Diagnosis of ataxic cerebral palsy is based on clinical assessment using standardized assessment tools. Diagnosis begins with the observation of slow motor development, abnormal muscle tone, and unusual posture in children that fail to reach developmental milestones. Diagnosis differs in adults and children because a child’s brain is still developing and acquiring new motor, linguistic, adaptive, and social skills. The testing strategy is based on the pattern of development of symptoms, the patient’s family history, and any factors that might influence the diagnosis, such as injury or trauma. Associated disabilities such as those previously described under symptoms associated with ataxic cerebral palsy, i.e., sensory impairment and cognitive dysfunction, are also helpful in diagnosing the disease.

In children, assessment of infantile reflexes is also a diagnostic tool, such as the Moro reflex and the Romberg Test. The Moro reflex is rarely present in infants after 6 months of age and is characterized as a response to a sudden loss of support that causes the infant to feel like it is falling. The infant will respond by abduction and adduction (or spreading and unspreading) of the arms, as well as crying. The Moro reflex is significant in evaluating the integration of the central nervous system and patients with ataxic cerebral palsy will show a persistence and exacerbation of the reflex. In addition, patients with ataxic cerebral palsy will rarely show a positive Romberg test, which indicates that there is localized cerebellar dysfunction.

Physical diagnostic tests, such as cerebral imaging using Computerized Tomography (CT), Magnetic Resonance Imaging (MRI), and ultrasound are also useful, but not preferred to clinical assessments. These neuroimaging techniques can show brain abnormalities that have been found in previous patients with cerebral palsy, i.e., focal infarction and various brain malformations, however in a study of 273 children who were born after 35 weeks of gestation and underwent neuroimaging studies, one-third of the infants showed normal studies. In addition, infants undergo neuroimaging studies once the infant has neurological findings suggestive of cerebral palsy.

For developmental diagnosis in children and infants, there are a number of milestones of motor, linguistic, adaptive, and social behavior, such as.

1. When the child could sit up on their own with or without support

2. Say their first words

3. Feed themselves

4. Play successfully with children of same age

Bell's palsy is a diagnosis of exclusion, meaning it is diagnosed by elimination of other reasonable possibilities. By definition, no specific cause can be determined. There are no routine lab or imaging tests required to make the diagnosis. The degree of nerve damage can be assessed using the House-Brackmann score.

One study found that 45% of patients are not referred to a specialist, which suggests that Bell’s palsy is considered by physicians to be a straightforward diagnosis that is easy to manage.

Other conditions that can cause similar symptoms include: herpes zoster, Lyme disease, sarcoidosis, stroke, and brain tumors.

Because the causes of CP are varied, a broad range of preventative 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. Prior to 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. 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 level of evidence has been shown for giving women antibiotics during preterm labour when their waters had not broken was associated with an increased risk of cerebral palsy in the child. Additionally, allowing a preterm birth to proceed rather than trying to delay the birth also had a moderate level of evidence for increased risk of cerebral palsy in the child.

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.

Current forms of prevention are focused during pregnancy, while others are focused immediately after birth. Some methods that have been used include prolonging the pregnancy using interventions such as 17-alpha progesterone, limiting the number of gestations during pregnancy (for pregnancies induced by assistive reproductive technology), antenatal steroid for mothers likely to deliver prematurely, high caffeine for premature births with extremely low birth weights.

The efficacy of acupuncture remains unknown because the available studies are of low quality (poor primary study design or inadequate reporting practices). There is very tentative evidence for hyperbaric oxygen therapy in severe disease.

Magnetic resonance imaging (MRI) is used to detect morphological brain abnormalities associated with ADCP in patients that are either at risk for ADCP or have shown symptoms thereof. The abnormalities chiefly associated with ADCP are lesions that appear in the basal ganglia. The severity of the disease is proportional to the severity and extent of these abnormalities, and is typically greater when additional lesions appear elsewhere in the deep grey matter or white matter. MRI also has the ability to detect brain malformation, periventricular leukomalacia (PVL), and areas affected by hypoxia-ischemia, all of which may play a role in the development of ADCP. The MRI detection rate for ADCP is approximately 54.5%, however this statistic varies depending on the patient’s age and the cause of the disease and has been reported to be significantly higher.

