Guillain-Barre Syndrome (GBS) & Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
Guillain-Barre Syndrome (GBS) & Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
Guillain-Barre Syndrome (GBS) and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) are both autoimmune neuropathies. This means they are diseases in which the immune system attacks its own nerves.
Appointment Information
A physician referral is required for the Peripheral Neuropathy Center. To schedule an appointment, call us at 734-936-9010 or have your physician call M-Line at 800-962-3555 to refer you as a patient.
What is GBS?
Guillain-Barré Syndrome (GBS) is an inflammatory disorder of the peripheral nerves outside the brain and spinal cord. One of its most common subtypes is called Acute Inflammatory Demyelinating Polyneuropathy (AIDP) or Landry’s Ascending Paralysis.
GBS is characterized by the rapid onset of numbness, weakness, and often paralysis of the legs, arms, breathing muscles, and face. Paralysis is typically ascending, meaning that it travels up the limbs from fingers and toes towards the torso. Loss of reflexes, such as the knee jerk, help solidify the diagnosis.
The cause of GBS is not clearly defined, though 60-80 percent of cases are preceded by a viral or bacterial infection. GBS is neither hereditary nor contagious. Ninety-five percent of patients recover to varying degrees. Recovery may take 6 months to 2 years and pain, numbness and muscle aches may persist.
What is CIDP?
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is a rare disorder of the peripheral nerves characterized by gradually increasing sensory loss and weakness associated with loss of reflexes. The covering of the nerves, called myelin, is damaged. CIDP can start at any age and is more frequent in men than women. It is neither hereditary nor contagious.
The number of new cases per year of CIDP is about 1-2 per 100,000 people, but as the disease can be present in a person for years prior to diagnosis, the prevalence reflecting the accumulation of cases over time may be slightly higher in some areas.
CIDP warrants early recognition and treatment, when appropriate. Left untreated, 30 percent of CIDP patients will progress to wheelchair dependence. Early recognition and proper treatment can avoid a significant amount of disability. Long term, relapses are expected, but remission is also possible.
How do GBS & CIPD compare?
GBS presents much more acutely, and reaches its most severe state in less than 4 weeks. CIDP presents more slowly and reaches its more severe state typically in over 8 weeks. Because of this, GBS is considered a classic acute autoimmune neuropathy while CIDP is a classic chronic autoimmune neuropathy.
A disease is called demyelinating when the myelin sheath, the protective covering that surrounds nerve fibers, is damaged. CIDP by definition almost always involves some degree of demyelination, while GBS can be both demyelinating and axonal (where the nerves are directly damaged by the disease).
How are GBS & CIDP treated?
Both patients with GBS and those with CIDP are treated at the Peripheral Neuropathy Center. The Peripheral Neuropathy Center is a designated center of the Neuropathy Association — one of a select few in the country. The center has also been named a Center of Excellence by the GBS | CDIP Foundation International.
How is Guillain-Barré syndrome (GBS) treated?
GBS is treated in the hospital. You may be given immunotherapy. If muscle weakness is severe, you may also have treatment to help you breathe, drink, and eat. You may need therapy to help you walk and talk again. Most people recover with few lasting symptoms. But recovery may take several months.
Locations
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Neurology Clinic | Taubman Center 1500 E Medical Center Dr
Floor 1 Reception C
Ann Arbor, MI 48109-5322Get Directions
Doctors
Benjamin Becker, MD
Clinical Assistant Professor
Neurology, Neuromuscular Medicine
Brian Christopher Callaghan, MD
Professor
Neurology, Electrodiagnostic Medicine, Clinical Neurophysiology
Melissa Anne Elafros, MD, PhD
Assistant Professor
Neurology
Gary W Gallagher, MD
Clinical Associate Professor
Neurology, Electrodiagnostic Medicine, Neuromuscular Medicine
Ann A Little, MD
Clinical Associate Professor
Neurology, Electrodiagnostic Medicine, Clinical Neurophysiology
Zachary Nathaniel London, MD
Clinical Professor
Neurology, Electrodiagnostic Medicine, Neuromuscular Medicine
Savannah Quigley, MD
Clinical Assistant Professor
Neurology, Electrodiagnostic Medicine, Neuromuscular Medicine
Amro Maher Stino, MD
Clinical Associate Professor
Neurology, Electrodiagnostic Medicine, Clinical Neurophysiology
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