In 1950, William Hammon at the University of Pittsburgh purified the gamma globulin component of the blood plasma of polio survivors. Hammon proposed the gamma globulin, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. The results of a large clinical trial were promising; the gamma globulin was shown to be about 80 percent effective in preventing the development of paralytic poliomyelitis. It was also shown to reduce the severity of the disease in patients who developed polio. Due to the limited supply of blood plasma gamma globulin was later deemed impractical for widespread use and the medical community focused on the development of a polio vaccine.

Paralytic poliomyelitis may be clinically suspected in individuals experiencing acute onset of flaccid paralysis in one or more limbs with decreased or absent tendon reflexes in the affected limbs that cannot be attributed to another apparent cause, and without sensory or cognitive loss.

A laboratory diagnosis is usually made based on recovery of poliovirus from a stool sample or a swab of the pharynx. Antibodies to poliovirus can be diagnostic, and are generally detected in the blood of infected patients early in the course of infection. Analysis of the patient's cerebrospinal fluid (CSF), which is collected by a lumbar puncture ("spinal tap"), reveals an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level. Detection of virus in the CSF is diagnostic of paralytic polio, but rarely occurs.

If poliovirus is isolated from a patient experiencing acute flaccid paralysis, it is further tested through oligonucleotide mapping (genetic fingerprinting), or more recently by PCR amplification, to determine whether it is "wild type" (that is, the virus encountered in nature) or "vaccine type" (derived from a strain of poliovirus used to produce polio vaccine). It is important to determine the source of the virus because for each reported case of paralytic polio caused by wild poliovirus, an estimated 200 to 3,000 other contagious asymptomatic carriers exist.

The CDC MMWR report advised, "To prevent infections in general, persons should stay home if they are ill, wash their hands often with soap and water, avoid close contact (such as touching and shaking hands) with those who are ill, and clean and disinfect frequently touched surfaces."

Unlike polio, acute flaccid myelitis can not currently be prevented with a vaccine.

Incomplete spinal cord injuries result in varied post injury presentations. There are three main syndromes described, depending on the exact site and extent of the lesion.

1. The central cord syndrome: most of the cord lesion is in the gray matter of the spinal cord, sometimes the lesion continues in the white matter.

2. The Brown–Séquard syndrome: hemi section of the spinal cord.

3. The anterior cord syndrome: a lesion of the anterior horns and the anterolateral tracts, with a possible division of the anterior spinal artery.

For most patients with ASIA A (complete) tetraplegia, ASIA B (incomplete) tetraplegia and ASIA C (incomplete) tetraplegia, the International Classification level of the patient can be established without great difficulty. The surgical procedures according to the International Classification level can be performed. In contrast, for patients with ASIA D (incomplete) tetraplegia it is difficult to assign an International Classification other than International Classification level X (others). Therefore, it is more difficult to decide which surgical procedures should be performed. A far more personalized approach is needed for these patients. Decisions must be based more on experience than on texts or journals.

The results of tendon transfers for patients with complete injuries are predictable. On the other hand, it is well known that muscles lacking normal excitation perform unreliably after surgical tendon transfers. Despite the unpredictable aspect in incomplete lesions tendon transfers may be useful. The surgeon should be confident that the muscle to be transferred has enough power and is under good voluntary control. Pre-operative assessment is more difficult to assess in incomplete lesions.

Patients with an incomplete lesion also often need therapy or surgery before the procedure to restore function to correct the consequences of the injury. These consequences are hypertonicity/spasticity, contractures, painful hyperesthesias and paralyzed proximal upper limb muscles with distal muscle sparing. Spasticity is a frequent consequence of incomplete injuries. Spasticity often decreases function, but sometimes a patient can control the spasticity in a way that it is useful to their function. The location and the effect of the spasticity should be analyzed carefully before treatment is planned. An injection of Botulinum toxin (Botox) into spastic muscles is a treatment to reduce spasticity. This can be used to prevent muscle shorting and early contractures.

Over the last ten years an increase in traumatic incomplete lesions is seen, due to the better protection in traffic.

Delayed diagnosis of cervical spine injury has grave consequences for the victim. About one in 20 cervical fractures are missed and about two-thirds of these patients have further spinal-cord damage as a result. About 30% of cases of delayed diagnosis of cervical spine injury develop permanent neurological deficits. In high-level cervical injuries, total paralysis from the neck can result. High-level tetraplegics (C4 and higher) will likely need constant care and assistance in activities of daily living, such as getting dressed, eating and bowel and bladder care. Low-level tetraplegics (C5 to C7) can often live independently.

Even with "complete" injuries, in some rare cases, through intensive rehabilitation, slight movement can be regained through "rewiring" neural connections, as in the case of the late actor Christopher Reeve.

