b.c. d. BOBATH EXERCISE (By. Terapi Latihan yang disusun oleh : Suharto, RPT Tahun 2000) 1. PENDAHULUAN Tehnik Bobath pertama kali ditemukan oleh Bertha Bobath, seorang fisioterapis. Metode ini juga dikenal dengan sebutan “ NDT” Neoro Developmental Treatment”. Tehink ini sering dignakan pada kasus-kasus gangguan motorik dan keseimbangan akibat post trauma cerebri dan post immobilisasi lama. Dalam pertumbuhan dan perkembangan motorik dikenal dua terminology, yatu keterlambatan perkembangan motorik atau motor delay dan kelainan motorik (motorik disorder). Keterlambatan perkembangan motorik dapat disebabkan oleh kurangnya stimulasi, social emosi, malnutrisi syndrom down dan microsefalus dan sebagainya. Dalam metode ini, factor yang sangat penting adalah righting rection dan equilibrium reaction yaitu penggunaan pola perkembangan motoris yang normal. 2. PRINSIF DASAR METODE BOBATH a. Inhibisi. Inhibisi atau menghambat. Yaitu menghambat pola gerak abnormal atau sikap tubuh abnormal. Tekniknya disebut juga RIP (Refleks Inhibiting Postur). Dengan mengatur posisi penderita kita dapat menghambat aktifitas reflex abnormal tertentu, misalnya untuk menghambat spastisitas ekstensor , kita mengatur posisi anak dalam posisi fleksi. Fasilitasi. Teknik ini kita kenal sangat banyak, namun pada saat ini, kita contohkan adalah memberikan posisi dan gerakan normal. Stimulasi. Dari namanya berarti menstimulir atau merangsang daerah tertentu untuk mendapatkan reaksi atau respon dari penderita. Teknik ini biasanya diberikan pada keadaan placid/hypotonus. Tekniknya dapat berupa kompressi, tapping, atau stroking. Dalam beberapa kasus sering juga diberikan goresan-goresan batu es. Dalam perkembangannya ketiga teknik tersebut dapat dikombinasikan. Key Point Of Control (KPOC) KPOC adalah tempat –tempat tertentu yang paling efektif untuk memberikan inhibisi, fasilitasi dan stimulasi. Biasanya sendi proximal, seperti panggul, bahu dan sebagainya. Meskipun yang lain juga dapat diberikan KPOC. 3. PEMBAHASAN Pada Metode Bobath ada beberapa jenis gerakan yang dapat diberikan antara lain: 1) Reaksi mengangkat/menegakkan. 2) Reaksi keseimbangan. Namun untuk postingan kali ini, penulis hanya akan membahas reaksi mengangkat/menegakkan. Karena pada tahap ini saja sangat banyak gerakan yang perlu diperhatikan. Oleh karena itu postingan berikutnya kita akan melanjutkan dengan Reaksi keseimbangan. 1. REAKSI MENGANGKAT/MENEGAKKAN. Yakni reaksi yang pertama kali muncul sejak lahir pada usia 10 - 12 bulan. Righting reaction terdiri dari : a. Neck Righting reaction. Dengan memutar kepala secara aktif atau pasif ke salah satu sisi, dalam posisi terlentang, maka akan terjadi rotasi seluruh tubuh ke sisi yang sama. Dengan gerakan ini diharapkan anak dapat melakukan gerakan miring atau rolling secara mandiri. b. Labirithine reaction. Reaksi yang terjadi adalah menegakkan kepala dalam posisi telungkup. Reaksi ini mula-mula lemah dan makin lama makin kuat, sehingga anak-anak dapat mengangkat kepala mereka sehingga muka vertical dan mulut horizontal. Reaksi ini timbul pada usia 1 – 6 bulan. c. Reaksi vertibular Reaksi ini timbul pada saat anak terlentang yakni dengan mengangkat kepala, sehingga dengan reaksi ini anak dapat mempertahankan kepalanya pada waktu diangkat ke posisi duduk. d. Body righting reaction. Reaksi ini berkaitan dengan labirithine righting reaction, yang berguna untuk mengatur posisi kepala di udara. Reaksi ini dapat ditimbulkan dengan menyentuhkan kaki ke lantai, akan diikuti dengan tegaknya kepala. f. Body Rigting reaction. .e.See more at: http://www.dpuf CEREBRAL PALSY Laura Rogers and Eric Wong Editors: Alexa Caturay and Sultan Chaudhry Faculty reviewer: Dr.5/1000 live births in the Western world. 2009 Mar. kemudian dikuti oleh pelvic atau sebaliknya. 2008 Dec. . communication. i. The ratio of affected males to females is 1. Peter Rosenbaum. behaviour. epilepsy.4:1. Professor. yakni mulai timbul setelah 6 bulan dan akan terus meningkat sejalan usia. the movement disorder is not secondary to another neurofunctional disability. and secondary musculoskeletal problems. and more children in the developing world. 18E CP affects approximately 2-2. Pediatr Neurol.q1mSUBuo. CP excludes transient disease processes. 