Cerebral palsy
Group of movement disorders that appear in early childhood / From Wikipedia, the free encyclopedia
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Cerebral palsy (CP) is a group of movement disorders that appear in early childhood.[1] Signs and symptoms vary among people and over time,[1][3] but include poor coordination, stiff muscles, weak muscles, and tremors.[1] There may be problems with sensation, vision, hearing, and speaking.[1]
Cerebral palsy | |
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A child with cerebral palsy being assessed by a physician | |
Specialty | |
Symptoms | |
Complications | |
Usual onset | Prenatal to early childhood[1] |
Duration | Lifelong[1] |
Causes | Often unknown[1] or brain injury |
Risk factors |
|
Diagnostic method | Based on child's development[1] |
Treatment | |
Medication | |
Frequency | 2.1 per 1,000[2] |
Often, babies with cerebral palsy do not roll over, sit, crawl or walk as early as other children of their age.[1] Other symptoms include seizures and problems with thinking or reasoning, each of which occur in about one-third of people with CP.[1] While symptoms may get more noticeable over the first few years of life, underlying problems do not worsen over time.[1]
Cerebral palsy is caused by abnormal development or damage to the parts of the brain that control movement, balance, and posture.[1][4] Most often, the problems occur during pregnancy, but they may also occur during childbirth or shortly after birth.[1] Often, the cause is unknown.[1] Risk factors include preterm birth, being a twin, certain infections during pregnancy, such as toxoplasmosis or rubella, exposure to methylmercury during pregnancy, a difficult delivery, and head trauma during the first few years of life.[1] About 2% of cases are believed to be due to an inherited genetic cause.[5]
A number of sub-types are classified, based on the specific problems present.[1] For example, those with stiff muscles have spastic cerebral palsy, those with poor coordination in locomotion have ataxic cerebral palsy, and those with writhing movements have dyskinetic cerebral palsy.[6] Diagnosis is based on the child's development over time.[1] Blood tests and medical imaging may be used to rule out other possible causes.[1]
Some of the causes of CP are preventable through immunization of the mother, and through efforts to prevent head injuries in children such as through improved safety.[1] There is no known cure for CP, but supportive treatments, medication and surgery may help many individuals.[1] This may include physical therapy, occupational therapy and speech therapy.[1] Mouse NGF has been shown to improve outcomes [7][8] and has been available in China since 2003.[9] Medications such as diazepam, baclofen and botulinum toxin may help relax stiff muscles.[1][10][11] Surgery may include lengthening muscles and cutting overly active nerves.[1] Often, external braces and Lycra splints and other assistive technology are helpful with mobility.[12][1] Some affected children can achieve near normal adult lives with appropriate treatment.[1] While alternative medicines are frequently used, there is no evidence to support their use.[1]
Cerebral palsy is the most common movement disorder in children.[13] It occurs in about 2.1 per 1,000 live births.[2] Cerebral palsy has been documented throughout history, with the first known descriptions occurring in the work of Hippocrates in the 5th century BCE.[14] Extensive study of the condition began in the 19th century by William John Little, after whom spastic diplegia was called "Little's disease".[14] William Osler first named it "cerebral palsy" from the German zerebrale Kinderlähmung (cerebral child-paralysis).[15] A number of potential treatments are being examined, including stem cell therapy.[1] However, more research is required to determine if it is effective and safe.[1]
Cerebral palsy is defined as "a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain."[16] While movement problems are the central feature of CP, difficulties with thinking, learning, feeling, communication and behavior often co-occur,[16][17] with 28% having epilepsy, 58% having difficulties with communication, at least 42% having problems with their vision, and 23–56% having learning disabilities.[18] Muscle contractions in people with cerebral palsy are commonly thought to arise from overactivation.[19]
Cerebral palsy is characterized by abnormal muscle tone, reflexes, or motor development and coordination. The neurological lesion is primary and permanent while orthopedic manifestations are secondary and progressive. In cerebral palsy unequal growth between muscle-tendon units and bone eventually leads to bone and joint deformities. At first, deformities are dynamic. Over time, deformities tend to become static, and joint contractures develop. Deformities in general and static deformities in specific (joint contractures) cause increasing gait difficulties in the form of tip-toeing gait, due to tightness of the Achilles tendon, and scissoring gait, due to tightness of the hip adductors. These gait patterns are among the most common gait abnormalities in children with cerebral palsy. However, orthopaedic manifestations of cerebral palsy are diverse.[20][21] Additionally, crouch gait (also described as knee flexion gait)[22] is prevalent among children who possess the ability to walk.[23] The effects of cerebral palsy fall on a continuum of motor dysfunction, which may range from slight clumsiness at the mild end of the spectrum to impairments so severe that they render coordinated movement virtually impossible at the other end of the spectrum.[24] Although most people with CP have problems with increased muscle tone, some have normal or low muscle tone. High muscle tone can either be due to spasticity or dystonia.[25]
