Modern concepts and rehabilitation of cerebral palsy I. Modern definition and classification of pediatric cerebral palsy 1. Many improvements have been proposed. In order to standardize the definition and classification of cerebral palsy worldwide, a revision of the definition and classification of pediatric cerebral palsy was proposed at an international symposium held in Bethesda, USA, from July 11 to 13, 2004, and a report on the definition and classification of pediatric cerebral palsy was published in April 2006 by Rosenbaum, then chairman of the Task Force on Definition. In this report, “Cerebral palsy is a group of persistent disorders of motor and postural development that cause limitations in movement and are non-progressive impairments (disturbances) that occur in the developing fetal and infant (infant) brain. The motor impairments of cerebral palsy are often accompanied by sensory, perceptual, cognitive, communication, and behavioral impairments, with epilepsy, and with secondary musculoskeletal problems.” In fact, this definition is based on the definition of the Surveillance Society for Cerebral Palsy in Europe (SCPE) with the addition of “musculoskeletal problems,” and after SCPE published its definition in 2000, many scholars expressed different opinions, including the question of whether co-occurring impairments should be included in the definition. Nevertheless, Miller, a leading expert on cerebral palsy from the United States (University of Pennsylvania), refrained from using the International Workshop definition, stating that “cerebral palsy is a heterogeneous group of non-progressive syndromes characterized by motor and postural abnormalities. These manifestations vary in severity and are due to abnormalities in the developing brain from a variety of causes. Although the disease itself does not progress, its neuropathological lesions and its clinical manifestations change as the brain matures.” Although this definition avoids the age of onset of cerebral palsy, its special emphasis on the feature of motor deficits and postural abnormalities, without including concurrent damage in the definition of cerebral palsy, is highly desirable. Currently, Miller’s discussion of cerebral palsy is used mostly around the world, and many hospitals in Germany are using this definition. In our opinion, no matter how cerebral palsy is defined, several key words are essential: first, it occurs in the fetal (fetal) and infant (infant) periods; second, it is a non-progressive injury and defect in the developing brain; and third, it is the resulting motor impairment and postural abnormalities. Therefore, the author believes that cerebral palsy should be defined as motor impairment and postural abnormalities caused by non-progressive damage and defects in the developing brain during the fetal and infant periods. This definition restricts the age to before infancy and childhood in order to emphasize the damage to the fetal and infant brain during the most vigorous development. This is also consistent with the principle annotated by the International Symposium that “although no definite upper age is proposed, damage to the brain before 2-3 years of age after birth is most important. It occurs before the development of functions such as walking and manipulation.” Cerebral palsy caused by causative factors after the neonatal period (so-called acquired cerebral palsy) must after all represent a minority (10-15%), especially the so-called acquired cerebral palsy observed clinically, although it is also an injury of the developing brain, its etiology is clear, its clinical manifestations are mainly spastic palsy, a few with tardive dyskinesia, which has its own specificity, and the treatment is mainly to restore the acquired motor functions and to allow their further development. Therefore, it is somewhat different from cerebral palsy caused by various reasons before the neonatal period. Hutton et al. (2002), a Scottish scholar, addressed this issue by referring to cerebral palsy caused by brain injury after the neonatal period until the age of 5 years as “late impairment cerebral palsy”, while cerebral palsy caused by various factors during the neonatal and fetal periods (classical cerebral palsy) is referred to as early impairment cerebral palsy. The incidence of cerebral palsy in Western Europe8 is about 1.5 times that of cerebral palsy. 