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Cerebral palsy

Cerebral palsy (CP) is a group of movement disorders that appear in early childhood. Signs and symptoms vary among people and over time, but include poor coordination, stiff muscles, weak muscles, and tremors. There may be problems with sensation, vision, hearing, and speech. Often, babies with cerebral palsy do not roll over, sit, crawl or walk as early as other children. Other symptoms include seizures and problems with thinking or reasoning. While symptoms may get more noticeable over the first years of life, underlying problems do not worsen over time.

Cerebral palsy is caused by abnormal development or damage to the parts of the brain that control movement, balance, and posture. Most often, the problems occur during pregnancy, but may occur during childbirth or shortly afterwards. Often, the cause is unknown. Risk factors include preterm birth, being a twin, certain infections or exposure to methylmercury during pregnancy, a difficult delivery, and head trauma during the first few years of life. About 2% of cases are believed to be due to an inherited genetic cause.

Sub-types are classified, based on the specific problems present. For example, those with stiff muscles have spastic cerebral palsy, poor coordination in locomotion have ataxic cerebral palsy, and writhing movements have dyskinetic cerebral palsy. Diagnosis is based on the child's development. Blood tests and medical imaging may be used to rule out other possible causes.

Some causes of CP are preventable through immunization of the mother, and efforts to prevent head injuries in children such as improved safety. There is no known cure for CP, but supportive treatments, medication and surgery may help individuals. This may include physical therapy, occupational therapy and speech therapy. Mouse NGF has been shown to improve outcomes and has been available in China since 2003. Medications such as diazepam, baclofen and botulinum toxin may help relax stiff muscles. Surgery may include lengthening muscles and cutting overly active nerves. Often, external braces and Lycra splints and other assistive technology are helpful with mobility. Some affected children can achieve near normal adult lives with appropriate treatment. While alternative medicines are frequently used, there is no evidence to support their use. Potential treatments are being examined, including stem cell therapy. However, more research is required to determine if it is effective and safe.

Cerebral palsy is the most common movement disorder in children, occurring in about 2.1 per 1,000 live births. It has been documented throughout history, with the first known descriptions occurring in the work of Hippocrates in the 5th century BCE. Extensive study began in the 19th century by William John Little, after whom spastic diplegia was called "Little's disease". William Osler first named it "cerebral palsy" from the German zerebrale Kinderlähmung (cerebral child-paralysis).

Signs and symptoms
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." While movement problems are the central feature of CP, difficulties with thinking, learning, feeling, communication and behavior often co-occur, with 28% having epilepsy, 58% having difficulties with communication, at least 42% having problems with their vision, and 2356% having learning disabilities. Muscle contractions in people with cerebral palsy-related high muscle tone are commonly thought to arise from overactivation. Although most people with CP have problems with increased muscle tone, some have low muscle tone instead. High muscle tone can either be due to spasticity or dystonia.

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 to high muscle tone and progressive. In cerebral palsy with high muscle tone, 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. Additionally, crouch gait (also described as knee flexion gait) is prevalent among children who possess the ability to walk. 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.

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. 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.

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. It can additionally cause choking.

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.

Children with CP may also have sensory processing issues. Adults with cerebral palsy have a higher risk of respiratory failure.

Skeleton
For bones to attain their normal shape and size, they require the stresses from normal musculature. People with cerebral palsy are at risk of low bone mineral density. The shafts of the bones are often thin (gracile), and become thinner during growth. When compared to these thin shafts (diaphyses), the centres (metaphyses) often appear quite enlarged (ballooning). Due to more than normal joint compression caused by muscular imbalances, articular cartilage may atrophy, leading to narrowed joint spaces. Depending on the degree of spasticity, a person with the spastic form of 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.

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. These children generally have fractures in the legs, whereas non-affected children mostly fracture their arms in the context of sporting activities.

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. Children may develop scoliosis before the age of 10 – estimated prevalence of scoliosis in children with CP is between 21% and 64%. Higher levels of impairment on the GMFCS are associated with scoliosis and hip dislocation. Scoliosis can be corrected with surgery, but CP makes surgical complications more likely, even with improved techniques. 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. Equinus deformity is managed by conservative methods especially when dynamic. If fixed/static deformity ensues surgery may become mandatory.

Growth spurts during puberty can make walking more difficult for people with CP and high muscle tone.

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. Gastro-oesophageal reflux is common in children with CP. Children with CP may have too little or too much sensitivity around and in the mouth. 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. Feeding difficulties are related to higher GMFCS levels. Dental problems can also contribute to difficulties with eating. Pneumonia is also common where eating difficulties exist, caused by undetected aspiration of food or liquids. 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. Grip strength impairments are less common.

Children with severe cerebral palsy, particularly with oropharyngeal issues, are at risk of undernutrition. Triceps skin fold tests have been found to be a very reliable indicator of malnutrition in children with cerebral palsy. Due to challenges in feeding, evidence has shown that children with cerebral palsy are at a greater risk of malnutrition.

Language
Speech and language disorders are common in people with cerebral palsy. The incidence of dysarthria is estimated to range from 31% to 88%, and around a quarter of people with CP are non-verbal. 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.

Early use of augmentative and alternative communication systems may assist the child in developing spoken language skills. Overall language delay is associated with problems of cognition, deafness, and learned helplessness. Children with cerebral palsy are at risk of learned helplessness and becoming passive communicators, initiating little communication. 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.

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. When children with cerebral palsy are in pain, they experience worse muscle spasms. 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. Pain in CP has a number of different causes, and different pains respond to different treatments.

There is also a high likelihood of chronic sleep disorders secondary to both physical and environmental factors. Children with cerebral palsy have significantly higher rates of sleep disturbance than typically developing children. 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. Chronic pain is under-recognized in children with cerebral palsy, even though three out of four children with cerebral palsy experience pain. Adults with CP also experience more pain than the general population.

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. Epilepsy is often found in the child before they are 1 year old, or also before they are four or five. 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. Obesity in people with cerebral palsy or a more severe Gross Motor Function Classification System assessment in particular are considered risk factors for multimorbidity. Other medical issues can be mistaken for being symptoms of cerebral palsy, and so may not be treated correctly.

Related conditions can include apraxia, sensory impairments, urinary incontinence, fecal incontinence, or behavioural disorders.

Seizure management is more difficult in people with CP as seizures often last longer. Epilepsy and asthma are common co-occurring diseases in adults with CP. The associated disorders that co-occur with cerebral palsy may be more disabling than the motor function problems.

Managing respiratory illnesses in children with severe CP is considered complex due to the need to manage oropharyngeal dysphagia of both food/drink and saliva, gastroesophageal reflux, motor disorders, upper airway obstruction during sleep, malnutrition, among other factors.

Causes
Cerebral palsy is due to abnormal development or damage occurring to the developing brain. This damage can occur during pregnancy, delivery, the first month of life, or less commonly in early childhood. Structural problems in the brain are seen in 80% of cases, most commonly within the white matter. More than three-quarters of cases are believed to result from issues that occur during pregnancy. Most children who are born with cerebral palsy have more than one risk factor associated with CP. Cerebral palsy is not contagious and cannot be contracted in adulthood. CP is almost always developed en utero, or prior to birth.

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.

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.

Preterm birth
Between 40% and 50% of all children who develop cerebral palsy were born prematurely. Most of these cases (75–90%) are believed to be due to issues that occur around the time of birth, often just after birth. Multiple-birth infants are also more likely than single-birth infants to have CP. They are also more likely to be born with a low birth weight.

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%. Among those born before 28 weeks of gestation it occurs in 8%. Genetic factors are believed to play an important role in prematurity and cerebral palsy generally. In those who are born between 34 and 37 weeks the risk is 0.4% (three times normal).

