How does cerebral palsy develop?

Sexual paralysis (cerebral?

palsy), referred to as cerebral palsy, usually refers to central movement disorders caused by non-progressive brain injury or brain developmental abnormality from before birth to one month after birth due to various reasons. Clinically, it is characterized by abnormal posture and muscle tone, muscle weakness, involuntary movements, and ****济调调, often accompanied by sensory, cognitive, communication, and behavioral disorders and secondary skeletal muscle abnormalities, and may be associated with seizures. Nonprogressive central movement disorders of various causes after the first month of life, sometimes called acquired?

cerebral?palsy, account for about 10% of pediatric cerebral palsies. The incidence of cerebral palsy is approximately 1.2-2.5?‰ (per 1,000 live births).

Western medical name: cerebral palsy English name: cerebral?palsy belongs to the department: internal medicine? -? Neurology Contagiousness: non-contagious

Catalog

Etiology and Risk Factors Pathology Clinical Manifestations Spastic hemiplegia (Spastic?

hemiplegia) Spastic biplegia? (Spastic?

diplegia) spastic quadriplegia? (Spastic?

quadriplegia)Dyskinesia (dyskinetic?

CP)**** Chiropractic Disorder (Ataxia?

CP)DiagnosisDifferential DiagnosisTreatmentPhysical TherapyOperational TherapyOrthotics ApplicationSpeech TherapyPsycho-behavioral TherapyFamily Training ProgramSpecial EducationMedicationSurgery TreatmentPreventionExpansionCauses and Risk Factors?

Pathology?

Clinical manifestations?

Spastic hemiplegia?

Spastic diplegia? (Spastic diplegia)?

Spastic quadriplegia? (Spastic quadriplegia)?

Dyskinetic CP?

Diagnosis of ****typical dyskinesia (Ataxia?CP)?

Differential diagnosis?

Treatment?

Physical therapy?

Operational therapy?

Orthotic applications?

Speech therapy?

Psychobehavioral therapy?

Home training programs?

Special education?

Medication?

