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 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.

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.

Spastic quadriplegia is generally caused by brain damage or disruptions in normal brain development preceding birth. According to the National Institutes of Health, there are four types of brain damage that can cause spastic quadriplegia. These include, damage to the white matter (periventricular leukomalacia), abnormal brain development (cerebral dysgenesis), bleeding in the brain (intracranial hemorrhage), and brain damage due to lack of oxygen (hypoxic-ischemic encephalopathy or intrapartum asphyxia).

The white matter of the brain is especially vulnerable between the 26th and 34th weeks of maturation, and damage to the white matter can interfere with the brain’s ability to transmit signals to the rest of the body. Spastic quadriplegia can be caused by a condition known as periventricular leukomalacia which results in the formation of lesions and holes in the white matter of the brain.

Prior to the 26th week of maturation, the fetal brain is particularly susceptible to various toxins whose effects can ultimately hinder normal development. Exposure of the brain to infectious agents is especially dangerous because they can trigger immune responses that activate cytokines and lead to inflammation of the brain. Some infections that have been linked to the development of spastic quadriplegia include meningitis, herpes, rubella, and encephalitis. A difference in blood types between the mother and the fetus can also initiate a problematic immune response and cause brain damage. Severe jaundice, can also lead to brain damage and spastic quadriplegia due to a buildup of bilirubin in the blood.

Bleeding in the brain caused by fetal strokes, blood clots, weak and malformed blood vessels, or high maternal blood pressure may also lead to brain damage causing spastic quadriplegia. Maternal infection, most specifically pelvic inflammatory disease, has been shown to increase the risk of fetal stroke.

Hypoxia, lack of oxygen to the brain, can also cause damage in the cerebral motor cortex and other brain regions. This lack of oxygen can be the result of placenta malfunction, womb rupture, umbilical cord damage, low maternal blood pressure or asphyxia during labor and delivery.

Children who experienced many complications during birth, such as, prematurity, insufficient oxygen, low birthweight, aspiration, head injury, or bleeding in the brain have a greater risk of developing spastic quadriplegia. Children whose mothers were ill during the pregnancy or did not receive adequate nutrition are also more likely to develop the disease.

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.

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.

Although HSP is a progressive condition, the prognosis for individuals with HSP varies greatly. It primarily affects the legs although there can be some upperbody involvement in some individuals. Some cases are seriously disabling while others are less disabling and are compatible with a productive and full life. The majority of individuals with HSP have a normal life expectancy.

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.

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.

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.

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).

Worldwide, the prevalence of all hereditary spastic paraplegias combined is estimated to be 2 to 6 in 100,000 people. A Norwegian study of more than 2.5 million people published in March 2009 has found an HSP prevalence rate of 7.4/100,000 of population – a higher rate, but in the same range as previous studies. No differences in rate relating to gender were found, and average age at onset was 24 years. In the United States, Hereditary Spastic Paraplegia is listed as a "rare disease" by the Office of Rare Diseases (ORD) of the National Institutes of Health which means that the disorder affects less than 200,000 people in the US population.

Spastic quadriplegia, also known as spastic tetraplegia, is a subset of spastic cerebral palsy that affects all four limbs (both arms and legs).

Compared to quadriplegia, spastic tetraplegia is defined by spasticity of the limbs as opposed to strict paralysis. It is distinguishable from other forms of cerebral palsy in that those afflicted with the condition display stiff, jerky movements stemming from hypertonia of the muscles.

Spastic quadriplegia, while affecting all four limbs more or less equally, can still present parts of the body as stiffer than others, such as one arm being tighter than another arm, and so forth. Spastic triplegia, meanwhile, involves three limbs (such as one arm and two legs, or one leg and two arms, etc.); spastic diplegia affects two limbs (commonly just the legs), spastic hemiplegia affects one or another entire side of the body (left or right); and spastic monoplegia involves a single limb.

Triplegia is a medical condition characterized by the paralysis of three limbs (Triplegia Muscle Anatomy) . A person with triplegia can be referred to as triplegic. While there is no typical pattern of involvement, it is usually associated with paralysis of both legs and one arm — but can also involve both arms and one leg. Triplegia can sometimes by considered a combination of hemiplegia (paralysis of arm and leg of one side of the body) overlaying diplegia (paralysis of both legs), or as quadriplegia (paralysis of four limbs) with less involvement in one extremity.

The condition is commonly associated with cerebral palsy, although conditions such as stroke can also lead to it. Triplegia has also been found to be due to an increase in intracranial pressure associated with hydrocephalus resulting from traumatic brain injury.

A similar condition is triparesis, in which the patient suffers from paresis in three limbs, meaning that the limbs are very weak, but not completely paralyzed.

In a case reported only due to its rarity, triplegia was reported following a tonsillectomy (surgical removal of the tonsils). An eight-year-old male patient was sent to Willard Parker Hospital on August 12, 1929 and had been diagnosed with poliomyelitis. After an unrelated, and routine, tonsillectomy there was complete flaccid paralysis and loss of feeling in both the legs, right arm, and muscles in the trunk.

The prognosis for those with spastic muscles depends on multiple factors, including the severity of the spasticity and the associated movement disorder, access to specialised and intensive management, and ability of the affected individual to maintain the management plan (particularly an exercise program). Most people with a significant UMN lesion will have ongoing impairment, but most of these will be able to make progress. The most important factor to indicate ability to progress is seeing improvement, but improvement in many spastic movement disorders may not be seen until the affected individual receives help from a specialised team or health professional.