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.

, it was unclear how much of a role birth asphyxia plays as a cause. It is unclear if the size of the placenta plays a role. it is evident that in advanced countries, most cases of cerebral palsy in term or near-term neonates have explanations other than asphyxia.

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. Most inherited cases are autosomal recessive. 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. 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.

Cerebellar hypoplasia is sometimes genetic and can cause ataxic cerebral palsy.

Early childhood
After birth, other causes include toxins, severe jaundice, lead poisoning, physical brain injury, stroke, abusive head trauma, incidents involving hypoxia to the brain (such as near drowning), and encephalitis or meningitis.

Others
Infections in the mother, even those not easily detected, can triple the risk of the child developing cerebral palsy. Infection of the fetal membranes known as chorioamnionitis increases the risk.

Intrauterine and neonatal insults (many of which are infectious) increase the risk.

Rh blood type incompatibility can cause the mother's immune system to attack the baby's red blood cells.

It has been hypothesised that some cases of cerebral palsy are caused by the death in very early pregnancy of an identical twin.

Diagnosis
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. 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. Symptoms and diagnosis typically occur by the age of two, although depending on factors like malformations and congenital issues, persons with milder forms of cerebral palsy may be over the age of five, if not in adulthood, when finally diagnosed.

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. Early diagnosis and intervention are seen as being a key part of managing cerebral palsy. Machine learning algorithms facilitate automatic early diagnosis, with methods such as deep neural network and geometric feature fusion producing high accuracy in predicting cerebral palsy from short videos. It is a developmental disability.

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 (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. There is a small risk associated with sedating children to facilitate a clear MRI.

The age when CP is diagnosed is important, but medical professionals disagree over the best age to make the diagnosis. 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. Infants may have temporary problems with muscle tone or control that can be confused with CP, which is permanent. 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. 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. However, these disorders get worse over time, and CP does not (although it may change in character). In infancy it may not be possible to tell the difference between them. In the UK, not being able to sit independently by the age of 8 months is regarded as a clinical sign for further monitoring. Fragile X syndrome (a cause of autism and intellectual disability) and general intellectual disability must also be ruled out. 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.

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. 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. 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.

Cerebral palsy is also classified according to the topographic distribution of muscle spasticity. 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).

Spastic
Spastic cerebral palsy is the type of cerebral palsy characterized by spasticity or high muscle tone often resulting in stiff, jerky movements. 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 of the brain, a specific portion of the cerebral cortex responsible for the planning and completion of voluntary movement. Spastic CP is the most common type of overall cerebral palsy, representing about 80% of cases. Botulinum toxin is effective in decreasing spasticity. It can help increase range of motion which could help mitigate CPs effects on the growing bones of children. 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.

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. Ataxic cerebral palsy is caused by damage to cerebellar structures. 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. 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.

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. DCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone. Clinical diagnosis of DCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques. Dyskinetic cerebral palsy is an extrapyramidal form of cerebral palsy. Dyskinetic cerebral palsy can be divided into two different groups; choreoathetosis and dystonia. 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.

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.

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. 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.

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.

Gait types 5 is also known as crouch gait.

Prevention
Because the causes of CP are varied, a broad range of preventive interventions have been investigated.

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. Before this, electronic fetal monitoring was widely used to prop up obstetric litigation.

In those at risk of an early delivery, magnesium sulphate appears to decrease the risk of cerebral palsy. It is unclear if it helps those who are born at term. 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. However, guidelines for the use of magnesium sulfate in mothers at risk of preterm labour are not strongly adhered to; in 2017 only 2 in 3 eligible women in the UK received the medication despite it being recommended by NICE guidelines. An NHS quality improvement programme increased its usage in England from 71% in 2018 to 83% in 2020.

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. 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. 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. Corticosteroids are sometimes taken by pregnant women expecting a preterm birth to provide neuroprotection to their baby. Taking corticosteroids during pregnancy is shown to have no significant correlation with developing cerebral palsy in preterm births.

Cooling high-risk full-term babies shortly after birth may reduce disability, but this may only be useful for some forms of the brain damage that causes CP.

Management

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. 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. 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. Although such cross-over benefit might happen, not enough high-quality studies have been done to demonstrate it.

Because cerebral palsy has "varying severity and complexity" across the lifespan, it can be considered a collection of conditions for management purposes. A multidisciplinary approach for cerebral palsy management is recommended, focusing on "maximising individual function, choice and independence" in line with the International Classification of Functioning, Disability and Health's goals. 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.

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. Intensive rehabilitation is practiced in certain countries, but obtaining reliable data on its medium and long-term effectiveness is challenging.

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.

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. 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. 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 needs to be standardised to ensure studies can be reproduced and readily compared and evaluated.

Orthotics in the concept of therapy
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. 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.

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. 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. The adjustment of the stiffness has a decisive influence on the gait pattern and on the energy cost of walking. 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.

Prognosis
CP is not a progressive disorder (meaning the brain damage does not worsen), but the symptoms can become more severe over time. A person with the disorder may improve somewhat during childhood if he or she receives extensive care, but once bones and musculature become more established, orthopedic surgery may be required. People with CP can have varying degrees of cognitive impairment or none whatsoever. The full intellectual potential of a child born with CP is often not known until the child starts school. People with CP are more likely to have learning disorders but have normal intelligence. Intellectual level among people with CP varies from genius to intellectually disabled, as it does in the general population, and experts have stated that it is important not to underestimate the capabilities of a person with CP and to give them every opportunity to learn.

The ability to live independently with CP varies widely, depending partly on the severity of each person's impairment and partly on the capability of each person to self-manage the logistics of life. Some individuals with CP require personal assistant services for all activities of daily living. Others only need assistance with certain activities, and still others do not require any physical assistance. But regardless of the severity of a person's physical impairment, a person's ability to live independently often depends primarily on the person's capacity to manage the physical realities of his or her life autonomously. In some cases, people with CP recruit, hire, and manage a staff of personal care assistants (PCAs). PCAs facilitate the independence of their employers by assisting them with their daily personal needs in a way that allows them to maintain control over their lives.

Puberty in young adults with cerebral palsy may be precocious or delayed. Delayed puberty is thought to be a consequence of nutritional deficiencies. There is currently no evidence that CP affects fertility, although some of the secondary symptoms have been shown to affect sexual desire and performance. Adults with CP were less likely to get routine reproductive health screening as of 2005. Gynecological examinations may have to be performed under anesthesia due to spasticity, and equipment is often not accessible. Breast self-examination may be difficult, so partners or carers may have to perform it. Men with CP have higher levels of cryptorchidism at the age of 21.

CP can significantly reduce a person's life expectancy, depending on the severity of their condition and the quality of care they receive. 5–10% of children with CP die in childhood, particularly where seizures and intellectual disability also affect the child. The ability to ambulate, roll, and self-feed has been associated with increased life expectancy. While there is a lot of variation in how CP affects people, it has been found that "independent gross motor functional ability is a very strong determinant of life expectancy". According to the Australian Bureau of Statistics, in 2014, 104 Australians died of cerebral palsy. The most common causes of death in CP are related to respiratory causes, but in middle age cardiovascular issues and neoplastic disorders become more prominent.

Self-care
For many children with CP, parents are heavily involved in self-care activities. Self-care activities, such as bathing, dressing, and grooming, can be difficult for children with CP, as self-care depends primarily on the use of the upper limbs. For those living with CP, impaired upper limb function affects almost 50% of children and is considered the main factor contributing to decreased activity and participation. As the hands are used for many self-care tasks, sensory and motor impairments of the hands make daily self-care more difficult. Motor impairments cause more problems than sensory impairments. The most common impairment is that of finger dexterity, which is the ability to manipulate small objects with the fingers. Compared to other disabilities, people with cerebral palsy generally need more help in performing daily tasks. Occupational therapists are healthcare professionals that help individuals with disabilities gain or regain their independence through the use of meaningful activities.

