A quarter of all people with Guillain–Barré syndrome develop weakness of the breathing muscles leading to respiratory failure, the inability to breathe adequately to maintain healthy levels of oxygen and/or carbon dioxide in the blood. This life-threatening scenario is complicated by other medical problems such as pneumonia, severe infections, blood clots in the lungs and bleeding in the digestive tract in 60% of those who require artificial ventilation.

The first symptoms of Guillain–Barré syndrome are numbness, tingling, and pain, alone or in combination. This is followed by weakness of the legs and arms that affects both sides equally and worsens over time. The weakness can take half a day to over two weeks to reach maximum severity, and then becomes steady. In one in five people, the weakness continues to progress for as long as four weeks. The muscles of the neck may also be affected, and about half experience involvement of the cranial nerves which supply the head and face; this may lead to weakness of the muscles of the face, swallowing difficulties and sometimes weakness of the eye muscles. In 8%, the weakness affects only the legs (paraplegia or paraparesis). Involvement of the muscles that control the bladder and anus is unusual. In total, about a third of people with Guillain–Barré syndrome continue to be able to walk. Once the weakness has stopped progressing, it persists at a stable level ("plateau phase") before improvement occurs. The plateau phase can take between two days and six months, but the most common duration is a week. Pain-related symptoms affect more than half, and include back pain, painful tingling, muscle pain and pain in the head and neck relating to irritation of the lining of the brain.

Many people with Guillain–Barré syndrome have experienced the signs and symptoms of an infection in the 3–6 weeks prior to the onset of the neurological symptoms. This may consist of upper respiratory tract infection (rhinitis, sore throat) or diarrhea.

In children, particularly those younger than six years old, the diagnosis can be difficult and the condition is often initially mistaken (sometimes for up to two weeks) for other causes of pains and difficulty walking, such as viral infections, or bone and joint problems.

On neurological examination, characteristic features are the reduced power and reduced or absent tendon reflexes (hypo- or areflexia, respectively). However, a small proportion has normal reflexes in affected limbs before developing areflexia, and some may have exaggerated reflexes. In the "Miller Fisher variant" subtype of Guillain–Barré syndrome (see below), a triad of weakness of the eye muscles, abnormalities in coordination, as well as absent reflexes can be found. The level of consciousness is normally unaffected in Guillain–Barré syndrome, but the Bickerstaff brainstem encephalitis subtype may feature drowsiness, sleepiness, or coma.

In order to diagnose Bickerstaff brainstem encephalitis, ataxia and ophthalmoplegia must be present. These are also diagnostic features of Miller Fisher syndrome, and so Bickerstaff's is only diagnosed if other features are present which exclude Miller Fisher syndrome. These may include drowsiness, coma or hyperreflexia. When the condition is defined in this way, a number of other features are commonly but not always found: among these are weakness of the limbs, the face, and/or the bulbar muscles; abnormalities of the pupils; and absent reflexes.

Like some other autoimmune diseases, the condition usually follows a minor infection, such as a respiratory tract infection or gastroenteritis.

Bickerstaff brainstem encephalitis is a rare inflammatory disorder of the central nervous system, first described by Edwin Bickerstaff in 1951. It may also affect the peripheral nervous system, and has features in common with both Miller Fisher syndrome and Guillain–Barré syndrome.

A patient presenting with Hyper IgM syndrome may be affected by simple infectious organisms in exposed regions like the respiratory system. Vaccination against pathogenic organisms may not help these individuals, because vaccinating them does not properly stimulate production of antibodies. Symptoms can include:

- Fever (recurrent infections)

- Low counts of IgA, IgG and IgE antibodies

- CD40L not reactive in T cells

- Recurrent sinopulmonary and GI infections with pyogenic bacteria and opportunistic organisms, and cutaneous manifestations including pyodermas extensive warts.

Gleich's syndrome or episodic angioedema with eosinophilia is a rare disease in which the body swells up episodically (angioedema), associated with raised antibodies of the IgM type and increased numbers of eosinophil granulocytes, a type of white blood cells, in the blood (eosinophilia). It was first described in 1984.