2. Regarding the incidence rate 14 research centers in 8 countries in Western Europe (2002): 2-3‰; Sweden has the best performance in prevention and treatment, which was reduced to 1.5‰, and now is 2.2‰. Northern Ireland (2001): 2.24‰. Japan: 2.0‰, reportedly declining. There is no comprehensive survey in China. Jiamusi University School of Rehabilitation Medicine: 1989 census of 80,000 urban and rural population: 2.1‰. WHO Rehabilitation Department (1993) recommended incidence rate of 3 per 1000 births with cerebral palsy. In 2002 Einspieler et al. reported that the incidence of cerebral palsy has not changed much during the last 40 years. Therefore, cerebral palsy remains a major target for prevention and treatment in the field of rehabilitation, especially in pediatric rehabilitation. Advances in perinatal medicine and neonatal monitoring and treatment have increased the chances of survival of very small immature (under 1500 g) and high-risk infants, but the incidence of cerebral palsy has not improved much. As a result, the incidence of cerebral palsy cannot be reduced in any country in the world. There are 600g survivors in China; 400g survivors in Western countries. The above facts suggest that obstetricians and neonatologists should make efforts to prevent the sequelae when treating high-risk children. The classification made at the International Symposium on Cerebral Palsy (2006) still basically follows the classification method of the American Association of Cerebral Palsy (AACP) in 1956, and proposes that the classification consists of four parts: First, motor abnormalities: according to the nature and type of motor disorders, they are classified into spasticity, dysmetria, dystonia, tardive dyskinesia, and tardive dyskinesia; according to the functional motor ability, the range of motor limitations, such as mouth movement and speech function. The second is the classification of concurrent impairments, such as seizures, visual and auditory impairments, and deficits in attention, behavior, communication, and cognition. The third is the anatomical classification, such as the anatomical distribution of movement disorders (limb, trunk, and medullary bulbar palsy signs, etc.) and imaging findings (ventricular enlargement, white matter loss, brain abnormalities, etc.). Fourth, the etiology and timing of the disease are easily classified, such as postnatal factors (encephalitis, meningitis, head trauma, etc.) and malformations of the brain, but prenatal factors are often presumed and difficult to classify. This is the problem that this international symposium was perplexed by and did not resolve, and is unlikely to do so. It is true that the proposed classification is important, such as the etiology and time of onset, the imaging findings, and the accompanying damage, which should be noted in the medical record if it is clear, as is now done by cerebral palsy practitioners in various countries, but it is far-fetched to use this as a principle for classification. In my opinion, the classification proposed by Miller in 1992 and revised in 2006 is the best one based on the combination of neurophysiology and damage site. poor hand function (poor hand function); asymmetric (asymmetric). Hemiplegia: upper extremity involved more than lower extremity (arm involved more than leg); lower extremity involved as much as or more than arm (leg involved more than upper extremity). Quadriplegia (quadriplegia) 2. dyskinetic (mainly dystonic) tardive dyskinesia (mainly athetoid) 3. ataxic (simple ataxia) diplegia (ataxic) The European Little Club classification of 1958 already eliminated this type, and according to Hagberg (2000), the so-called hypotonic type is merely a concomitant of other disorders (such as epilepsy and mental retardation), or developmentally dependent hypotonia, which can eventually reach normal. Eventually, muscle tone may reach full normal. The lack of reference to the concept of mixed type in this classification is a slight shortcoming, since tardive dyskinesia with spasticity is a common clinical manifestation, and therefore, in those cases where the “components” of the manifestations are similar or significant, a mixed type should be diagnosed and the composition of the impairment should be indicated, such as tardive dyskinesia + spastic biparesis, which is This is important for guiding training. The 2006 International Symposium on Cerebral Palsy did not avoid this issue and stated in the classification instructions that those with both tardive dyskinesia and spasticity can be diagnosed as mixed type. Our clinical practice over the years has proven that this classification is the most realistic and easy to operate. In 2000, the Society for Surveillance of Cerebral Palsy in Europe (SCPE) classified cerebral palsy into 3 types. One is spastic