Symptoms can include, but are not limited to lack of consciousness, aggression, seizures, depression, hemiparesis, ataxia, apraxia, coma, etc. There will also be lesions in the corpus callosum.

Marchiafava-Bignami disease is routinely diagnosed with the use of an MRI due to the fact that the majority of clinical symptoms are non-specific. Before the use of such imaging equipment, it was unable to be diagnosed until autopsy. The patient usually has a history of alcoholism or malnutrition and neurological symptoms are sometimes present and can help lead to a diagnosis. MBD can be told apart from other neural diseases due to the symmetry of the lesions in the corpus callosum as well as the fact that these lesions don’t affect the upper and lower edges.

There are two clinical subtypes of MBD

Type A- Stupor and coma predominate. Radiological imaging shows involvement of the entire corpus callosum. This type is also associated with symptoms of the upper motor neurons.

Type B- This type has normal or only mildly impair mental status and radiological imaging shows partial lesions in the corpus callosum.

As of 2007, fewer than 500 Yakut individuals have been infected with VE. Viliuisk Encephalomyelitis is classified as a progressive neurological disorder that ultimately ends in the death of the infected individual. The disease has three distinguishable phases: The acute form, the progressive form, and the chronic form.

The acute form is the most rapid and most violent of all the stages. It begins with the characteristic rigidity of the muscles, accompanied by slurred speech, severe headaches, and exaggeration of cold-like symptoms. Patients usually die within weeks of the initial symptoms. Routine post-mortem examinations yield: severe inflammation of the brain lining, clusters of dead cells and tissue, and largely increased amounts of macrophages and lymphocytes.

The progressive form is the most common case. Patients initially experience acute-like symptoms which are not as severe, and subside within a few weeks. Following the sub-acute phase, the patients experience a few mild symptoms including some behavioral changes, incoordination, and difficulty in speech. Eventually the disease developed fully and those infected were stricken with the characteristic symptoms of rigidity, slurred speech, and deterioration of cognitive functions. Ultimately, brain function depreciates rapidly resulting in death.

Many patients who undergo the chronic form claim never to have had an acute attack. These patients endure varying measures of impairment and suffer mental deterioration for the remainder of their lives. Usually they live to be very old and succumb to other diseases.

In almost all cases there are changes characteristic of VE. Early onset shows an increased number of lymphocytes and increased protein concentration — which reduces over many years. These factors help neurologists determine the form of VE based on progression. The trademark changes in the brain include: thickened inflamed meninges, necrotic cortical lesions, increased number of lymphocytes, and neuronal death.

Viliuisk Encephalomyelitis (VE) is a fatal progressive neurological disorder found only in the Sakha (Iakut/Yakut) population of central Siberia. About 15 new cases are reported each year. VE is a very rare disease and little research has been conducted. The causative agents, origin of the disease, and involved candidate genes are currently unknown, but much research has been done in pursuit of the answers.

Those inflicted with the disease survive for a period of only a few months to several years. VE follows three main courses of infection: an acute form, a sub-acute form subsiding into a progressive form, and a chronic form. Initially, the infected patients experience symptoms such as: severe headaches, delirium, lethargy, meningism, bradykinesia, and incoordination. A small percentage of patients die during the acute phase as result of a severe coma. In all cases the disease is fatal.

Most symptoms of people with post-viral cerebellar ataxia deal to a large extent with the movement of the body. Some common symptoms that are seen are clumsy body movements and eye movements, difficulty walking, nausea, vomiting, and headaches.

Differential diagnosis may include:

- Opsoclonus-myoclonus-ataxia syndrome

- Miller-Fisher syndrome

- Meningoencephalitis

- Cerebral abscess

- Tumor

- Hydrocephalus

- Inner-ear Disease

- Acute Vestibulitis

- Acute Labyrinthitis

Symptoms of OBS vary with the disease that is responsible. However, the more common symptoms of OBS are confusion; impairment of memory, judgment, and intellectual function; and agitation. Often these symptoms are attributed to psychiatric illness, which causes a difficulty in diagnosis.

Acute cerebellar ataxia usually follows 2–3 weeks after an infection. Onset is abrupt. Vomiting may be present at the onset but fever and nuchal rigidity characterestically are absent. Horizontal nystagmus is present is approximately 50% of cases.

- Truncal ataxia with deterioration of gait

- Slurred speech and nystagmus

- Afebrile

Acute hemorrhagic edema of infancy (also known as "Acute hemorrhagic edema of childhood", "Finkelstein's disease", "Infantile postinfectious iris-like purpura and edema", "Medallion-like purpura", "Purpura en cocarde avec oedema" and "Seidlmayer syndrome") is a skin condition that affects children under the age of two with a recent history of upper respiratory illness, a course of antibiotics, or both. The disease was first described in 1938 by Finkelstein and later by Seidlmayer as “Seidlmayer cockade purpura”.