Its cause is unknown, but it is unrelated to capillary leak syndrome (which may cause similar swelling episodes) and eosinophilia-myalgia syndrome (which features eosinophilia but alternative symptoms). Some studies have shown that edema attacks are associated with degranulation (release of enzymes and mediators from eosinophils), and others have demonstrated antibodies against endothelium (cells lining blood vessels) in the condition.

Gleich's syndrome is not a form of the idiopathic hypereosinophilic syndrome in that there is little or no evidence that it leads to organ damage. Rather, recent studies report that a subset of T cells (a special form of lymphocyte blood cell) found in several Gleich syndrome patients have an abnormal immunophenotype, i.e. they express CD3-, CD4+ cluster of differentiation cell surface antigens. These same aberrant T cell immunophenotypes are found in lymphocyte-variant eosinophilia, a disease in which the aberrant T cells overproduce cytokines such as interleukin 5 which simulate the proliferation of eosinophil precursor cells and are thereby responsible for the eosinophilia. It is suggested that most forms of Gleich's syndrome are due to a similar aberrant T cell mechanism and are a subtype of lymphocyte-variant eosinophilia.

Gleich syndrome has a good prognosis. Attack severity may improve with steroid treatment.

Hyper IgM Syndrome Type 1 (HIGM-1) is the X-linked variant of the Hyper-IgM syndrome. The affected individuals are virtually always male, because males only have one X chromosome, received from their mothers. Their mothers are not symptomatic, even though they are carriers of the allele, because the trait is recessive. Male offspring of these women have a 50% chance of inheriting their mother's mutant allele.

The following is a list of common signs and symptoms found with neonatal meningitis.

- Fever

- poor appetite

- anterior fontanelle bulging

- seizure

- jitteriness

- dyspnea

- irritability

- anorexia

- vomiting

- diarrhea

- abdominal distention (increase in abdominal size)

- neck rigidity

- cyanosis

- jaundice

- and sunset eyes (downward gaze of the eyes)

- abnormal body temperature (hypo-or hyperthermia)

- change of activity (lethargy or irritability)

Unfortunately these symptoms are unspecific and may point to many different conditions.

Neonatal meningitis is a serious medical condition in infants. Meningitis is an inflammation of the meninges (the protective membranes of the central nervous system (CNS)) and is more common in the neonatal period (infants less than 44 days old) than any other time in life and is an important cause of morbidity and mortality globally. Mortality is roughly half in developing countries and ranges from 8%-12.5% in developed countries.

Symptoms seen with neonatal meningitis are often unspecific that may point to several conditions, such as sepsis (whole body inflammation). These can include fever, irritability, and dyspnea. The only method to determine if meningitis is the cause of these symptoms is lumbar puncture (LP; an examination of the cerebrospinal fluid).

The most common causes of neonatal meningitis is bacterial infection of the blood, known as bacteremia (specifically Group B "Streptococci" (GBS; "Streptococcus agalactiae"), "Escherichia coli", and "Listeria monocytogenes"). Although there is a low mortality rate in developed countries, there is a 50% prevalence rate of neurodevelopmental disabilities in "E. coli" and GBS meningitis, while having a 79% prevalence for non-"E. coli" Gram-negative caused meningitis. Delayed treatment of neonatal meningitis may cause include cerebral palsy, blindness, deafness, and learning deficiencies.

Clinical features of CRPS have been found to be inflammation resulting from the release of certain pro-inflammatory chemical signals from the nerves, sensitized nerve receptors that send pain signals to the brain, dysfunction of the local blood vessels' ability to constrict and dilate appropriately, and maladaptive neuroplasticity.

The signs and symptoms of CRPS usually initially manifest near the site of a (typically minor) injury. The most common symptoms are pain sensations, including burning, stabbing, grinding, and throbbing. Moving or touching the limb is often intolerable. The patient may also experience muscle spasms; local swelling; extreme sensitivity to things such as wind and water, touch and vibrations; abnormally increased sweating; changes in skin temperature (usually hot but sometimes cold) and color (bright red or a reddish violet); softening and thinning of bones; joint tenderness or stiffness; changes in nail and hair growth and/or restricted or painful movement. Drop attacks (falls), almost fainting, and fainting spells are infrequently reported, as are visual problems. The symptoms of CRPS vary in severity and duration. Since CRPS is a systemic problem, potentially any organ can be affected.