2007 Feb.109:8-14.html#sthash. CP is often accompanied by disturbances of sensation. cognition. perception. Pediatrics (McMaster University) Definition Dev Med Child Neurol Suppl.51(4):775-86.e. Merupakan modifikasi dari Neck Righting reaction. Essentials of Obstetrics and Gynecology. Etiology Clin Obstet Gynecol. Cerebral palsy (CP) is a heterogeneous group of movement disorders with various etiologies. Dengan memutar kepala ke samping diikuti oleh rotasi bahu. non-progressive pathology that formed in utero or early infancy(before 2-3 years of age). Penglihatn sangat berperan dalam mengatur posisi kepala dan tubuh. Optikal righting reaction Gerakan yang terakhir untuk righting reaction adalah Optikal righting reaction. The primary functional difficulty is in movement and posture. CP is associated with a permanent.40(3):168-74. Dengan reaksi ini memungkinkan anak dapat membalikkan badan dari posisi tengkurap ke posisi terlentang. 5E (Hacker) Nelson Textbook of Pediatrics. Reaksi ini terdapat pada usia 6 – 8 bulan.fisio-usman.net/2012/12/normal-0-false-false-false-in-x-nonex. .Antenatal (~7080% of causes) Prematurity and low birth weight Greater risk of CP with preterm deliveries (but since most deliveries happen close to term. most infants with CP (75%) are born after 36 weeks). Prevalence of CP in the surviving twin was found to be 15x higher than average. Multiple gestation Increases the risk of antenatal complications. as fetuses with cerebral abnormalities tend to be delivered either preterm or postterm. Parturition is hypothesized to be partially related to fetal brain maturity. cytomegalovirus. o Chorioamnionitis is an infection of the chorion and amnion.o There is a U-shaped association between CP and gestational age. enterovirus). See Pathophysiology for details. Underdeveloped fetal brains are more susceptible to inflammation and inflammatory cytokines.304(9):976-82. such as preterm labour. IVH may cause PVL or ischemia in other parts of the brain. o o Periventricular leukomalacia (PVL) is a condition of underdeveloped white matter in the brain surrounding the ventricles. other infections (varicella zoster. The mechanism may be related to the physiological changes that trigger labour. Twinning is the single strongest risk factor for the development of CP. and death of a co-twin. syphilis. and other causes of third trimester bleeding) seem to lead to premature delivery. adenovirus. conferring the same risks for CP as a premature infant according to some evidence. Intraventricular hemorrhage (IVH) is predominantly associated with prematurity and is due to fragility of developing blood vessels in the infant’s brain. 2010 Sep 1. Pregnancy complications in the mother Thrombophilias can lead to placental vascular injury and clotting of the fetal vessels. Infections Fetoplacental and uterine infection or inflammation can cause initiation of preterm labour. where incidence of CP is increased in both preterm and postterm babies. which can lead to CNS injury and CP. These cytokines are hypothesized to be responsible for the development of PVL. TORCHS infections are associated with approximately 5% of all CP cases. PVL is discussed in thePathophysiology section below. the two membranes surrounding the developing fetus. Hemorrhage and preeclampsia (placental abruption. o TORCHS is an acronym for perinatal infections: toxoplasmosis. low birth weight. It is the leading cause of CP in preterm infants. It is the most frequently associated maternal infection in CP. Death of a co-twin in utero has been shown to induce neuropathologic changes that can lead to CP in the surviving twin. growth restriction. placenta previa. herpes simplex virus. . JAMA. rubella. Although both pathologies increase the risk of CP. PVL is more closely related to CP and is the leading cause in preterm infants. thus preterm infants have . In women with premature rupture of membranes. Pediatric Ophthalmology: Current Thought and a Practical Guide. and to increase the seizure threshold in mothers with preeclampsia) may reduce the risk of CP according to some studies. Intraventricular hemorrhage (IVH) IVH describes bleeding from the subependymal matrix (the origin of fetal brain cells) into the ventricles of the brain. Both IVH and PVL cause CP because the corticospinal tracts. 