cerebral palsy, which is characterized by the presence of abnormal posture and/or movements, increased muscle tone (which does not have to be continuous), and the presence of pathological reflexes (increased reflexes, hyperreflexia and/or cone bundle signs, such as Babinski’s sign) in only two of the three manifestations. Spastic cerebral palsy was also classified as unilateral and bilateral, with unilateral involvement of one limb of the body (i.e., hemiparesis) and bilateral involvement of both limbs, thus eliminating the concept of quadriplegia and diplegia. The second is the ataxic type, which is characterized by abnormal posture and/or movement patterns and a loss of orderly muscle coordination to the point where movements are performed with abnormal force, rhythm, and precision. The third is the dyskinetic type, which is characterized by abnormal posture and/or movement, as well as by involuntary, uncontrollable, repetitive, and occasionally stereotyped movements, and is divided into two subtypes: the dystonic type, which is characterized by decreased movement (reduced activity, i.e., rigid movements) and hypertonicity (usually increased tension); and the choreographic tardive dyskinetic type, which is characterized by excessive activity (increased activity). The choreoathetosis type is dominated by hyperactivity (increased activity, i.e., variable and vigorous movements) and hypotonia (usually reduced tone). Although this classification is clearer for each type, the division of the spastic type into unilateral and bilateral paresis and the elimination of the concept of quadriplegia and biparesis are difficult to accept. Therefore, this idea was politely rejected at the International Symposium in 2006. In the 2000 report of SCPE, the Hierarchical classification tree of cerebral palsy was proposed as a diagnostic procedure for cerebral palsy subtypes. This diagnostic procedure is quite important for clinical workers and is described as follows: whether there is a continuous increase in muscle tone in one or more limbs ← —–→ no ↓ ↓ both sides of the body are ↓ whether muscle tone changes whether both are involved ↓ ↓ ↓ ↓ ↓ yes no yes ——→ whether there is generalized hypotonia ↓ ↓ ↓ and with signs of dystonia bilateral spasticity unilateral spasticity involuntary movements ↓ ↓ ↓ CP sexual CP type CP yes no ↓ ↓ ↓ ↓ Decreased activity Increased activity Dyscalculia CP Increased tone for those who cannot be classified Hypotonia ↓ ↓ Dystonia Choreoathetosis CP The diagnostic procedure (hierarchical classification tree) of this subtype of cerebral palsy is concise and helps clinical thinking and judgment, but its classification of bilateral and unilateral spastic cerebral palsy is not shared by most scholars. Unilateral spastic cerebral palsy, i.e. hemiplegia, is well understood; however, the elimination of quadriplegia and diplegia, and the inclusion of those with tardive dyskinesia or dystonia in the category of bilateral cerebral palsy, is really unacceptable. In our opinion, it is more reasonable and clinically appropriate to diagnose those with all four limbs involved as spastic quadriplegia and those with better upper limb function than lower limbs as spastic diplegia. this was also recognized in the report of the 2006 International Cerebral Palsy Symposium; this was also done in Miller’s 2006 classification of cerebral palsy. Second, etiology currently believes that the endogenous cause of the occurrence of cerebral palsy is primarily genetic susceptibility, while the exogenous cause consists of prenatal, perinatal, and postnatal factors. Most of the accidents that occur at birth are due to prenatal factors, and the detection rate of prenatal factors has increased (advanced screening techniques, especially the development of prenatal diagnosis). The combination of prenatal and perinatal factors is the largest cause of cerebral palsy (2002, Rotta). Among the prenatal factors (52%), intrauterine infections, especially TORCH infection syndrome, should be given adequate attention. teratogenic viral infections at 3 months of age – Rubella virus, Cytomegalovirus; Toxoplasma and Herpes infections during pregnancy. Herpes virus infections. In recent years, it has been reported that delivery through the birth canal predisposes to herpes virus infection. This is followed by early pregnancy abnormalities, bleeding from sexual organs, genetic disorders, maternal hypertension, diabetes mellitus, renal disease, anemia and gestational toxicity. Other factors such as toxic encephalopathy (heavy metals, CO, benzene, organophosphorus, excessive alcohol