Movement and posture limitations are aspects of all CP types and as a result, CP has historically been diagnosed based on parental reporting of developmental motor delays such as failure to sit upright, reach for objects, crawl, stand, or walk at the appropriate age. Diagnosis of ADCP is also based on clinical assessment used in conjunction with milestone reporting. The majority of ADCP assessments now use the Gross Motor Function Classification System (GMFCS) or the International Classification of Functioning, Disability and Health (formerly the International Classification of Impairments Disease, and Handicaps), measures of motor impairment that are effective in assessing severe CP. ADCP is typically characterized by an individual’s inability to control their muscle tone, which is readily assessed via these classification systems.

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. Much of childhood therapy is aimed at improving gait and walking. Approximately 60% of people with CP are able to walk independently or with aids at adulthood. 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. A Cochrane review published in 2004 found a trend toward 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 (selective dorsal rhizotomy).

In any manifestation of spastic CP, clonus of the affected limb(s) may intermittently result, as well as muscle spasms, each of which results from the pain and/or stress of the tightness experienced, indicating especially hard-working and/or exhausted musculature. The spasticity itself can and usually does also lead to very early onset of muscle-stress symptoms like arthritis and tendinitis, especially in ambulatory individuals in their mid-20s and early-30s. As compared to other types of CP, however, and especially as compared to hypotonic CP or more general paralytic mobility disabilities, spastic CP is typically more easily manageable by the person affected, and medical treatment can be pursued on a multitude of orthopaedic and neurological fronts throughout life.

Physical therapy and occupational therapy regimens of assisted stretching, strengthening, functional tasks, and/or targeted physical activity and exercise are usually the chief ways to keep spastic CP well-managed, although if the spasticity is too much for the person to handle, other remedies may be considered, such as various antispasmodic medications, botox, baclofen, or even a neurosurgery known as a selective dorsal rhizotomy (which eliminates the spasticity by eliminating the nerves causing it).

The muscle spasticity can cause gait patterns to be awkward and jerky. The constant spastic state of the muscle can lead to bone and tendon deformation, further complicating the patient's mobility. Many patients with spastic hemiplegia are subjected to canes, walkers and even wheelchairs. Due to the decrease in weight bearing, patients are at a higher risk of developing osteoporosis. An unhealthy weight can further complicate mobility. Patients with spastic hemiplegia are a high risk for experiencing seizures. Oromotor dysfunction puts patients at risk for aspiration pneumonia. Visual field deficits can cause impaired two-point discrimination. Many patients experience the loss of sensation in the arms and legs on the affected side of the body. Nutrition is essential for the proper growth and development for a child with spastic hemiplegia.

A thorough medical history and physical examination, including a neurological examination, are the first steps in making a diagnosis. This alone may be sufficient to diagnose Bell's Palsy, in the absence of other findings. Additional investigations may be pursued, including blood tests such as ESR for inflammation, and blood sugar levels for diabetes. If other specific causes, such as sarcoidosis or Lyme disease are suspected, specific tests such as angiotensin converting enzyme levels, chest x-ray or Lyme titer may be pursued. If there is a history of trauma, or a tumour is suspected, a CT scan may be used.

In the industrialized world, the incidence of overall cerebral palsy, which includes but is not limited to spastic diplegia, is about 2 per 1000 live births. Thus far, there is no known study recording the incidence of CP in the overall nonindustrialized world. Therefore, it is safe to assume that not all spastic CP individuals are known to science and medicine, especially in areas of the world where healthcare systems are less advanced. Many such individuals may simply live out their lives in their local communities without any medical or orthopedic oversight at all, or with extremely minimal such treatment, so that they are never able to be incorporated into any empirical data that orthopedic surgeons or neurosurgeons might seek to collect. It is shocking to note that—as with people with physical disability overall—some may even find themselves in situations of institutionalization, and thus barely see the outside world at all.

