Etiology. There is no one specific cause. List of congenital problems can result in the infant and child with CP;

Transcription

1 Cerebal Palsy 1

2 Definition Is an umbrella term covering a group of nonprogressive but often changing motor impairment syndromes that may or may not involve sensory deficits, that are caused by a nonprogressive deficits, lesion, or anomaly of the developing the brain, and that can be in part a developmental diagnosis. Cerebal Palsy 2

3 Definition 2 Is a neurodevelopmental impairment caused by a nonprogressive lesion in single or multiple locations in the immature brain. This lesion leads to a persistent disorder of movements and posture appearing early in infant s life. Cerebal Palsy 3

4 Etiology There is no one specific cause. List of congenital problems can result in the infant and child with CP; Schizencephaly segmental deficit that cause a cleft in the brain. Lissencephaly decrease cerebral gyri. Cortical dysgenesis disorder of brain cortex formation Cerebal Palsy 4

5 Etiology Half of the created neurons die off (apoptosis), in particular during midgestation. Axons and synapses are also eliminated during normal development for the first decade or more. This shaping of NS is guided by neurochemichal processes and neural activity. When there are changes in the formation of the developing nervous system, the result can be an infant with CP. Cerebal Palsy 5

6 Etiology Immature brain has much more plasticity, the response to injury is much different and makes diagnosis and prognosis difficult. Prenatal events are responsible for about 75% of all CP. Prenatal asphyxia is cause 6% to 8% of CP. 10% to 18% of CP is caused postnatally. Cerebal Palsy 6

7 Etiology The potential cause of cerebral palsy are known to be occur in the; Antenatal or prenatal stage. Perinatal or neonatal stage. Postnatal or postneonatal stage. Cerebal Palsy 7

8 Antenatal causes of CP Vascular event such as a middle cerebral artery infarct. Maternal infarctions during the first and second trimesters such as rubella, cytomegalovirus, and toxoplasmosis. Less common: metabolic disorders, maternal ingestion of toxins, and rare genetic syndromes. Cerebal Palsy 8

9 Perinatal causes of CP Obstructed labor. Cord prolapse. Antepartum hemorrhage. Hypoxic-ischemic encephalopathy. Neonatal stroke, usually MCA. Severe hypoglycemia Untreated jaundice and severe neonatal infection. Cerebal Palsy 9

10 Postneonatal causes of CP Metabolic encephalopathy; Storage disorder. Intermedullary metabolism disorder. Metabolic metabolism. Miscellaneous disorder. Toxicity such as alcohol. Infections; Meningitis, septicemia, and malaria. Cerebal Palsy 10

11 Postneonatal causes of CP Injuries; Cerebrovascular accident. Following surgery for congenital malformations. Near-drowing. Trauma. Motor vehicle accident. Child abuse such as shaken baby syndrome. Cerebal Palsy 11

12 Classification They classify it according to; 1. Topography. 2. Types (the best for PT). 3. Severity. 4. Pathology. 5. Cerebral imaging techniques. Types of CP; 1. Spastic (70%). 2. Dyskinetic and movement disorders (Athetosis) (20%). 3. Ataxic (10%). 4. Hypotonic. Cerebal Palsy 12

13 a) Spastic CP Spasticity is a disorder of tone characterized by initial increased resistance to stretch. Within this types there are; Diaplegic CP: both legs are affected and more affected than arms. Hemiplegic CP: one side of the body is more affected than the other. Quadreplegic CP tetraplegic : all four limbs are affected. Cerebal Palsy 13

14 b) Dyskinesia and movement disorders It s a group of disorders where the movement is generally uncontrolled and involuntary and includes; Athetosis. Regidity. Tremor. Dystonia. Ballismus. Choreoathetosia. Cerebal Palsy 14

15 Term Athetosis Rigidity Tremor Dystonia Rigidity Tremor Definition is involuntary movement, slow and writhing. Abnormal in timing, direction and spatial characteristics. Usually are large motion of the more proximal joints. less common, felt as resistance to both active and passive movement, is not velocity dependent rhythmic movement of small magnitude, usually in smaller joints. is involuntary movement, slow and writhing. Abnormal in timing, direction and spatial characteristics. Usually are large motion of the more proximal joints. less common, felt as resistance to both active and passive movement, is not velocity dependent. rhythmic movement of small magnitude, usually in smaller joints. Cerebal Palsy 15

