DUSN may be caused by a helminthic infection with Toxocara canis, Baylisascaris procyonis, or Ancylostoma caninum. The characteristic lesions are believed to result from a single nematode migrating within the subretinal space. Although previously thought to be endemic in some areas, that belief was likely due to under awareness. DUSN has been diagnosed in patients in many countries and climates including America, Brazil, China and India.

Diffuse unilateral subacute neuroretinitis (DUSN) is a rare condition that occurs in otherwise healthy, often young patients and is due to the presence of a subretinal nematode.

ARN is associated with people who have latent herpes viruses that have been reactivated. The most common causes of the disease have been linked to VSV, HSV-1, HSV-2, and CMV respectively.

ARN cases have been reported in patients who have AIDS, are immunocompromised and in children. The disease is not limited to a specific gender. Most cases have been reported in young adults though children and the elderly can be affected.

Specific genetic markers in Caucasians in the United States have shown elevated risk for disease development (HLA-DQw7 and Bw62, DR4) as well as HLA-Aw33, B44, and DRw6 in the Japanese population.

According to recent research not a single theory is able to explain the cause fully. However current plausible theories include infection with "Toxoplasma gondii", Herpes simplex virus, Rubella, neurogenic causes, and autoimmune pathology.

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

In a study done published by the British Journal of Ophthalmology, the cases of ARN/BARN reported in 2001-2002 in the UK, Varicella Zoster Virus was the most common culprit for the disease and presented mostly in men than in women.

Researchers have also looked at two cases of ARN in patients who have been diagnosed with an immunodeficiency virus. The disease presented itself more so in the outer retina until it progressed far enough to then affect the inner retina. The patients were not so responsive to the antiviral agents given to them through an IV, acyclovir specifically. The cases progressed to retinal detachment. The patients tested positive for the herpes virus. Researchers are now wondering if this type of ARN is specific to those who have the immunodeficiency virus.

Patients usually do not require treatment due to benign nature of the disease. In case cataract develops patients generally do well with cataract surgery.

Affected individuals are typically 20 to 50 years old. The female to male ratio is 2:1. By definition, there is no history of either surgical or accidental ocular trauma. VKH is more common in Asians, Latinos, Middle Easterners, American Indians, and Mexican Mestizos; it is much less common in Caucasians and in blacks from sub-Saharan Africa.

VKH is associated with a variety of genetic polymorphisms that relate to immune function. For example, VKH has been associated with human leukocyte antigens (HLA) HLA-DR4 and DRB1/DQA1, copy-number variations (CNV) of complement component 4, a variant IL-23R locus and with various other non-HLA genes. HLA-DRB1*0405 in particular appears to play an important susceptibility role.

Multiple evanescent white dot syndrome (MEWDS) is an uncommon inflammatory condition of the retina that typically affects otherwise healthy young females in the second to fourth decades of life.

The typical patient with MEWDS is a healthy middle aged female age 15-50. There is a gender disparity as women are affected with MEWDS four times more often than men. Roughly 30% of patients have experienced an associated viral prodrome. Patients present with acute, painless, unilateral change in vision.

Although there is sometimes a preceding viral infection, or skin or eye trauma, the exact underlying initiator of VKH disease remains unknown. However, VKH is attributed to aberrant T-cell-mediated immune response directed against self-antigens found on melanocytes. Stimulated by interleukin 23 (IL-23), T helper 17 cells and cytokines such as interleukin 17 (IL-17) appear to target proteins in the melanocyte.

Lisch epithelial corneal dystrophy (LECD), also known as band-shaped and whorled microcystic dystrophy of the corneal epithelium, is a rare form of corneal dystrophy first described in 1992 by Lisch et al. In one study it was linked to chromosomal region Xp22.3, with as yet unknown candidate genes.

The main features of this disease are bilateral or unilateral gray band-shaped and feathery opacities. They sometimes take on a form of a whirlpool, repeating the known pattern of corneal epithelium renewal. Abrasion of the epithelium in 3 patients brought only temporary relief, with abnormal epithelium regrowth in several months.

Epithelial cells in the zones of opacity were shown to have diffuse cytoplasmic vacuoles with as yet unestablished content.

The prognosis is favorable in most patients with an isolated cutaneous abnormality. In the majority of cases, both the vivid red marking and the difference in circumference of the extremities regress spontaneously during the first year of life. It is theorized that this may be due to the normal maturation process, with thickening of the epidermis and dermis. Improvements for some patients can continue for up to 10 years, while in other cases, the marbled skin may persist for the patient's lifetime.

One study reported an improvement in lesions in 46% of patients within 3 years. If CMTC persists into adulthood, it can result in complaints due to paresthesia, increased sensitivity to cold and pain, and the formation of ulcers.

Few reports included long-term follow up of CMTC into adolescence and adulthood. While about 50% of patients seem to show definite improvement in the reticular vascular pattern, the exact incidence and cause of persistent cases are unknown.

Fewer than 100 cases of CMTC have been published worldwide. Petrozzi reported the first case of CMTC in the United States in 1970. CMTC is believed to be more common than suspected, as studies have shown that milder forms of the disease are not being recognized as CMTC.

The pathophysiology is still unclear, with most cases occurring sporadically, although rare cases were reported in families. Studies indicated the primary involvement of capillaries, venules and veins, and possibly also that of arterioles and lymphatics.

