FAQs

First of all, thank you for your donations. Because of them, a patient is getting support from a liaison somewhere at this moment. Without your contributions, we wouldn’t be able to help with such critical support. Other than in-person visits from Liaisons—survivors of GBS or CIDP themselves or their caregivers—the Foundation offers a broad range of support from its Global Medical Advisory Board, Liaisons and Volunteers as well the employees and board members that lead the organization. More details can be found on the GET SUPPORT section of the site.

We appreciate all the ideas our volunteers share with us. And our liaisons are happy to work with you on a local level to help shape those ideas into reality. For any fundraising activities, please contact the main office at 610-667-0131 or email info@gbs-cidp.org to get things started. They’ll be glad to work with you and the liaison as necessary.

For the latest Covid-19 information, please visit our Covid-19 portal.

As you have probably experienced over the recent years, insurance coverage and issues evolve rapidly. For more information, see the HEALTH & INSURANCE section of the ALL ABOUT ADVOCACY page. If you have any questions or concerns about a specific insurance issue, don’t hesitate to contact our office either by phone 610-667-0131 or via email at info@gbs-cidp.org.

There is no research to support that GBS or CIDP is contagious or hereditary.

Due to the rareness of these disorders, some medical professionals aren’t familiar with them. But that is where our work comes in by raising awareness globally. There are many ways you can help spread the word so more people, including medical professionals, learn about these disorders. Contact your local liaison today to learn more about how.

As you have probably experienced over the recent years, insurance coverage and issues evolve rapidly. For more information, see the HEALTH & INSURANCE section of the ALL ABOUT ADVOCACY page. If you have any questions or concerns about a specific insurance issue, don’t hesitate to contact our office either by phone 610-667-0131 or via email at info@gbs-cidp.org.

There is no research to support that GBS or CIDP is contagious or hereditary.

It’s even more rare to have multiple episodes of GBS, but it can happen. Since the causes of GBS or unknown, there’s technically nothing you can do to control the possibility. But we do believe you should stay positive and focused on the recovery process and healthy living.

Due to the rareness of these disorders, some medical professionals aren’t familiar with them. But that is where our work comes in by raising awareness globally. There are many ways you can help spread the word so more people, including medical professionals, learn about these disorders. Contact your local liaison today to learn more about how.

It appears from Brazilian researchers and neurologists that the preliminary media reports might be somewhat misleading on this link as the actual cases of GBS that can be clearly linked to preceding Zika virus infection have been small when attempts have been made to better clarify the relationship by skilled clinical neurologists. As of this time we do not have enough evidence to make this type of estimate.

Susceptibility to Zika virus is a function of mosquito exposure in endemic areas, and has nothing to do with having had prior GBS; 80% of patients infected with the Zika virus have no symptoms, and the remainder develop a benign viral syndrome manifest by fever, aches and pains, headache, rash and conjunctivitis that resolves over 7-11 days. Having had a prior episode of GBS should have no bearing on the risk of Zika infection.

Patients should be directed to the CDC website for the most current travel recommendations. There is, as of now, no proven association between a history of prior GBS and developing recurrent GBS upon traveling to an endemic area, as the exact relationship between the Zika virus and any trigger to a first episode of GBS has yet to be scientifically substantiated. Pregnant women (regardless of prior GBS status) are strongly discouraged from traveling to the affected regions.

Since CB is the major physiologic phenomenon underlying MMN, understanding the cause of the block can lead to treatments directed at the specific target.

Progress: Initially the CB in MMN was thought to be caused by the stripping off of the insulation of the axon (myelin). This demyelination is known to cause CB in other diseases including the demyelinating form of GBS as well as CIDP. However, we know that the acute motor axonal form (AMAN) form of GBS has CB without demyelination. It has been shown in AMAN that the target of the antibodies in AMAN are directed at a region of the axon that produces the fast transmission of impulses down the nerve- the Node of Ranvier. AMAN has similar antibodies to those found in MMN and there is now increasing evidence that the CB in MMN is also due to an attack of the Node of Ranvier or its adjacent regions. This knowledge is likely to provide investigators the opportunity to develop treatments directed at specific targets in this region.

Progress: Although challenges remain, it is clear that there are aspects of the anatomy and electrophysiologic properties of the nerve fibers that are different between motor and sensory nerves. This makes the motor fibers more vulnerable to the immunologic attack as well as to development of CB.