16 c) Ataxic CP Is primarily a disorder of balance and control in the timing of coordinated movements along with weakness, coordination, a wide-based gate, and a noted tremor. This type results from a deficits in cerebellum. Often occur in combination with spasticity and athetosis. Cerebal Palsy 16

17 d) Hypotonic CP Not correlated with a particular neural lesion. Can be permanent but is more often transient in the evolution of athetosis or spasticity and may not represent a specific type of CP. Cerebal Palsy 17

18 Cerebal Palsy 18

19 The gross motor function classification system (GMFCS) Standardized system to measure the severity of movement disability in CP children. There are five levels; Level 1, Walks without Limitations. Level 2, Walks with Limitations. Level 3, Walks Using a Hand-Held Mobility Device. Level 4, Self-Mobility with Limitations; May Use Powered Mobility. Level 5, Transported in a Manual Wheelchair. Cerebal Palsy 19

20 Assessment and Evaluation Purpose of assessment is to; Discover the functional abilities and strength of the child. Determine the primary and secondary impairments. Discover the desired functional and participation outcomes of the child and/or family. Cerebal Palsy 20

21 1. Assessment of movement Observation. Held by the arms of mother or caregiver. Come into the clinic with wheelchair. Enter the clinic ambulatory. Examine individual aspect of motor function. Functional antigravity control; Supine, prone, side-lying, sitting, quadruped, kneeling, half kneeling, standing and walking. Cerebal Palsy 21

22 Continue If the child processes higher level skill; Climbing stairs, navigating ramps or curbs, unilateral stance, running, jumping, hopping, galloping and skipping. Child who functions from a wheelchair; Alignment and mobility of body, shifting of weight, propulsion of wheelchair, management of wheelchair and its parts and transfer to and from wheelchair. Cerebal Palsy 22

23 2. Assessment of postural control Find answers to the following questions; 1. Dose the child have a variety of ways to transition between postures or only stereotypic choices? 2. Dose the child actively push into the supporting surface with the pelvis and extremities? 3. Is the child able to repeat movements or tasks and make small changes in his or her motor performance? Cerebal Palsy 23

24 3. Assessment of postural tone Tone; is how the muscle and group of muscle feels under the clinicians hands when the joints of a body part are moved through a particular range. Tone; describe the impairments of spasticity and abnormal extensibility. Stiffness; describe the resistance to movement felt when a limb or the trunk is moved in space. feel the child transition between postures and move the limb through the space. The most effective and efficient means of treatment is to gain postural stability and the need for compensatory stiffness is eliminated. Cerebal Palsy 24

25 Stiffness signs Increased stiffness; Distal fixing (toe curling and fisting). Difficulty moving a body segments through a range. Asymmetric posture. Retracted lips and tongue. Decreased stiffness; Excessive collapse of body segments. Loss of postural alignment. Inability to sustain a posture against gravity. Fluctuating stiffness level; sign of booth increased and decreased stiffness, mainly seen in athetosis and ataxia CP. Cerebal Palsy 25

26 4. Musculoskeletal assessment Due to spasticity, increased or decreased stiffness, weakness, or static positioning the child may exhibit a muscle shortening and/or soft tissue contracture, and over time bony deformities. There are a lot of points we should take care of; 1. Goniometric measurements. 2. Evaluation of the spine. 3. Thoracic movement. 4. Evaluation of the shoulder girdle and upper extremities. 5. Examination of the hip and pelvis. 6. Femoral anteversion. 7. Examination of the knee. 8. Tibial torsion. 9. Examination of the foot. 10. Discrepancy in leg length. Cerebal Palsy 26

