About 2% of all CP cases are inherited, with glutamate decarboxylase-1 being one of the possible enzymes involved. Most inherited cases are autosomal recessive.

In babies that 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.

Approximately 2-2.5 per thousand children born in the western world have cerebral palsy, with increasing incidence in twin and premature births. Ataxic cerebral palsy accounts for 5 to 10% of all cases. The cause of cerebral palsy, in particular its ataxic subtype is unknown, but thought to be due to malformation or damage in the cerebellum and its many connections. The majority of cases that present malformation of the cerebellum are congenital, however acquired ataxic cerebral palsy can result from meningitis, trauma, birth complications, and encephalopathies (septic, acute, disseminated, and toxic). In addition, maternal viral infections may cause damage to the fetal brain due to increase in inflammatory cytokines produced during infection. Brain injury can occur during prenatal, perinatal, or postnatal periods. Most cases of cerebral palsy, approximately 80%, are acquired prenatally from unknown causes. Incidence increases with decreasing gestational period—fewer than 32 weeks of gestation and birth weight less than 5 Ib 8 oz or 2500g.

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.

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.

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

In some cases, spastic cerebral palsy is caused by genetic factors.

The genetic factors for spastic cerebral palsy include:

Although it has its origins in a brain injury, spastic CP can largely be thought of as a collection of orthopaedic and neuromuscular issues because of how it manifests symptomatically over the course of the person's lifespan. It is therefore not the same as "brain damage" and it need not be thought of as such. Spastic quadriplegia in particular, especially if it is combined with verbal speech challenges and strabismus, may be misinterpreted by the general population as alluding to cognitive dimensions to the disability atop the physical ones, but this is false; the intelligence of a person with any type of spastic CP is unaffected by the condition "of the spasticity itself".

In spastic cerebral palsy in children with low birth weights, 25% of children had hemiplegia, 37.5% had quadriplegia, and 37.5% had diplegia.

The incidence of cerebral palsy has increased in the past 40 years. It has been estimated that in the United States cerebral palsy occurs in 4 out every 1000 births. Of these births about 20–30% of them have spastic hemiplegia. Spasticity overall, is the more common type of cerebral palsy, whereas as non-spastic cerebral palsy is less common. Studies show that spastic type cerebral palsy is on the rise, and the occurrence of diplegia type is decreasing. The prevalence of cerebral palsy is higher in areas of low socioeconomic status. This could potentially be because cerebral palsy incidence increases as birth weight decreases.

There are several ways of getting diplegia in the arms. It is very common for people with Cerebral Palsy to have diplegia of the arms. Although most people with Cerebral Palsy have diplegia in their legs, some people have diplegia in their arms. Other ways of getting paralysis of both arms is through a traumatic event or injury.

The number of new cases of Bell's palsy is about 20 per 100,000 population per year. The rate increases with age. Bell’s palsy affects about 40,000 people in the United States every year. It affects approximately 1 person in 65 during a lifetime.

A range of annual incidence rates have been reported in the literature: 15, 24, and 25–53 (all rates per 100,000 population per year). Bell’s palsy is not a reportable disease, and there are no established registries for people with this diagnosis, which complicates precise estimation.

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.

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.

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.

Spastic diplegia's particular type of brain damage inhibits the proper development of upper motor neuron function, impacting the motor cortex, the basal ganglia and the corticospinal tract. Nerve receptors in the spine leading to affected muscles become unable to properly absorb gamma amino butyric acid (GABA), the amino acid that regulates muscle tone in humans. Without GABA absorption to those particular nerve rootlets (usually centred, in this case, around the sectors L1-S1 and L2-S2), affected nerves (here, the ones controlling the legs) perpetually fire the message for their corresponding muscles to permanently, rigidly contract, and the muscles become permanently hypertonic (spastic).

