Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired autoimmune disease of the peripheral nervous system characterized by progressive weakness and impaired sensory function in the legs and arms.

In its traditional manifestation, chronic inflammatory demyelinating polyneuropathy is characterized by symmetric, progressive limb weakness and sensory loss, which typically starts in the legs.

[5][6][7] Numerous reports have outlined a range of clinical patterns that are thought to be chronic inflammatory demyelinating polyneuropathy variations.

[4] Chronic inflammatory demyelinating polyneuropathy (or polyradiculoneuropathy) is considered an autoimmune disorder destroying myelin, the protective covering of the nerves.

Typical early symptoms are "tingling" (sort of electrified vibration or paresthesia) or numbness in the extremities, frequent (night) leg cramps, loss of reflexes (in knees), muscle fasciculations, "vibration" feelings, loss of balance, general muscle cramping and nerve pain.

Despite these limitations, early diagnosis and treatment is favoured in preventing irreversible axonal loss and improving functional recovery.

However, only a small number of convincingly identified specific targets for such a response have been found in chronic inflammatory demyelinating polyneuropathy.

[20] Individuals with chronic inflammatory demyelinating polyneuropathy have evidence of activation of T cells in the systemic immune compartment; however, antigen specificity is still largely unknown.

This was supported by the detection of oligoclonal IgG bands in the cerebrospinal fluid[23] and immunoglobulin as well as complement deposition on myelinated nerve fibers.

There is serologic evidence of recent Campylobacter jejuni infection in a small number of individuals with chronic inflammatory demyelinating polyneuropathy.

Because carbohydrate epitopes are expressed in both microbial lipopolysaccharides and nerve glycolipids, this discovery may, in rare cases, point to molecular mimicry as the root cause of chronic inflammatory demyelinating polyneuropathy.

[25] Apart from myelin-directed antibodies, other serum components that can cause demyelination as well as conduction block include complement, cytokines, and other inflammatory mediators.

Comparison of the proximal and distal latencies of equivalent segments of two nerves in the same limb reveals that these patients with acquired demyelinating neuropathy frequently have a differential slowing of conduction velocity.

[26] An MRI can show proximal nerve or root enlargement and gadolinium enhancement, which indicate active inflammation as well as demyelination in the brachial plexus[27] or cauda equina.

The acronym CANOMAD refers to a rare chronic ataxic neuropathy linked to disialosyl (ganglioside) antibodies, IgM paraprotein, ophthalmoplegia, and cold agglutinins.

In such cases, presence of clinical characteristics suggestive of CIDP are critical, justifying full investigations, including sural nerve biopsy.

Despite less definitive published evidence of efficacy, corticosteroids are considered standard therapies because of their long history of use and cost effectiveness.

[citation needed] Non-cytotoxic immunosuppressive treatments usually include the anti-rejection transplant drugs azathioprine (Imuran/Azoran) and mycophenolate mofetil (Cellcept).

[citation needed] In severe cases of CIDP, when second-line immunomodulatory drugs are not efficient, autologous hematopoietic stem cell transplantation (HSCT) is sometimes performed.

[42] (In MS, the ASTIMS RCT provides evidence for superior effect of HSCT to the then-best practice for treatment of aggressive MS.[42] The more recent MIST RCT confirmed its superiority in MS.[43]) Physical therapy and occupational therapy may improve muscle strength, activities of daily living, mobility, and minimize the shrinkage of muscles and tendons and distortions of the joints.

[citation needed] Ongoing specialist community support, information, advice, and guidance is available from a range of Charities, Non-Government Organisations (NGOs), and Patient Advisory Groups around the world.

In the United Kingdom this is provided by GAIN (Guillain–Barré and Associated Inflammatory Neuropathies),[44] in the USA it is provided by GBS/CIDP Foundation International,[45] and in The European Union by a range of organisations under the umbrella of EPODIN (European Patient Organization for Disimmune & Inflammatory Neuropathies)[46] As in multiple sclerosis, another demyelinating condition, it is not possible to predict with certainty how CIDP will affect patients over time.

However, many individuals are left with residual numbness, weakness, tremors, fatigue and other symptoms which can lead to long-term morbidity and diminished quality of life.

[citation needed] In 1982 Lewis et al. reported a group of patients with a chronic asymmetrical sensorimotor neuropathy mostly affecting the arms with multifocal involvement of peripheral nerves.