Progress: It is still not entirely clear whether the GM1 antibodies are the specific cause of MMN. However, it is known that GM1 is prominent at the nodes of Ranvier and is different in structure in sensory nerve fibers compared to the motor nerves which would potentially make the motor fibers more vulnerable to antibody attacks and that similar antibodies cause AMAN, a purely motor disorder. However, reproducing MMN in animals has not been accomplished by either giving them GM1 antibodies or stimulating the animal to make the antibodies.

The fact that only 35-50% of patients with MMN had the antibodies (in most reports) was particularly troubling. This issue may have been resolved with a recent study from Dr. Hugh Willison’s laboratory (MAB member) that the antibodies are detected in over 85% of patients with MMN if the test combines MMN with other similar glycoproteins (gangliosides). This detection of antibodies to complexes of gangliosides, if confirmed, will not only give us a better understanding of the disease but also provide an important diagnostic test that will more definitively determine if someone has MMN.

Progress: There remains a great deal of work that is needed to answer these questions but progress is being made. Recognizing that the primary site of attack in MMN is at the Node of Ranvier now points to the axon as being primarily involved. Attack on the nodes does not only cause CB, but also affects the energy transport down the nerve fiber which over time can cause degeneration of the must vulnerable aspects of the nerve, the distal twigs that are farthest from the cell body. This concept is being considered in other disorders that affect the nodes but needs further study in MMN. Some of the axonal elements at the nodes of ranvier may be amenable to therapy.

Challenges: The fact that there are no treatments other than IVIg that have been proven to be effective has been very disappointing. There are a number of challenges to identifying new treatments.

1. MMN is a hard disorder to study treatments. It is very rare and requires many centers to recruit patients. This is very expensive and it is difficult to obtain funding to support such an effort.
2. Developing outcome measures that can accurately and sensitively determine if a treatment is effective is an important requirement for good clinical trials. The GBS-CIDP FI supported Peripheral Neuropathy Outcome Measure Study (PERINOMS) has developed and validated a number of outcome measures that can be used in clinical trials in MMN and other immune neuropathies.
3. We know that MMN is both under-diagnosed and mis-diagnosed. The potential for the antibody testing against GM1 complexes providing specific and sensitive diagnostic information will help improve our diagnostic accuracy which will improve our ability to determine if a treatment is effective.
4. We need a better understanding of the natural history of the disease, the different symptoms and signs that encompass MMN. Having a more specific way of determining who has MMN will be a big step in this regard. Some larger series have provided important information but an international registry and database is needed.

The ARDA study is designed to assess the safety and effectiveness of the investigational study drug compared to a placebo for the treatment of adults living with MMN. Participants enrolled in the study will be randomly assigned by a computer to either receive the investigational drug or a placebo. Participants will have 2 out of 3 chances to receive the study drug.

The study will consist of a screening period to ensure eligibility, followed by IVIG study treatment period to confirm that the disease responds to study treatment. There is then a 4 month treatment period, followed by an optional long-term extension and a 9-month safety follow-up period. All participants will be monitored and supported by the study team.

To learn more, visit https://clinicaltrials.gov/ct2/show/NCT05225675 or email clinicaltrials@argenx.com

It appears from Brazilian researchers and neurologists that the preliminary media reports might be somewhat misleading on this link as the actual cases of GBS that can be clearly linked to preceding Zika virus infection have been small when attempts have been made to better clarify the relationship by skilled clinical neurologists. As of this time we do not have enough evidence to make this type of estimate.

Susceptibility to Zika virus is a function of mosquito exposure in endemic areas, and has nothing to do with having had prior GBS; 80% of patients infected with the Zika virus have no symptoms, and the remainder develop a benign viral syndrome manifest by fever, aches and pains, headache, rash and conjunctivitis that resolves over 7-11 days. Having had a prior episode of GBS should have no bearing on the risk of Zika infection.

Patients should be directed to the CDC website for the most current travel recommendations. There is, as of now, no proven association between a history of prior GBS and developing recurrent GBS upon traveling to an endemic area, as the exact relationship between the Zika virus and any trigger to a first episode of GBS has yet to be scientifically substantiated. Pregnant women (regardless of prior GBS status) are strongly discouraged from traveling to the affected regions.

For the latest Covid-19 information, please visit our Covid-19 portal.