The pain of CRPS is continuous although varies in severity. It is widely recognized that it can be heightened by emotional or physical stress.

Previously it was considered that CRPS had three stages; it is now believed that people affected by CRPS do not progress through these stages sequentially. These stages may not be time-constrained and could possibly be event-related, such as ground-level falls or re-injuries of previously damaged areas. Thus, rather than a progression of CRPS from bad to worse, it is now thought, instead, that such individuals are likely to have one of the three following types of disease progression:

1. "Stage" one is characterized by severe, burning pain at the site of the injury, muscle spasms, joint stiffness, restricted mobility, rapid hair and nail growth, and vasospasm. The vasospasm is that which causes the changes in the color and temperature of the skin. Some may experience hyperhydrosis (increased sweating). In mild cases this stage lasts a few weeks, in which it can subside spontaneously or respond rapidly to treatment (physical therapy, pain specialist).

2. "Stage" two is characterized by more intense pain. Swelling spreads, hair growth diminishes, nails become cracked, brittle, grooved and spotty, osteoporosis becomes severe and diffuse, joints thicken, and muscles atrophy.

3. "Stage" three is characterized by irreversible changes in the skin and bones, while the pain becomes unyielding and may involve the entire limb. There is marked muscle atrophy, severely limited mobility of the affected area, and flexor tendon contractions (contractions of the muscles and tendons that flex the joints). Occasionally the limb is displaced from its normal position, and marked bone softening and thinning is more dispersed.

Zika virus infections have been strongly associated with Guillain–Barré syndrome (GBS), which is a rapid onset of muscle weakness caused by the immune system damaging the peripheral nervous system, and which can progress to paralysis. While both GBS and Zika infection can simultaneously occur in the same individual, it is difficult to definitively identify Zika virus as the cause of GBS. Several countries affected by Zika outbreaks have reported increases in the rate of new cases of GBS. During the 2013–2014 outbreak in French Polynesia there were 42 reported cases of GBS over a 3-month period, compared to between 3 and 10 annually prior to the outbreak.

Most people who are infected have no or few symptoms. Otherwise the most common signs and symptoms of Zika fever are fever, rash, conjunctivitis (red eyes), muscle and joint pain, and headache, which are similar to signs and symptoms of dengue and chikungunya fever. The time from a mosquito bite to developing symptoms is not yet known, but is probably a few days to a week. The disease lasts for several days to a week and is usually mild enough that people do not have to go to a hospital.

Due to being in the same family as dengue, there has been concern that it could cause similar bleeding disorders. However that has only been documented in one case, with blood seen in semen, also known as hematospermia.

Camisa disease (or Vohwinkel variant with ichthyosis) is the variant form of Vohwinkel syndrome, characterized by ichthyosis and normal hearing.

It is associated with loricrin.

It was characterized in 1984 and 1988.

Complex regional pain syndrome (CRPS), also known as reflex sympathetic dystrophy (RSD), is a long term pain syndrome that often worsens with time. It is characterized by severe pain out of proportion to the original injury and is often accompanied by sensitivity, swelling, and changes in the skin. It may initially affect one limb and then spread throughout the body; 35% of affected people report symptoms throughout their whole body.

The cause of CRPS is unknown though CRPS is associated with dysregulation of the central nervous system and autonomic nervous system resulting in abnormal temperature control and pain of the affected limb(s) resulting in functional impairment and disability. Precipitating factors include injury and surgery, although there are cases where no identifiable injury had occurred at the original site. CRPS is not caused by psychological factors, yet the constant pain and reduced quality of life are known to cause psychological problems (such as increased depression and anxiety). Although "research does not reveal support for specific personality or psychopathology predictors of the condition," CRPS is associated with psychosocial effects, including impaired social and occupational function. It is classified as an amplified musculoskeletal pain syndrome.