consumption, etc.), exposure to radiation and use of drugs (hormones and anticancer drugs) are also important. Among the perinatal factors (33%), intrauterine and postnatal asphyxia are the most important (including emergency cesarean delivery). Volpe reported (2002) that 20% of neonatal HIE are due to prenatal hypoxia, 35% to perinatal hypoxia, 35% to prenatal with perinatal hypoxia, and only 10% to postnatal hypoxia. Chronic hypoxia during pregnancy (placental dysfunction or fetal nutritional deprivation, etc.) has received attention, and sequelae of brain damage can occur in these infants despite good vital indicators and normal Apgar scores at birth. Immature infants and pathological jaundice (kernicterus) are still an important part of the three major causes (plus asphyxia), but in some developed countries, due to the aggressive control of pathological jaundice, cerebral palsy due to kernicterus has been greatly reduced, so that involuntary motor cerebral palsy accounts for only 10-12% of the total and is mostly caused by HIE due to asphyxia. Pregnancy toxicity, intracranial hemorrhage and hypoglycemia (lactation weakness) have received attention. Inadequate breastfeeding is almost the leading factor for the development of cerebral palsy in immature children (56%). Postnatal factors (12%) are mostly head trauma and intracranial infections (encephalitis, meningitis). Scholars generally agree that prevention and treatment of those factors that lead to fetal and neonatal hypoxia are extremely important to improve the prognosis of brain injury. Early diagnosis and early treatment of the importance of 1, infancy and early childhood brain development is the most vigorous (the fastest within 18 months), plasticity (born brain weight 370g, 6 months 700g, 2 years old up to 1000g, 7 years old up to 1400g close to adults); 2 years before the age of the fastest myelination, up to 75%. Synaptic modifications are extremely active at this time. The number of brain cells is fixed at birth: 14 billion – the basis of function, no regeneration but functional compensation is possible. In recent years, it has been reported that the hippocampus still has neural stem cells that can regenerate neurogenesis . 2, not far down the abnormal path, easy to pull back to normal or near normal developmental track. Especially to avoid the fixation of posture, contracture and deformity. 3, cerebral palsy is fixed around 2 years old, the diagnosis before 1 year old is called early diagnosis, and the diagnosis before 4-6 months is super early diagnosis. If early treatment or early intervention is possible, the consequences can be quite significant. Currently, scholars in various countries are trying to explore early diagnosis and strive to diagnose cerebral palsy before the age of 6 months. In the past, the commonly used Vojta’s seven postural reflexes were no longer used by most scholars because of their poor accuracy and the vague concept of the term “central coordination disorder”. Since 1993, Sporns and Edelman proposed the “neurogenic group selection” theory of neural control of motor development, emphasizing that motor development is the result of the interaction between genes and environmental factors, and that “experience-dependent” motor development plays a dominant role in this process. Motor development plays a dominant role. In recent years, Prechtl et al. (1997) analyzed the early development of infants (before 6 months of age) using video techniques, observing “general movements (GMs)”, especially “fidgety movements (FMs)”, to determine the development of the infant. Prechtl et al. (1997) showed that the paucity of general movements and the accompanying spasticity were predictive indicators for the later onset of cerebral palsy. (2002) showed that the paucity of restless movements, “upper limb circular movements” and finger spreading were predictive indicators of later onset of involuntary cerebral palsy. The emergence of CT and MR plays an important role in the diagnosis of cerebral palsy and the determination of brain lesions, and is an important examination tool. CT is superior to MR in observing calcification and water content (cerebral edema); while MR is clearer in observing myelination (white matter), and the 3D cross-section is more conducive to detecting lesions. Imaging only determines the nature and distribution of the lesion, although it is related to the clinical type (e.g., periventricular white matter softening associated with double palsy), but clinical typing still depends on clinical examination and evaluation. Multicystic encephalomalacia (MCE) is a condition in which there are numerous cysts in both hemispheres of the brain. It is seen in one of the twin fetuses as a stillbirth, when the mother has a severe respiratory impairment, still DIC caused by multiple infarcts along the vascular pathway, necrosis after neuroglial hyperplasia to form sacs. Clinically, it is severe cerebral palsy, all quadriplegia (spastic or mixed type); rare, accounting for less than 10%. 