Babies born with severe cerebral palsy often have irregular posture; their bodies may be either very floppy or very stiff. Birth defects, such as spinal curvature, a small jawbone, or a small head sometimes occur along with CP. Symptoms may appear or change as a child gets older. Babies born with cerebral palsy do not immediately present with symptoms.[26] Classically, CP becomes evident when the baby reaches the developmental stage at 6 to 9 months and is starting to mobilise, where preferential use of limbs, asymmetry, or gross motor developmental delay is seen.[21]
Drooling is common among children with cerebral palsy, which can have a variety of impacts including social rejection, impaired speaking, damage to clothing and books, and mouth infections.[27][28] It can additionally cause choking.[28][29]
An average of 55.5% of people with cerebral palsy experience lower urinary tract symptoms, more commonly excessive storage issues than voiding issues. Those with voiding issues and pelvic floor overactivity can deteriorate as adults and experience upper urinary tract dysfunction.[30]
Children with CP may also have sensory processing issues.[31] Adults with cerebral palsy have a higher risk of respiratory failure.[32]
Skeleton
For bones to attain their normal shape and size, they require the stresses from normal musculature.[33] People with cerebral palsy are at risk of low bone mineral density.[34] The shafts of the bones are often thin (gracile),[33] and become thinner during growth. When compared to these thin shafts (diaphyses), the centres (metaphyses) often appear quite enlarged (ballooning).[35] Due to more than normal joint compression caused by muscular imbalances, articular cartilage may atrophy,[36]: 46 leading to narrowed joint spaces. Depending on the degree of spasticity, a person with CP may exhibit a variety of angular joint deformities. Because vertebral bodies need vertical gravitational loading forces to develop properly, spasticity and an abnormal gait can hinder proper or full bone and skeletal development. People with CP tend to be shorter in height than the average person because their bones are not allowed to grow to their full potential. Sometimes bones grow to different lengths, so the person may have one leg longer than the other.[37][38]
Children with CP are prone to low trauma fractures, particularly children with higher Gross Motor Function Classification System (GMFCS) levels who cannot walk. This further affects a child's mobility, strength, and experience of pain, and can lead to missed schooling or child abuse suspicions.[33] These children generally have fractures in the legs, whereas non-affected children mostly fracture their arms in the context of sporting activities.[39]
Hip dislocation and ankle equinus or plantar flexion deformity are the two most common deformities among children with cerebral palsy. Additionally, flexion deformity of the hip and knee can occur. Torsional deformities of long bones such as the femur and tibia are also encountered, among others.[20][40] Children may develop scoliosis before the age of 10 – estimated prevalence of scoliosis in children with CP is between 21% and 64%.[41] Higher levels of impairment on the GMFCS are associated with scoliosis and hip dislocation.[20][42] Scoliosis can be corrected with surgery, but CP makes surgical complications more likely, even with improved techniques.[41] Hip migration can be managed by soft tissue procedures such as adductor musculature release. Advanced degrees of hip migration or dislocation can be managed by more extensive procedures such as femoral and pelvic corrective osteotomies. Both soft tissue and bony procedures aim at prevention of hip dislocation in the early phases or aim at hip containment and restoration of anatomy in the late phases of disease.[20] Equinus deformity is managed by conservative methods especially when dynamic. If fixed/static deformity ensues surgery may become mandatory.[40]
Growth spurts during puberty can make walking more difficult for people with CP.[43]
Eating
Due to sensory and motor impairments, those with CP may have difficulty preparing food, holding utensils, or chewing and swallowing. An infant with CP may not be able to suck, swallow or chew.[44] Gastro-oesophageal reflux is common in children with CP.[29] Children with CP may have too little or too much sensitivity around and in the mouth.[44] Poor balance when sitting, lack of control of the head, mouth, and trunk, not being able to bend the hips enough to allow the arms to stretch forward to reach and grasp food or utensils, and lack of hand-eye coordination can make self-feeding difficult.[45] Feeding difficulties are related to higher GMFCS levels.[29] Dental problems can also contribute to difficulties with eating.[45] Pneumonia is also common where eating difficulties exist, caused by undetected aspiration of food or liquids.[29] Fine finger dexterity, like that needed for picking up a utensil, is more frequently impaired than gross manual dexterity, like that needed for spooning food onto a plate.[46][non-primary source needed] Grip strength impairments are less common.[46][non-primary source needed]