Hypotheses that have been proposed include: environmental/external factors; peripheral neural dysfunction; failure of the development of mesodermic vessels in an early embryonic stage; autosomal dominant inheritance with incomplete penetrance and, finally, the theory of Happle.

Prognosis is poor, however, current analysis suggests that those associated with thymoma, benign or malignant, show a less favorable prognosis (CASPR2 Ab positive).

Lucio's phenomenon is treated by anti-leprosy therapy (dapsone, rifampin, and clofazimine), optimal wound care, and treatment for bacteremia including antibiotics. In severe cases exchange transfusion may be helpful.

In children and some adults, FSGS presents as a nephrotic syndrome, which is characterized by edema (associated with weight gain), hypoalbuminemia (low serum albumin, a protein in the blood), hyperlipidemia and hypertension (high blood pressure). In adults, it may also present as kidney failure and proteinuria, without a full-blown nephrotic syndrome.

There are currently several known genetic causes of the hereditary forms of FSGS.

Some researchers found SuPAR as a cause of FSGS.

Another gene that has been associated with this syndrome is the COL4A5 gene.

"N"-Methyl D-aspartate receptor (NMDAR) Ab encephalitis is the most common Ab-mediated autoimmune encephalopathy. It was first described in 2005 as a paraneoplastic syndrome associated with ovarian teratomas in young women and the antigenic target was determined in 2007, associated with antibodies against NR1 or NR2 subunits of the NMDA receptor. Irani et al. in 2010 presented NMDAR Ab encephalitis in a predominantly non-paraneoplastic disorder of both sexes.

The main pathological features of this disease are a vasculitis affecting all cutaneous vessels.

There are by five characteristic features:

- colonisation of endothelial cells by acid-fast bacilli

- endothelial proliferation and marked thickening of vessel walls to the point of obliteration

- angiogenesis

- vascular ectasia

- thrombosis of the superficial and mid-dermal blood vessels

The likely pathogenesis is endothelial cell injury due to colonization/invasion followed by proliferation, angiogensis, thrombosis and vessel ectasia.

Crossed dystopia (syn.unilateral fusion cross fused renal ectopia) is a rare form of renal ectopia where both kidneys are on the same side of the spine. In many cases, the two kidneys are fused together, yet retain their own vessels and ureters. The ureter of the lower kidney crosses the midline to enter the bladder on the contralateral side. Both renal pelvis can lie one above each other medial to the renal parenchyma (unilateral long kidney) or the pelvis of the crossed kidney faces laterally (unilateral "S" shaped kidney). Urogram is diagnostic.

The anomaly can be diagnosed through ultrasound of urography, but surgical intervention is only necessary if there are other complications, such as tumors or pyelonephritis.

Encephalocraniocutaneous lipomatosis (ECCL), otherwise known as Haberland syndrome, is a rare condition primarily affecting the brain, eyes, and skin of the head and face. It is characterized by unilateral subcutaneous and intracranial lipomas, alopecia, unilateral porencephalic cysts, epibulbar choristoma and other ophtalmic abnormalities.

It was named after Haberland and Perou who first described it.

Rowell's Syndrome was described by Professor Neville Rowell and colleagues in 1963. Patients with the syndrome have lupus erythematosus (discoid or systemic), annular lesions of the skin like erythema multiforme associated with a characteristic pattern of immunological abnormalities. It is uncommon but occurs worldwide.

Rowell's syndrome has been reported to occur with all subtypes of LE (systemic, acute, subacute or discoid).

The cause is generally either paraneoplastic syndrome or idiopathic. In idiopathic AAG, the body's own immune system damages a receptor in the autonomic ganglia, which is part of a peripheral nerve fibre. If the AAG is paraneoplastic, they have a form of cancer, and their immune system has produced paraneoplastic antibodies in response to the cancer.

In dairy breeds, the disease may occur in calves between birth and 4 months of age. In rustic breeds or beef cattle, heifers and young steers up to 12 months of age can be affected. In calves, muscles in upper portion of the front legs and the hind legs are degraded, causing the animal to have a stiff gait and it may have difficulty standing. The disease may also present in the form of respiratory distress.

EN is associated with a wide variety of conditions, including:

- Idiopathic

In about 30–50% of cases, the cause of EN is unknown.

- Infection

- Streptococcal infection which, in children, is by far the most common precipitant,

- Primary infection of Tuberculosis

- "Mycoplasma pneumoniae"

- "Histoplasma capsulatum"

- "Yersinia"

- Epstein-Barr virus

- "Coccidioides immitis" (Valley fever)

- Cat scratch disease

- Autoimmune disorders, including

- Inflammatory bowel disease (IBD)

- Behçet's disease

- Sarcoidosis

- Pregnancy

- Medications, including

- Sulfonamides

- Penicillins

- Oral contraceptives

- Bromides

- Hepatitis B vaccination

- Cancer, including

- Non-Hodgkins lymphoma (NHL)

- Carcinoid tumours

- Pancreatic cancer

EN may also be due to excessive antibody production in lepromatous leprosy leading to deposition of immune complexes.

There is an association with the HLA-B27 histocompatibility antigen, which is present in 65% of patients with erythema nodosum.

A useful mnemonic for causes is SORE SHINS (Streptococci, OCP, Rickettsia, Eponymous (Behçet), Sulfonamides, Hansen's Disease (Leprosy), IBD, NHL, Sarcoidosis.