The site and type of brachial plexus injury determine the prognosis. Avulsion and rupture injuries require timely surgical intervention for any chance of recovery. For milder injuries involving buildup of scar tissue and for neurapraxia, the potential for improvement varies, but there is a fair prognosis for spontaneous recovery, with a 90–100% return of function.

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.

Brachial plexus injury is found in both children and adults, but there is a difference between children and adults with BPI.

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

Anatomically, damage to the axillary nerve or suppression of it causes the palsy. This suppression, referred to as entrapment, causes the nerve pathway to become smaller and impulses cannot move through the nerve as easily. Furthermore, if trauma causes damage to the myelin sheath, or injures the nerve another way, this will also reduce the ability of nerve impulse flow.

Usually, an outside force is acting to suppress the nerve, or cause nerve damage. Most commonly, shoulder dislocation or fractions in the shoulder can cause the palsy. Contact sports such as football and hockey can cause the injury Other cases have been caused by repeated crutch pressure or injuries accidentally caused by health professionals (iatrogenesis). Furthermore, following an anterior shoulder operation; damage to the axillary nerve is possible and has been documented by various surgeons, thus causing axillary nerve palsy. Other possible causes include: deep infection, pressure from a cast or splint, fracture of the humerus, or nerve disorders in which the nerves become inflamed.

There are rare causes of axillary nerve palsy that do occur. For instance, axillary nerve palsy can occur after there is blunt trauma in the shoulder area without any sort of dislocation or fracture. Examples of this blunt trauma may include: being hit by heavy an object, falling on shoulder, a strong blow while participating in boxing, or motor vehicle accidents. Another rare cause of axillary nerve palsy can occur after utilizing a side birthing position. When the patient lies on their side for a strenuous amount of time, they can develop axillary nerve palsy. This rare complication of labor can occur due to the prolonged pressure on the axillary nerve while in a side-birth position. Some patients who are diagnosed with nodular fasciitis may develop axillary nerve palsy if the location of the rapid growth is near the axilla. In the case of Nodular Fasciitis, a fibrous band or the growth of a schwannoma can both press against the nerve, causing axillary nerve palsy.

An injury to the axillary nerve normally occurs from a direct impact of some sort to the outer arm, though it can result from injuring a shoulder via dislocation or compression of the nerve. The axillary nerve comes from the posterior cord of the brachial plexus at the coracoid process and provides the motor function to the deltoid and teres minor muscles. An EMG can be useful in determining if there is an injury to the axillary nerve. The largest numbers of axillary nerve palsies arise due to stretch injuries which are caused by blunt trauma or iatrogenesis. Axillary nerve palsy is characterized by the lack of shoulder abduction greater than 30 degrees with or without the loss of sense in the low two thirds of the shoulder. Normally the patients that have axillary nerve palsy are involved in blunt trauma and have a number of shoulder injuries. Surgery is not always required to solve the problem (information from: Midha, Rajiv, Zager, Eric. Surgery of Peripheral Nerves: A Case-Based Approach. Thieme Medical Publishers, Inc. 2008.)

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 appearance of the affected arm (or arms) depends on the individual case. In some cases the arm may lack the ability to straighten or rotate but otherwise function normally giving the overall appearance of the arm to be stiff and crooked. Whereas in other circumstances the arm has little to no control and has a "loose" appearance. Treatment such as physiotherapy, massage and electrical stimulation can help to prevent this early on (or throughout) the patient's life by strengthening the arm.

In some cases, again, individuals may suffer a great deal of discomfort. For example, they may experience a severe cramping pain that lasts for some time and is particularly painful after they have slept, running from the shoulder all the way down to the wrist. Although pain does not affect everyone with Erb's Palsy, it can be extremely uncomfortable to those that it does and can even cause patients to be physically sick or faint. This extreme nerve pain is mostly common during the final stages of growth and almost always eases off in time. Other pains that Erb's Palsy sufferers might endure include strained muscle, stiffness, circulatory problems and cramp. Different factors are dependent on the severity of the condition and can vary, so whilst some patient experience a lot of pain, some patients may experience no pain at all and for their affected arm to simply be visually crooked.

Discomfort with the shoulder blade is also extremely common in Erb's palsy as the shoulder is often at risk of dislocation. This can result, again, in sickness or lack of sleep.

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.

Klumpke Palsy is listed as a 'rare disease' by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH). This means that Klumpke palsy, or a subtype of Klumpke palsy, affects fewer than 200,000 people in the US population.

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.

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.