Children with severe cerebral palsy, particularly with oropharyngeal issues, are at risk of undernutrition.[47] Triceps skin fold tests have been found to be a very reliable indicator of malnutrition in children with cerebral palsy.[45]
Language
Speech and language disorders are common in people with cerebral palsy. The incidence of dysarthria is estimated to range from 31% to 88%,[48] and around a quarter of people with CP are non-verbal.[49] Speech problems are associated with poor respiratory control, laryngeal and velopharyngeal dysfunction, and oral articulation disorders that are due to restricted movement in the oral-facial muscles. There are three major types of dysarthria in cerebral palsy: spastic, dyskinetic (athetotic), and ataxic.[50]
Early use of augmentative and alternative communication systems may assist the child in developing spoken language skills.[49] Overall language delay is associated with problems of cognition, deafness, and learned helplessness.[51] Children with cerebral palsy are at risk of learned helplessness and becoming passive communicators, initiating little communication.[51][52] Early intervention with this clientele, and their parents, often targets situations in which children communicate with others so that they learn that they can control people and objects in their environment through this communication, including making choices, decisions, and mistakes.[51]
Pain and sleep
Pain is common and may result from the inherent deficits associated with the condition, along with the numerous procedures children typically face.[53] When children with cerebral palsy are in pain, they experience worse muscle spasms.[54] Pain is associated with tight or shortened muscles, abnormal posture, stiff joints, unsuitable orthosis, etc. Hip migration or dislocation is a recognizable source of pain in CP children and especially in the adolescent population. Nevertheless, the adequate scoring and scaling of pain in CP children remains challenging.[20] Pain in CP has a number of different causes, and different pains respond to different treatments.[55]
There is also a high likelihood of chronic sleep disorders secondary to both physical and environmental factors.[56] Children with cerebral palsy have significantly higher rates of sleep disturbance than typically developing children.[57] Babies with cerebral palsy who have stiffness issues might cry more and be harder to put to sleep than non-disabled babies, or "floppy" babies might be lethargic.[58] Chronic pain is under-recognized in children with cerebral palsy,[59] even though three out of four children with cerebral palsy experience pain.[60] Adults with CP also experience more pain than the general population.[61]
Associated disorders
Associated disorders include intellectual disabilities, seizures, muscle contractures, abnormal gait, osteoporosis, communication disorders, malnutrition, sleep disorders, and mental health disorders, such as depression and anxiety.[62] In addition to these, functional gastrointestinal abnormalities contributing to bowel obstruction, vomiting, and constipation may also arise. Adults with cerebral palsy may have ischemic heart disease, cerebrovascular disease, cancer, and trauma more often.[63] Obesity in people with cerebral palsy or a more severe Gross Motor Function Classification System assessment in particular are considered risk factors for multimorbidity.[64] Other medical issues can be mistaken for being symptoms of cerebral palsy, and so may not be treated correctly.[65]
Related conditions can include apraxia, sensory impairments, urinary incontinence, fecal incontinence, or behavioural disorders.[66]
Seizure management is more difficult in people with CP as seizures often last longer.[67] Epilepsy and asthma are common co-occurring diseases in adults with CP.[68] The associated disorders that co-occur with cerebral palsy may be more disabling than the motor function problems.[29]
Cerebral palsy is due to abnormal development or damage occurring to the developing brain.[69] This damage can occur during pregnancy, delivery, the first month of life, or less commonly in early childhood.[69] Structural problems in the brain are seen in 80% of cases, most commonly within the white matter.[69] More than three-quarters of cases are believed to result from issues that occur during pregnancy.[69] Most children who are born with cerebral palsy have more than one risk factor associated with CP.[70] Cerebral palsy is not contagious and cannot be contracted in adulthood. CP is almost always developed en utero, or prior to birth.[71]