In the case of cerebral palsy, which is caused by damage to the motor cortex either before, during (10%), or after birth, some people with tetraplegia are gradually able to learn to stand or walk through physical therapy.

Quadriplegics can improve muscle strength by performing resistance training at least three times per week. Combining resistance training with proper nutrition intake can greatly reduce co-morbidities such as obesity and type 2 diabetes.

Diagnosis of post-polio syndrome can be difficult, since the symptoms are hard to separate from complications due to the original poliomyelitis infection, and from the normal infirmities of aging. There is no laboratory test for post-polio syndrome, nor are there any other specific diagnostic criteria. Three important criteria are recognized, including: previous diagnosis of polio, long interval after recovery and the gradual onset of weakness.

In general, PPS is a diagnosis of exclusion whereby other possible causes of the symptoms are eliminated. Neurological examination aided by other laboratory studies can help to determine what component of a neuromuscular deficit occurred with polio and what components are new and to exclude all other possible diagnoses. Objective assessment of muscle strength in PPS patients may not be easy. Changes in muscle strength are determined in specific muscle groups using various muscle scales which quantify strength, such as the Medical Research Council (MRC) scale. Magnetic resonance imaging (MRI), neuroimaging, and electrophysiological studies, muscle biopsies, or spinal fluid analysis may also be useful in establishing a PPS diagnosis.

Six of ten children in Denver were sent home for outpatient treatment; some with mild symptoms have recovered from temporary limb weakness, while the fate of those more severely affected remains unclear. Intensive physical therapy and occupational therapy may be beneficial for recovery.

The diagnosis of viral meningitis is made by clinical history, physical exam, and several diagnostic tests. Most importantly, cerebrospinal fluid (CSF) is collected via lumbar puncture (also known as spinal tap). This fluid, which normally surrounds the brain and spinal cord, is then analyzed for signs of infection. CSF findings that suggest a viral cause of meningitis include an elevated white blood cell count (usually 10-100 cells/µL) with a lymphocytic predominance in combination with a normal glucose level. Increasingly, cerebrospinal fluid PCR tests have become especially useful for diagnosing viral meningitis, with an estimated sensitivity of 95-100%. Additionally, samples from the stool, urine, blood and throat can also help to identify viral meningitis.

In certain cases, a CT scan of the head should be done before a lumbar puncture such as in those with poor immune function or those with increased intracranial pressure.

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.

Because symptoms of ALS can be similar to those of a wide variety of other, more treatable diseases or disorders, appropriate tests must be conducted to exclude the possibility of other conditions. One of these tests is electromyography (EMG), a special recording technique that detects electrical activity in muscles. Certain EMG findings can support the diagnosis of ALS. Another common test measures nerve conduction velocity (NCV). Specific abnormalities in the NCV results may suggest, for example, that the person has a form of peripheral neuropathy (damage to peripheral nerves) or myopathy (muscle disease) rather than ALS. While a magnetic resonance imaging (MRI) is often normal in people with early stage ALS, it can reveal evidence of other problems that may be causing the symptoms, such as a spinal cord tumor, multiple sclerosis, a herniated disk in the neck, syringomyelia, or cervical spondylosis.

Based on the person's symptoms and findings from the examination and from these tests, the physician may order tests on blood and urine samples to eliminate the possibility of other diseases, as well as routine laboratory tests. In some cases, for example, if a physician suspects the person may have a myopathy rather than ALS, a muscle biopsy may be performed.

Viral infectious diseases such as human immunodeficiency virus (HIV), human T-cell leukemia virus (HTLV), Lyme disease, syphilis and tick-borne encephalitis can in some cases cause ALS-like symptoms. Neurological disorders such as multiple sclerosis, post-polio syndrome, multifocal motor neuropathy, CIDP, spinal muscular atrophy, and spinal and bulbar muscular atrophy can also mimic certain aspects of the disease and should be considered.

ALS must be differentiated from the "ALS mimic syndromes" which are unrelated disorders that may have a similar presentation and clinical features to ALS or its variants. Because of the prognosis carried by this diagnosis and the variety of diseases or disorders that can resemble ALS in the early stages of the disease, people with ALS symptoms should always obtain a specialist neurological opinion in order to rule out alternative diagnoses. Myasthenic syndrome, also known as Lambert–Eaton syndrome, can mimic ALS, and its initial presentation can be similar to that of myasthenia gravis (MG), a treatable autoimmune disease sometimes mistaken for ALS.

Benign fasciculation syndrome is another condition that mimics some of the early symptoms of ALS but is accompanied by normal EMG readings and no major disablement.