The abnormally high muscle tone that results creates lifelong difficulty with all voluntary and passive movement in the legs, and in general creates stress over time—depending on the severity of the condition in the individual, the constant spasticity ultimately produces pain, muscle/joint breakdown including tendinitis and arthritis, premature physical exhaustion (i.e., becoming physically exhausted even when you internally know that you have more energy than you are able to use), contractures, spasms, and progressively worse deformities/mis-alignments of bone structure around areas of the tightened musculature as the person's years progress. Severe arthritis, tendinitis, and similar breakdown can start as early as the spastic diplegic person's mid-20s (as a comparison, typical people with normal muscle tone are not at risk of arthritis, tendinitis, and similar breakdown until well into their 50s or 60s, if even then).

No type of CP is officially a progressive condition, and indeed spastic diplegia does not clinically "get worse" given the nerves, damaged permanently at birth, neither recover nor degrade. This aspect is clinically significant because other neuromuscular conditions with similar surface characteristics in their presentations, like most forms of multiple sclerosis, indeed do degrade the body over time and do involve actual progressive worsening of the condition, including the spasticity often seen in MS. However, spastic diplegia is indeed a chronic condition; the symptoms themselves cause compounded effects on the body that are typically just as stressful on the human body as a progressive condition is. Despite this reality and the fact that muscle tightness is the symptom of spastic diplegia and not the cause, symptoms rather than cause are typically seen as the primary area of focus for treatment, especially surgical treatment, except when a selective dorsal rhizotomy is brought into consideration, or when an oral baclofen regimen is attempted.

Unlike any other condition that may present with similar effects, spastic diplegia is entirely congenital in origin—that is, it is almost always acquired shortly before or during a baby's birth process. Things like exposure to toxins, traumatic brain injury, encephalitis, meningitis, drowning, or suffocation do not tend to lead to spastic diplegia in particular or even cerebral palsy generally. Overall, the most common cause of spastic diplegia is Periventricular leukomalacia, more commonly known as neonatal asphyxia or infant hypoxia—a sudden in-womb shortage of oxygen-delivery through the umbilical cord. This sudden lack of oxygen is also almost always combined with premature birth, a phenomenon that, even by itself, would inherently risk the infant developing some type of CP. On the other hand, the presence of certain maternal infections during pregnancy such as congenital rubella syndrome can also lead to spastic diplegia, since such infections can have similar end results to infant hypoxia.

The severity of impairment and related prognosis is dependent on the location and severity of brain lesions. Up to 50% of patients will achieve some degree of ambulation. Speech problems, such as dysarthria, are common to these patients.

The cause of PBP is unknown. One form of PBP is found to occur within patients that have a CuZn-superoxide dismutase (SOD1) mutation. Progressive bulbar palsy patients that have this mutation are classified with FALS patients, Familial ALS (FALS) accounts for about 5%-10% of all ALS cases and is caused by genetic factors. Within these, about 20-25% are linked to the SOD1 mutation. It is not currently known if and how the decreased SOD1 activity contributes to Progressive Bulbar Palsy or FALS, and studies are being done in patients and transgenic mice to help further understand the impact of this gene on the disease.

A case study was done on a 42-year-old woman who complained of muscle weakness 10 months prior to admission in the hospital. Upon neurological examination, the patient showed muscle atrophy, fasciculation in all limbs and decreased deep tendon reflexes. The patient’s older brother, father, and paternal uncle had previously all died of ALS or an ALS type syndrome. The patient developed Progressive Bulbar Palsy, became dependent on a respirator, and had two episodes of cardiac arrest. The patient died from pneumonia two years after the onset of the disease. After studying the patient, it was found that the patient had a two base pair deletion in the 126th codon in exon 5 of the SOD1 gene. This mutation produced a frameshift mutation, which led to a stop codon at position 131. SOD1 activity was decreased by about 30%. The patient’s histological examination showed severe reduction in lower motor neurons. Upon further study, this case proved to be important because it demonstrated that SOD1 mutations might not effect steady neuropathological changes, and that environmental and genetic factors might affect the phenotype of the SOD1 mutations.

CP in general is a non-progressive, neurological condition that results from brain injury and malformation occurring before cerebral development is complete. ADCP is associated with injury and malformations to the extrapyramidal tracts in the basal ganglia or the cerebellum. Lesions to this region principally arise via hypoxic ischemic brain injury (HIBI) or bilirubin encephalopathy.