Treatment involves a multidisciplinary approach involving medications, physical and occupational therapy, psychological treatments, and neuromodulation. Despite this, the results are often unsatisfactory, especially if treatment is delayed.

Inflammatory demyelinating diseases (IDDs), sometimes called Idiopathic (IIDDs) because the unknown etiology of some of them, and sometimes known as borderline forms of multiple sclerosis, is a collection of multiple sclerosis variants, sometimes considered different diseases, but considered by others to form a spectrum differing only in terms of chronicity, severity, and clinical course.

Multiple Sclerosis for some people is a syndrome more than a single disease. It can be considered among the acquired demyelinating syndromes with a multiphasic instead of monophasic behaviour. Multiple sclerosis also has a prodromal stage in which an unknown underlying condition, able to damage the brain, is present, but no lesion has still developed.

Progressive inflammatory neuropathy (PIN) is a disease that was identified in a report, released on January 31, 2008, by the Centers for Disease Control and Prevention. The first known outbreak of this neuropathy occurred in southeastern Minnesota in the United States. The disease was reported among pig slaughterhouse workers who appeared at various care facilities in the area reporting similar neurological symptoms. The disease was later identified at pork processing plants in Indiana and Nebraska as well. The condition is characterized by acute paralysis, pain, fatigue, numbness, and weakness, especially in extremities. It was initially believed that workers might have contracted the disease through inhaling aerosols from pig brains blown through a compressed-air hose and that this exposure to pig neural tissue induced an autoimmune response that might have produced their mysterious peripheral neuropathy. These suspicions were confirmed in reports and investigations conducted at the Mayo Clinic in Rochester, Minnesota.

Over 40 laboratory tests were initially conducted to rule out various pathogens and environmental toxins. These tests were used to try to identify potential viruses carried by humans, pigs, or both, including rotoviruses, adenoviruses, hepatitis A, and hepatitis E. They also tried to identify bacteria such as salmonella and escherichia coli (e. coli), and parasites such as Giardia and cryptosporidium that could be causing the symptoms. All were ruled out.

Neurodegenerative diseases were considered specifically because of the similarity of symptoms and animal involvement thus included investigation of prion associated diseases such as bovine spongiform encephalopathy (BSE), chronic wasting disease (CWD), and variant Creutzfeldt–Jakob disease (vCJD). These all have highly transmissible pathogenic agents that induce brain damage. Since no pathogenic agent had been found, these diseases were ruled out as being related.

Next two very similar neuropathies were ruled out. Guillain–Barré syndrome (GBS) induces an acute autoimmune response which affects the Schwann cells in the peripheral nervous system. GBS is usually triggered by an infection that causes weakness and tingling that may lead to muscle loss. This condition may be life-threatening if muscle atrophy ascends to affect the pulmonary or cardiac systems. So far, no infectious agents have been found that relate to the current disease, progressive infammatory neuropathy. They looked at chronic inflammatory demyelinating polyneuropathy (CIDP) which is characterized by progressive weakness and sensory impairment in the arms and legs. Damage occurs to the myelin sheath in the peripheral nervous system. As doctors at the Mayo Clinic were beginning to note, the problem they were seeing in progressive inflammatory neuropathy was occurring in the spinal nerve roots.

The conjunctiva provides lining for the inside of the eyelid as well as a coating for the sclera, the white portion of the eyeball. It typically serves to provide lubrication for the eye through the production of mucus and tears. When infected with AHC, patients will experience painful, red eyes, swelling of the conjunctival tissue, and frequent mucus discharge from the eyes accompanied by excessive tearing and subconjunctival hemorrhaging. This hemorrhaging is caused by the rupture of blood vessels beneath the conjunctiva giving the eyes a bright red appearance. Some patients also experience blurry vision and fever in addition to the common symptoms and one in every ten thousand cases exhibits paralysis similar to that of polio.

