Some of the rarer auto-antibodies (e.g., NMDAR) have no commercially available assay and can only be measured by a very small number of research laboratories worldwide, further delaying diagnosis by weeks or months. Most patients with limbic encephalitis are initially diagnosed with herpes simplex encephalitis, because the two syndromes cannot be distinguished clinically. HHV-6 (human herpes virus 6) encephalitis is also clinically indistinguishable from limbic encephalitis.There are two sets of diagnostic criteria used. The oldest are those proposed by Gultekin et al. in 2000. A revised set of criteria were proposed by Graus and Saiz in 2005. The main distinction between the two sets of criteria is whether or not the detection of a paraneoplastic antibody is needed for diagnosis. Antibodies against intracellular neuronal antigens
The main antibodies within this group are those against Hu, Ma2, CV2, amphiphysin and Ri. The syndrome of anti-Ma2 encephalitis may be clinically mistaken for Whipples disease. Antibodies against cell membrane antigens
The main antibodies within this group are those against N-methyl-D-aspartate receptors (NMDAR) and the voltage-gated potassium channel-complex (VGKC-complex). Anti-NMDAR encephalitis is strongly associated with benign tumours of the ovary (usually teratomata or dermoid cysts). Anti-VGKC-complex encephalitis is most often not associated with tumours.Patients with NMDAR encephalitis are frequently young women who present with fever, headache and fatigue. This is often misdiagnosed as influenza, but progresses to severe behavioural and personality disturbance, delusions, paranoia and hallucinations. Patients may therefore initially be admitted to a psychiatric ward for acute psychosis or schizophrenia. The disease then progresses to catatonia, seizures and loss of consciousness.
Antidesmoglein antibodies can also be detected in a blood sample using the ELISA technique. Classification
Pemphigus is a group of autoimmune blistering diseases that may be classified into these types:
Pemphigus vulgaris
Pemphigus vegetans
Pemphigus vegetans of Hallopeau
Pemphigus vegetans of Neumann
Pemphigus foliaceus, of which there several forms:
Pemphigus erythematosus or Senear–Usher Syndrome
Endemic pemphigus foliaceus with its three variants, Fogo Selvagem, the new variant endemic pemphigus Foliaeus and Tunisian endemic pemphigus foliaceus
Paraneoplastic pemphigus
IgA pemphigus, of which there several forms:
Subcorneal pustular dermatosis
Intraepidermal neutrophilic IgA dermatosis
Drug induced pemphigus

Treatment
If not treated, pemphigus can be fatal, usually from overwhelming opportunistic infection of lesions. The most common treatment is the administration of oral steroids, especially prednisone, often in high doses. The side effects of corticosteroids may require the use of so-called steroid-sparing or adjuvant drugs. One of the most dangerous side effects of high-dosage steroid treatments is intestinal perforations, which may lead to sepsis. Steroids and other medications being taken to treat pemphigus may also mask the effects of the perforations. Patients on high dosages of oral steroids should closely monitor their gastrointestinal health. As lesions are usually terribly painful, pain medication likely complicate and exacerbate the gastrointestinal issues caused by steroids. Treatment options
Topical steroids, such as clobetasol
Intralesional injection of steroids, such as dexamethasone
Immunosuppressant drugs, such as CellCept (mycophenolic acid): In recent years, adjuvant drugs, especially biologics, have shown great promise. Serum- or plasma-pooled products, such as intravenous gamma globulin (IVIG) may be useful in severe cases, especially paraneoplastic pemphigus.