Productivity
The effects of sensory, motor, and cognitive impairments affect self-care occupations in children with CP and productivity occupations. Productivity can include but is not limited to, school, work, household chores, or contributing to the community.

Play is included as a productive occupation as it is often the primary activity for children. If play becomes difficult due to a disability, like CP, this can cause problems for the child. These difficulties can affect a child's self-esteem. In addition, the sensory and motor problems experienced by children with CP affect how the child interacts with their surroundings, including the environment and other people. Not only do physical limitations affect a child's ability to play, the limitations perceived by the child's caregivers and playmates also affect the child's play activities. Some children with disabilities spend more time playing by themselves. When a disability prevents a child from playing, there may be social, emotional and psychological problems, which can lead to increased dependence on others, less motivation, and poor social skills.

In school, students are asked to complete many tasks and activities, many of which involve handwriting. Many children with CP have the capacity to learn and write in the school environment. However, students with CP may find it difficult to keep up with the handwriting demands of school and their writing may be difficult to read. In addition, writing may take longer and require greater effort on the student's part. Factors linked to handwriting include postural stability, sensory and perceptual abilities of the hand, and writing tool pressure.

Speech impairments may be seen in children with CP depending on the severity of brain damage. Communication in a school setting is important because communicating with peers and teachers is very much a part of the "school experience" and enhances social interaction. Problems with language or motor dysfunction can lead to underestimating a student's intelligence. In summary, children with CP may experience difficulties in school, such as difficulty with handwriting, carrying out school activities, communicating verbally, and interacting socially.

Leisure
Leisure activities can have several positive effects on physical health, mental health, life satisfaction, and psychological growth for people with physical disabilities like CP. Common benefits identified are stress reduction, development of coping skills, companionship, enjoyment, relaxation and a positive effect on life satisfaction. In addition, for children with CP, leisure appears to enhance adjustment to living with a disability.

Leisure can be divided into structured (formal) and unstructured (informal) activities. Children and teens with CP engage in less habitual physical activity than their peers. Children with CP primarily engage in physical activity through therapies aimed at managing their CP, or through organized sport for people with disabilities. It is difficult to sustain behavioural change in terms of increasing physical activity of children with CP. Gender, manual dexterity, the child's preferences, cognitive impairment and epilepsy were found to affect children's leisure activities, with manual dexterity associated with more leisure activity. Although leisure is important for children with CP, they may have difficulties carrying out leisure activities due to social and physical barriers.

Children with cerebral palsy may face challenges when it comes to participating in sports. This comes with being discouraged from physical activity because of these perceived limitations imposed by their medical condition.

Participation and barriers
Participation is involvement in life situations and everyday activities. Participation includes self-care, productivity, and leisure. In fact, communication, mobility, education, home life, leisure, and social relationships require participation, and indicate the extent to which children function in their environment. Barriers can exist on three levels: micro, meso, and macro. First, the barriers at the micro level involve the person. Barriers at the micro level include the child's physical limitations (motor, sensory and cognitive impairments) or their subjective feelings regarding their ability to participate. For example, the child may not participate in group activities due to lack of confidence. Second, barriers at the meso level include the family and community. These may include negative attitudes of people toward disability or lack of support within the family or in the community.

One of the main reasons for this limited support appears to be the result of a lack of awareness and knowledge regarding the child's ability to engage in activities despite his or her disability. Third, barriers at the macro level incorporate the systems and policies that are not in place or hinder children with CP. These may be environmental barriers to participation such as architectural barriers, lack of relevant assistive technology, and transportation difficulties due to limited wheelchair access or public transit that can accommodate children with CP. For example, a building without an elevator can prevent the child from accessing higher floors.

A 2013 review stated that outcomes for adults with cerebral palsy without intellectual disability in the 2000s were that "60–80% completed high school, 14–25% completed college, up to 61% were living independently in the community, 25–55% were competitively employed, and 14–28% were involved in long term relationships with partners or had established families". Adults with cerebral palsy may not seek physical therapy due to transport issues, financial restrictions and practitioners not feeling like they know enough about cerebral palsy to take people with CP on as clients.

Aging
Children with CP may not successfully transition into using adult services because they are not referred to one upon turning 18, and may decrease their use of services. Quality of life outcomes tend to decline for adults with cerebral palsy. Because children with cerebral palsy are often told that it is a non-progressive disease, they may be unprepared for the greater effects of the aging process as they head into their 30s. Young adults with cerebral palsy experience problems with aging that non-disabled adults experience "much later in life". 25% or more adults with cerebral palsy who can walk experience increasing difficulties walking with age. Hand function does not seem to have similar declines. Chronic disease risk, such as obesity, is also higher among adults with cerebral palsy than the general population. Common problems include increased pain, reduced flexibility, increased spasms and contractures, post-impairment syndrome and increasing problems with balance. Increased fatigue is also a problem. When adulthood and cerebral palsy is discussed,, it is not discussed in terms of the different stages of adulthood. About half of people with CP report some loss of function as of their 40s.

Like they did in childhood, adults with cerebral palsy experience psychosocial issues related to their CP, chiefly the need for social support, self-acceptance, and acceptance by others. Workplace accommodations may be needed to enhance continued employment for adults with CP as they age. Rehabilitation or social programs that include salutogenesis may improve the coping potential of adults with CP as they age.

Epidemiology
Cerebral palsy occurs in about 2.1 per 1000 live births. In those born at term rates are lower at 1 per 1000 live births. Within a population it may occur more often in poorer people. The rate is higher in males than in females; in Europe it is 1.3 times more common in males.

There was a "moderate, but significant" rise in the prevalence of CP between the 1970s and 1990s. This is thought to be due to a rise in low birth weight of infants and the increased survival rate of these infants. The increased survival rate of infants with CP in the 1970s and 80s may be indirectly due to the disability rights movement challenging perspectives around the worth of infants with a disability, as well as the Baby Doe Law. Between 1990 and 2003, rates of cerebral palsy remained the same.

As of 2005, advances in the care of pregnant mothers and their babies did not result in a noticeable decrease in CP. This is generally attributed to medical advances in areas related to the care of premature babies (which results in a greater survival rate). Only the introduction of quality medical care to locations with less-than-adequate medical care has shown any decreases. The incidence of CP increases with premature or very low-weight babies regardless of the quality of care. , there is a suggestion that both incidence and severity are slightly decreasing – more research is needed to find out if this is significant, and if so, which interventions are effective. It has been found that high-income countries have lower rates of children born with cerebral palsy than low or middle-income countries.

Prevalence of cerebral palsy is best calculated around the school entry age of about six years; the prevalence in the U.S. is estimated to be 2.4 out of 1000 children.

History
Cerebral palsy has affected humans since antiquity. A decorated grave marker dating from around the 15th to 14th century BCE shows a figure with one small leg and using a crutch, possibly due to cerebral palsy. The oldest likely physical evidence of the condition comes from the mummy of Siptah, an Egyptian Pharaoh who ruled from about 1196 to 1190 BCE and died at about 20 years of age. The presence of cerebral palsy has been suspected due to his deformed foot and hands.

The medical literature of the ancient Greeks discusses paralysis and weakness of the arms and legs; the modern word palsy comes from the Ancient Greek words παράλυση or πάρεση, meaning paralysis or paresis respectively. The works of the school of Hippocrates (460c. 370 BCE), and the manuscript On the Sacred Disease in particular, describe a group of problems that matches up very well with the modern understanding of cerebral palsy. The Roman Emperor Claudius (10 BCE54 CE) is suspected of having CP, as historical records describe him as having several physical problems in line with the condition. Medical historians have begun to suspect and find depictions of CP in much later art. Several paintings from the 16th century and later show individuals with problems consistent with it, such as Jusepe de Ribera's 1642 painting The Clubfoot.

