Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) Frequently Asked Questions

A. CIDP is a neurological disorder characterized by gradually (over a time period of months or years) increasing weakness of the legs and arms. It is caused by damage to the protective covering of the nerves, called myelin. Symptoms are variable and may be mild to debilitating.

A. A patient with CIDP typically presents with difficulty walking which progressively worsens over 2 months or more. Weakness, tingling or other abnormal sensations may also be experienced, and usually begin in the fingers or toes (on both sides of the body). Physical examination will usually show loss of reflexes, such as the knee and ankle jerk. Evaluation by a neurologist will often include an electrical test, a nerve conduction velocity-electromyography study. Your doctor may obtain blood and urine tests, including analysis of proteins, to look for causes of CIDP. CIDP is usually a chronic condition, which means that it may require long-term treatment.

A. Although the exact cause is unknown, it is believed that the immune system, which is normally protective, perceives myelin as foreign and attacks it. Just what starts this process is not clear. Some patients are found to have abnormal proteins in their blood, and these may facilitate damage. Over time, the destruction of myelin leads to weakness, numbness and tingling in the arms and legs.

A. Several treatment options are available. These include steroids, plasmapheresis and intravenous immune globulin (IVIG). The goals of treatment are to stop further damage to the myelin, prevent damage to the nerve fibers (axons), alleviate symptoms and prevent relapse, and if possible, create an environment that allows the myelin to regenerate. In patients with CIDP, IVIG has been shown to reduce disability, prevent relapse and even improve quality of life.[1]

1. Donofrio PD, Bril V, Dalakas MC, et al. Safety and tolerability of immune globulin intravenous in chronic inflammatory demyelinating polyradiculoneuropathy. Arch Neurol. 2010 Sep;67(9):1082-8.