27 5. Evaluation of gait The child ambulate by acquiring antigravity movement components of the neck, trunk, and extremities while in prone, supine, and side-lying positions. Stability is increased as the strength is gained. Immature gait pattern is characterized by; Uneven step length. Excessive flexion of hip and knee during swing phase. Immobility of pelvis without pelvis tilting or rotation. Abduction and external rotation through swing phase. Wide base of support. Pronation of the foot. Contact with the floor with foot flat. Hyperextension of the knee throughout stance phase. Cerebal Palsy 27

28 Mature component of gait Its providing a useful framework for evaluating the gait in CP children; Pelvic tilt. Pelvic rotation. Knee flexion at midstance. Heel strike. Mature mechanism of the foot and knee. Mature base of support. Synchronous movement of the upper extremities. Cerebal Palsy 28

29 Gait in cerebral palsy In spastic diplegia; have limited mobility in (lumber spine, pelvis and hip joint) and shows limited asymmetric pelvic tilt or pelvic rotation during gait. In order to compensate the lack of mobility, these children tend to shift their weight and maintain balance by using excessive mobility through the head, neck, upper trunk and upper extremities. Cerebal Palsy 29

30 Gait in cerebral palsy Hips; Flexed during stance. Full extension of hip is never achieved. Excessive adduction and internal rotation, in severe cases the medial aspect of the knees may approximate. Knees; Either flexed or hyperextend during stance depending on the function of pelvic, lumbar, and ankle musculature. Feet; Valgus outside the lateral dimension of the trunk. Or, close together in narrow base of support in planter flexion with heels off the floor. Cerebal Palsy 30

31 Gait in cerebral palsy In hemiplegia; Asymmetry. Shifting weight to the involved side is brief and incomplete. Limbs on the involved side is retracted and rotated posteriorly. Arm swing occurs on the uninvolved side. Shoulder hyperextension and elbow flexion on the involved side. Lower extremities, stiffness in extension and greater mobility in flexion. Ambulate without assistive devices. Cerebal Palsy 31

32 Gait in cerebral palsy In athetosis; Low postural tone fluctuate to higher level of stiffness. Lower extremities usually lifted high into flexion and placed down in stance into extension with adduction, internal rotation, and planter flexion. Hip slightly flexed. Lumber spine hyperextended. Thoracic spine rounded with capital hyperextension. Cerebal Palsy 32

33 Cerebal Palsy 33

34 Therapeutic intervention Tx Must be guided by functional outcome and/or the participation outcomes. The interventions are; Therapeutic exercise. Neurodevelopmental treatment (Bobath). Sensory integration (SI). Electrical stimulation (ES). Conductive education. Alternative interventions. Neuromedical and neurosurgical interventions. Orthopedic surgical interventions. Orthotics (Bracing). Cerebal Palsy 34

35 1. Therapeutic exercise Therapeutic exercise should be developed in relation; Assessment of the child. Identified long-term and short-term functional outcomes. The functional abilities. The impairment goals of the child. Strength training improve identified parameters of gait and improve muscle performance. Cerebal Palsy 35

36 1. Therapeutic exercise Four point must do to have an effective strength training program; 1. Understand the process. 2. Child put maximal or near-maximal effort. 3. Be motivated and be able to accomplish the task. 4. Family support the child and the program. Start the program according to the situation of the child, wither against gravity or with gravity eliminated. Cerebal Palsy 36

37 1. Therapeutic exercise External support The therapist hands or a piece of equipment used to provide initial support to; Maintain alignment. Reduce the stiffness. Initiate weight shift. Support movement. The support point start from proximal to distal; trunk, shoulder, or pelvis points provide greater amount of support and stability. Cerebal Palsy 37

38 2. Neurodevelopmental treatment (Bobath) Clinical application of NDT is used for neurological impaired children CP and hemiplegia in adult. Bobath s found that the general characteristics found on CP patients are; Retardation of normal motor development with persistence of primitive total pattern of earliest childhood. Release of tonic reflexes. Poor head control and Lack of trunk rotation. Normal active movement delay. Absence of balance and other adaptive reactions. Cerebal Palsy 38

39 2. Neurodevelopmental treatment (Bobath) The aim of treatment; 1. Inhibit abnormal reflex activity and facilitate normal postural reaction, which are: Righting. Equilibrium. Protective reaction. 2. Guide the child through the normal sequence of motor development; Rolling over, sitting, quadruped, crawling, standing, and walking. Cerebal Palsy 39