While in certain cases there is no identifiable cause, typical causes include problems in intrauterine development (e.g. exposure to radiation, infection, fetal growth restriction), hypoxia of the brain (thrombotic events, placental insufficiency, umbilical cord prolapse), birth trauma during labor and delivery, and complications around birth or during childhood.[51][72][73]
In Africa birth asphyxia, high bilirubin levels, and infections in newborns of the central nervous system are main cause. Many cases of CP in Africa could be prevented with better resources available.[74]
Preterm birth
Between 40% and 50% of all children who develop cerebral palsy were born prematurely.[75] Most of these cases (75–90%) are believed to be due to issues that occur around the time of birth, often just after birth.[69] Multiple-birth infants are also more likely than single-birth infants to have CP.[76] They are also more likely to be born with a low birth weight.[77]
In those who are born with a weight between 1 kg (2.2 lbs) and 1.5 kg (3.3 lbs) CP occurs in 6%.[2] Among those born before 28 weeks of gestation it occurs in 8%.[78][lower-alpha 1] Genetic factors are believed to play an important role in prematurity and cerebral palsy generally.[79] In those who are born between 34 and 37 weeks the risk is 0.4% (three times normal).[80]
Term infants
In babies who are born at term risk factors include problems with the placenta, birth defects, low birth weight, breathing meconium into the lungs, a delivery requiring either the use of instruments or an emergency Caesarean section, birth asphyxia, seizures just after birth, respiratory distress syndrome, low blood sugar, and infections in the baby.[81]
As of 2013[update], it was unclear how much of a role birth asphyxia plays as a cause.[82] It is unclear if the size of the placenta plays a role.[83] As of 2015[update] it is evident that in advanced countries, most cases of cerebral palsy in term or near-term neonates have explanations other than asphyxia.[73]
Genetics
Cerebral palsy is not commonly considered a genetic disease. About 2% of all CP cases are expected to be inherited, with glutamate decarboxylase-1 being one of the possible enzymes involved.[5] Most inherited cases are autosomal recessive.[5] However, the vast majority of CP cases are connected to brain damage during birth and in infancy. There is a small percentage of CP cases caused by brain damage that stemmed from the prenatal period, which is estimated to be less than 5% of CP cases overall.[84] Moreover, there is no one reason why some CP cases come from prenatal brain damage, and it is not known if those cases have a genetic basis.[84]
Cerebellar hypoplasia is sometimes genetic[85] and can cause ataxic cerebral palsy.[86]
Early childhood
After birth, other causes include toxins, severe jaundice,[87] lead poisoning, physical brain injury, stroke,[88] abusive head trauma, incidents involving hypoxia to the brain (such as near drowning), and encephalitis or meningitis.[87]
Others
Infections in the mother, even those not easily detected, can triple the risk of the child developing cerebral palsy.[89] Infection of the fetal membranes known as chorioamnionitis increases the risk.[90]
Intrauterine and neonatal insults (many of which are infectious) increase the risk.[91]
Rh blood type incompatibility can cause the mother's immune system to attack the baby's red blood cells.[1]
It has been hypothesised that some cases of cerebral palsy are caused by the death in very early pregnancy of an identical twin.[92]
The diagnosis of cerebral palsy has historically rested on the person's history and physical examination and is generally assessed at a young age. A general movements assessment, which involves measuring movements that occur spontaneously among those less than four months of age, appears most accurate.[93][94] Children who are more severely affected are more likely to be noticed and diagnosed earlier. Abnormal muscle tone, delayed motor development and persistence of primitive reflexes are the main early symptoms of CP.[45] Symptoms and diagnosis typically occur by the age of two,[95] although depending on factors like malformations and congenital issues,[96] persons with milder forms of cerebral palsy may be over the age of five, if not in adulthood, when finally diagnosed.[97]
Cognitive assessments and medical observations are also useful to help confirm a diagnosis. Additionally, evaluations of the child's mobility, speech and language, hearing, vision, gait, feeding and digestion are also useful to determine the extent of the disorder.[96] Early diagnosis and intervention are seen as being a key part of managing cerebral palsy.[98] Machine learning algorithms facilitate automatic early diagnosis, with methods such as deep neural network[99] and geometric feature fusion[100] producing high accuracy in predicting cerebral palsy from short videos. It is a developmental disability.[93]