Surgical treatmentsPrevention unfolds

Editorial Causes and Risk FactorsThere are many causes of cerebral palsy, but no cause can be found in more than one-third of cases. Sometimes multiple factors may also be present in some cases. Prenatal factors are the most common and include genetic and chromosomal disorders, congenital infections, malformations or hypoplasia of brain development, and fetal cerebral ischemia and hypoxia resulting in softening of the white matter around the ventricles or damage to the basal ganglia. Perinatal factors are brain injuries that occur from the beginning of labor to one week after birth, including cerebral edema, neonatal shock, intracerebral hemorrhage, sepsis or central nervous system infection, and ischemic-hypoxic encephalopathy. Perinatal factors may be an important cause of cerebral palsy in preterm infants. Late postneonatal factors include CNS infections, cerebrovascular disease, head trauma, poisoning, and various other causes of nonprogressive brain injury occurring from 1 week to 3 or 4 years of age. Premature birth and intrauterine growth retardation, although not direct causes of cerebral palsy, are important risk factors for cerebral palsy. Maternal intrauterine inflammation, or chorioamnionitis, has received increasing attention as a potential risk factor. [1] Edit Pathology Pathologic changes are related to etiology and the susceptibility of the developing brain to damage from various pathogenic factors. Early gestational pathogenic factors mainly cause neuronal proliferation and migratory abnormalities, which can occur in anencephalic gyrus, megalencephalic gyrus, multiple cerebellar gyrus, cerebral fissure malformations, and neuronal ectasia. The most common pathological changes in preterm infants are periventricular white matter softening and periventricular hemorrhagic infarcts. The type of pathology in term infants is complex and varied, often associated with hypoxic-ischemic brain damage. The marble state, on the other hand, is characterized by neuronal loss and neurogliosis with increased myelination in the basal ganglia and thalamus, resulting in a marble-like texture, which is a typical alteration of karyorrhexis and is also seen in hypoxic-ischemic brain injury. Editorial Clinical presentation Symptoms of cerebral palsy manifest in infancy, often with complaints of abnormal postures and backward motor development. Although the child's brain damage or abnormal brain development is nonprogressive, the clinical presentation often changes as the brain injury is repaired and the developmental process occurs. For example, severe neonatal ischemic-hypoxic encephalopathy is often characterized by hypotonia in early infancy, which gradually changes to hypertonia. Balance dysfunction can only be manifested when the infant develops to sitting or even standing. Secondary changes such as joint contractures and spinal deformities also develop gradually. They can be accompanied by epilepsy, mental retardation, sensory disturbances, and behavioral disorders. These concomitant disorders can sometimes be the primary disability in children with cerebral palsy. Clinically, according to the nature of the movement disorders, they can be categorized as spastic, involuntary movement, ****济失调型, hypotonic and mixed types, etc. And according to the distribution of the affected limbs, they are categorized as monoparesis, hemiparesis, diplegia, trilobal palsy and quadriplegia. Several specific clinical syndromes that are common are described below. Spastic hemiplegia (Spastic?hemiplegia) is the most common and involves one side of the limb, with most of the upper limbs being more severely affected than the lower limbs, and the distal limbs being more severely affected than the proximal limbs, while the face is often not involved. Most children present with symptoms after 3 months of age, which are characterized by hypermobility of the affected limb, persistent clenching of the fist, absence of the gripping reflex, flexion and rotation of the forearm, and a circle gait. In some patients, the affected limb may initially show hypotonia, which later turns into spasticity. This type is often associated with mental retardation and epilepsy. Epileptic seizures are partial or secondary to generalized seizures. Strabismus is common. Spastic diplegia? (Spastic?diplegia) is characterized by increased muscle tone in both lower limbs. This type is most often seen in premature infants. Children often present with hypotonia in both lower limbs within 1-3 months. This is followed by the so-called dystonic phase, in which the child induces tonic straightening of the lower limbs and crosses them in a scissor-like manner when the child is in the upright position and the soles of the feet are touching the examination bed. Finally, the spastic phase occurs, with hip and knee flexion, internal rotation of the lower limbs, scissor gait, and in severe cases, inability to walk independently. The upper limbs are less severely affected, often showing abnormal posture of the upper limbs when walking, but the functional involvement of the hands is not obvious. The combination of this type with epilepsy is rare, accounting for about 1/5. about 2/3 of the patients have normal intelligence or critical state. Strabismus is common. Spastic quadriplegia? (Spastic?quadriplegia) is seen in children with severe asphyxia. There is increased muscle tone in all four limbs, often in the form of