From what "is" known, the incidence of spastic diplegia is higher in males than in females; the Surveillance of Cerebral Palsy in Europe (SCPE), for example, reports a M:F ratio of 1.33:1. Variances in reported rates of incidence across different geographical areas in industrialized countries are thought to be caused primarily by discrepancies in the criteria used for inclusion and exclusion.

When such discrepancies are taken into account in comparing two or more registers of patients with cerebral palsy and also the extent to which children with mild cerebral palsy are included, the incidence rates still converge toward the average rate of 2:1000.

In the United States, approximately 10,000 infants and babies are born with CP each year, and 1200–1500 are diagnosed at preschool age when symptoms become more obvious. It is interesting to note that those with extremely mild spastic CP may not even be aware of their condition until much later in life: Internet chat forums have recorded men and women as old as 30 who were diagnosed only recently with their spastic CP.

Overall, advances in care of pregnant mothers and their babies has not resulted in a noticeable decrease in CP; in fact, because medical advances in areas related to the care of premature babies has resulted in a greater survival rate in recent years, it is actually "more" likely for infants with cerebral palsy to be born into the world now than it would have been in the past. Only the introduction of quality medical care to locations with less-than-adequate medical care has shown any decreases in the incidences of CP; the rest either have shown no change or have actually shown an increase. The incidence of CP increases with premature or very low-weight babies regardless of the quality of care.

Usually occurs within 2 periods:

1. With premature babies

2. full diagnosis usually between ages 2–5 years

Diplegia is usually not diagnosed before the age of 2 years yet the symptoms and signs of the earlier stages are typical and should enable the diagnosis to be made before the contractures have occurred. Parents suspecting diplegia should take their child to the doctor to potentially get an earlier diagnosis.

As age increases, spasticity makes for more noticeable effects in bones and joints and muscle function. This is often mistakenly said to mean that "spasticity increases as people with spastic CP age", which is a misrepresentation of the knock-on effects of spasticity with age. The clinical reality is that spasticity intensities remain constant but an increasing age in to middle-adulthood and the early elder years self-evidently changes the body structure, body response times and body adaptiveness capabilities markedly, leading to very different interplays between the body's spasticity and the body itself as the body 'degrades' across the twilight years.

That being said, cerebral palsy, including spastic cerebral palsy, is notable for a glaring overall research deficiency—the fact that it is one of the very few "major" groups of conditions on the planet in human beings for which medical science has not yet (as of 2011) collected wide-ranging empirical data on the development and experiences of young adults, the middle aged and older adults. An especially puzzling aspect of this lies in the fact that cerebral palsy as defined by modern science was first "discovered" and specifically addressed well over 100 years ago and that it would therefore be reasonable to expect by now that at least some empirical data on the adult populations with these conditions would have long since been collected, especially over the second half of the 20th century when existing treatment technologies rapidly improved and new ones came into being. The vast majority of empirical data on the various forms of cerebral palsy is concerned near-exclusively with children (birth to about 10 years of age) and sometimes pre-teens and early teens (11–13). Some doctors attempt to provide their own personal justifications for keeping their CP specialities purely paediatric, but there is no objectively apparent set of reasons backed by any scientific consensus as to why medical science has made a point of researching adult cases of multiple sclerosis, muscular dystrophy and the various forms of cancer in young and older adults, but has failed to do so with CP.