Most people with Bell's palsy start to regain normal facial function within 3 weeks—even those who do not receive treatment. In a 1982 study, when no treatment was available, of 1,011 patients, 85% showed first signs of recovery within 3 weeks after onset. For the other 15%, recovery occurred 3–6 months later. After a follow-up of at least 1 year or until restoration, complete recovery had occurred in more than two-thirds (71%) of all patients. Recovery was judged moderate in 12% and poor in only 4% of patients. Another study found that incomplete palsies disappear entirely, nearly always in the course of one month. The patients who regain movement within the first two weeks nearly always remit entirely. When remission does not occur until the third week or later, a significantly greater part of the patients develop sequelae. A third study found a better prognosis for young patients, aged below 10 years old, while the patients over 61 years old presented a worse prognosis.

Major complications of the condition are chronic loss of taste (ageusia), chronic facial spasm, facial pain and corneal infections. To prevent the latter, the eyes may be protected by covers, or taped shut during sleep and for rest periods, and tear-like eye drops or eye ointments may be recommended, especially for cases with complete paralysis. Where the eye does not close completely, the blink reflex is also affected, and care must be taken to protect the eye from injury.

Another complication can occur in case of incomplete or erroneous regeneration of the damaged facial nerve. The nerve can be thought of as a bundle of smaller individual nerve connections that branch out to their proper destinations. During regrowth, nerves are generally able to track the original path to the right destination - but some nerves may sidetrack leading to a condition known as synkinesis. For instance, regrowth of nerves controlling muscles attached to the eye may sidetrack and also regrow connections reaching the muscles of the mouth. In this way, movement of one also affects the other. For example, when the person closes the eye, the corner of the mouth lifts involuntarily.

Around 9% of patients have some sort of sequelae after Bell's palsy, typically the synkinesis already discussed, or spasm, contracture, tinnitus and/or hearing loss during facial movement or crocodile tear syndrome. This is also called gustatolacrimal reflex or Bogorad's Syndrome and involves the sufferer shedding tears while eating. This is thought to be due to faulty regeneration of the facial nerve, a branch of which controls the lacrimal and salivary glands. Gustatorial sweating can also occur.

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.

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.

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.

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.

Klumpke's paralysis is a form of paralysis involving the muscles of the forearm and hand, resulting from a brachial plexus injury in which the eighth cervical (C8) and first thoracic (T1) nerves are injured either before or after they have joined to form the lower trunk. The subsequent paralysis affects, principally, the intrinsic muscles of the hand (notably the interossei, thenar and hypothenar muscles) and the flexors of the wrist and fingers (notably flexor carpi ulnaris and ulnar half of the flexor digitorum profundus). Forearm pronators and wrist flexors may be involved, as may dilators of the iris and elevators of the eyelid (both of which may be seen in the case of associated Horner's syndrome). The classic presentation of Klumpke's palsy is the “claw hand” where the forearm is supinated and the wrist and fingers are flexed. If Horner syndrome is present, there is miosis (constriction of the pupils) in the affected eye.

The injury can result from difficulties in childbirth. The most common aetiological mechanism is caused by a traumatic vaginal delivery. The risk is greater when the mother is small or when the infant is of large weight. Risk of injury to the lower brachial plexus results from traction on an abducted arm, as with an infant being pulled from the birth canal by an extended arm above the head or with someone catching himself by a branch as he falls from a tree. Lower brachial plexus injuries should be distinguished from upper brachial plexus injuries, which can also result from birth trauma but give a different syndrome of weakness known as Erb's palsy.

Other trauma, such as motorcycle accidents, that have similar spinal cord injuries to C-8 & T-1, also show the same symptom's of Klumpke's paralysis.

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 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.

In many cases recovery happens spontaneously and no treatment is needed. This spontaneous recovery can occur because distance between the injury location and the deltoid muscle is small. Spontaneous recovery may take as long as 12 months.

In order to combat pain and inflammation of nerves, medication may be prescribed.

Surgery is an option, but it has mixed results within the literature and is usually avoided because only about half of people who undergo surgery see any positive results from it. Some suggest that surgical exploration should be considered if no recovery occurs after 3 to 6 months. Some surgical options include nerve grafting, neurolysis, or nerve reconstruction. Surgery results are typically better for younger patients (under 25) and for nerve grafts less than six centimeters.

For some, recovery does not occur and surgery is not possible. In these cases, most patients’ surrounding muscles can compensate, allowing them to gain a satisfactory range of motion back. Physical therapy or Occupational therapy will help retrain and gain muscle tone back.

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.

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.

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.

Medical procedures are the most common cause of injury to the spinal accessory nerve. In particular, radical neck dissection and cervical lymph node biopsy are among the most common surgical procedures that result in spinal accessory nerve damage. London notes that a failure to rapidly identify spinal accessory nerve damage may exacerbate the problem, as early intervention leads to improved outcomes.

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.