1E (Wilson) Preterm infants The premature neonatal brain is susceptible to two main pathologies: intraventricular hemorrhage (IVH) andperiventricular leukomalacia (PVL). as steroids inhibit cytokine production.93(2):F153-61. thus preventing PVL.Perinatal Birth asphyxia (~10%) is commonly associated with CP. This may be due to increased survival rates of premature and low birth weight babies. Pathophysiology Arch Dis Child Fetal Neonatal Ed. course through the periventricular region. 2008 Mar. but further research is needed before it is used specifically as a neuroprotective agent for preterm births. Corticosteroids reduce the risk of CP. antibiotics reduce the risk of chorioamnionitis. but there is not a clear association between CP and the quality of perinatal care. the incidence of CP has remained constant. Antibiotics used to treat bacterial vaginosis may reduce the rate of preterm delivery. The term PVL describes white matter in the periventricular region that is underdeveloped or damaged (“leukomalacia”). composed of descending motor axons. The blood vessels around the ventricles develop late in the third trimester. Postnatal Non-accidental injury Head trauma Meningitis/encephalitis (including cerebral malaria in the developing world) Cardiopulmonary arrest Obstetrical care (protective factors) Magnesium sulfate (used for tocolysis for preterm labour. Despite the advancement of prenatal and obstetrical care in the past 30 years. CP is associated with complicated labour and delivery. underdeveloped periventricular blood vessels. . Periventricular leukomalacia (PVL) IVH is a risk factor for PVL. The pathogenesis of PVL arises from two important factors: (1) ischemia/hypoxia and (2) infection/inflammation. but PVL is a separate pathological process. predisposing them to increased risk of IVH. The risk of CP increases with the severity of IVH. . . the periventricular white matter is susceptible to ischemic damage. it is limited in preterm infants due to immature vasoregulatory mechanisms and underdevelopment of arteriolar smooth muscles. Infections also activate microglial cells. Neuroscience. interferon γ and TNF-α) that are toxic to premyelinating oligodendrocytes. an important antioxidant).. discussion 53-61. Since preterm and even term neonates have low cerebral blood flow. which is essential for white matter development. Term infants Circulation and autoregulation of cerebral blood flow are similar to that of an adult in a full term infant.g. thromboembolic stroke). 3E (Purves) Clinical Neuroanatomy.9 Suppl 1:3-9. Infection and inflammation: This process involves microglial (brain macrophage) cell activation and cytokine release.e. 26E (Waxman) . however. 18E Eur J Neurol. o Basal ganglia damage can cause extrapyramidal or dyskinetic CP.. low production of glutathione. This is the most common area of injury. Ischemic and hemorrhagic injuries tend to follow similar patterns of those in adults: o Watershed areas where the three major cerebral arteries end in the cortex. Glutamate is increased because hypoxia causes white matter cells to reduce reuptake of glutamate due to lack of energy to operate glutamate pumps. IVH is hypothesized to cause PVL because iron-rich blood causes ironmediated conversion of hydrogen peroxide to hydroxyl radical. Glutamate is also released from microglial cells during the inflammatory response. decreased cerebral blood flow in the brain overall). Premyelinating oligodendrocytes have immature defences against reactive oxygen species (e. Although collateral blood flow from two arterial sources protects the area when one artery is blocked (e. which stimulates reactive oxidative species release.g. contributing to oxidative damage. Clinical features Nelson Textbook of Pediatrics. which produces cytokines(e.g. which release free radicals..Ischemia/hypoxia: The periventricular white matter of the neonatal brain is supplied by the distal segments of adjacent cerebral arteries. Intrauterine infections activate the fetal immune system. which causes damage to a specific cell type in the developing brain called the oligodendrocyte. Autoregulation of cerebral blood flow usually protects the fetal brain from hypoperfusion. this watershed zone is susceptible to damage from cerebral hypoperfusion (i. Theoligodendrocytes are a type of supportive brain cell that wraps around neurons to form the myelin sheath. Excitotoxicity is a process where increased extracellular glutamate levels stimulate oligodendrocytes to increase calcium influx. 