40 2. Neurodevelopmental treatment (Bobath) 3. Normal integration of both sides of the body is sought while associated reactions are avoided. 4. Normal responses once elicited, are always repeated. Opportunity is given to practice the new ability in functionally meaningful ways. 5. Voluntary control of normal responses is encouraged. Cerebal Palsy 40

41 3. Sensory integration (SI) Sensory integration is done very carefully and stopped if the response becomes abnormal or hyperactive. The kinds of sensory integration includes; 1. Weight bearing with pressure and resistance. 2. Placing and holding. 3. Tapping e.g. joint compression. Cerebal Palsy 41

42 4. Electrical stimulation It has been conducted toward the patients who are unable to follow a muscle training program or who are too weak to do strengthening in isolation. The two methods that have been used; 1. Neuromuscular electrical stimulation (NMES). It could be functional electrical stimulation (FES). 2. Threshold electrical stimulation (TES). Cerebal Palsy 42

43 4. Electrical stimulation Studies found that NMES was effective in strengthening the quadriceps of 13-year-old with spastic diplegic cerebral palsy for the development of new skills like stair climbing. TES is a low-level, subcontractionelectrical stimulation applied during sleep. To increase the blood flow to result of muscle bulk enlargement. Cerebal Palsy 43

44 5. Conductive education Address all aspect of development; Motor, cognitive, communication, psychological and activity of daily living. In order to improve the child s orthofunction which is; the capacity of individual to respond to biologic and social demands made upon them. Aimed toward the independence of the child. Cerebal Palsy 44

45 5. Conductive education The ideal program meets; 5 days/week, 6 hours/day, with the length varying between 5 weeks to 1 year. Common features across programs include; Group work using a highly structures framework. The use of task series. The use of rhythmic intention. The use of specific equipment. Cerebal Palsy 45

46 6. Alternative interventions Its to improve the functional level and to break the routine of child s tired of going to therapy sessions. 1. Therapeutic aquatics hydro. 2. Hippotherapy horse approach. 3. Yoga. 4. Karate. 5. Dance classes. 6. Tumbling sliding. To build on the child s strength toward functional skills. Its more fun and not therapy in the mind of child. Cerebal Palsy 46

47 7. Neuromedical and neurosurgical interventions 1. Muscle relaxants. 2. Neuromuscular blocks. 3. Selective dorsal rhizotomy. 4. Intrathecalbaclofen pump. Cerebal Palsy 47

48 8. Orthopedic surgical intervention 1. The spine. 2. The hip; Subluxation/dislocation. Adduction tightness. Flexion tightness. Internal rotation deformity. 3. The knee; knee flexion deformity. 4. The ankle and foot; Equinus deformity. Pesvalgus. Varus deformity. Cerebal Palsy 48

49 9. Orthotics Bracing Physical therapy contribution must include assessment of; Available range of motion passive and active. Foot alignment and flexibility both in weight bearing and non-weight bearing. Voluntary control of movement in the leg, ankle, and foot. Current functional abilities. Desired functional and participatory outcomes of the child and family. Cerebal Palsy 49

50 9. Orthotics Bracing Types; 1. Inhibitive casts. 2. Dynamic ankle-foot orthosis. 3. Articulating ankle-foot orthosis. 4. Floor reaction orthosis. 5. Supramalleolar orthosis. 6. Shoe insert. Cerebal Palsy 50

51 Additional points Home management. CP in schools. Its multidisciplinary approach; General pediatrician, neurologist, orthopedic surgeon, podiatrist, ophthalmologist, physiatrist, and the medical complications indicate such as; gastroenterologist, earnose-throat specialists, nutritionists, and psychiatrists. Cerebal Palsy 51

52 Case study Cerebal Palsy 52

53 Thank you Cerebal Palsy 53

54 Reference, Pediatric physical therapy, JAN S. TECKLIN, fourth edition. Chapter 5, page (179 to 230) Cerebal Palsy 54