2, Bilateral basal ganglia, thalamic lesion (BBTL) Basal nucleus or thalamic consistency high signal (T2), characteristic. It is presumed to be a necrotizing lesion. Most often seen in those with severe intrauterine hypoxia. It is mostly tetraplegia (mainly chorea-hypoparalysis), which is not uncommon and accounts for 20-30% of mature children with cerebral palsy. 3.Border zone infarct (BI) is a necrotic infarct in the border zone of the anterior and middle cerebral arteries or the middle and posterior cerebral arteries (parsagittal area), which is a state of circulatory insufficiency and insufficient cerebral blood perfusion (mild to moderate). Mostly quadriplegia or diplegia (spastic type). 4.Middle cerebral artery infarct (MCAI) causes hemiparesis without exception (spastic type). It presents with large brain masses of softening and necrosis. It is characterized by the absence of symptoms at the time of occurrence and the appearance of abnormal symptoms several months later. The above four are mostly seen in mature children with cerebral palsy.5 Periventricular leukomalacia (PVL) is a characteristic abnormality seen in immature children. Short-term severe ischemia (asphyxia) causes hypoxia of the ventricles and their adjacent white matter, destruction of the periventricular white matter, uneven density, and unshaped enlargement of the ventricles. Most of them are diplegic (spastic type), sometimes they can be severe diplegic with quadriplegia, or hemiplegia, etc. In recent years, it has been found that it has gestational age-dependent features (immature children occur after birth; mature children occur before birth). 6, intracerebral hemorrhagic lesion (posthemorrhagic lesion, PHL) This includes subarachnoid hemorrhage, ventricular hemorrhage and parenchymal hemorrhage. Here mainly refers to the ventricular hemorrhage, the severe cases spread to the brain parenchyma, divided into 4 levels, 3, 4 often cause sequelae of brain injury, mostly seen in premature low birth weight babies. Intraventricular hemorrhage, enlargement of the ventricles, disruption of the shape of the ventricles, and even hematoma formation in the brain parenchyma, mostly cause diplegia (spastic type). Subarachnoid hemorrhage often accompanies HIE and is seen in mature infants, especially in breech deliveries, and often causes cerebral palsy. It is rare, accounting for only 10% of cases. 7. Co-injury of the cortex and basal ganglia This is mostly caused by severe hypotension. The presence of cortical atrophy, thinning of the gyrus, deepening of the sulcus, and even the myxoid gyrus suggest extensive cortical damage, often resulting in mental retardation, convulsive seizures, and visual disturbances (cortical blindness); basal ganglia atrophy, uneven density, and long T1 and long T2 signals. Mostly tetraplegia (mixed type), severe disease. 8. Non-specific abnormalities of the gap between the brain and the skull opening (CT somatotype), with various causes, the extent of which often does not parallel the clinical course. Hypotonia and developmental delay are often present, mostly benign, later turning to normal development; some have long-term hypotonia and developmental delay residual, which can hardly be said to be benign. 9, congenital brain malformation (congenital brain malformation) 1) abnormalities of neural tube closure (disorders of neural tube closure) cranioschisis, cranial suture closure incomplete (cranioschisis or dysraphic disorders). Chiari-II malformation (Chiari-II malformation): narrowing of the midbrain aqueduct. Dandy-Walker syndrome: congenital atresia of the Magendie (middle) foramen and Luschka (lateral) foramen of the 4th ventricle, or rarely, stenosis. agenesis of corpus callosum (brain beam) defect: common in gestational toxicity. 