2002 May. . UMN lesions can cause positive or negative signs: o Positive signs include muscle overactivity and spasticity. generally due to reduced descending excitatory signals from the brain. leading to a net disinhibition of the spinal reflexes. The motor nuclei of cranial nerves in the brainstem are also lower motor neurons because they directly attach to muscles in the head and neck.g. . The location of damage can be divided into upper motor neuron or lower motor neuron. UMN synapse onto lower motor neurons at the ventral horn of the spinal cord at the level which the neuron leaves the cord. it does not require input from the brain). generally due to reduced descending inhibitory signals from the brain. o Negative signs include weakness or loss of dexterity. The pathology in CP is in the upper motor neurons. Upper motor neurons travel through the pyramidal tracts (i. Rosenbloom L (2012). The faster the velocity of stretching. CNS) that control movement of muscles. Lower motor neuron (LMN) Includes neurons from ventral horn of the spinal cord grey matter that exit the spinal cord and attach to skeletal muscles. the stronger the reflex. They function to modulate and refine movement rather than directly cause movement. The extrapyramidal tracts link the cerebellum and basal ganglia with LMN.e. LMNs relay signals from the UMNs to skeletal muscles to initiate excitation-contraction coupling. allowing individual units of a muscle to contract in a synchronized manner. which increases muscle tone (contraction) as the muscle is passively stretched.e. corticospinal tracts). Rosenbaum P. passively stretching a muscle group (e.. stretching the biceps by passively extending the elbow) causes contraction of the same muscle group to prevent overstretching and injury. unlike the upper motor neurons in the pyramidal tracts. The clinical features of neurological disorders depend on the location of damage to the nervous system. It is characteristic of an UMN lesion where there is disturbance of the supraspinal excitatory and inhibitory neurons.. From Diagnosis to Adult Life. o Spasticity is defined as a velocity-dependent increase in the tonic stretch reflex. Cerebral Palsy. Spasticity: Injury to descending UMNs that usually provide inhibitory signals to the spinal reflexes causes net disinhibition. o Note that lesions in the extrapyramidal tracts do not cause these UMN signs. London: Mac Keith Press. This tonic stretch reflex is a spinal reflex (i. Tonic stretch reflex: Normally. Upper motor neuron (UMN) Includes neurons in the brain and spinal cord (central nervous system. This reflex is normally minimal or not present. In LMN lesions. where individual sacromeres (contractile units in muscles) fire and contract at random. Unilateral ankle clonus (usually). Comparison of UMN and LMN lesion clinical presentations Upper motor neuron lesion Lower motor neuron lesion Spasticity Flaccid paralysis Increased tone Hyperactive deep reflexes Clonus Babinski sign Decreased or absent deep tendon reflexes Fasciculations and fibrillations Severe muscle atrophy (from disuse) Little to no muscle atrophy Common clinical presentations Spastic hemiplegia Affects one side of the body more than the other (though both sides may be affected).. there is no neural input to muscles. Upper limb affected more than lower. Brisk deep tendon reflexes.e. The lack of excitation-contraction coupling causes fasciculations in the muscles. Cognitive abnormalities in 25% of cases.g. o On affected side: Growth differences of hand and thumbnail. and then towards it (i. Weakness of hand and foot dorsiflexors. Hand preference obvious at an early age. o Circumductive gait: one leg is stiff and upon stepping it is rotated away from the body. due to increased tone in the gastrocnemius muscles. e. Their function is to provide muscle tone to skeletal muscles. gastrocnemius and sartorius. Delayed walking (18-24 months) with a circumductive gait. Babinski sign. Spasticity has a greater effect on the postural (antigravity) muscles. . The stiffness in the affected leg limits flexion and the patient has to raise the pelvis to