The modern understanding of CP as resulting from problems within the brain began in the early decades of the 1800s with a number of publications on brain abnormalities by Johann Christian Reil, Claude François Lallemand and Philippe Pinel. Later physicians used this research to connect problems in the brain with specific symptoms. The English surgeon William John Little (18101894) was the first person to study CP extensively. In his doctoral thesis he stated that CP was a result of a problem around the time of birth. He later identified a difficult delivery, a preterm birth and perinatal asphyxia in particular as risk factors. The spastic diplegia form of CP came to be known as Little's disease. At around this time, a German surgeon was also working on cerebral palsy, and distinguished it from polio. In the 1880s British neurologist William Gowers built on Little's work by linking paralysis in newborns to difficult births. He named the problem "birth palsy" and classified birth palsies into two types: peripheral and cerebral.

Working in the US in the 1880s, Canadian-born physician William Osler (18491919) reviewed dozens of CP cases to further classify the disorders by the site of the problems on the body and by the underlying cause. Osler made further observations tying problems around the time of delivery with CP, and concluded that problems causing bleeding inside the brain were likely the root cause. Osler also suspected polioencephalitis as an infectious cause. Through the 1890s, scientists commonly confused CP with polio.

Before moving to psychiatry, Austrian neurologist Sigmund Freud (18561939) made further refinements to the classification of the disorder. He produced the system still being used today. Freud's system divides the causes of the disorder into problems present at birth, problems that develop during birth, and problems after birth. Freud also made a rough correlation between the location of the problem inside the brain and the location of the affected limbs on the body and documented the many kinds of movement disorders.

In the early 20th century, the attention of the medical community generally turned away from CP until orthopedic surgeon Winthrop Phelps became the first physician to treat the disorder. He viewed CP from a musculoskeletal perspective instead of a neurological one. Phelps developed surgical techniques for operating on the muscles to address issues such as spasticity and muscle rigidity. Hungarian physical rehabilitation practitioner András Pető developed a system to teach children with CP how to walk and perform other basic movements. Pető's system became the foundation for conductive education, widely used for children with CP today. Through the remaining decades, physical therapy for CP has evolved, and has become a core component of the CP management program.

In 1997, Robert Palisano et al. introduced the Gross Motor Function Classification System (GMFCS) as an improvement over the previous rough assessment of limitation as either mild, moderate, or severe. The GMFCS grades limitation based on observed proficiency in specific basic mobility skills such as sitting, standing, and walking, and takes into account the level of dependency on aids such as wheelchairs or walkers. The GMFCS was further revised and expanded in 2007.

Economic impact
It is difficult to directly compare the cost and cost-effectiveness of interventions to prevent cerebral palsy or the cost of interventions to manage CP. Access Economics has released a report on the economic impact of cerebral palsy in Australia. The report found that, in 2007, the financial cost of cerebral palsy (CP) in Australia was A$1.47 billion or 0.14% of GDP. Of this:
 * A$1.03 billion (69.9%) was productivity lost due to lower employment, absenteeism, and premature death of Australians with CP
 * A$141 million (9.6%) was the DWL from transfers including welfare payments and taxation forgone
 * A$131 million (9.0%) was other indirect costs such as direct program services, aides and home modifications, and the bringing-forward of funeral costs
 * A$129 million (8.8%) was the value of the informal care for people with CP
 * A$40 million (2.8%) was direct health system expenditure

The value of lost well-being (disability and premature death) was a further A$2.4 billion.

In per capita terms, this amounts to a financial cost of A$43,431 per person with CP per annum. Including the value of lost well-being, the cost is over $115,000 per person per annum.

Individuals with CP bear 37% of the financial costs, and their families and friends bear a further 6%. The federal government bears around one-third (33%) of the financial costs (mainly through taxation revenues forgone and welfare payments). State governments bear under 1% of the costs, while employers bear 5% and the rest of society bears the remaining 19%. If the burden of disease (lost well-being) is included, individuals bear 76% of the costs.

The average lifetime cost for people with CP in the US is US$921,000 per individual, including lost income.

In the United States, many states allow Medicaid beneficiaries to use their Medicaid funds to hire their own PCAs, instead of forcing them to use institutional or managed care.

In India, the government-sponsored program called "NIRAMAYA" for the medical care of children with neurological and muscular deformities has proved to be an ameliorating economic measure for persons with such disabilities. It has shown that persons with mental or physically debilitating congenital disabilities can lead better lives if they have financial independence.

Use of the term
"Cerebral" means "of, or pertaining to, the cerebrum or the brain" and "palsy" means "paralysis, generally partial, whereby a local body area is incapable of voluntary movement". It has been proposed to change the name to "cerebral palsy spectrum disorder" to reflect the diversity of presentations of CP.

Many people would rather be referred to as a person with a disability (people-first language) instead of as "handicapped". "Cerebral Palsy: A Guide for Care" at the University of Delaware offers the following guidelines:

"Impairment is the correct term to use to define a deviation from normal, such as not being able to make a muscle move or not being able to control an unwanted movement. Disability is the term used to define a restriction in the ability to perform a normal activity of daily living which someone of the same age can perform. For example, a three-year-old child who is not able to walk has a disability because a normal three-year-old can walk independently. A handicapped child or adult is one who, because of the disability, is unable to achieve the normal role in society commensurate with his age and socio-cultural milieu. As an example, a sixteen-year-old who is unable to prepare his own meal or care for his own toilet or hygiene needs is handicapped. On the other hand, a sixteen-year-old who can walk only with the assistance of crutches but who attends a regular school and is fully independent in activities of daily living is disabled but not handicapped. All disabled people are impaired, and all handicapped people are disabled, but a person can be impaired and not necessarily be disabled, and a person can be disabled without being handicapped."

The term "spastic" denotes the attribute of spasticity in types of spastic CP. In 1952 a UK charity called The Spastics Society was formed. The term "spastics" was used by the charity as a term for people with CP. The word "spastic" has since been used extensively as a general insult to disabled people, which some see as extremely offensive. They are also frequently used to insult non-disabled people when they seem overly uncoordinated, anxious, or unskilled in sports. The charity changed its name to Scope in 1994. In the United States the word spaz has the same usage as an insult but is not generally associated with CP.

Media
Maverick documentary filmmaker Kazuo Hara criticises the mores and customs of Japanese society in an unsentimental portrait of adults with cerebral palsy in his 1972 film Goodbye CP. Focusing on how people with cerebral palsy are generally ignored or disregarded in Japan, Hara challenges his society's taboos about physical handicaps. Using a deliberately harsh style, with grainy black-and-white photography and out-of-sync sound, Hara brings a stark realism to his subject.

Spandan (2012), a film by Vegitha Reddy and Aman Tripathi, delves into the dilemma of parents whose child has cerebral palsy. While films made with children with special needs as central characters have been attempted before, the predicament of parents dealing with the stigma associated with the condition and beyond is dealt in Spandan. In one of the songs of Spandan "Chal chaal chaal tu bala" more than 50 CP kids have acted. The famous classical singer Devaki Pandit has given her voice to the song penned by Prof. Jayant Dhupkar and composed by National Film Awards winner Isaac Thomas Kottukapally.

My Left Foot (1989) is a drama film directed by Jim Sheridan and starring Daniel Day-Lewis. It tells the true story of Christy Brown, an Irishman born with cerebral palsy, who could control only his left foot. Christy Brown grew up in a poor, working-class family, and became a writer and artist. It won the Academy Award for Best Actor (Daniel Day-Lewis) and Best Actress in a Supporting Role (Brenda Fricker). It was also nominated for Best Director, Best Picture and Best Writing, Screenplay Based on Material from Another Medium. It also won the New York Film Critics Circle Award for Best Film for 1989.