There is no known cure for cerebral palsy, however there is a large array of treatments proven effective at improving quality of life and relieving some of the symptoms associated with CP, especially SHCP. Some treatments are aimed at improving mobility, strengthening muscle and improving coordination. Although CP is due to permanent damage and is not progressive in nature, without treatment the symptoms can become worse, intensifying in pain and severity, and create complications that were not initially present. Some treatments are preventative measures to help prevent further complications, such as complete paralysis of the arm due to non-use and subsequent worsening hypertonia and joint contracture. Others forms of treatment are corrective in nature. Many treatments target symptoms that are indirectly related to or caused by the SHCP. Many of these treatments are common for other forms of CP as well. Treatment is individualized based on each case and the specific needs of the patient. Treatments are often combined with other forms of treatment and a long term treatment plan is created and continuously evaluated. Treatment can include the following:

- "Physical therapy" – Physical therapy is the most common form of treatment (source needed). It may include sensory stimulation, stretching, strengthening and positioning. Constraint-induced movement therapy is a newer form of physical therapy for SHCP that involves casting or splinting the unaffected arm to promote use of the affected arm (Taub). The theory behind constraint-induced movement therapy is that new neural pathways are created. Alternative forms of physical therapy include yoga and dance. Physical therapy may also include the use of braces while not actively involved with the therapist.

- "Occupational therapy" – Occupational therapy evaluates and treats patients through selected activities in order to enable people to function as effectively and independently as possible in daily life. Occupational therapy is geared toward the individual to achieve optimal results and performance while learning to cope with their disability.

- "Speech therapy" – Due to difficulties in speech, speech therapy is often necessary. Aside from helping with understanding language and increasing communication skills, speech therapists can also assist children that have difficulty eating and drinking.

- "Behavioral therapy" — Psychotherapy and counseling are heavily used in treatment of individuals with SHPD to help them cope emotionally with their needs and frustrations. Counseling through social work can be very beneficial for social issues and adjustments to society. Psychotherapy becomes a more important aspect of therapy when more serious issues such as depression become problematic. Play therapy is a common treatment for all young children with or without disabilities, but can be very useful helping children with SHCP. This therapy again is individualized geared to improve emotional and social development; reduce aggression; improve cooperation with others; assist a child in processing a traumatic event or prepare for an upcoming event such as surgery.

- "Surgery" – Although surgery may become necessary in some cases, physical therapy and the consistent use of braces can help mitigate the need for surgery. Surgical procedures are painful with long and difficult recoveries and do not cure the condition. Most common, is surgery that effectively lengthens the muscle. This type of surgery is usually performed on the legs, but can be performed on the arms as well. Surgeries also may be necessary to realign joints. Other, less popular surgical techniques try to reduce spasticity by severing selected overactive nerves that control muscles. This procedure, known as selective dorsal root rhizotomy, is still somewhat controversial, and is generally used only on the lower extremities of severe cases. Other experimental surgical techniques are also being investigated. The benefits of surgery can also be negated or reversed if the patient does not participate in physical therapy and braces (or casts) are not worn regularly.

- "Medicinal" – Medication targeting symptoms associated with spasticity is also a relatively new treatment that is utilized, but is still in the early stages of development. Drugs such as baclofen, benzodiazepines (e.g., diazepam), tizanidin, and sometimes dantrolene have shown promise in the effort to diminish spasticity. Botulinum toxin ("Botox") type A may reduce spasticity a few months at a time and has frequently been considered a beneficial treatment for children with SHCP and other forms of CP. Botox has been shown to be especially beneficial to reducing spasticity in the gastrocnemius (calf) muscle. This therapy can improve range of motion, reduce deformity, improve response to occupational and physical therapy, and delay the need for surgery. Botox injections have also shown advantages for upper extremities. There is still some doubt for the effectiveness, and some side effects to the relaxed muscles have been a loss of strength for patients with some muscle control. Casting, in conjunction with Botox injections may be an additional option for better results. Research is constantly investing in new improvements and more experimental therapy and treatment.

