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.

Patients with stiff person syndrome (SPS) suffer progressive stiffness in their truncal muscles, which become rigid and stiff because the lumbar and abdominal muscles engage in constant contractions. Initially, stiffness occurs in the thoracolumbar paraspinal and

abdominal muscles. It later affects the proximal leg and abdominal wall muscles. The stiffness leads to a change in posture, and patients develop a rigid gait. Persistent lumbar hyperlordosis often occurs as it progresses. The muscle stiffness initially fluctuates, sometimes for days or weeks, but eventually begins to consistently impair mobility. As the disease progresses, patients sometimes become unable to walk or bend. Chronic pain is common and worsens over time but sometimes acute pain occurs as well. Stress, cold weather, and infections lead to an increase in symptoms, and sleep decreases them.

SPS patients suffer superimposed spasms and extreme sensitivity to touch and sound. These spasms primarily occur in the proximal limb and axial muscles. There are co-contractions of agonist and antagonist muscles. Spasms usually last for minutes and can recur over hours. Attacks of spasms are unpredictable and are often caused by fast movements, emotional distress, or sudden sounds or touches. In rare cases, facial muscles, hands, feet, and the chest can be affected and unusual eye movements and vertigo occur. There are brisk stretch reflexes and clonus occurs in patients. Late in the disease's progression, hypnagogic myoclonus can occur. Tachycardia and hypertension are sometimes also present.

Because of the spasms, patients may become increasingly fearful, require assistance, and lose the ability to work, leading to depression, anxiety, and phobias, including agoraphobia and dromophobia. Most patients are psychologically normal and respond reasonably to their situations.

Paraneoplastic SPS tends to affect the neck and arms more than other variations. It progresses very quickly, is more painful, and is more likely to include distal pain than classic SPS. Patients with paraneoplastic SPS generally lack other autoimmune issues but may have other paraneoplastic conditions.

Stiff-limb syndrome is a variant of SPS. This syndrome develops into full SPS about 25 percent of the time. Stiffness and spasms are usually limited to the legs and hyperlordoisis generally does not occur. The stiffness begins in one limb and remains most prominent there. Sphincter and brainstem issues often occur with stiff-limb syndrome. Progressive encephalomyelitis with rigidity, another variant of the condition, includes symptoms of SPS with brainstem issues and autonomic disturbances. It involves polio-encephalomyelitis in the spine and brainstem. There is cerebellar and brainstem involvement. In some cases, the limbic system is affected, as well. Most patients have upper motoneuron issues and autonomic disturbances. Jerking man syndrome or jerking SPS is another subtype of the condition. It begins like classical SPS and progresses for several years, up to 14 in some cases. It is then distinguished by the development of myoclonus as well as seizures and ataxia in some cases.

Stiff person syndrome (SPS), also known as stiff man syndrome (SMS), is a rare neurologic disorder of unclear cause characterized by progressive rigidity and stiffness. The stiffness primarily affects the truncal muscles and is superimposed by spasms, resulting in postural deformities. Chronic pain, impaired mobility, and lumbar hyperlordosis are common symptoms.

SPS occurs in about one in a million people and is most commonly found in middle-aged people. A small minority of patients have the paraneoplastic variety of the condition. Variants of the condition, such as stiff-limb syndrome which primarily affects a specific limb, are often seen.

SPS was first described in 1956. Diagnostic criteria were proposed in the 1960s and refined two decades later. In the 1990s and 2000s the roles of antibodies in the condition became more clear. SPS patients generally have GAD antibodies, which seldom occur in the general population. In addition to blood to tests for GAD, electromyography tests can help confirm the condition's presence.

Benzodiazepine-class drugs are the most common treatment; they are used for symptom relief from stiffness. Other common treatments include Baclofen, intravenous immunoglobin and rituximab. There has been limited but encouraging success with stem-cell treatment.

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.