swing the leg out to lift the leg enough to clear the ground. which leads to flaccid paralysis due to lack of resting muscle tone and subsequent atrophyfrom disuse.. Tiptoe walking on one side. a semicircle shape). On exam: o Circumductive gait. Seizure disorder presenting before 2 years of age in 1/3 of children. Spastic diplegia . On exam: o Increased tone and spasticity in all limbs. Most common neuropathologic lesion is PVL. dyskinetic) o o o o Less common than spastic CPs. High association with cognitive deficiencies and seizure disorders. Increased difficulty swallowing due to supranuclear bulbar palsies. First clinical signs appear around the time when the child starts to crawl. may be present. On exam: Infants are usually hypotonic with poor head control and head lag. Athetoid (extrapyramidal. o Scissoring posture of legs when held in the air supported by the axillae due to spasticity in the hip adductor muscles. like vision. which can cause the child to have aspiration pneumonias. o Decreased spontaneous movements. o Commando crawl: the child uses arms in a normal reciprocal manner but drags legs behind rather than using legs as well. Normal intellectual development is common. Upper extremities more affected than lower extremities. o Brisk reflexes. Variably increased tone with rigidity and dystonia with age. o Bilateral Babinski sign. but may also include basal ganglia damage. . Minimal risk of seizure disorder. Most common neuropathologic feature is PVL. Motor impairment to all extremities. o Atrophy and impaired growth of legs in severe cases. o Brisk reflexes and plantar extension responses. o Ankle clonus. o Flexion contractures of knees and elbows commonly present in late childhood. but many children still have learning disabilities. o Tiptoe walking. Other deficits in sensory areas. 15-20% of patients with CP. Feeding and speech difficulties due to affected oropharyngeal muscles. On exam: o Spasticity of the legs. Bilateral spasticity of the limbs with legs more affected than arms. Strongly associated with white matter damage in utero between 20-34 weeks of gestation. Delay in speech and the presence of visual abnormalities are common. Spastic quadriplegia (‘total body involvement’) Most severe form of CP. posture. Examine and rule out the possibility of degenerative diseases. Rosenbaum P. General assessment Suspicions of CP are commonly based on a positive history of adverse perinatal or antenatal events. Normal intellectual development in many patients. Rosenbloom L (2012). Assessing chewing abilities or oromotor functioning is also important in determining any safety concerns with regards to feeding. CP is essentially a clinical diagnosis – there are no pathognomonic signs or diagnostic tests. ability to sit independently. asymmetry. etc. 2010 Mar. 18E. and presence of independent mobility is important. Diagnosis Pediatr Neurol. which is a 5-level classification scheme used to evaluate gross motor function in children with CP. Neuropathologic lesions of the basal ganglia and thalamus (signals are relayed by the extrapyramidal tracts) are most common. Growth curves: crossing major percentile lines raises concerns for growth and developmental disorder CP is non-progressive but can change its clinical manifestations throughout childhood. When independent mobility is present. Specific attention to head posture. . Assessing speech production and clarity. Most commonly associated with birth asphyxia. such changes are important to discuss with parents. Nelson Textbook of Pediatrics. Observations of the child while being held by their caregiver include: movements. From Diagnosis to Adult Life. head control. muscular dystrophy. suspicions are often raised by parental or family observations of developmental delays. gait.42(3):177-80. Seizure disorders are uncommon. London: Mac Keith Press. and abnormalities of posture should be assessed. If no positive history. Functional assessment It can be helpful to refer to the Gross Motor Function Classification System (GMFCS). metabolic genetic disorders. metabolic disorders. and anomalies of the cervical spinal cord and skull. Other causes: kernicterus (now rare in the Western world due to maternal blood group screening and immunization against Rh factor). spinal cord lesions/tumours. Cerebral