–39, 45, 46]. Physical therapists instruct patients and families on the proper use of walkers and/or other gait adaptive equipment.
Physical therapy involves the practice of postural transferring, such as rolling, sitting, crawling, kneeling, standing and walking [36–39, 43–47]. The largest benefit of therapy to the child with CP is in the treatment of problematic conditions when they occur, including muscle atrophy or tightening [33–36], loss in joint range of motion [41–44], muscle spasticity [43, 44, 48], pain in muscles and joints, joint inflammation, and/or contractures (muscle rigidity) [43, 44].
Occupational therapists teach techniques for easier dressing and other forms of self-care. They instruct on how to use splints for the hand and/or wrist to aid in eating, or other devices to help the child to reach and/or grasp objects. The goal of therapy is to ensure that a child achieves the highest level of functional performance within their home, school, public, and work environments [30, 32].
Occupational therapy employs adaptive processes to teach a child to perform tasks required in the normal course of a day. This is accomplished by focusing on identifying adaptive methods a child can learn to complete tasks, breaking down essential tasks into smaller steps, often modified, capitalizing on the need for accomplishment, pride, enjoyment, and independence, developing in a child a sense of place in their environment, at school, and in the community [30, 32, 49, 50].
Speech therapy can be helpful in improving oral motor control and swallowing. Some children with cerebral palsy have difficulty controlling the muscles in their face, throat, neck, and head. This can lead to troubles with speech, chewing, and swallowing [51]. It can also cause drooling and affect the overall ability to interact and learn. Those who also have difficulty hearing may have a hard time understanding spoken language.
Speech and language therapy seek to improve a child’s speech and communication by strengthening the muscles used for speech, increasing oral motor skills, and by improving their understanding of speech and language [51, 52]. It can also can help with swallowing disorders, such as dysphagia. Speech therapy is also helpful in addressing verbal fluency, which may be affected by both motor (oral motor control) and cognitive (memory and perception) losses [52].
Movement disorders cause not only pain and discomfort, but also depression, social isolation and low quality of life, owing to the embarrassment caused by the involuntary movements. Motor rehabilitation can minimize pain and isolation; thus, adherence to motor rehabilitation is important for achieving positive results [30, 53]. To ensure repetition and, therefore, motor learning, patients and caregivers must be instructed to practice at home the exercises performed at therapy sessions [30, 53].
Treatment should begin as early as possible, with the goal of therapy formulated to improve care, optimize motor function, prevent orthopedic deformities, and address associated impairments. Rehabilitative programs have a direct benefit for parent–child relationships, social and emotional status, confidence, and self-esteem [54].
Clinical Scales
Gross Motor Function Measure
Motor function may be assessed with Gross Motor Function Measure (GMFM ). The GMFM is a widely used, criterion-referenced, clinical observation tool, with a scale from 0 to 100, that was developed and validated for children with CP. It has excellent reliability and demonstrates the ability to evaluate meaningful change in gross motor function in children diagnosed with CP [55].
The GMFM measures gross motor function when carrying out lying and rolling, crawling and kneeling, sitting, standing, and walk–run–jump activities. It focuses on the extent of the achievement of a variety of gross motor activities (mainly mobility skills and activities requiring postural control such as sitting, kneeling, and standing on one foot) that a typically developing 5-year-old can accomplish [55].
Gross Motor Function Classification System
Children with CP can be categorized using the Gross Motor Function Classification System (GMFCS ) into five levels where level I is the greatest mobility; “the child walks without restriction: limitations in more advanced gross motor skills” to level V; “self-mobility is severely limited, even with the use of assistive technology” [56]. The GMFCS is a reliable and valid system that classifies children with CP according to their age-specific gross motor activity.
The GMFCS describes the major functional characteristics of children with CP at each level within the following age windows: before the second birthday; between the age of 2 years and the 4th birthday; between the age of 4 years and the 6th birthday; and between the ages of 6 and 12 years.
Pediatric Evaluation of Disability Inventory
The Pediatric Evaluation of Disability Inventory (PEDI ) was developed as a comprehensive functional assessment instrument for rehabilitation. It has three domains: self-care, mobility, and social function. Caregiver assistance in complex activities and environmental modifications/equipment can be described. PEDI can be used as a parent report/structured interview instrument or by professionals observing the child’s functional behavior in a hospital or outpatient setting.
The self-care domain has 73 items, mobility has 59, and social function has 65 items. There are eight questions on self-care and five on social function, scoring 5 for independent, 4 for supervised, 3 for minimal assistance, 20 for moderate assistance, 1 for maximum assistance, and 0 for full assistance. Lower scores mean greater dependence [57].
Spastic Cerebral Palsy Treatment
Spasticity causes muscle stiffness and weakness, and decreases daily functional activities, including standing and walking [48]. A variety of antispasticity interventions are available for the treatment of children with CP, including physical therapy, oral medications, neurolytic blocking agents, intrathecal baclofen pumps, tendon-lengthening procedures, and selective dorsal rhizotomy.
Physical Therapy
In general, physical therapy programs are tailored to the needs of children. Physical therapy assessment of children with CP includes history, functional level, neuromotor characteristics (spasticity, muscular synergies, voluntary movement description, transferring description, joint range of motion, strength), sensory systems (visual, vestibular, proprioceptive, hearing, tactile), perception, respiratory, and cardiac functions. Based on this evaluation, objectives are established and a treatment is proposed [58].