There are several types of immune-mediated neuropathies recognised. These include

- Chronic inflammatory demyelinating polyneuropathy (CIPD) with subtypes:

- Classical CIDP

- CIDP with diabetes

- CIDP/monoclonal gammopathy of undetermined significance

- Sensory CIDP

- Multifocal motor neuropathy

- Multifocal acquired demyelinating sensory and motor neuropathy (Lewis-Sumner syndrome)

- Multifocal acquired sensory and motor neuropathy

- Distal acquired demyelinating sensory neuropathy

- Guillain-Barre syndrome with subtypes:

- Acute inflammatory demyelinating polyradiculoneuropathy

- Acute motor axonal neuropathy

- Acute motor and sensory axonal neuropathy

- Acute pandysautonomia

- Miller Fisher syndrome

- IgM monoclonal gammopathies with subtypes:

- Waldenstrom's macroglobulinemia

- Mixed cryoglobulinemia, gait ataxia, late-onset polyneuropathy syndrome

- Myelin-associated glycoprotein-associated gammopathy, polyneuropathy, organomegaly, endocrinopathy, M-protein and skin changes syndrome (POEMS)

For this reason a diagnosis of chronic inflammatory demyelinating polyneuropathy needs further investigations.

The diagnosis is usually provisionally made through a clinical neurological examination. Patients usually present with a history of weakness, numbness, tingling, pain and difficulty in walking. They may additionally present with fainting spells while standing up or burning pain in extremities. Some patients may have sudden onset of back pain or neck pain radiating down the extremities, usually diagnosed as radicular pain. These symptoms are usually progressive and may be intermittent.

Autonomic system dysfunction can occur; in such a case, the patient would complain of orthostatic dizziness, problems breathing, eye, bowel, bladder and cardiac problems. The patient may also present with a single cranial nerve or peripheral nerve dysfunction.

On examination the patients may have weakness, and loss of deep tendon reflexes (rarely increased or normal). There may be atrophy (shrinkage) of muscles, fasciculations (twitching) and loss of sensation. Patients may have multi-focal motor neuropathy, as they have no sensory loss.

Most experts consider the necessary duration of symptoms to be greater than 8 weeks for the diagnosis of CIDP to be made.

Typical diagnostic tests include:

- Electrodiagnostics – electromyography (EMG) and nerve conduction study (NCS). In usual CIDP, the nerve conduction studies show demyelination. These findings include:

1. a reduction in nerve conduction velocities;

2. the presence of conduction block or abnormal temporal dispersion in at least one motor nerve;

3. prolonged distal latencies in at least two nerves;

4. absent F waves or prolonged minimum F wave latencies in at least two motor nerves. (In some case EMG/NCV can be normal).

- Serum test to exclude other autoimmune diseases.

- Lumbar puncture and serum test for anti-ganglioside antibodies. These antibodies are present in the branch of CIDP diseases comprised by anti-GM1, anti-GD1a, and anti-GQ1b.

- Sural nerve biopsy; biopsy is considered for those patients in whom the diagnosis is not completely clear, when other causes of neuropathy (e.g., hereditary, vasculitic) cannot be excluded, or when profound axonal involvement is observed on EMG.

- Ultrasound of the periferal nerves may show swelling of the affected nerves

- MRI can also be used in the diagnosic workup

In some cases electrophysiological studies fail to show any evidence of demyelination. Though conventional electrophysiological diagnostic criteria are not met, the patient may still respond to immunomodulatory treatments. In such cases, presence of clinical characteristics suggestive of CIDP are critical, justifying full investigations, including sural nerve biopsy.

Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated inflammatory disorder of the peripheral nervous system. The disorder is sometimes called chronic relapsing polyneuropathy (CRP) or chronic inflammatory demyelinating polyradiculoneuropathy (because it involves the nerve roots). CIDP is closely related to Guillain–Barré syndrome and it is considered the chronic counterpart of that acute disease. Its symptoms are also similar to progressive inflammatory neuropathy. An asymmetrical variant of CIDP is known as Lewis-Sumner Syndrome.

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.

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.

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.

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.

The most common and defining features of BGS are craniosynostosis and radial ray deficiency. The observations of these features allow for a diagnosis of BGS to be made, as these symptoms characterize the syndrome. Craniosynostosis involves the pre-mature fusion of bones in the skull. The coronal craniosynostosis that is commonly seen in patients with BGS results in the fusion of the skull along the coronal suture. Because of the changes in how the bones of the skull are connected together, people with BGS will have an abnormally shaped head, known as brachycephaly. Features commonly seen in those with coronal craniosynostosis are bulging eyes, shallow eye pockets, and a prominent forehead. Radial ray deficiency is another clinical characteristic of those with BGS, and results in the under-development (hypoplasia) or the absence (aplasia) of the bones in the arms and the hands. These bones include the radius, the carpal bones associated with the radius and the thumb. Oligodactyly can also result from radial ray deficiency, meaning that someone with BGS may have fewer than five fingers. Radial ray deficiency that is associated with syndromes (such as BGS) occurs bi-laterally, affecting both arms.