The presence of anti-MOG autoantibodies has been associated with the following conditions

- Some cases of aquaporin-4-seronegative neuromyelitis optica: NMO derived from an antiMOG associated encephalomyelitis,

- Some cases of acute disseminated encephalomyelitis, specially the recurrent ones (MDEM)

- Some cases of multiple sclerosis

- isolated optic neuritis or transverse myelitis

- Recurrent optic neuritis. The repetition of an idiopatic optic neuritis is considered a distinct clinical condition, and it has been found to be associated with anti-MOG autoantibodies

The anti-mog spectrum in children is equally variated: Out of a sample of 41 children with MOG-antibodies 29 had clinical NMOSD (17 relapsing), 8 had ADEM (4 relapsing with ADEM-ON), 3 had a single clinical event CIS, and 1 had a relapsing tumefactive disorder. Longitudinal myelitis was evident on MRI in 76[percent]. It has also been noted that percentage of children with anti-mog antibodies respect a demyelinating sample is higher than for adults

Acute hemorrhagic conjunctivitis (AHC) (also spelled acute haemorrhagic conjunctivitis) is a derivative of the highly contagious conjunctivitis virus, otherwise known as pink eye. Symptoms include excessively red, swollen eyes as well as subconjuntival hemorrhaging. Currently, there is no known treatment and patients are required to merely endure the symptoms while the virus runs its five- to seven-day course. While it was first identified in Ghana, the virus has now been seen in China, India, Egypt, Cuba, Singapore, Taiwan, Japan, Pakistan, Thailand, and the United States.

The initial scratch or wound caused by a bite from a carrier rodent results in mild inflammatory reactions and ulcerations. The wounds may heal initially, but reappear with the onset of symptoms. The symptoms include recurring fever, with body temperature 101–104°F (38–40°C). The fever lasts for 2–4 days, but recurs generally at 4–8 weeks. This cycle may continue for months or years. The other symptoms include regional lymphadenitis, malaise, and headache. The complications include myocarditis, endocarditis, hepatitis, splenomegaly, and meningitis.

Affected individuals typically develop symptoms including high fevers, shaking, chills, fatigue, headaches, vomiting, and general illness within 48 hours of the initial infection. The erythematous skin lesion enlarges rapidly and has a sharply demarcated, raised edge. It appears as a red, swollen, warm, and painful rash, similar in consistency to an orange peel. More severe infections can result in vesicles (pox or insect bite-like marks), blisters, and petechiae (small purple or red spots), with possible skin necrosis (death). Lymph nodes may be swollen, and lymphedema may occur. Occasionally, a red streak extending to the lymph node can be seen.

The infection may occur on any part of the skin, including the face, arms, fingers, legs, and toes; it tends to favour the extremities. Fat tissue and facial areas, typically around the eyes, ears, and cheeks, are most susceptible to infection. Repeated infection of the extremities can lead to chronic swelling (lymphangitis).

The signs of sepsis are non-specific and include:

- Body temperature changes

- Breathing problems

- Diarrhea

- Low blood sugar (hypoglycemia)

- Reduced movements

- Reduced sucking

- Seizures

- Bradycardia

- Swollen belly area

- Vomiting

- Yellow skin and whites of the eyes (jaundice)

A heart rate above 160 can also be an indicator of sepsis, this tachycardia can present up to 24 hours before the onset of other signs.

It is characterized by a deficiency in biliary copper excretion that causes deformations in the skeleton. These include projections on the back of the skull (parasagittal bone exostoses arising from the occipital bone—the so-called "occipital horns") as well as deformities of the elbow, radial head dislocation, hammer-shaped lateral ends of the clavicles, and abnormalities of the hips and pelvis.

OHS presents in early to middle childhood. Children may present with features such as:

Erysipelas is an acute infection typically with a skin rash, usually on any of the legs and toes, face, arms, and fingers. It is an infection of the upper dermis and superficial lymphatics, usually caused by beta-hemolytic group A "Streptococcus" bacteria on scratches or otherwise infected areas. Erysipelas is more superficial than cellulitis, and is typically more raised and demarcated. The term is from Greek ἐρυσίπελας, meaning "red skin".