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.

Other causes may include:

- Diabetes mellitus

- Facial nerve paralysis, sometimes bilateral, is a common manifestation of sarcoidosis of the nervous system, neurosarcoidosis.

- Bilateral facial nerve paralysis may occur in Guillain–Barré syndrome, an autoimmune condition of the peripheral nervous system.

- Moebius syndrome is a bilateral facial paralysis resulting from the underdevelopment of the VII cranial nerve (facial nerve), which is present at birth. The VI cranial nerve, which controls lateral eye movement, is also affected, so people with Moebius syndrome cannot form facial expression or move their eyes from side to side. Moebius syndrome is extremely rare, and its cause or causes are not known.

Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus. The facial nucleus itself can be affected by infarcts of the pontine arteries.

The facial nerve is the seventh of 12 cranial nerves. This cranial nerve controls the muscles in the face. Facial nerve palsy is more abundant in older adults than in children and is said to affect 15-40 out of 100,000 people per year. This disease comes in many forms which include congenital, infectious, traumatic, neoplastic, or idiopathic. The most common cause of this cranial nerve damage is Bell's palsy (idiopathic facial palsy) which is a paralysis of the facial nerve. Although Bell's palsy is more prominent in adults it seems to be found in those younger than 20 or older than 60 years of age. Bell's Palsy is thought to occur by an infection of the herpes virus which may cause demyelination and has been found in patients with facial nerve palsy. Symptoms include flattening of the forehead, sagging of the eyebrow, and difficulty closing the eye and the mouth on the side of the face that is affected. The inability to close the mouth causes problems in feeding and speech. It also causes lack of taste, acrimation, and sialorrhea.

The use of steroids can help in the treatment of Bell's Palsy. If in the early stages, steroids can increase the likelihood of a full recovery. This treatment is used mainly in adults. The use of steroids in children has not been proven to work because they seem to recover completely with or without them. Children also tend to have better recovery rates than older adults. Recovery rate also depends on the cause of the facial nerve palsy (e.g. infections, perinatal injury, congenital dysplastic). If the palsy is more severe patients should seek steroids or surgical procedures. Facial nerve palsy may be the indication of a severe condition and when diagnosed a full clinical history and examination are recommended.

Although rare, facial nerve palsy has also been found in patients with HIV seroconversion. Symptoms found include headaches (bitemporal or occipital), the inability to close the eyes or mouth, and may cause the reduction of taste. Few cases of bilateral facial nerve palsy have been reported and is said to only effect 1 in every 5 million per year.

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.

The most common cause of Erb's palsy is dystocia, an abnormal or difficult childbirth or labor. For example, it can occur if the infant's head and neck are pulled toward the side at the same time as the shoulders pass through the birth canal. The condition can also be caused by excessive pulling on the shoulders during a cephalic presentation (head first delivery), or by pressure on the raised arms during a breech (feet first) delivery. Erb's palsy can also affect neonates affected by a clavicle fracture unrelated to dystocia.

A similar injury may be observed at any age following trauma to the head and shoulder, which cause the nerves of the plexus to violently stretch, with the upper trunk of the plexus sustaining the greatest injury. Injury may also occur as the result of direct violence, including gunshot wounds and traction on the arm, or attempting to diminish shoulder joint dislocation. The level of damage to the constituent nerves is related to the amount of paralysis.

Klumpke's paralysis (or Klumpke's palsy or Dejerine–Klumpke palsy) is a variety of partial of the lower roots of the brachial plexus. The brachial plexus is a network of spinal nerves that originates in the back of the neck, extends through the axilla (armpit), and gives rise to nerves to the upper limb. (see picture - click to enlarge). It is named after Augusta Déjerine-Klumpke.

The fetal and neonatal brain is a rapidly changing, developing structure. Because neural structures are still developing and connections are still being formed at birth, many medications that are successful for treatment and protection in the adult central nervous system (CNS) are ineffective in infants. Moreover, some adult treatments have actually been shown to be toxic to developing brains.