angulation. It may be accompanied by supranuclear bulbar palsy, which is characterized by dysphagia and dysarthria. About half of the children have epilepsy and mental retardation. Dyskinetic CP accounts for about 10% of cases, with hypoxic brain injury and neonatal kernicterus as the main causes. Infants have hypotonia in the early stage, and then gradually develop extrapyramidal symptoms, such as or hand-foot movement and other manifestations. Children may have salivation, dysphagia, speech disorders and so on. Deep tendon reflexes of the lower limbs are normal or enhanced. There may be persistent primitive reflexes. Intelligence is mostly normal or critical. About 1/4 patients have epilepsy. Those caused by kernicterus are mostly characterized by hand and foot movement, sensory deafness, and dental enamel hypoplasia. ***The ataxia type (Ataxia? CP) accounts for about 10% of cases. In infancy, it is characterized by hypotonia, balance disorder, and backward motor development. By early childhood, signs such as poor distance discrimination and intentional tremor may be found. There are no signs of pyramidal fasciculations. Mental retardation is not uncommon but not severe. Ancillary imaging tests provide evidence of cerebral pathologic changes and are helpful in the diagnosis of the cause of cerebral palsy and prognosis. Ultrasound of the neonatal head can be performed at the bedside and can easily detect lesions such as paraventricular white matter softening and intracranial hemorrhage. MRI of the head is better than cranial CT for showing fine structural brain abnormalities, but cranial CT is better for showing calcifications. Electroencephalogram is required in patients with seizures. Visual and auditory evoked potentials and audiograms may be performed if visual or auditory deficits are suspected. Blood/urine amino acid and organic acid analyses are needed to exclude inborn metabolic defects. Enzymatic and genetic tests may be performed to exclude the corresponding cerebral degenerative disease. Assessment of motor function and daily living skills in cerebral palsy can help determine the severity of cerebral palsy, and can also be used as a basis for the effectiveness of rehabilitation therapy. Commonly used motor function assessment scales include the following two types.1. Gross Motor Function Measurement (GMFM) The GMFM is a gross motor function assessment tool, available in 88-item and 66-item versions, which assesses the gross motor skills of children with cerebral palsy in five functional areas, including recumbent position and turning, sitting, crawling and kneeling, standing and walking, and running and jumping. The individual items in each energy zone were ranked in order from easy to difficult. Scores for each zone are expressed as a percentage, with 100% representing the ability to perform all movements in that zone. The scale can reflect the effects of rehabilitation more sensitively and is suitable for the assessment of gross motor skills in children with cerebral palsy, the setting of rehabilitation goals and the monitoring of rehabilitation efficacy. As there is no norm established according to age, it is not possible to assess the level of motor development. 2. Peabody Motor Development Scale (PMDS) This scale measures the level of gross and fine motor development, ****249 items. The gross motor subtest includes four categories of items: reflexes, posture, movement, and practical manipulation, and the results are expressed as gross motor developmental age or developmental quotient; the fine motor subtest includes two categories of grasping and visual-motor integration, and the results are expressed as fine motor developmental age or developmental quotient; and the results are finally summed up as total developmental age or developmental quotient. The Peabody Motor Development Scale is used to assess motor function in children with motor delays and mild or moderate severity of cerebral palsy. In children with cerebral palsy, due to the extremely slow progress in certain aspects of motor ability, a decrease in motor development quotient with actual age can occur, and it is best to reflect the changes in the child in terms of developmental age. Edit Diagnosis The diagnosis of cerebral palsy is based primarily on history and neurologic examination. Typical cerebral palsy tends to be characterized by lagging motor development, postural abnormalities, and signs of central movement disorders. Asking for a history of abnormalities during pregnancy, the perinatal period, and the neonatal period may suggest the cause of cerebral palsy. Imaging may reveal evidence of brain damage. Cerebral palsy requires the exclusion of inherited metabolic and neurodegenerative disorders. Cerebral palsy often lacks specific signs in the early stages and is difficult to distinguish from generalized motor delays, even in the early stages when there are no obvious motor delays. The assessment of the quality of spontaneous generalized movements (GMs) has been developed in the last few years.GMs are a unique form of movement during the immature brain period and are present from the fetus to 4 months after full term. Studies have shown that the quantity of GMs does not directly correlate with motor development; it is the quality of GMs that is an important indicator of brain injury. Persistent, spastic-synchronous GMs accurately predict cerebral palsy. A small-amplitude, dance-like movement called fidgety?