2) Abnormalities of ventricular formation (disorders of diventiculation) Abnormalities of septum pellucidum-optic tract formation (septo-optic dysplasia). Holoprosencephaly or forebrain anomalies (holoproencephaly). (3) Disorders of sulcation and migration (lissencephaly): early fetal injury. Schizencephaly: hypoxic-ischemic damage in early fetal life. Gray matter ectopic (heterotopias): abnormal gray matter migration process. Thick or giant gyrus (pachygyria) often anencephalic-thick gyrus (agyria-pachygyria); early fetal damage. Multiple microcephalic gyri (polymicrogyria): mid-fetal hypoxia. V. Treatment and rehabilitation of cerebral palsy Treatment of cerebral palsy should be comprehensive. Various treatment methods should complement each other. Emphasis should be placed on both training (PT, OT, ST) and the promotion of the ability of daily living (ADL). Education and psychotherapy are also indispensable elements. The effect will be better if Chinese herbal medicine, massage and acupuncture are added to the treatment. However, in all cases, training therapy is still the dominant treatment method because it is consistent with both neurodevelopmental laws and the “neurogenic group selection theory”. The following are only the main treatment methods. 1.Medication 1）Brain hydrolysis protein solution: brain activator, brain peptide, etc. Brain tissue hydrolysis solution is 75% amino acid mixture, 25% is small molecule peptide. It may be due to the brain peptides it contains, especially containing nerve cell growth factor to play a role in promoting brain development and repair. It is effective in clinical use at home and abroad (Hartbauer, 2001), and no serious side effects have been found so far. 2) Symptomatic drugs: These drugs can only relieve the symptoms and cannot fundamentally change the course of cerebral palsy, so they should be used in moderation. The main anti-spasticity drugs are: balofen (GABAb receptor agonist), etc. Sometimes levodopa/carbidopa, methyldopa, sodium valproate, and nitroprusside are used for those with dystonia, but the dosage should be controlled to the extent that it does not interfere with training treatment. 3) Other brain cell nourishing drugs: cytidyl phosphorylcholine, piracetam (anti-spasticity drugs that promote information transmission and act on the cortex), gangliosides, nerve growth factor, etc., are effective. 2, injection botulinum toxin injection (botulinum toxin injection): act on the neuromuscular junction to block the release of acetylcholine, reduce muscle tone and release spasm. Baclofen medullary injection (baclofen intrathecal administration) or baclofen pump burial is used to relieve spasticity. The former has many side effects; the latter supplies baclofen automatically and can be added at any time, but it is prone to blockage and infection, resulting in failure. 3.SurgerySurgery is an auxiliary measure for cerebral palsy rehabilitation, and preoperative and postoperative training is very important. Orthopedic surgery: Achilles tendon lengthening, adductor cut, tendon transfer, bone orthopedic, etc. Selective dorsal rhyzotomy (SDR): T2-S1 proportionally cut the posterior root fibers to break the γ-loop. It is indicated for spastic biparesis, but the long-term results are not reliable. The side effects of cystorectal disorders should not be ignored. The choice of indications is the key factor for success. 4.Ueda method manual technique This is a kind of anti-spasticity treatment manual technique developed by Mr. Masa Ueda (director of the second Rango Gakuen, Aichi Prefectural Physical and Mental Disability Child Healing Center, Japan) in 1988. he came to China to give lectures in October 1998. Basic theories: 1) Subtractive development – He believes that a large number of brain cells die at birth, and development is toward simplification and simplification. He believes that the relationship between the limbs and the brain is like that of a mayor with citizens, and that the condition of the peripheral parts has a great influence on the central and motor development, and that the impairment of the peripheral parts is not always determined by the brain. In the case of motor disorders, it is also important to correct the endings to produce correct movement and posture, i.e., “endings pointing” rather than “brain pointing”. 