Call the Midwife (2012–) has featured two episodes with actor Colin Young, who himself has cerebral palsy, playing a character with the same disability. His storylines have focused on the segregation of those with disabilities in the UK in the 1950s, and also romantic relationships between people with disabilities.

Micah Fowler, an American actor with CP, stars in the ABC sitcom Speechless (2016–2019), which explores both the serious and humorous challenges a family faces with a teenager with CP.

9-1-1 (2018–) is a procedural drama series on Fox. From season 2 onwards, it features Gavin McHugh (who himself has cerebral palsy) in the recurring role as Christopher Diaz – a young child who has cerebral palsy.

Special (2019) is a comedy series that premiered on Netflix on 12 April 2019. It was written, produced and stars Ryan O'Connell as a young gay man with mild cerebral palsy. It is based on O'Connell's book I'm Special: And Other Lies We Tell Ourselves.

Australian drama serial The Heights (2019–) features a character with mild cerebral palsy, teenage girl Sabine Rosso, depicted by an actor who herself has mild cerebral palsy, Bridie McKim.

6,000 Waiting (2021) is a documentary by Michael Joseph McDonald. It is the first film to depict a person with cerebral palsy parachuting. It tells the story of three men with cerebral palsy seeking to live in their communities instead of institutions. Upon seeing the film, American politician Stacey Abrams interviewed one of the film's protagonists and publicly stated that her top priority was deinstitutionalization through Medicaid expansion.

Notable cases

 * Christy Brown was the basis for the Academy Award-winning film, My Left Foot.
 * Two sons of Canadian rock musician Neil Young, Zeke and Ben. In 1986, Young helped found the Bridge School, an educational organization for children with severe verbal and physical disabilities, and its annual supporting Bridge School Benefit concerts, together with his wife Pegi.
 * Nicolas Hamilton, a British racing driver competing in BTCC. He is the half-brother of Formula 1 driver Lewis Hamilton.
 * Geri Jewell, who had a regular role in the prime-time series The Facts of Life.
 * Josh Blue, winner of the fourth season of NBC's Last Comic Standing, whose act revolves around his CP. Blue was also on the 2004 U.S. Paralympic soccer team.
 * Jason Benetti, play-by-play broadcaster for ESPN, Fox Sports, Westwood One, and Time Warner covering football, baseball, lacrosse, hockey, and basketball. From 2016 until 2023, he was the television play-by-play announcer for Chicago White Sox home games. Since 2024, Benetti has been the play-by-play announcer for the Detroit Tigers.
 * Jack Carroll, British comedian and runner-up in the seventh season of Britain's Got Talent.
 * Abbey Curran, an American beauty queen who represented Iowa at Miss USA 2008 and was the first contestant with a disability to compete.
 * Robert Griswold, swimmer
 * Francesca Martinez, British stand-up comedian and actress.
 * Evan O'Hanlon, Australian Paralympian, the fastest athlete with cerebral palsy in the world.
 * Arun Shourie's son Aditya, about whom he has written a book Does He Know a Mother's Heart
 * Maysoon Zayid, the self-described "Palestinian Muslim virgin with cerebral palsy, from New Jersey", who is an actress, stand-up comedian, and activist. Zayid has been a resident of Cliffside Park, New Jersey. She is considered one of America's first Muslim women comedians and the first person ever to perform standup in Palestine and Jordan.
 * RJ Mitte, an American actor best known for his role as Walter White Jr. in Breaking Bad. He is also a celebrity ambassador for United Cerebral Palsy.
 * Zach Anner, an American comedian, actor, and writer. He had a television series on Oprah Winfrey's OWN called Rollin' With Zach and is the author of If at Birth You Don't Succeed.
 * Kaine, a member of the American hip-hop duo The Ying Yang Twins, has a mild form of cerebral palsy that causes him to limp.
 * Hannah Cockroft, is a British wheelchair athlete specialising in sprint distances in the T34 classification. She holds the Paralympic and world records for the 100 metres, 200 metres and 400 metres in her classification.
 * Keah Brown, American disability rights activist, author and journalist.
 * Kuli Kohli, Indian-British writer, poet, activist.
 * Simon James Stevens, a British disability issues consultant and activist, who starred in I'm Spazticus and founded Wheelies virtual nightclub
 * The Roman Emperor Claudius is hypothesized to have had cerebral palsy on the basis of his reported symptoms.
 * Rosie Jones, a British comedian and actress, is incorporating her cerebral palsy into her comedic style.
 * Christopher Nolan, an Irish Poet and Author, he wrote Damn-Burst of Dreams, The Banyan Tree, and Under The Eye Of The Clock. He passed away in 2009.
 * Lost Voice Guy British Comedian

Litigation
Because of the perception that cerebral palsy is mostly caused by trauma during birth, as of 2005, 60% of obstetric litigation was about cerebral palsy, which Alastair MacLennan, Professor of Obstetrics and Gynaecology at the University of Adelaide, regards as causing an exodus from the profession. In the latter half of the 20th century, obstetric litigation about the cause of cerebral palsy became more common, leading to the practice of defensive medicine.

title: Cerebral palsy


text:
Parkinsonism

Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia (slowed movements), rigidity, and postural instability. Both hypokinetic (bradykinesia and akinesia) as well as hyperkinetic (cogwheel rigidity and tremors at rest) features are displayed by Parkinsonism. These are the four motor symptoms found in Parkinson's disease (PD) – after which it is named – dementia with Lewy bodies (DLB), Parkinson's disease dementia (PDD), and many other conditions. This set of symptoms occurs in a wide range of conditions and may have many causes, including neurodegenerative conditions, drugs, toxins, metabolic diseases, and neurological conditions other than PD.

Signs and symptoms
Parkinsonism is a clinical syndrome characterized by the four motor symptoms found in Parkinson's disease: tremor, bradykinesia (slowed movements), rigidity, and postural instability.

Parkinsonism gait problems can lead to falls and serious physical injuries. Other common symptoms include:
 * Tremors, as rest tremor (when resting, mostly in the hands) and/or postular tremor
 * Short, shuffling gait
 * Slow movements (bradykinesia)
 * Loss of sound perception leading to soft speech, hypophonia
 * Difficulty sleeping
 * Dry skin
 * Apathy
 * Lack of facial expressions
 * Balance problems
 * Frequent falls
 * Very small handwriting
 * Rigid, stiff muscles
 * Cogwheeling (jerky feeling in arm or leg)
 * Upgaze impairment
 * Plastic, dead feeling resistance known as "lead-pipe rigidity".

Conditions
Parkinsonism occurs in many conditions.

Neurological
Neurodegenerative conditions and Parkinson-plus syndromes that can cause parkinsonism include:
 * Corticobasal degeneration
 * Dementia with Lewy bodies
 * The relationship (if any) with essential tremor is not clear.
 * Frontotemporal dementia (Pick's disease)
 * Gerstmann–Sträussler–Scheinker syndrome
 * Huntington's disease
 * Lytico-bodig disease (ALS complex of Guam)
 * Multiple system atrophy (Shy–Drager syndrome)
 * Neuroacanthocytosis
 * Neuronal ceroid lipofuscinosis
 * Olivopontocerebellar atrophy
 * Pantothenate kinase-associated neurodegeneration, also known as neurodegeneration with brain iron accumulation
 * Parkin mutation causing hereditary juvenile dystonia
 * Parkinson's disease
 * Parkinson's disease dementia
 * Progressive supranuclear palsy
 * Wilson's disease
 * X-linked dystonia parkinsonism (Lubag syndrome)

Infectious

 * Creutzfeldt–Jakob disease
 * Encephalitis lethargica
 * HIV infection and AIDS

Toxins
Evidence exists to show a link between exposure to pesticides and herbicides and PD; a two-fold increase in risk was seen with paraquat or maneb/mancozeb exposure.