Palsy. Therefore. dysmorphic features. and the clinician must do so by continuing to reassess children as they develop. Health care professionals usually involved in the care of children with CP include: o Developmental pediatricians Monitor and promote the child’s development. Child Development Teams act as excellent liaisons between the different health care professionals. o Can at times be ‘normal’ in the face of clear clinical findings. * It is very important to differentiate whether a delay or difference constitutes an abnormality. Children with CP often have multiple developmental issues that are best managed by a multidisciplinary team of health care professionals. Tests for thrombophilia in those where a stroke is the suspected cause. Rosenbloom L (2012). Management Nelson Textbook of Pediatrics. The time for reassessment is dependent on the normal achievement of specific developmental milestones. Rosenbaum P. o Location and extent of lesion.g. and are able to provide a structured program for treatment. Additional tests Hearing and vision testing Genetic screening in those with congenital malformations or if evidence of a genetic disorder. suitable to each child’s needs. . 18E.. Cerebral Palsy. London: Mac Keith Press.Characteristic features of CP based on age* Age Characteristics that may indicate CP < 6 months > 6 months Asymmetric tonic neck reflex: reaches with one hand while the other is in a fist > 10 months Mobilizes/crawls not using all limbs (e. Connect with other health care professionals as needed. From Diagnosis to Adult Life. commando crawl of spastic diplegia) Head lags when infant is picked up from supine position Feels stiff or floppy in your arms Scissoring of legs when picked up Brain imaging is one of the most useful diagnostic tools Confirmation of brain/spinal cord lesion via MRI. Occupational therapists Implement the use of assistive devices (e. minimizing spasticity. o Prognosis for motor function depends on the type and severity of motor impairment. Energy-rich supplements may be needed. 2008 Jul. Nutritionists Malnutrition may be seen in children with feeding difficulties. Orthopedic surgeons Chronic muscle weakness or spasticity can cause orthopedic deformities that need surgical correction.g. Dev Med Child Neurol. The development of speech language and the provision of non-verbal communication systems as necessary. walkers. o These trends can be divided into 5 distinct motor development curves which children can be categorized into to assist with providing further prognostic information for parents. and adaptations) that can be made to the home to accommodate the child. wheelchairs. o Individuals with CP on average have a life expectancy that is 44% of normal (this can be applied to countries with varying life expectancy rates). o o o o o Support children and families with the patient’s development in the context of their individual family and community. The use of the GMFCS (in the Ontario Motor Growth Study) has been shown to be an effective tool in assessing outcomes for individuals with CP. Pediatrics.g. dislocation of the hips due to spasticity of the thigh adductors. Food must be given in a form that the child is able to chew and swallow..288(11):1357-63. appropriate toys. as these children often have difficulties with chewing and swallowing. Speech therapists Assist with feeding.50(7):487-93. ankle-foot orthosis (AFOs). and preventing contractures. 2002 Sep 18. deformity of the ankle from calf muscle spasticity. e. Physiotherapists Assist with the development of muscle control. . JAMA.. Enteral feeding may also be necessary if oral intake is insufficient to maintain nutrition via surgical placement of G-tube or GJtube. o Motor assessments have been used alongside growth charts to characterize gross motor development over time. 2008 Dec. 2011 Aug. Prognosis Clin Obstet Gynecol.51(4):816-28.128(2):e299-307. overcoming weakness. .e. Research has shown that the strongest predictors of early mortality are immobility and impaired feeding ability (i. Shortest life expectancy is associated with individuals who are unable to lift their head in prone position. intellectual. hearing.o o Mortality risk increases with increasing number of impairments (e.. .g. vision). the need for tube feeding).