Treatment of OBS varies with the causative disorder or disease. It is important to note that it is not a primary diagnosis and a cause needs to be sought out and treated.

Patients present with acute unilateral decreased vision, photopsias and central or paracentral scotoma. An antecedent viral prodrome occurs in approximately one-third of cases. Myopia is commonly seen in patients.

Eye exam during the acute phase of the disease reveals multiple discrete white to orange spots at the level of the RPE or deep retina, typically in a perifoveal location (around the fovea).

Acute cerebellar ataxia of childhood is a childhood condition characterized by an unsteady gait, most likely secondary to an autoimmune of postinfectious cause, drug induced or paraneoplastic. Most common virus causing acute cerebellar ataxia are Chickenpox virus and Epstein Barr Virus. It is a diagnosis of exclusion.

MEWDS is a self limited disease with excellent visual recovery within 2-10 weeks. However residual symptoms including photopsia may persist for months.

Marburg acute multiple sclerosis, also known as Marburg multiple sclerosis or acute fulminant multiple sclerosis, is considered one of the multiple sclerosis borderline diseases, which is a collection of diseases classified by some as MS variants and by others as different diseases. Other diseases in this group are neuromyelitis optica (NMO), Balo concentric sclerosis, and Schilder's disease. The graver course is one form of malignant multiple sclerosis, with patients reaching a significant level of disability in less than five years from their first symptoms, often in a matter of months.

Sometimes Marburg MS is considered a synonym for tumefactive MS, but not for all authors.

Some discrepancy exists as to whether acute zonal occult outer retinopathy (AZOOR) is actually considered a white dot syndrome. However, AZOOR may definitely be related to other diseases included in the white dot syndrome group. AZOOR occurs in young to middle age adults and may eventually progress to retinal cell death. Symptoms include acute visual field loss and photopsias. Suspected causes for AZOOR include autoimmune, viral, and fungal.

White dot syndromes are inflammatory diseases characterized by the presence of white dots on the fundus, the interior surface of the eye. The majority of individuals affected with white dot syndromes are younger than fifty years of age. Some symptoms include blurred vision and visual field loss. There are many theories for the etiology of white dot syndromes including infectious, viral, genetics and autoimmune.

Classically recognized white dot syndromes include:

- Acute posterior multifocal placoid pigment epitheliopathy (APMPPE)

- Birdshot chorioretinopathy

- Multiple evanescent white dot syndrome (MEWDS)

- Acute zonal occult outer retinopathy (AZOOR)

- Multifocal choroiditis and panuveitis (MCP)

- Punctate inner choroiditis (PIC)

- Serpiginous choroiditis

Sydenham's chorea (SC) or chorea minor (historically referred to as St Vitus's dance) is a disorder characterized by rapid, uncoordinated jerking movements primarily affecting the face, hands and feet. Sydenham's chorea results from childhood infection with Group A beta-haemolytic "Streptococcus" and is reported to occur in 20–30% of patients with acute rheumatic fever (ARF). The disease is usually latent, occurring up to 6 months after the acute infection, but may occasionally be the presenting symptom of rheumatic fever. Sydenham's chorea is more common in females than males and most patients are children, below 18 years of age. Adult onset of Sydenham's chorea is comparatively rare and the majority of the adult cases are associated with exacerbation of chorea following childhood Sydenham's chorea.

Sydenham's chorea is characterized by the abrupt onset (sometimes within a few hours) of neurologic symptoms, classically chorea, usually affecting all four limbs. Other neurologic symptoms include behavior change, dysarthria, gait disturbance, loss of fine and gross motor control with resultant deterioration of handwriting, headache, slowed cognition, facial grimacing, fidgetiness and hypotonia. Also, there may be tongue fasciculations ("bag of worms") and a "milk sign", which is a relapsing grip demonstrated by alternate increases and decreases in tension, as if hand milking.

Non-neurologic manifestations of acute rheumatic fever are carditis, arthritis, erythema marginatum, and subcutaneous nodules.

The PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) syndrome is similar, but is not characterized by Sydenham's motor dysfunction. PANDAS presents with tics and/or a psychological component (e.g., OCD) and occurs much earlier, days to weeks after GABHS infection rather than 6–9 months later. It may be confused with other conditions such as lupus and Tourette syndrome.

Movements cease during sleep, and the disease usually resolves after several months. Unlike in Huntington's disease, which is generally of adult onset and associated with an unremitting autosomal dominant movement disorder and dementia, neuroimaging in Sydenham's chorea is normal and other family members are unaffected. Other disorders that may be accompanied by chorea include abetalipoproteinemia, ataxia-telangiectasia, biotin-thiamine-responsive basal ganglia disease, Fahr disease, familial dyskinesia-facial myokymia (Bird-Raskind syndrome) due to an ADCY5 gene mutation, glutaric aciduria, Lesch-Nyhan syndrome, mitochondrial disorders, Wilson disease, hyperthyroidism, lupus erythematosus, pregnancy (chorea gravidarum), and side effects of certain anticonvulsants or psychotropic agents.