Chronic manganese (Mn) exposure has been shown to produce a parkinsonism-like illness characterized by movement abnormalities. This condition is not responsive to typical therapies used in the treatment of PD, suggesting an alternative pathway than the typical dopaminergic loss within the substantia nigra. Manganese may accumulate in the basal ganglia, leading to the abnormal movements that characterize parkinsonism. A mutation of the SLC30A10 gene, a manganese efflux transporter necessary for decreasing intracellular Mn, has been linked with the development of this parkinsonism-like disease. The Lewy bodies typical to PD are not seen in Mn-induced parkinsonism.

Agent Orange may be a cause of parkinsonism, although evidence is inconclusive and further research is needed.

Other toxins that have been associated with parkinsonism are:
 * Annonaceae
 * Carbon monoxide
 * Carbon disulfide
 * Cyanide
 * Ethanol
 * Hexane
 * Mercury
 * Methanol
 * MPTP
 * Rotenone
 * Toluene (inhalant abuse: "huffing")

Vascular

 * Binswanger's disease (subcortical leukoencephalopathy)
 * Vascular dementia (multi-infarct)
 * Dural arteriovenous fistula / dAVF (reversible parkinsonism through fistula treatment)
 * Dural arteriovenous malformation / dAVM (reversible through dAVM treatment)

Other

 * Chronic traumatic encephalopathy (boxer's dementia or pugilistic encephalopathy)
 * Damage to the brain stem (especially dopaminergic nuclei of the substantia nigra), basal ganglia (especially globus pallidus) and the thalamus.
 * Hypothyroidism
 * Orthostatic tremor
 * Paraneoplastic syndrome: neurological symptoms caused by antibodies associated with cancers
 * Rapid onset dystonia parkinsonism
 * Autosomal recessive juvenile parkinsonism

Differential diagnosis
Secondary parkinsonism, including vascular parkinsonism and drug-induced parkinsonism.

Drug-induced parkinsonism
About 7% of people with parkinsonism developed symptoms as a result of side effects of medication, mainly neuroleptic antipsychotics especially the phenothiazines (such as perphenazine and chlorpromazine), thioxanthenes (such as flupentixol and zuclopenthixol) and butyrophenones (such as haloperidol), and rarely, antidepressants. Yet another drug that can induce parkinsonism is the antihistaminic medication cinnarizine, usually prescribed for motion sickness; this is because besides antagonizing histamine receptors this drug antagonizes the dopamine D2 receptors. The incidence of drug-induced parkinsonism increases with age. Drug-induced parkinsonism tends to remain at its presenting level and does not worsen like Parkinson's disease.

Implicated medications include:
 * Antipsychotics
 * Lithium
 * Metoclopramide
 * MDMA (addiction and frequent use)
 * Tetrabenazine
 * Cinnarizine

Society and culture
In the United States, the 2021 National Defense Authorization Act (NDAA) added parkinsonism to the list of presumptive conditions associated with Agent Orange exposure, enabling affected service members to receive Veterans Affairs disability benefits.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Parkinsonism


text:
Nuclear shell model

In nuclear physics, atomic physics, and nuclear chemistry, the nuclear shell model utilizes the Pauli exclusion principle to model the structure of atomic nuclei in terms of energy levels. The first shell model was proposed by Dmitri Ivanenko (together with E. Gapon) in 1932. The model was developed in 1949 following independent work by several physicists, most notably Maria Goeppert Mayer and J. Hans D. Jensen, who received the 1963 Nobel Prize in Physics for their contributions to this model, and Eugene Wigner, who received the Nobel Prize alongside them for his earlier groundlaying work on the atomic nuclei.

The nuclear shell model is partly analogous to the atomic shell model, which describes the arrangement of electrons in an atom, in that a filled shell results in better stability. When adding nucleons (protons and neutrons) to a nucleus, there are certain points where the binding energy of the next nucleon is significantly less than the last one. This observation that there are specific magic quantum numbers of nucleons (2, 8, 20, 28, 50, 82, and 126) that are more tightly bound than the following higher number is the origin of the shell model.

The shells for protons and neutrons are independent of each other. Therefore, there can exist both "magic nuclei", in which one nucleon type or the other is at a magic number, and "doubly magic quantum nuclei", where both are. Due to variations in orbital filling, the upper magic numbers are 126 and, speculatively, 184 for neutrons, but only 114 for protons, playing a role in the search for the so-called island of stability. Some semi-magic numbers have been found, notably Z = 40, which gives the nuclear shell filling for the various elements; 16 may also be a magic number.

To get these numbers, the nuclear shell model starts with an average potential with a shape somewhere between the square well and the harmonic oscillator. To this potential, a spin-orbit term is added. Even so, the total perturbation does not coincide with the experiment, and an empirical spin-orbit coupling must be added with at least two or three different values of its coupling constant, depending on the nuclei being studied. The magic numbers of nuclei, as well as other properties, can be arrived at by approximating the model with a three-dimensional harmonic oscillator plus a spin–orbit interaction. A more realistic but complicated potential is known as the Woods–Saxon potential.

Modified harmonic oscillator model
Consider a three-dimensional harmonic oscillator. This would give, for example, in the first three levels ("ℓ" is the angular momentum quantum number):

Nuclei are built by adding protons and neutrons. These will always fill the lowest available level, with the first two protons filling level zero, the next six protons filling level one, and so on. As with electrons in the periodic table, protons in the outermost shell will be relatively loosely bound to the nucleus if there are only a few protons in that shell because they are farthest from the center of the nucleus. Therefore, nuclei with a full outer proton shell will have a higher nuclear binding energy than other nuclei with a similar total number of protons. The same is true for neutrons.

This means that the magic numbers are expected to be those in which all occupied shells are full. In accordance with the experiment, we get 2 (level 0 full) and 8 (levels 0 and 1 full) for the first two numbers. However, the full set of magic numbers does not turn out correctly. These can be computed as follows:

 * In a three-dimensional harmonic oscillator the total degeneracy of states at level n is $${(n+1)(n+2)\over 2}$$.
 * Due to the spin, the degeneracy is doubled and is $$(n+1)(n+2)$$.
 * Thus, the magic numbers would be$$ \sum_{n=0}^k (n+1)(n+2) = \frac{(k+1)(k+2)(k+3)} 3 $$for all integer k. This gives the following magic numbers: 2, 8, 20, 40, 70, 112, ..., which agree with experiment only in the first three entries. These numbers are twice the tetrahedral numbers (1, 4, 10, 20, 35, 56, ...) from the Pascal Triangle.

In particular, the first six shells are: where for every ℓ there are 2ℓ+1 different values of ml and 2 values of ms, giving a total of 4ℓ+2 states for every specific level.
 * level 0: 2 states (ℓ = 0) = 2.
 * level 1: 6 states (ℓ = 1) = 6.
 * level 2: 2 states (ℓ = 0) + 10 states (ℓ = 2) = 12.
 * level 3: 6 states (ℓ = 1) + 14 states (ℓ = 3) = 20.
 * level 4: 2 states (ℓ = 0) + 10 states (ℓ = 2) + 18 states (ℓ = 4) = 30.
 * level 5: 6 states (ℓ = 1) + 14 states (ℓ = 3) + 22 states (ℓ = 5) = 42.

These numbers are twice the values of triangular numbers from the Pascal Triangle: 1, 3, 6, 10, 15, 21, ....