Specific treatment programs at the different levels of functional independence at a particular moment show better results than general therapy programs, but both approaches have positive effects on gait speed and gross motor function [38]. Most studies address the outcomes after physiotherapy programs for children with hemiplegia or diplegia [30, 32, 36, 37, 43, 44], but some studies also show improvement in children with quadriplegia [35, 53].
Passive Muscle Stretching
Passive muscle stretching is used for individuals with spastic CP to reduce the tightness or contracture of soft tissues. Manual stretching can increase the range of movements, reduce spasticity, and even improve walking efficiency in children with spasticity . Sustained stretching of longer duration showed greater improvement in the range of movements and reduced spasticity of muscles around targeted joints [41].
Prolonged passive muscle stretching while standing on a tilt-table decreases the resistance to passive ankle joint movements in children with CP [42]. A daily standing program with hip abduction provided acetabular development and maintained hip abduction range of motion in the spastic adductor muscles in ambulatory children with spastic diplegia CP , when performed during the first years of life [43, 44].
Muscle Strengthening by Functional Training
According to neurodevelopmental treatment principles, the motor problems of CP arise fundamentally from central nervous system dysfunction, which interferes with the development of normal postural control against gravity and impedes normal motor development [45, 59]. The goal is the establishment of normal motor development and function and/or the prevention of contractures and deformities. The approach focuses on sensorimotor components of muscle tone, reflexes and abnormal movement patterns, postural control, sensation, perception, and memory [59].
Handling techniques that control various sensory stimuli have been used to inhibit spasticity, abnormal reflexes, and abnormal movement patterns. Neurodevelopmental treatment is used to facilitate normal muscle tone, equilibrium responses, and movement patterns. The normal developmental sequence is advocated as a framework for treatment. Neurodevelopmental treatment focusing on sit-to-stand transfer enables children with spastic diplegia to perform these movements more efficiently, with selective muscle control. Results can be observed after the first session of treatment [45].
A dynamic postural stability training program improves balance control and gait parameters in children with CP. The program has eight levels of difficulty and consists in keeping balance while standing on a platform. It has resulted in improvements in stability indices and gait parameters in children with spastic CP [39].
One study showed that trunk–hip strengthening exercises are effective for improvement in trunk and hip muscle activation. The exercises also improved the position of the pelvis, with a decrease in anterior pelvic tilt motion during standing in children with spastic diplegia [37]. The association of neurodevelopmental treatment and progressive functional training can increase the muscle thickness of the quadriceps femoris and rectus femoris and improve the mobility of children with spastic CP [36].
Children with moderate to severe cerebral palsy also benefit from muscle strengthening. Children classified as IV or V in the GMFCS are at risk for low bone mass for chronological age, which compounds the risk in adulthood for progressive deformity and chronic pain. A regular program of seated speed, resistance, and power training exercises improve bone mineral density and prevent spinal deformity and back pain in adulthood [35, 56]. Some patients also report improved bowel and bladder control, and increased energy levels [35].
A daily physiotherapy program, based on motor learning principles, was feasible and improved overall development, even in children with cerebral palsy at GMFCS level V, which is the lowest motor function level [53]. After 4 consecutive weeks of 2 h of PT intervention based on motor learning principles 5 days a week, children showed improvements in motor function, language, and cognitive skills [53].
Electrical Stimulation
Electrical stimulation has been applied in children with CP to increase strength and range of motion, reduce spasticity, and improve the performance of activities [33]. Neuromuscular electrical stimulation activates muscles in isolation when aimed at reducing impairments such as weakness or spasticity, whereas threshold electrical stimulation affects muscles at subcontraction levels (often during sleep) when aimed at increasing circulation [34].
In contrast, functional electrical stimulation causes muscles to contract during the performance of an activity such as sitting, standing up from a chair, walking, or reaching for and manipulating objects [33]. Therefore, electrical stimulation has been recommended as an additional tool during functional practice of children with CP [34].
Constraint-Induced Movement Therapy and Bimanual Intense Therapy
Constraint-induced movement therapy attempts to promote hand function by using intensive practice using the affected hand while restraining the less-affected hand [32]. Impaired hand function is among the most functionally disabling symptoms of children with unilateral cerebral palsy . Recent approaches providing intensive upper extremity training are promising: constraint-induced movement therapy, when children perform tasks with the affected hand, and bimanual training (hand–arm bimanual intensive therapy), when children perform tasks that require both hands.
Constraint-induced movement therapy and bimanual training improve dexterity and bimanual upper extremity use; however, training must have a high intensity. Ninety hours of constraint-induced movement therapy and bimanual training lead to greater improvements than 60 h of the same treatments [30]. Bimanual training may allow direct practice of functionally meaningful goals, and such practice may transfer to unpracticed goals and improve bimanual coordination. Increased dosing frequency may be needed for older children and combined approaches may be useful, but require sufficient intensity.
The constraint-induced movement therapy has been recently proposed in the context of a day camp model for children aged 5–9 years with spastic hemiplegic cerebral palsy. The intervention resulted in significant improvement in distal control of the affected limb. It is interesting to mention that increased social function was also observed after the intervention. All improvements were maintained at the 3-month follow-up assessment [32].
Another recent study showed the positive effects of a home-based, intensive bimanual intervention with children with unilateral spastic cerebral palsy . Trained caregivers provided 90 h of intensive, bimanual hand–arm therapy in the home after which children demonstrated significant improvements in hand function [30].
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