Doublecortin positive cells, Similar to stem cells, are extremely adaptable and, when extracted from a brain, cultured and then re-injected in a lesioned area of the same brain, they can help repair and rebuild it. The treatment using them would take some time to be available for general public use, as it has to clear regulations and trials.

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 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.

While moderate to severe traumatic brain injury is a risk for ALS, it is unclear if mild traumatic brain injury increases rates.

In 1994 the National Institute for Occupational Safety and Health (NIOSH) reported a nonsignificant increase in nervous system disorders due to four cases of ALS among National Football League (NFL) players. It was unclear if this was due to chance or not. Another study from 2012 also found a possible increase in ALS in NFL football players. An older study did not find an increased risk among high school football players. A 2007 review found an increased risk among soccer players. ALS may also occur more often among the US military veterans however the reason is unknown. This may be due to head injury.

After the 2012 report was released, some NFL players involved in the legal settlement with the NFL complained that the NFL, which initially agreed to pay $765 million, was not doing enough to help players. The judge in the case concurred, and the NFL then agreed to pay an unlimited amount of damages for players found to have ALS, Parkinson's disease, Alzheimer's disease and dementia.

About 5–10% of cases are directly inherited from a person's parents. Overall, first-degree relatives of an individual with ALS have a 1% risk of developing ALS.

A defect on chromosome 21, which codes for superoxide dismutase, is associated with about 20% of familial cases of ALS, or about 2% of ALS cases overall. This mutation is believed to be transmitted in an autosomal dominant manner, and has over a hundred different forms of mutation. The most common ALS-causing mutation is a mutant "SOD1" gene, seen in North America; this is characterized by an exceptionally rapid progression from onset to death. The most common mutation found in Scandinavian countries, D90A-SOD1, is more slowly progressive than typical ALS, and people with this form of the disorder survive for an average of 11 years.

In 2011, a genetic abnormality known as a hexanucleotide repeat was found in a region called C9orf72, which is associated with ALS combined with frontotemporal dementia ALS-FTD, and accounts for some 6% of cases of ALS among white Europeans.

Transverse myelitis is a neurological condition in which the spinal cord is inflamed. The inflammation damages nerve fibers, and causes them to lose their myelin coating leading to decreased electrical conductivity in the central nervous system. "Transverse" implies that the inflammation extends across the entire width of the spinal cord. Partial transverse myelitis and partial myelitis are terms used to define inflammation of the spinal cord that affects part of the width of the spinal cord.

Doublecortin (DCX or XLIS) mutations are responsible for X-linked disorders. While LIS1 mutations tend to cause severe malformations in the posterior brain, DCX mutations focus much of their destruction on anterior malformations and are linked to lissencephaly in males and subcortical band heterotopias in females. Women with DCX mutations tend to have an anteriorly-predominant subcortical band heterotopia and pachygyria.

Spastic

For details on the most common form of cerebral palsy, see spastic diplegia.

Spastic cerebral palsy is by far the most common type, occurring in 70% to 80% of all cases. Moreover, spastic CP accompanies one of the other types in 30% of all cases. People with this type are hypertonic and have a neuromuscular condition stemming from damage to the corticospinal tract or the motor cortex that affects the nervous system's ability to receive gamma amino butyric acid in the area(s) affected by the disability. Spastic CP is further classified by topography dependent on the region of the body affected; these include:

Spastic hemiplegia (one side being affected). Generally, injury to muscle-nerves controlled by the brain's left side will cause a right body deficit, and vice versa. Typically, people that have spastic hemiplegia are the most ambulatory, although they generally have dynamic equinus on the affected side and are primarily prescribed ankle-foot orthoses to prevent said equinus.[11]

Spastic diplegia (the lower extremities are affected with little to no upper-body spasticity). The most common form of the spastic forms. Most people with spastic diplegia are fully ambulatory and have a scissors gait. Flexed knees and hips to varying degrees are common. Hip problems, dislocations, and in three-quarters of spastic diplegics, also strabismus (crossed eyes), can be present as well. In addition, these individuals are often nearsighted. The intelligence of a person with spastic diplegia is unaffected by the condition.

Spastic tetraplegia (all four limbs affected equally). People with spastic quadriplegia are the least likely to be able to walk, or if they can, to want to walk, because their muscles are too tight and it is too much effort to do so. Some children with quadriplegia also have hemiparetic tremors, an uncontrollable shaking that affects the limbs on one side of the body and impairs normal movement.

Occasionally, terms such as monoplegia, paraplegia, triplegia, and pentaplegia may also be used to refer to specific manifestations of the spasticity.

The cause of polymicrogyria is unclear. It is currently classified as resulting from abnormalities during late neuronal migration or early cortical organization of fetal development. Evidence for both genetic and non-genetic causes exists. Polymicrogyria appears to occur around the time of neuronal migration or early cortical development. Non-genetic causes include defects in placental oxygenation and in association with congenital infections, particularly cytomegalovirus.

An association with the gene WDR62 has been identified.

Because pachygyria is a structural defect no treatments are currently available other than symptomatic treatments, especially for associated seizures. Another common treatment is a gastrostomy (insertion of a feeding tube) to reduce possible poor nutrition and repeated aspiration pneumonia.