Including a spin-orbit interaction
We next include a spin–orbit interaction. First, we have to describe the system by the quantum numbers j, mj and parity instead of ℓ, ml and ms, as in the hydrogen–like atom. Since every even level includes only even values of ℓ, it includes only states of even (positive) parity. Similarly, every odd level includes only states of odd (negative) parity. Thus we can ignore parity in counting states. The first six shells, described by the new quantum numbers, are where for every j there are 2j +  1 different states from different values of mj.
 * level 0 (n = 0): 2 states (j = $1/undefined$). Even parity.
 * level 1 (n = 1): 2 states (j = $1/undefined$) + 4 states (j = $1/undefined$) = 6. Odd parity.
 * level 2 (n = 2): 2 states (j = $1/undefined$) + 4 states (j = $1/undefined$) + 6 states (j = $1/undefined$) = 12. Even parity.
 * level 3 (n = 3): 2 states (j = $1/undefined$) + 4 states (j = $1/undefined$) + 6 states (j = $1/undefined$) + 8 states (j = $1/undefined$) = 20. Odd parity.
 * level 4 (n = 4): 2 states (j = $1/undefined$) + 4 states (j = $1/undefined$) + 6 states (j = $1/undefined$) + 8 states (j = $1/undefined$) + 10 states (j = $1/undefined$) = 30. Even parity.
 * level 5 (n = 5): 2 states (j = $1/undefined$) + 4 states (j = $1/undefined$) + 6 states (j = $1/undefined$) + 8 states (j = $1/undefined$) + 10 states (j = $1/undefined$) + 12 states (j = $1/undefined$) = 42. Odd parity.

Due to the spin–orbit interaction, the energies of states of the same level but with different j will no longer be identical. This is because in the original quantum numbers, when $$\scriptstyle \vec{s}$$ is parallel to $$\scriptstyle \vec{l}$$, the interaction energy is positive, and in this case j = ℓ + s = ℓ + $1/undefined$. When $$\scriptstyle \vec{s}$$ is anti-parallel to $$\scriptstyle \vec{l}$$ (i.e. aligned oppositely), the interaction energy is negative, and in this case j =  ℓ  −  s  =  ℓ  −  $3/2$. Furthermore, the strength of the interaction is roughly proportional to ℓ.

For example, consider the states at level 4:
 * The 10 states with j = $1/undefined$ come from ℓ = 4 and s parallel to ℓ. Thus they have a positive spin–orbit interaction energy.
 * The 8 states with j = $3/2$ came from ℓ = 4 and s anti-parallel to ℓ. Thus they have a negative spin–orbit interaction energy.
 * The 6 states with j = $5/2$ came from ℓ = 2 and s parallel to ℓ. Thus they have a positive spin–orbit interaction energy. However, its magnitude is half compared to the states with j = $1/undefined$.
 * The 4 states with j = $3/2$ came from ℓ = 2 and s anti-parallel to ℓ. Thus they have a negative spin–orbit interaction energy. However, its magnitude is half compared to the states with j = $5/2$.
 * The 2 states with j = $7/2$ came from ℓ = 0 and thus have zero spin–orbit interaction energy.

Changing the profile of the potential
The harmonic oscillator potential $$V(r) = \mu \omega^2 r^2 /2$$ grows infinitely as the distance from the center r goes to infinity. A more realistic potential, such as the Woods–Saxon potential, would approach a constant at this limit. One main consequence is that the average radius of nucleons' orbits would be larger in a realistic potential. This leads to a reduced term $$\scriptstyle \hbar^2 l(l+1)/ 2m r^2$$ in the Laplace operator of the Hamiltonian operator. Another main difference is that orbits with high average radii, such as those with high n or high ℓ, will have a lower energy than in a harmonic oscillator potential. Both effects lead to a reduction in the energy levels of high ℓ orbits.

Predicted magic numbers

Together with the spin–orbit interaction, and for appropriate magnitudes of both effects, one is led to the following qualitative picture: at all levels, the highest j states have their energies shifted downwards, especially for high n (where the highest j is high). This is both due to the negative spin–orbit interaction energy and to the reduction in energy resulting from deforming the potential into a more realistic one. The second-to-highest j states, on the contrary, have their energy shifted up by the first effect and down by the second effect, leading to a small overall shift. The shifts in the energy of the highest j states can thus bring the energy of states of one level closer to the energy of states of a lower level. The "shells" of the shell model are then no longer identical to the levels denoted by n, and the magic numbers are changed.

We may then suppose that the highest j states for n = 3 have an intermediate energy between the average energies of n = 2 and n = 3, and suppose that the highest j states for larger n (at least up to n = 7) have an energy closer to the average energy of n −  1. Then we get the following shells (see the figure)

and so on.
 * 1st shell: 2 states (n = 0, j = $1/undefined$).
 * 2nd shell: 6 states (n = 1, j = $3/2$ or $5/2$).
 * 3rd shell: 12 states (n = 2, j = $7/2$, $9/2$ or $1/undefined$).
 * 4th shell: 8 states (n = 3, j = $3/2$).
 * 5th shell: 22 states (n = 3, j = $5/2$, $7/2$ or $9/2$; n = 4, j = $11/2$).
 * 6th shell: 32 states (n = 4, j = $1/undefined$, $1/undefined$, $9/2$ or $7/2$; n = 5, j = $5/2$).
 * 7th shell: 44 states (n = 5, j = $9/2$, $3/2$, $7/2$, $1/undefined$ or $1/undefined$; n = 6, j = $1/undefined$).
 * 8th shell: 58 states (n = 6, j = $3/2$, $1/undefined$, $3/2$, $5/2$, $7/2$ or $1/undefined$; n = 7, j = $3/2$).

Note that the numbers of states after the 4th shell are doubled triangular numbers. Spin–orbit coupling causes so-called 'intruder levels' to drop down from the next higher shell into the structure of the previous shell. The sizes of the intruders are such that the resulting shell sizes are themselves increased to the next higher doubled triangular numbers from those of the harmonic oscillator. For example, 1f2p has 20 nucleons, and spin–orbit coupling adds 1g9/2 (10 nucleons), leading to a new shell with 30 nucleons. 1g2d3s has 30 nucleons, and adding intruder 1h11/2 (12 nucleons) yields a new shell size of 42, and so on.

The magic numbers are then

 * 2
 * 8 =  2  +  6
 * 20 =  2  +  6  +  12
 * 28 =  2  +  6  +  12  +  8
 * 50 =  2  +  6  +  12  +  8  +  22
 * 82 =  2  +  6  +  12  +  8  +  22  +  32
 * 126 =  2  +  6  +  12  +  8  +  22  +  32  +  44
 * 184 =  2  +  6  +  12  +  8  +  22  +  32  +  44  +  58

and so on. This gives all the observed magic numbers and also predicts a new one (the so-called island of stability) at the value of 184 (for protons, the magic number 126 has not been observed yet, and more complicated theoretical considerations predict the magic number to be 114 instead).

Another way to predict magic (and semi-magic) numbers is by laying out the idealized filling order (with spin–orbit splitting but energy levels not overlapping). For consistency, s is split into j = 1⁄2 and j = -1⁄2 components with 2 and 0 members respectively. Taking the leftmost and rightmost total counts within sequences bounded by / here gives the magic and semi-magic numbers.

