Inflammation, and frequently concomitant demyelination,[3][4][5] cause impaired transmission of neural signals and leads to aberrant nerve function.

Neuritis is often conflated with neuropathy, a broad term describing any disease process which affects the peripheral nervous system.

Common causes include autoimmune diseases, such as multiple sclerosis; infection, either bacterial, such as leprosy, or viral, such as varicella zoster; post-infectious immune reactions, such as Guillain-Barré syndrome; or a response to physical injury, as frequently seen in sciatica.

[12] Rapid identification of an infectious cause of neuritis dictates treatment approach and often has a much more positive long term prognosis than other etiologies.

It presents with a low number of anesthetic, anhydrotic skin plaques with few bacilli, the result of a granulomatous process which destroys cutaneous nerves.

[15] Lepromatous leprosy, seen when the host lacks resistance to the organism, presents with widespread skin lesions and palpably enlarged nerves.

The first stage of Lyme disease frequently presents with a pathognomonic "bull's eye" rash, erythema migrans, as well as fever, malaise, and arthralgias.

Roughly 15% of untreated patients will then develop neurological manifestations, classically characterized by cranial neuropathy, radiculoneuritis, and a lymphocytic meningitis.

[16] Herpes reactivation is often treated with acyclovir, although evidence for its efficacy in controlling peripheral neurological manifestation of disease remain poor.

As the disease process progresses, diffuse infiltrative lymphocytosis syndrome may include a lymphocytic inflammation of peripheral nerves which results in a painful symmetric polyneuropathy.

[16] AIDP, which represents the vast majority of Guillain-Barré cases, classically presents with an acute onset, ascending paralysis which begins in the distal extremities.

This carcinomatous polyneuropathy is associated with the presence of antibodies against onconeural antigen, Hu, Yo, amphiphysin, or CV2/CRMP5, which recognize and bind to both tumor cells and peripheral nervous system neurons.

Treatment of paraneoplastic syndromes aim for both elimination of tumor tissue via conventional oncologic approach as well as immunotherapy options such as steroids, plasmapheresis or IVIG.

[32] Deficiency of vitamin B12 causes subacute combined degeneration, a disease classically associated with a central demyelinating process; however, it also presents with a painful peripheral neuropathy.

[33] Many classes of medication may have toxic effects on peripheral nerves, these iatrogenic neuropathies are an increasingly common form of neuritis.

[35] Management of these medication induced neuropathies center around discontinuation of the offending agents, although patients will frequently continue to worsen for several weeks after cessation of administration.