Once a person is diagnosed with cerebral palsy, further diagnostic tests are optional. Neuroimaging with CT or MRI is warranted when the cause of a person's cerebral palsy has not been established. An MRI is preferred over CT, due to diagnostic yield and safety. When abnormal, evidence from neuroimaging may suggest the timing of the initial damage. The CT or MRI is also capable of revealing treatable conditions, such as hydrocephalus, porencephaly, arteriovenous malformation, subdural hematomas and hygromas, and a vermian tumour[101] (which a few studies suggest are present 5–22% of the time). Furthermore, abnormalities detected by neuroimaging may indicate a high likelihood of associated conditions, such as epilepsy and intellectual disability.[102] There is a small risk associated with sedating children to facilitate a clear MRI.[97]
The age when CP is diagnosed is important, but medical professionals disagree over the best age to make the diagnosis.[94] The earlier CP is diagnosed correctly, the better the opportunities are to provide the child with physical and educational help, but there might be a greater chance of confusing CP with another problem, especially if the child is 18 months of age or younger.[94] Infants may have temporary problems with muscle tone or control that can be confused with CP, which is permanent.[94] A metabolism disorder or tumors in the nervous system may appear to be CP; metabolic disorders, in particular, can produce brain problems that look like CP on an MRI.[1] Disorders that deteriorate the white matter in the brain and problems that cause spasms and weakness in the legs, may be mistaken for CP if they first appear early in life.[94] However, these disorders get worse over time, and CP does not[94] (although it may change in character).[1] In infancy it may not be possible to tell the difference between them.[94] In the UK, not being able to sit independently by the age of 8 months is regarded as a clinical sign for further monitoring.[97] Fragile X syndrome (a cause of autism and intellectual disability) and general intellectual disability must also be ruled out.[94] Cerebral palsy specialist John McLaughlin recommends waiting until the child is 36 months of age before making a diagnosis because, by that age, motor capacity is easier to assess.[94]
Classification
CP is classified by the types of motor impairment of the limbs or organs, and by restrictions to the activities an affected person may perform.[103] The Gross Motor Function Classification System-Expanded and Revised and the Manual Ability Classification System are used to describe mobility and manual dexterity in people with cerebral palsy, and recently the Communication Function Classification System, and the Eating and Drinking Ability Classification System have been proposed to describe those functions.[104] There are three main CP classifications by motor impairment: spastic, ataxic, and dyskinetic. Additionally, there is a mixed type that shows a combination of features of the other types. These classifications reflect the areas of the brain that are damaged.[105]
Cerebral palsy is also classified according to the topographic distribution of muscle spasticity.[106] This method classifies children as diplegic, (bilateral involvement with leg involvement greater than arm involvement), hemiplegic (unilateral involvement), or quadriplegic (bilateral involvement with arm involvement equal to or greater than leg involvement).[107][106]
Spastic
Spastic cerebral palsy is the type of cerebral palsy characterized by spasticity or high muscle tone often resulting in stiff, jerky movements.[108] Itself an umbrella term encompassing spastic hemiplegia, spastic diplegia, spastic quadriplegia and – where solely one limb or one specific area of the body is affected – spastic monoplegia. Spastic cerebral palsy affects the motor cortex[108] of the brain, a specific portion of the cerebral cortex responsible for the planning and completion of voluntary movement.[109] Spastic CP is the most common type of overall cerebral palsy, representing about 80% of cases.[110] Botulinum toxin is effective in decreasing spasticity.[10] It can help increase range of motion which could help mitigate CPs effects on the growing bones of children.[10] There may be an improvement in motor functions in the children and ability to walk. however, the main benefit derived from botulinum toxin A comes from its ability to reduce muscle tone and spasticity and thus prevent or delay the development of fixed muscle contractures.[10][111]
Ataxic
Ataxic cerebral palsy is observed in approximately 5–10% of all cases of cerebral palsy, making it the least frequent form of cerebral palsy.[112] Ataxic cerebral palsy is caused by damage to cerebellar structures.[113] Because of the damage to the cerebellum, which is essential for coordinating muscle movements and balance, patients with ataxic cerebral palsy experience problems in coordination, specifically in their arms, legs, and trunk. Ataxic cerebral palsy is known to decrease muscle tone.[114] The most common manifestation of ataxic cerebral palsy is intention (action) tremor, which is especially apparent when carrying out precise movements, such as tying shoe laces or writing with a pencil. This symptom gets progressively worse as the movement persists, making the hand shake. As the hand gets closer to accomplishing the intended task, the trembling intensifies, which makes it even more difficult to complete.[107]
Dyskinetic