3) Motor development cannot always be explained by a predetermined pattern of maturation of the brain, but motor experience is also important. The experience of movement is also important. This has been confirmed by the recent “neurogenic group selection” theory. In short, this manual technique is an “opposite excitation” inhibiting manual technique. For example, triceps spasms such as ankle plantar flexion and pointed foot, which occur in cerebral palsy, also have a role in the excitatory circuit of the tibialis anterior muscle. After strong plantar flexion, the tibialis anterior muscle is rested and relaxed to the maximum extent, and the opposite excitatory circuit is closed, while the opposite inhibitory circuit is opened (awakened), thus relieving the triceps spasm. Introduction to the basic hand techniques of the Ueda method: 1) Neck-Torso hand technique Neck method: In the supine position, turn the face slowly to one side while the other hand lifts the shoulder on the side of the face and the cervical spine is fully rotated back, hold for 3 minutes. Shoulder nail – pelvic method: two people operate, shoulder nail belt and pelvic belt gyrate in opposite direction – “twist twist”. (2) The upper limb method of hand technique of the extremities: make a fist of the forearm to rotate before full flexion and press to the chest for 3 minutes; open the hand and finger dorsal flexion of the forearm to rotate back and abduct 90-110 degrees, then immediately flex the position, repeat 15 times, and finally hold the flexion position for 3 minutes. Lower extremity method: hold the mother toe with one hand, push the heel with the other hand, maximum plantar flexion of the ankle joint, full flexion of the toe for 3 minutes; push the mother toe with one hand, all flexion of the lower extremity, hold the heel with the other hand, dorsiflexion of the ankle joint to maintain a mild inversion position of the arch, interact with the plantar flexion position of the ankle joint 15 times; then maintain the plantar flexion position for 3 minutes. Diagonal method: one side of the upper limb method flexion phase (or extension phase) and the other side of the lower limb method extension phase (or flexion phase) together, alternating (two people operate). Advantages and disadvantages of the Ueda method: simple and standardized operation, quick release of spasticity (immediate effect); local rather than overall treatment, not psychosomatic treatment, limited use; theoretical basis is not easy to understand. 5.Vojta method – neurophysiological approach uses the stimulation of the trigger to induce a reflexive movement. Through the repeated occurrence of movement, the normal reflex pathway is promoted and the abnormal reflex pathway and movement are suppressed to achieve the therapeutic purpose. It is also called neurophysiologically intensive manual technique. Mobility is essential. There are three elements: postural responsiveness, rising mechanism and phase-motor ability. Rolling and crawling are the basic forms of locomotion. This method has two types of manual techniques and variations: reflexive prone climbing (R-K) and reflexive turning (R-U). Note: the departure posture is the most important, the pressure of the evoked band should be in place (part, strength, direction and time), and the main evoked band and the auxiliary evoked band should be cooperated and used flexibly. Effects of the Vojta method: brain plasticity (plasticity) – reconfiguration; promotion of myelination; promotion of inter-synaptic transmission; positive feedback loops; reinforcement in space (combination of evoked bands) and time (application of resistance); conversion of muscle contraction direction (centripetal → centrifugal). Advantages and disadvantages of the Vojta method: the technique is simple, standardized and easy to learn, but difficult to master; it is effective for all types of cerebral palsy; it is reliable for infants, especially those with poor vertical head (leader); the child is crying and “painful”, which is not in line with the rule of “development and learning through play “The “normalization” rate of 92% for early treatment of Vojta is not credible. Only Germany is prevalent, Japan is also carried out more widely, other developed countries basically do not use. We have used for many years with good results. 6, Peto method of guided education treatment (conductive education treatment) This is a method developed by Dr. Hungarian Yali Peto in 1945, also called group guidance therapy. It is a kind of education and training program developed for organized disabled people through education. It is a training and educational program for people with disabilities through education. It is a training and educational program for people with disabilities that includes activities of daily living and eating. The instructor (1 person) leads and demonstrates, breaks down the movements into 5 steps, and leads a group of children with disabilities (15-20 children) to train collectively, giving full play to the initiative of the children, learning from each other and promoting each other, while other trainers (6-7 people) provide individual counseling. This method requires a guidance and education team including doctors, physical therapists, occupational (occupational) therapists, speech therapists, social workers, caregivers, teachers and family members to work together to develop a program of education and training. It is a combination of group training and individual instruction. Mostly used in community rehabilitation. Also applicable to adults. The child should have a certain level of intelligence and is generally suitable for children with disabilities from 2-3 years of age. Currently prevalent in Western countries. However, in our country, it is difficult for the family to accept the hospitalization because it depends on the child’s own ability, so it is suitable for community rehabilitation. 