movements is often seen transiently in small healthy infants. They begin after 6 weeks of corrected age, are most pronounced at 9-12 weeks, and subside until they disappear at 14-20 weeks. The lack of restless movements is highly suggestive of neurologic abnormalities and an early sign of cerebral palsy. Editorial Differential diagnosis Some inherited metabolic or degenerative disorders may progress slowly, such as heterozygous cerebral white matter dystrophy and familial spastic paraplegia, which are not easily differentiated from cerebral palsy in the early stages and may be misdiagnosed. Glutaric acidemia type 1 is easily mistaken for dyskinetic cerebral palsy, whereas arginase deficiency is easily mistaken for bilateral paralytic cerebral palsy. Hypotonia in infancy must be differentiated from lower motor neuron palsy, in which tendon reflexes are often diminished or absent. In infantile hypotonia, special attention must be paid to the exclusion of inherited metabolic disorders. Spastic diplegia sometimes needs to be differentiated from dopa-responsive dystonia. Editorial Treatment The treatment plan should aim to maximize the improvement of the child's function and enhance his or her quality of life, minimize secondary joint deformities and soft tissue contractures, and delay or avoid surgical treatment as much as possible. Commonly used treatments include: Physical therapy improves motor function and enhances self-care by increasing joint mobility, adjusting muscle tone, and improving motor control, coordination, strength, and endurance. Commonly used techniques include: postural therapy, soft tissue stretching, muscle tone adjustment techniques, functional active activity strengthening training, muscle strength and endurance training, balance and coordination control, physical factor assisted therapy (physiotherapy) and so on. Occupational therapy mainly includes fine hand function training, training of daily living activities, production of supports and aids, and simple modification of living environment facilities. The application of orthotics is often used in conjunction with orthotics in rehabilitation therapy to limit abnormal joint movement, improve stability, assist in controlling muscle spasm, maintain muscle length, prevent deformity, and assist in improving motor function. The key to the application of orthotics lies in the selection of the best wearing period and type according to the individual situation of the child, therefore, it should be decided by the rehabilitation physician, therapist and orthotist*** in the same discussion. Speech therapy is evaluated by physicians and speech therapists, and treatment is based on different types of speech disorders, such as motor control training of the jaw, mouth and lips, tongue muscles, soft palate, as well as comprehension and expression ability training. Psycho-behavioral therapy for children with cerebral palsy is sometimes accompanied by abnormal psycho-behavioral problems, such as autism, hyperactivity, emotional instability and other symptoms. A healthy family environment, increased socialization with peers, and early psycho-behavioral intervention are key to preventing and treating psycho-behavioral disorders. The family training program therapist should develop a family training program for the child and his or her parents. The focus of the program should be on improving function and preventing secondary disabilities, but in particularly severe cases, easing care and reducing the burden on the family should be the primary goals. It usually includes: understanding of the child's condition and organization of daily living; targeted muscle strength and joint mobility training; stretching of spastic muscles; strengthening of functional active activities; and use of assistive devices such as orthotics, chairs, standing frames, and wheelchairs. Special education pediatric rehabilitation should also include special education for different levels of intelligence, therefore, the establishment of institutions integrating medical treatment, care and education is a good model for providing comprehensive and continuous services for children. Medications commonly used include neurotrophic drugs and muscle relaxants. Medication is used only when necessary and it cannot replace functional training. Numerous studies and clinical practice have proved that botulinum toxin A intramuscular injection is a safe and effective treatment for spasticity. Generally, the effect of reducing spasticity can be maintained for 3~8 months, at this time, individualized comprehensive treatment should be carried out in a timely manner, such as functional muscle training, soft tissue pulling, wearing orthotics, etc., in order to give full play to the maximum opportunity for rehabilitation brought about by hypotonia. Spasticity will gradually increase 4~6 months after injection, but usually the effect of motor function improvement will not disappear, and can be injected again if necessary. Surgery When muscle contractures and joint deformities are severe, orthopedic surgery is an option and should be done as much as possible in a single operation to complete all areas that need orthopedic treatment for better functional improvement after surgery. Selective posterior spinal nerve rhizotomy may be used in children with extensive spasticity of the muscles of the lower extremities and essentially normal muscle strength. Regardless of the type of surgery, there should be a standardized rehabilitation program before and after the surgery. In conclusion, on the basis of a full understanding of the child's pathologic problems and the indications for various methods, the purpose of treatment should be clearly defined, and the correct