Most cases of ALS, however, are correctly diagnosed, with the error rate of diagnosis in large ALS clinics is less than 10%. One study examined 190 people who met the MND/ALS diagnostic criteria, complemented with laboratory research in compliance with both research protocols and regular monitoring. Thirty of these people (16%) had their diagnosis completely changed during the clinical observation development period. In the same study, three people had a false negative diagnosis of MG, which can mimic ALS and other neurological disorders, leading to a delay in diagnosis and treatment. MG is eminently treatable; ALS is not.

No test can provide a definite diagnosis of ALS, although the presence of upper and lower motor neuron signs in a single limb is strongly suggestive. Instead, the diagnosis of ALS is primarily based on the symptoms and signs the physician observes in the person and a series of tests to rule out other diseases. Physicians obtain the person's full medical history and usually conduct a neurologic examination at regular intervals to assess whether symptoms such as muscle weakness, atrophy of muscles, hyperreflexia, and spasticity are worsening.

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.

It has been proposed that viral meningitis might lead to inflammatory injury of the vertebral artery wall.

The Meningitis Research Foundation is conducting a study to see if new genomic techniques can the speed, accuracy and cost of diagnosing meningitis in children in the UK. The research team will develop a new method to be used for the diagnosis of meningitis, analysing the genetic material of microorganisms found in CSF (cerebrospinal fluid). The new method will first be developed using CSF samples where the microorganism is known, but then will be applied to CSF samples where the microorganism is unknown (estimated at around 40%) to try and identify a cause.

In general, PPS is not life-threatening. The major exception are patients left with severe residual respiratory difficulties, who may experience new severe respiratory impairment. Studies have shown that, compared to control populations, PPS patients lack any elevation of antibodies against the poliovirus, and because no poliovirus is excreted in the feces, it is not considered a recurrence of the original polio. Further, there is no evidence that the poliovirus can cause a persistent infection in humans. PPS has been confused with amyotrophic lateral sclerosis (ALS), which progressively weakens muscles. PPS patients do not have an elevated risk of ALS.

There have been no sufficient longitudinal studies on the prognosis of post-polio syndrome; however, speculations have been made by several physicians based on experience. Fatigue and mobility usually return to normal over a long period of time. The prognosis also differs depending upon different causes and factors affecting the individual. An overall mortality rate of 25 percent exists due to possible respiratory paralysis of persons with post-polio syndrome; otherwise, post-polio syndrome is usually non-lethal.

Prognosis can be abruptly changed for the worse by the use of anesthesia, such as during surgery.

Rubella virus specific IgM antibodies are present in people recently infected by rubella virus, but these antibodies can persist for over a year, and a positive test result needs to be interpreted with caution. The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.

Currently, the commonly accepted international standard for the clinical case definition is the one published by the International Pediatric MS Study Group, revision 2007.

Diagnosis of pseudobulbar palsy is based on observation of the symptoms of the condition. Tests examining jaw jerk and gag reflex can also be performed. It has been suggested that the majority of patients with pathological laughter and crying have pseudobulbar palsy due to bilateral corticobulbar lesions and often a bipyrimidal involvement of arms and legs. To further confirm the condition, MRI can be performed to define the areas of brain abnormality.

Standard titer measles vaccine is recommended at 9 months of age in low-income countries where measles infection is endemic and often fatal. Many observational studies have shown that measles-vaccinated children have substantially lower mortality than can be explained by the prevention of measles-related deaths. Many of these observational studies were natural experiments, such as studies comparing the mortality before and after the introduction of measles vaccine and other studies where logistical factors rather than maternal choice determined whether a child was vaccinated or not.

These findings were later supported in randomized trials from 2003 to 2009 in Guinea-Bissau. An intervention group of children given standard titer measles vaccine at 4.5 and 9 month of age had a 30% reduction in all-cause mortality compared to the children in the control group, which were only vaccinated against measles at 9 month of age.

In a recent WHO-commissioned review based on four randomized trials and 18 observational studies, it was concluded that "There was consistent evidence of a beneficial effect of measles vaccine, although all observational studies were assessed as being at risk of bias and the GRADE rating was of low confidence. There was an apparent difference between the effect in girls and boys, with girls benefitting more from measles vaccination", and furthermore "estimated effects are in the region of a halving of mortality risk" and "if these effects are real then they are not fully explained by deaths that were established as due to measles". Based on the evidence, the WHO's Strategic Advisory Group of Experts on Immunization concluded that "the non-specific effects on all-cause mortality warrant further research".

The live attenuated BCG vaccine developed against tuberculosis has been shown to have strong beneficial effects on the ability to combat non-tuberculosis infections.