There is a rapid onset of clinical signs over the period of 2–7 days, beginning with anorexia, lethargy, and hyperbilirubinemia (icterus and discolored urine). Signs of hepatic encephalopathy (ataxia, blindness, aggression, and coma) and fever can also occur. Other signs include photodermatitis, hemorrhagic diathesis, dependent edema, and colic. The reason for colic is unknown, but is thought to be due to rapid decrease in the size of the liver, and the increased risk of gastric impaction. Rarely, weight loss can occur.

Acne fulminans begins as pain and inflammation in the joints. It eventually progresses into a swelling of the lymph nodes located at the base of the neck, causing inflexibility in the neck within weeks after the nodes swell. This swelling will eventually decrease, but this decrease will be accompanied by an increased inflammation and swelling of the joints, as well as a complete loss of appetite, though these symptoms are often ignored. After some time, the disease will cause an extreme loss of weight and atrophy of the muscles, leading to the decline of physical abilities.

Acute, tender, erythematous plaques, nodes, pseudovesicles and, occasionally, blisters with an annular or arciform pattern occur on the head, neck, legs, and arms, particularly the back of the hands and fingers. The trunk is rarely involved. Fever (50%); arthralgia or arthritis (62%); eye involvement, most frequently conjunctivitis or iridocyclitis (38%); and oral aphthae (13%) are associated features.

Sweet described a disease with four features: fever; leukocytosis; acute, tender, red plaques; and a dermal infiltrate of neutrophils. This led to the name acute febrile neutrophilic dermatosis. Larger series of patients showed that fever and neutrophilia are not consistently present. The diagnosis is based on the two constant features, a typical eruption and the characteristic histologic features; thus the eponym "Sweet's syndrome" is used.

Acne fulminans (also known as "acute febrile ulcerative acne") is a severe form of the skin disease, acne, which can occur after unsuccessful treatment for another form of acne, acne conglobata. The condition is thought to be an immunologically induced disease in which elevated level of testosterone causes a rise in sebum and population of "Propionibacterium acnes" bacteria. The increase in the amount of "P acnes" or related antigens may trigger the immunologic reaction in some individuals and lead to an occurrence of acne fulminans. In addition to testosterone, isotretinoin may also precipitate acne fulminans, possibly related to highly increased levels of "P acnes antigens" in the patient's immune system. Acne fulminans is a rare disease. Over the past several years, fewer cases of this disease have occurred, possibly because of earlier and better treatment of acne. Approximately 100 patients with acne fulminans have been described.

It took its name from Otto Marburg. It can be diagnosed "in vivo" with an MRI scan.

If Marburg disease occurs in the form of a single large lesion, it can be radiologically indistinguishable from a brain tumor or abscess. It is usually lethal, but it has been found to be responsive to Mitoxantrone and Alemtuzumab, and it has also been responsive to autologous stem cell transplantation. Recent evidence shows that Marburg's presents a heterogeneous response to medication, as does standard MS.

Porphyria is a group of diseases in which substances called porphyrins build up, negatively affecting the skin or nervous system. The types that affect the nervous system are also known as acute porphyria, as symptoms are rapid in onset and last a short time. Symptoms of an attack include abdominal pain, chest pain, vomiting, confusion, constipation, fever, high blood pressure, and high heart rate. The attacks usually last for days to weeks. Complications may include paralysis, low blood sodium levels, and seizures. Attacks may be triggered by alcohol, smoking, hormonal changes, fasting, stress, or certain medications. If the skin is affected, blisters or itching may occur with sunlight exposure.

Most types of porphyria are inherited from a person's parents and are due to a mutation in one of the genes that make heme. They may be inherited in an autosomal dominant, autosomal recessive, or X-linked dominant manner. One type, porphyria cutanea tarda, may also be due to increased iron in the liver, hepatitis C, alcohol, or HIV/AIDS. The underlying mechanism results in a decrease in the amount of heme produced and a build-up of substances involved in making heme. Porphyrias may also be classified by whether the liver or the bone marrow is affected. Diagnosis is typically by blood, urine, and stool tests. Genetic testing may be done to determine the specific mutation.

Treatment depends on the type of porphyria and a person's symptoms. The treatment of porphyria of the skin generally involves the avoidance of sunlight. The treatment for acute porphyria may involve giving intravenous heme or a glucose solution. Rarely a liver transplant may be carried out.

The frequency of porphyria is unclear. It is estimated that it affects 1 to 100 per 50,000 people. Rates vary around the world. Porphyria cutanea tarda is believed to be the most common type. The disease was described at least as early as 370 BC by Hippocrates. The underlying mechanism was first described by Felix Hoppe-Seyler in 1871. The name "porphyria" is from the Greek πορφύρα, "porphyra", meaning "purple", a reference to the color of the urine that may occur during an attack.