A variety of methods may be used to diagnose axillary nerve palsy. The health practitioner may examine the shoulder for muscle atrophy of the deltoid muscle. Furthermore, a patient can also be tested for weakness when asked to raise the arm. The deltoid extension lag sign test is one way to evaluate the severity of the muscle weakness. During this test, the physician stands behind the patient and uses the patient's wrist to elevate the arm. Then, the patient is told to hold this position without the doctor's assistance. If the patient cannot hold this position on their own and an angular drop occurs, the angular lag is observed as an indicator of axillary nerve palsy. When the shoulder is at its maximum extension, only the posterior area of the deltoid muscle and the axillary nerve are working to raise the arm. Therefore, no other muscles can provide compensation, which allows the test to be an accurate measure of the axillary nerve’s dysfunction.

Additional testing includes electromyography (EMG) and nerve conduction tests. However, these should not be done right after the injury because results will be normal. These tests must be executed weeks after the initial injury and onset of symptoms. An MRI (magnetic resonance imaging) or X-Ray may also be done by a doctor.

PBP is aggressive and relentless, and there were no treatments for the disease as of 2005. However, early detection of PBP is the optimal scenario in which doctors can map out a plan for management of the disease. This typically involves symptomatic treatments that are frequently used in many lower motor disorders.

The most common cause of diplegia in the legs is Cerebral Palsy. Paralysis of the legs may also be caused by trauma, injury, or genetics but this is very rare

Facial nerve paralysis may be divided into supranuclear and infranuclear lesions.

As a matter of everyday maintenance, muscle stretching, range of motion exercises, yoga, contact improvisation, modern dance, resistance training, and other physical activity regimens are often utilized by those with spastic CP to help prevent contractures and reduce the severity of symptoms.

Major clinical treatments for spastic diplegia are:

- Baclofen (and its derivatives), a gamma amino butyric acid (GABA) substitute in oral (pill-based) or intrathecal form. Baclofen is essentially chemically identical to the GABA that the damaged, over-firing nerves cannot absorb, except that it has an extra chemical 'marker' on it that makes the damaged nerves 'think' it is a different compound, and thus those nerves will absorb it. Baclofen is noted for being the sole medication available for GABA-deficiency-based spasticity which acts on the actual cause of the spasticity rather than simply reducing symptomatology as muscle relaxants and painkillers do. The intrathecal solution is a liquid injected into the spinal fluid for trial, and if successful in reducing spasticity, thereafter administered via an intrathecal pump, which has variously been proven potentially very dangerous on one or another level with long-term use (see article), including sudden and potentially lethal baclofen overdose, whereas the oral route, which comes in 10- or 20-milligram tablets and the dosage of which can be gently titrated either upward or downward, as well as safely ceased entirely, has not.

- Antispasmodic muscle relaxant chemicals such as tizanidine and botulinum toxin (Botox), injected directly into the spastic muscles; Botox wears off every three months.

- Phenol and similar chemical 'nerve deadeners', injected selectively into the over-firing nerves in the legs on the muscle end to reduce spasticity in their corresponding muscles by preventing the spasticity signals from reaching the legs; Phenol wears off every six months.

- Orthopedic surgery to release the spastic muscles from their hypertonic state, a usually temporary result because the spasticity source is the nerves, not the muscles; spasticity can fully reassert itself as little as one year post-surgery.

- Selective dorsal rhizotomy, a neurosurgery directly targeting and eliminating ("cutting" or "lesioning") the over-firing nerve rootlets and leaving the properly firing ones intact, thereby permanently eliminating the spasticity but compelling the person to spend months re-strengthening muscles that will have been severely weakened by the loss of the spasticity, due to the fact of those muscles not really having had actual strength to begin with.

Progressive Bulbar Palsy is slow in onset, with symptoms starting in most patients around 50–70 years of age. PBP has a life expectancy typically between 6 months and 3 years from onset of first symptoms. It is subtype of the Motor Neurone Diseases (MND) accounting for around 1 in 4 cases. Amyotrophic lateral sclerosis (ALS) is another sub-type. Pure PBP without any EMG or clinical evidence of abnormalities in the legs or arms is possible, albeit extremely rare. Moreover, about twenty-five percent of patients with PBP eventually develop the widespread symptoms common to ALS.

EMG &NCV can help to treatment with the diagnosis of the location and severity of the lesion.