7, Bobath method (Bobath hand technique, Bobath approach) Dr. Karel Bobath is a Czech, later went to the United Kingdom. Dr. Karel Bobath was a Czech national who went to England and engaged in 2-3 specialties such as orthopedic surgery and finally pediatrics. He married Berta Bobath from Australia (who was engaged in dance gymnastics) and the two of them were very concerned about children with disabilities and embarked on the path of treating them. Now, through the efforts and development of scholars in various countries, it has been developed into the “Neurodevelopmental Therapy Manual Technique”. History of the Bobath Method: 1943: Handling was found to be effective in the treatment of hemiplegia, and was then applied to cerebral palsy. 1945: Development of reflex inhibitory posture (RIP). 1953: Kabet’s intrinsic neuromuscular facilitation (PNF) was introduced. 1960: Promoted early diagnosis, early treatment and mother-child admission. 1967: The theory of inhibition and facilitation through the key point was established. 1970: The Bobath method was introduced in Japan (Osaka), and the Bobath Hospital was established in Osaka in 1982. Mr. and Mrs. Bobath died in January 1991, and they were sorely missed. This method has a sound theoretical basis and is a treatment method developed based on neurophysiology and neurodevelopmental science. Features of the Bobath Method: All-round: training treatment in all aspects of somatic (physical), homework, language, education, audiovisual, communication (communication), ADL (activities of daily living), social activities, etc. Diagnosis-evaluation (assessment) and treatment become one and complement each other. Training in games: Easy and enjoyable to accomplish training goals. Combination of facilitating and inhibiting manual techniques: facilitating normal (postural) development (vertical response and balance response, etc.); inhibiting abnormal (postural) development (primitive reflex and nervous reflex). Follow developmental rules: three facets of developmental elements; head-collateral principle; principle of central part-end; principle of developmental stages and continuity; principle of pattern competition; principle of active and passive; principle of key point. Live and learn depending on the person, the type, and the condition. Continuous exploration, never ending: Anyone can create new hand techniques as long as they master the principles and principles. Examples of specific hand techniques: vertical head: prone position support and sitting position movement, available round roll and training ball, preferably mediated by sitting position tilt trunk. Roll over: driven by the limbs (vertical response). Four crawl: “rowing boat”, “bridge”, weight movement from the hip and trunk (training hip separation and interaction, balance). Focus on training the components of movement patterns. Stance: exploration while doing so, top-down erection, body movement, stance balance. Flexion against jerk; abduction and external rotation against internal rotation or rotation forward. Training principles for spastic type: release psychological barriers such as stubbornness, restlessness, fear, dependence and lack of self-confidence; control movement with movement; avoid the effect of tension reflex on casual movement; plenty of sensory stimulation; experience the sensation of normal muscle tone, movement pattern and posture. Principles of tardive dyskinesia training: address emotional instability and desire for dissatisfaction; restrain with stillness; center pointing; symmetry; vertical head first (leader) – trunk → caudal, vertical head and shoulder girdle stability is the basis of whole body stability; avoid supine position (ATNR and TLR); counteract TLR; emphasize ADL; treat 24/7, even during sleep; repeat Establish normal movement patterns; during exercise training, balance movement response (vertical response and balance response) should be induced by weight movement.