Dyskinetic cerebral palsy (sometimes abbreviated DCP) is primarily associated with damage to the basal ganglia and the substantia nigra in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic-ischemic brain injury.[115] DCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone.[107] Clinical diagnosis of DCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques.[116][117] Dyskinetic cerebral palsy is an extrapyramidal form of cerebral palsy.[118] Dyskinetic cerebral palsy can be divided into two different groups; choreoathetosis and dystonia.[107] Choreo-athetotic CP is characterized by involuntary movements, whereas dystonic CP is characterized by slow, strong contractions, which may occur locally or encompass the whole body.[106]
Mixed
Mixed cerebral palsy has symptoms of dyskinetic, ataxic and spastic CP appearing simultaneously, each to varying degrees, and both with and without symptoms of each. Mixed CP is the most difficult to treat as it is extremely heterogeneous and sometimes unpredictable in its symptoms and development over the lifespan.[119][120][121][122]
Gait Classification
In patients with spastic hemiplegia or diplegia, various gait patterns can be observed, the exact form of which can only be described with the help of complex gait analysis systems. In order to facilitate interdisciplinary communication in the interdisciplinary team between those affected, doctors, physiotherapists and orthotists, a simple description of the gait pattern is useful. J. Rodda and H. K. Graham already described in 2001 how gait patterns of CP patients can be more easily recognized and defined gait types which they compared in a classification. They also described that gait patterns can vary with age.[123] Building on this, the Amsterdam Gait Classification was developed at the free university in Amsterdam, the VU medisch centrum.
A special feature of this classification is that it makes different gait patterns very easy to recognize and can be used in CP patients in whom only one leg and both legs are affected. According to the Amsterdam Gait Classification, five gait types are described. To assess the gait pattern, the patient is viewed visually or via a video recording from the side of the leg to be assessed. At the point in time at which the leg to be viewed is in mid stance and the leg not to be viewed is in mid swing, the knee angle and the contact of the foot with the ground are assessed on the one hand.[124]
Classification of the gait pattern according to the Amsterdam Gait Classification: In gait type 1, the knee angle is normal and the foot contact is complete. In gait type 2, the knee angle is hyperextended and the foot contact is complete. In gait type 3, the knee angle is hyperextended and foot contact is incomplete (only on the forefoot). In gait type 4, the knee angle is bent and foot contact is incomplete (only on the forefoot). With gait type 5, the knee angle is bent and the foot contact is complete.[124]
Gait types 5 is also known as crouch gait.[125]
Because the causes of CP are varied, a broad range of preventive interventions have been investigated.[126]
Electronic fetal monitoring has not helped to prevent CP, and in 2014 the American College of Obstetricians and Gynecologists, the Royal Australian and New Zealand College of Obstetricians and Gynaecologists, and the Society of Obstetricians and Gynaecologists of Canada have acknowledged that there are no long-term benefits of electronic fetal monitoring.[73] Before this, electronic fetal monitoring was widely used to prop up obstetric litigation.[127]
In those at risk of an early delivery, magnesium sulphate appears to decrease the risk of cerebral palsy.[128] It is unclear if it helps those who are born at term.[129] In those at high risk of preterm labor a review found that moderate to severe CP was reduced by the administration of magnesium sulphate, and that adverse effects on the babies from the magnesium sulphate were not significant. Mothers who received magnesium sulphate could experience side effects such as respiratory depression and nausea.[130] However, guidelines for the use of magnesium sulfate in mothers at risk of preterm labour are not strongly adhered to;[131] in 2017 only 2 in 3 eligible women in the UK received the medication despite it being recommended by NICE guidelines.[132] An NHS quality improvement programme increased its usage in England from 71% in 2018 to 83% in 2020.[133][134]
Caffeine is used to treat apnea of prematurity and reduces the risk of cerebral palsy in premature babies, but there are also concerns of long term negative effects.[135] A moderate quality level of evidence indicates that giving women antibiotics during preterm labor before her membranes have ruptured (water is not yet not broken) may increase the risk of cerebral palsy for the child.[136] Additionally, for preterm babies for whom there is a chance of fetal compromise, allowing the birth to proceed rather than trying to delay the birth may lead to an increased risk of cerebral palsy in the child.[136] Corticosteroids are sometimes taken by pregnant women expecting a preterm birth to provide neuroprotection to their baby.[137] Taking corticosteroids during pregnancy is shown to have no significant correlation with developing cerebral palsy in preterm births.[136]