Some of the other clinical characteristics sometimes associated with this disorder are growth retardation and poikiloderma. Although the presentation of BGS may differ between individuals, these characteristics are often observed. People with BGS may have stunted growth, short stature and misshapen kneecaps. Poikiloderma may also be present in people with this syndrome, meaning that their skin may have regions of hyperpigmentation and hypopigmentation, or regions where the skin is missing (atrophy).

Individuals with KSS present initially in a similar way to those with typical CPEO. Onset is in the first and second decades of life.

The first symptom of this disease is a unilateral ptosis, or difficulty opening the eyelids, that gradually progresses to a bilateral ptosis. As the ptosis worsens, the individual commonly extends their neck, elevating their chin in an attempt to prevent the eyelids from occluding the visual axis. Along with the insidious development of ptosis, eye movements eventually become limited causing a person to rely more on turning the head side to side or up and down to view objects in the peripheral visual field.

In virology, defective interfering particles (DIPs), also known as defective interfering viruses, are spontaneously generated virus mutants in which a critical portion of the particle's genome has been lost due to defective replication. DIPs are derived from and associated with their parent virus, and particles are classed as DIPs if they are rendered non-infectious due to at least one essential gene of the virus being lost or severely damaged as a result of the defection. A DIP can usually still penetrate host cells, but requires another fully functional virus particle (the 'helper' virus) to co-infect a cell with it, in order to provide the lost factors. The existence of DIPs has been known about for decades, and they can occur within nearly every class of both DNA and RNA viruses.

KSS results in a pigmentation of the retina, primarily in the posterior fundus. The appearance is described as a "salt-and-pepper" appearance. There is diffuse depigmentation of the retinal pigment epithelium with the greatest effect occurring at the macula. This is in contrast to retinitis pigmentosa where the pigmentation is peripheral. The appearance of the retina in KSS is similar to that seen in myotonic dystrophy type 1 (abbreviated DM1). Modest night-blindness can be seen in patients with KSS. Visual acuity loss is usually mild and only occurs in 40–50% of patients.

Young's syndrome, also known as azoospermia sinopulmonary infections, sinusitis-infertility syndrome and Barry-Perkins-Young syndrome, is a rare condition that encompasses a combination of syndromes such as bronchiectasis, rhinosinusitis and reduced fertility. In individuals with this syndrome, the functioning of the lungs is usually normal but the mucus is abnormally viscous. The reduced fertility (azoospermia) is due to functional obstruction of sperm transport down the genital tract at the epididymis where the sperms are found in viscous, lipid-rich fluid. The syndrome was named after Donald Young, the urologist who first made observations of the clinical signs of the syndrome in 1972. There have been several studies undertaken suggesting that contact with mercury might cause the syndrome.

A variant of Young's syndrome has been observed in an individual, showing slightly different signs and symptoms.

Pickardt's syndrome may cause difficulties in differential diagnosis of pituitary adenomas, as both suprasellar hormone-inactive adenomas and prolactinomas may be associated with increased prolactin levels, central hypgogonadism and central hypothyroidism. Usually, the prolactin levels are higher in case of a true prolactinoma, but the concentration ranges overlap.

Stage IV, or the late motor deterioration stage, can last for years or decades. Prominent features include reduced mobility, curvature of the spine, and muscle weakness, rigidity, spasticity, and increased muscle tone with abnormal posturing of an arm, leg. Girls who were previously able to walk may stop walking. Cognition, communication, or hand skills generally do not decline in stage IV. Repetitive hand movements may decrease and eye gaze usually improves.

Stage III, or the plateau or pseudo-stationary stage, usually begins between ages 2 and 10 and can last for years. Apraxia, motor problems, and seizures are prominent during this stage. However, there may be improvement in behavior, with less irritability, crying, and autistic-like features. In stage III there may be more interest in the surroundings and alertness, attention span, and communication skills may improve. Many girls remain in this stage for most of their lives.

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:

Some NMO patients present double positive for autoantibodies to AQP4 and MOG. These patients have MS-like brain lesions, multifocal spine lesions and retinal and optic nerves atrophy.

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.

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.