I read with interest the article about Ralph Neas and his battle with Guillain-Barré syndrome (GBS) [“With help, I survived a rare disorder,” Jan. 11]. Increased public and physician awareness of the syndrome will help in early diagnosis and treatment, which reduces the disability from GBS.
Since Mr. Neas’s illness in 1979, two treatments are available to treat GBS in addition to supportive care. Plasma exchange, in which the plasma in a patient’s blood is removed in an effort to get rid of circulating factors causing the disease, and intravenous immunoglobulin, a human blood product, shorten the time a patient is paralyzed and speed up the time when rehabilitation can begin. Even with these treatments, many are left with weakness, severe pain and fatigue that impairs daily living.
While the exact cause of GBS is unknown, research suggests that GBS patients develop antibodies against common infectious organisms. Those antibodies mistakenly identify the nerve as similar to the organism and attack the nerve. Not everyone exposed to a given infection gets GBS, and only certain infectious agents lead to GBS. These observations lead to the conclusion that GBS is due to a match (or mismatch) between a specific inciting agent and a susceptible individual who comes into contact with it.
More GBS research is needed to prevent GBS and to find better treatments. Lessons learned from treating this autoimmune disease will benefit the many other autoimmune diseases that also lack effective treatments.
David R. Cornblath, MD, Member, Board of Directors and Medical Advisory Board, GBS-CIDP Foundation International and Professor of Neurology at The Johns Hopkins University School of Medicine