 * s(2,0)/p(4,2) > 2,2/6,8, so (semi)magic numbers 2,2/6,8
 * d(6,4):s(2,0)/f(8,6):p(4,2) > 14,18:20,20/28,34:38,40, so 14,20/28,40
 * g(10,8):d(6,4):s(2,0)/h(12,10):f(8,6):p(4,2) > 50,58,64,68,70,70/82,92,100,106,110,112, so 50,70/82,112
 * i(14,12):g(10,8):d(6,4):s(2,0)/j(16,14):h(12,10):f(8,6):p(4,2) > 126,138,148,156,162,166,168,168/184,198,210,220,228,234,238,240, so 126,168/184,240

The rightmost predicted magic numbers of each pair within the quartets bisected by / are double tetrahedral numbers from the Pascal Triangle: 2, 8, 20, 40, 70, 112, 168, 240 are 2x 1, 4, 10, 20, 35, 56, 84, 120, ..., and the leftmost members of the pairs differ from the rightmost by double triangular numbers: 2 − 2 = 0, 8 − 6 = 2, 20 − 14 = 6, 40 − 28 = 12, 70 − 50 = 20, 112 − 82 = 30, 168 − 126 = 42, 240 − 184 = 56, where 0, 2, 6, 12, 20, 30, 42, 56, ... are 2 × 0, 1, 3, 6, 10, 15, 21, 28, ... .

Other properties of nuclei
This model also predicts or explains with some success other properties of nuclei, in particular spin and parity of nuclei ground states, and to some extent their excited nuclear states as well. Take (oxygen-17) as an example: Its nucleus has eight protons filling the first three proton "shells", eight neutrons filling the first three neutron "shells", and one extra neutron. All protons in a complete proton shell have zero total angular momentum, since their angular momenta cancel each other. The same is true for neutrons. All protons in the same level (n) have the same parity (either +1 or −1), and since the parity of a pair of particles is the product of their parities, an even number of protons from the same level (n) will have +1 parity. Thus, the total angular momentum of the eight protons and the first eight neutrons is zero, and their total parity is +1. This means that the spin (i.e. angular momentum) of the nucleus, as well as its parity, are fully determined by that of the ninth neutron. This one is in the first (i.e. lowest energy) state of the 4th shell, which is a d-shell (ℓ = 2), and since p = (−1)$5/2$, this gives the nucleus an overall parity of +1. This 4th d-shell has a j = $9/2$, thus the nucleus of is expected to have positive parity and total angular momentum $1/undefined$, which indeed it has.

The rules for the ordering of the nucleus shells are similar to Hund's Rules of the atomic shells, however, unlike its use in atomic physics, the completion of a shell is not signified by reaching the next n, as such the shell model cannot accurately predict the order of excited nuclei states, though it is very successful in predicting the ground states. The order of the first few terms are listed as follows: 1s, 1p$3/2$, 1p$5/2$, 1d$7/2$, 2s, 1d$11/2$... For further clarification on the notation refer to the article on the Russell–Saunders term symbol.

For nuclei farther from the magic quantum numbers one must add the assumption that due to the relation between the strong nuclear force and total angular momentum, protons or neutrons with the same n tend to form pairs of opposite angular momentum. Therefore, a nucleus with an even number of protons and an even number of neutrons has 0 spin and positive parity. A nucleus with an even number of protons and an odd number of neutrons (or vice versa) has the parity of the last neutron (or proton), and the spin equal to the total angular momentum of this neutron (or proton). By "last" we mean the properties coming from the highest energy level.

In the case of a nucleus with an odd number of protons and an odd number of neutrons, one must consider the total angular momentum and parity of both the last neutron and the last proton. The nucleus parity will be a product of theirs, while the nucleus spin will be one of the possible results of the sum of their angular momenta (with other possible results being excited states of the nucleus).

The ordering of angular momentum levels within each shell is according to the principles described above – due to spin–orbit interaction, with high angular momentum states having their energies shifted downwards due to the deformation of the potential (i.e. moving from a harmonic oscillator potential to a more realistic one). For nucleon pairs, however, it is often energetically favourable to be at high angular momentum, even if its energy level for a single nucleon would be higher. This is due to the relation between angular momentum and the strong nuclear force.

The nuclear magnetic moment of neutrons and protons is partly predicted by this simple version of the shell model. The magnetic moment is calculated through j, ℓ and s of the "last" nucleon, but nuclei are not in states of well-defined ℓ and s. Furthermore, for odd-odd nuclei, one has to consider the two "last" nucleons, as in deuterium. Therefore, one gets several possible answers for the nuclear magnetic moment, one for each possible combined ℓ and s state, and the real state of the nucleus is a superposition of them. Thus the real (measured) nuclear magnetic moment is somewhere in between the possible answers.

The electric dipole of a nucleus is always zero, because its ground state has a definite parity. The matter density (ψ$1/undefined$, where ψ is the wavefunction) is always invariant under parity. This is usually the situation with the atomic electric dipole.

Higher electric and magnetic multipole moments cannot be predicted by this simple version of the shell model for reasons similar to those in the case of deuterium.

Including residual interactions

For nuclei having two or more valence nucleons (i.e. nucleons outside a closed shell), a residual two-body interaction must be added. This residual term comes from the part of the inter-nucleon interaction not included in the approximative average potential. Through this inclusion, different shell configurations are mixed, and the energy degeneracy of states corresponding to the same configuration is broken.

These residual interactions are incorporated through shell model calculations in a truncated model space (or valence space). This space is spanned by a basis of many-particle states where only single-particle states in the model space are active. The Schrödinger equation is solved on this basis, using an effective Hamiltonian specifically suited for the model space. This Hamiltonian is different from the one of free nucleons as, among other things, it has to compensate for excluded configurations.

One can do away with the average potential approximation entirely by extending the model space to the previously inert core and treating all single-particle states up to the model space truncation as active. This forms the basis of the no-core shell model, which is an ab initio method. It is necessary to include a three-body interaction in such calculations to achieve agreement with experiments.

Collective rotation and the deformed potential
In 1953 the first experimental examples were found of rotational bands in nuclei, with their energy levels following the same J(J+1) pattern of energies as in rotating molecules. Quantum mechanically, it is impossible to have a collective rotation of a sphere, so this implied that the shape of these nuclei was non-spherical. In principle, these rotational states could have been described as coherent superpositions of particle-hole excitations in the basis consisting of single-particle states of the spherical potential. But in reality, the description of these states in this manner is intractable, due to a large number of valence particles—and this intractability was even greater in the 1950s when computing power was extremely rudimentary. For these reasons, Aage Bohr, Ben Mottelson, and Sven Gösta Nilsson constructed models in which the potential was deformed into an ellipsoidal shape. The first successful model of this type is now known as the Nilsson model. It is essentially the harmonic oscillator model described in this article, but with anisotropy added, so the oscillator frequencies along the three Cartesian axes are not all the same. Typically the shape is a prolate ellipsoid, with the axis of symmetry taken to be z. Because the potential is not spherically symmetric, the single-particle states are not states of good angular momentum J. However, a Lagrange multiplier $$-\omega\cdot J$$, known as a "cranking" term, can be added to the Hamiltonian. Usually the angular frequency vector ω is taken to be perpendicular to the symmetry axis, although tilted-axis cranking can also be considered. Filling the single-particle states up to the Fermi level produces states whose expected angular momentum along the cranking axis $$\langle J_x\rangle$$ is the desired value.

Related models
Igal Talmi developed a method to obtain the information from experimental data and use it to calculate and predict energies which have not been measured. This method has been successfully used by many nuclear physicists and has led to a deeper understanding of nuclear structure. The theory which gives a good description of these properties was developed. This description turned out to furnish the shell model basis of the elegant and successful interacting boson model.

A model derived from the nuclear shell model is the alpha particle model developed by Henry Margenau, Edward Teller, J. K. Pering, T. H. Skyrme, also sometimes called the Skyrme model. Note, however, that the Skyrme model is usually taken to be a model of the nucleon itself, as a "cloud" of mesons (pions), rather than as a model of the nucleus as a "cloud" of alpha particles.

title: Nuclear shell model