Several studies have suggested that BCG vaccination may reduce atopy, particularly when given early in life. Furthermore, in multiple observational studies BCG vaccination has been shown to provide beneficial effects on overall mortality. These observations encouraged randomised controlled trials to examine BCG vaccination's beneficial non-specific effects on overall health. Since BCG vaccination is recommended to be given at birth in countries that have a high incidence of tuberculosis it would have been unethical to randomize children into 'BCG' vs. 'no BCG' groups. However, many low-income countries delay BCG vaccination for low-birth-weight (LBW) infants; this offered the opportunity to directly test the effect of BCG on overall mortality.

In the first two randomised controlled trials receipt of BCG+OPV at birth vs. OPV only ('delayed BCG') was associated with strong reductions in neonatal mortality; these effects were seen as early as 3 days after vaccination. BCG protected against sepsis as well as respiratory infections.

Among BCG vaccinated children, those who develop a BCG scar or a positive skin test (TST) are less likely to develop sepsis and exhibit an overall reduction in child mortality of around 50%.

In a recent WHO-commissioned review based on five clinical trials and nine observational studies, it was concluded that "the results indicated a beneficial effect of BCG on overall mortality in the first 6–12 months of life. Relevant follow-up in some of the trials was short, and all of the observational studies were regarded as being at risk of bias, so the confidence in the findings was rated as very low according to the GRADE criteria and "There was a suggestion that BCG vaccination may be more beneficial the earlier it is given". Furthermore, "estimated effects are in the region of a halving of mortality risk" and "any effect of BCG vaccine on all-cause mortality is not likely to be attributable to any great extent to fewer deaths from tuberculosis (i.e. to a specific effect of BCG vaccine against tuberculosis)". Based on the evidence, the WHO's Strategic Group of Experts on Immunization concluded that "the non-specific effects on all-cause mortality warrant further research".

Most patients reported in the literature have been given treatments suitable for autoimmune neurological diseases, such as corticosteroids, plasmapheresis and/or intravenous immunoglobulin, and most have made a good recovery. The condition is too rare for controlled trials to have been undertaken.

Anti-GQ1b antibodies are found in two-thirds of patients with this condition. This antibody is also found in almost all cases of Miller Fisher syndrome. The EEG is often abnormal, but shows only slow wave activity, which also occurs in many other conditions, and so is of limited value in diagnosis. Similarly, raised CSF protein levels and pleocytosis are frequent but non-specific. It was originally thought that raised CSF protein without pleocytosis ('albuminocytological dissociation') was a characteristic feature, as it is in Guillain–Barré syndrome, but this has not been supported in more recent work. In only 30% of cases is a MRI brain scan abnormal. Nerve conduction studies may show an axonal polyneuropathy.

Infantile Progressive Bulbar palsy is a rare type of progressive bulbar palsy that occurs in children. The disease exists in both rapid and slow onsets, and involves inflammation of the gray matter of the bulb. Infantile PBP is a disease that manifests itself in two forms: Fazio Londe syndrome (FL) and Brown-Vialetto-Van-Laere syndrome (BVVL).

Rubella infections are prevented by active immunisation programs using live attenuated virus vaccines. Two live attenuated virus vaccines, RA 27/3 and Cendehill strains, were effective in the prevention of adult disease. However their use in prepubertal females did not produce a significant fall in the overall incidence rate of CRS in the UK. Reductions were only achieved by immunisation of all children.

The vaccine is now usually given as part of the MMR vaccine. The WHO recommends the first dose be given at 12 to 18 months of age with a second dose at 36 months. Pregnant women are usually tested for immunity to rubella early on. Women found to be susceptible are not vaccinated until after the baby is born because the vaccine contains live virus.

The immunisation program has been quite successful. Cuba declared the disease eliminated in the 1990s, and in 2004 the Centers for Disease Control and Prevention announced that both the congenital and acquired forms of rubella had been eliminated from the United States.

Screening for rubella susceptibility by history of vaccination or by serology is recommended in the United States for all women of childbearing age at their first preconception counseling visit to reduce incidence of congenital rubella syndrome (CRS). It is recommended that all susceptible non-pregnant women of childbearing age should be offered rubella vaccination. Due to concerns about possible teratogenicity, use of MMR vaccine is not recommended during pregnancy. Instead, susceptible pregnant women should be vaccinated as soon as possible in the postpartum period.

In regards to the diagnosis of spinal and bulbar muscular atrophy, the "AR Xq12" gene is the focus. Many mutations are reported and identified as missense/nonsense, that can be identified with 99.9% accuracy. Test for this gene in the majority of affected patients yields the diagnosis.

A diagnosis usually can be made by the presenting signs and symptoms alone. If the diagnosis is unclear, a throat swab or stool specimen may be taken to identify the virus by culture. The common incubation period (the time between infection and onset of symptoms) ranges from three to six days. Early detection of HFMD is important in preventing an outbreak in the pediatric population.