Cooling high-risk full-term babies shortly after birth may reduce disability,[138] but this may only be useful for some forms of the brain damage that causes CP.[95]
Over time, the approach to CP management has shifted away from narrow attempts to fix individual physical problems – such as spasticity in a particular limb – to making such treatments part of a larger goal of maximizing the person's independence and community engagement.[139]: 886 However, the evidence base for the effectiveness of intervention programs reflecting the philosophy of independence has not yet caught up: effective interventions for body structures and functions have a strong evidence base, but evidence is lacking for effective interventions targeted toward participation, environment, or personal factors.[139] There is also no good evidence to show that an intervention that is effective at the body-specific level will result in an improvement at the activity level or vice versa.[139] Although such cross-over benefit might happen, not enough high-quality studies have been done to demonstrate it.[139]
Because cerebral palsy has "varying severity and complexity" across the lifespan,[104] it can be considered a collection of conditions for management purposes.[95] A multidisciplinary approach for cerebral palsy management is recommended,[104] focusing on "maximising individual function, choice and independence" in line with the International Classification of Functioning, Disability and Health's goals.[97] The team may include a paediatrician, a health visitor, a social worker, a physiotherapist, an orthotist, a speech and language therapist, an occupational therapist, a teacher specialising in helping children with visual impairment, an educational psychologist, an orthopaedic surgeon, a neurologist and a neurosurgeon.[140]
Various forms of therapy are available to people living with cerebral palsy as well as caregivers and parents. Treatment may include one or more of the following: physical therapy; occupational therapy; speech therapy; water therapy; drugs to control seizures, alleviate pain, or relax muscle spasms (e.g. benzodiazepines); surgery to correct anatomical abnormalities or release tight muscles; braces and other orthotic devices; rolling walkers; and communication aids such as computers with attached voice synthesisers.[141] Intensive rehabilitation is practiced in certain countries, but obtaining reliable data on its medium and long-term effectiveness is challenging.[142]
Surgical intervention in CP children may include various orthopaedic or neurological surgeries to improve quality of life, such as tendon releases, hip rotation, spinal fusion, (selective dorsal rhizotomy) or placement of an intrathecal baclofen pump.[23][139][143]
A Cochrane review published in 2004 found a trend toward the benefit of speech and language therapy for children with cerebral palsy but noted the need for high-quality research.[144] A 2013 systematic review found that many of the therapies used to treat CP have no good evidence base; the treatments with the best evidence are medications (anticonvulsants, botulinum toxin, bisphosphonates, diazepam), therapy (bimanual training, casting, constraint-induced movement therapy, context-focused therapy, fitness training, goal-directed training, hip surveillance, home programmes, occupational therapy after botulinum toxin, pressure care) and surgery. There is also research on whether the sleeping position might improve hip migration, but there are not yet high-quality evidence studies to support that theory.[145] Research papers also call for an agreed consensus on outcome measures which will allow researchers to cross-reference research. Also, the terminology used to describe orthoses[146] needs to be standardised to ensure studies can be reproduced and readily compared and evaluated.
To improve the gait pattern, orthotics can be included in the therapy concept. An orthosis can support physiotherapeutic treatment in setting the right motor impulses in order to create new cerebral connections.[147] The orthosis must meet the requirements of the medical prescription. In addition, the orthosis must be designed by the orthotist in such a way that it achieves the effectiveness of the necessary levers, matching the gait pattern, in order to support the proprioceptive approaches of physiotherapy. The characteristics of the stiffness of the orthosis shells and the adjustable dynamics in the ankle joint are important elements of the orthosis to be considered.[148]
Due to these requirements, the development of orthoses has changed significantly in recent years, especially since around 2010. At about the same time, care concepts were developed that deal intensively with the orthotic treatment of the lower extremities in cerebral palsy.[149] Modern materials and new functional elements enable the rigidity to be specifically adapted to the requirements that fits to the gait pattern of the CP patient.[150] The adjustment of the stiffness has a decisive influence on the gait pattern and on the energy cost of walking.[151][152][153] It is of great advantage if the stiffness of the orthosis can be adjusted separately from one another via resistances of the two functional elements in the two directions of movement, dorsiflexion and plantar flexion.[154]