As previously noted, there are often few signs of white matter injury in newborns. Occasionally, physicians can make the initial observations of extreme stiffness or poor ability to suckle. The preliminary diagnosis of PVL is often made using imaging technologies. In most hospitals, premature infants are examined with ultrasound soon after birth to check for brain damage. Severe white matter injury can be seen with a head ultrasound; however, the low sensitivity of this technology allows for some white matter damage to be missed. Magnetic resonance imaging (MRI) is much more effective at identifying PVL, but it is unusual for preterm infants to receive an MRI unless they have had a particularly difficult course of development (including repeated or severe infection, or known hypoxic events during or immediately after birth). No agencies or regulatory bodies have established protocols or guidelines for screening of at-risk populations, so each hospital or doctor generally makes decisions regarding which patients should be screened with a more sensitive MRI instead of the basic head ultrasound.

PVL is overdiagnosed by neuroimaging studies and the other white matter lesions of the brain are underestimated. It is important to differentiate PVL from the following major white matter lesions in the cerebral hemispheres: edematous hemorrhagic leukoencephalopathy (OGL), telentsefalny gliosis (TG), diffuse leukomalacia (DFL), subcortical leukomalacia (SL), periventricular hemorrhagic infarction (PHI), intracerebral hemorrhage ( ICH), multicystic encephalomalacia (ME), subendymal pseudocyst. Diffuse white matter lesions of the cerebral hemispheres of the brain, accompanied by softening and spreading to the central and subcortical areas are more likely DFL, PHI and ME.

Some babies recover on their own; however, some may require specialist intervention.

Neonatal/pediatric neurosurgery is often required for avulsion fracture repair. Lesions may heal over time and function return. Physiotherapeutic care is often required to regain muscle usage.

Although range of motion is recovered in many children under one year in age, individuals who have not yet healed after this point will rarely gain full function in their arm and may develop arthritis.

The three most common treatments for Erb's Palsy are: Nerve transfers (usually from the opposite arm or limb), Sub Scapularis releases and Latissimus Dorsi Tendon Transfers.

Nerve transfers are usually performed on babies under the age of 9 months since the fast development of younger babies increases the effectiveness of the procedure. They are not usually carried out on patients older than this because when the procedure is done on older infants, more harm than good is done and can result in nerve damage in the area where the nerves were taken from. Scarring can vary from faint scars along the lines of the neck to full "T" shapes across the whole shoulder depending on the training of the surgeon and the nature of the transplant.

Subscapularis releases, however, are not time limited. Since it is merely cutting a "Z" shape into the subscapularis muscle to provide stretch within the arm, it can be carried out at almost any age and can be carried out repeatedly on the same arm; however, this will compromise the integrity of the muscle.

Latissimus Dorsi Tendon Transfers involve cutting the Latissimus Dorsi in half horizontally in order to 'pull' part of the muscle around and attach it to the outside of the biceps. This procedure provides external rotation with varying degrees of success. A side effect may be increased sensitivity of the part of the biceps where the muscle will now lie, since the Latissimus Dorsi has roughly twice the number of nerve endings per square inch of other muscles.

Preventing or delaying premature birth is considered the most important step in decreasing the risk of PVL. Common methods for preventing a premature birth include self-care techniques (dietary and lifestyle decisions), bed rest, and prescribed anti-contraction medications. Avoiding premature birth allows the fetus to develop further, strengthening the systems affected during the development of PVL.

An emphasis on prenatal health and regular medical examinations of the mother can also notably decrease the risk of PVL. Prompt diagnosis and treatment of maternal infection during gestation reduces the likelihood of large inflammatory responses. Additionally, treatment of infection with steroids (especially in the 24–34 weeks of gestation) have been indicated in decreasing the risk of PVL.

It has also been suggested that avoiding maternal cocaine usage and any maternal-fetal blood flow alterations can decrease the risk of PVL. Episodes of hypotension or decreased blood flow to the infant can cause white matter damage.