In September 2022, The MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Project was joined by doctors all over the world to talk all things MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease in a face-to-face question and answer panel at the Harvard Faculty Club, Cambridge, MA. Dr. Michael Levy, Dr. Sudarshini (Darshi) Ramanathan, Dr. John J. Chen, Dr. Tanuja Chitnis, Dr. Elias Sotirchos, Dr. Brenda Banwell and Dr. Jonathan Sanotoro answered 11 essential questions that we did not have time to answer during the panel discussion which originated from the MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease community.
OnInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. behalf of The MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Project and the entire MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease community, we would like to thank these doctors and all other doctors and researchers who attended the round-table in Boston to help accelerate research in MOG Antibody DiseaseOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease and continuously provide insightful information to not only the patients and their carers, but to colleagues, doctors and scientists globally. This includes: Testing for the MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodiesA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. a cell-based assayA laboratory test used to: • Measure the presence or amount of a specific substance: in a sample, such as blood, urine, or tissue.
• Determine the potency or activity: of a drug or other substance.
• Analyze the purity: of a chemical compound.
• Identify and quantify: biomarkers related to a disease or condition.
, predicting relapsesWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community)., differentiating between adult and paediatric phenotypes, for the new clinical trials that have just launched for MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , mood and anxiety disorders, fatigue and sleeping difficulties, effective treatment options and more!
This video presentation would not be possible without a grant from UCB Pharma Company. You can view the entire video onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. our YouTube Channel here as well as onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. our website page here under “Special Presentation Videos” which also contains a link to download a PDF of the transcript.
Questions and Answers
1. Are there any theories that vision loss can be progressive once it gets to a certain point? Some people in the community believe their vision has decreased significantly despite no clinically confirmed relapses.
There are theories that vision loss can become progressive despite no additional relapsesWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community)., after a severe attack that causes a lot of damage. In this regard, it is similar to other severe optic nerveThe cranial nerves that relay messages from your eyes to your brain to create visual images. These nerves extend from the retina in the back of the eyes to the part of the brain that processes what we see. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), they may be the target of inflammation or lesions, sometimes causing visual disruption or blindness. injuries. There are not many patients where this occurs with MOG antibody diseaseOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , but there may be some. In addition, patients with optic nerveThe cranial nerves that relay messages from your eyes to your brain to create visual images. These nerves extend from the retina in the back of the eyes to the part of the brain that processes what we see. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), they may be the target of inflammation or lesions, sometimes causing visual disruption or blindness. damage will notice significant fluctuations in their vision from hour-to-hour due to being more sensitive to different lighting conditions, etc.
2. When a patient presents with possible relapse symptoms but they show no signs of active disease on their MRI, what are the recommended next steps to confirm the symptoms are tied to MOGAD vs. a different disease or another medical condition?
There is no set workup in this circumstance, but rather it all depends onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. the symptoms. For example, if the symptom is neuropathic pain, the workup might include looking for nerve root compression or medication toxicity. For vision loss, the workup may include an ophthalmological exam. It is important to rule out a pseudo-relapseThe recurrence of neurologic symptoms often due to an exacerbating factor or trigger such as heat or sickness. Pseudo-relapses can often be distinguished clinically from relapses by their fluctuance in severity and improvement over 24-48 hours. Pseudo-relapses will never show any new or worsening lesions on MRI. which can occur because of heat or fever and not due to a true biological relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community)..
3. When an adult or pediatric patient exhibits psychological symptoms, how do physicians distinguish the separation between MOGAD symptoms and other causes?
Adult situations: MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. psychological symptoms that occur in adults include fatigue and maybe depression. These may also be due to other causes and are often not distinguishable. In most cases, the contribution by MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. cannot be separated from non-MOG causes, and they are treated similarly. It is important to remember that the prevalence of anxiety and depression in the general community is rather high, and in MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease patients, these mood disturbances may have predated the onset of MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , or be reactive to a new diagnosis of MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease . It is critical to actively target management of anxiety and depression, as this may affect a patient’s quality of life significantly.
Paediatric situations: MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. psychological symptoms that occur in children may include confusion, attention problems, anxiety and many others. Some of these symptoms occur when MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. inflammationA process of the immune system that involves chemicals released by immune cells (i.e. white blood cells) inducing localized heat, swelling, redness, and pain to an area that occurs when tissue becomes damaged or infected from a pathogen, and usually results in the desctruction and removal of the pathogen and/or healing to the tissue. In the case of myelin oligodendrocyte glycoprotein antibody disease (MOGAD), inflammation is the result of the incorrect targeting of the myelin oligodendrocyte glycoprotein (MOG) by the immune system, resulting in damage to myelin sheaths. is active in the brain and some occur long after inflammationA process of the immune system that involves chemicals released by immune cells (i.e. white blood cells) inducing localized heat, swelling, redness, and pain to an area that occurs when tissue becomes damaged or infected from a pathogen, and usually results in the desctruction and removal of the pathogen and/or healing to the tissue. In the case of myelin oligodendrocyte glycoprotein antibody disease (MOGAD), inflammation is the result of the incorrect targeting of the myelin oligodendrocyte glycoprotein (MOG) by the immune system, resulting in damage to myelin sheaths. has subsided. In children, most psychological symptoms would be attributed to MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. as the most likely cause.
4. We have met some other MOGAD patients with other autoimmune conditions such as; psoriasis, Hashimoto’s, myasthenia gravis, rheumatoid arthritis, and giant cell arteritis. How can a doctor distinguish between symptoms from these diseases and symptoms from MOGAD?
Symptoms from MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease can generally be referred to a lesionIn relation to MOGAD, an area of damage or scarring in the central nervous system. It is caused by inflammation that results from the immune system attacking the myelin sheath around nerves. Lesions can be found on the brain, spine, or optic nerves. in the brain, optic nerveThe cranial nerves that relay messages from your eyes to your brain to create visual images. These nerves extend from the retina in the back of the eyes to the part of the brain that processes what we see. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), they may be the target of inflammation or lesions, sometimes causing visual disruption or blindness. or spinal cord. For example, if the symptom is vision problems and there is a new inflamed lesionIn relation to MOGAD, an area of damage or scarring in the central nervous system. It is caused by inflammation that results from the immune system attacking the myelin sheath around nerves. Lesions can be found on the brain, spine, or optic nerves. in the optic nerveThe cranial nerves that relay messages from your eyes to your brain to create visual images. These nerves extend from the retina in the back of the eyes to the part of the brain that processes what we see. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), they may be the target of inflammation or lesions, sometimes causing visual disruption or blindness., the problem is likely to be attributable to MOG antibody diseaseOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease . Giant cell arteritis also causes vision loss but those attacks are generally not visible onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. MRIA noninvasive imaging technique that uses strong magnetic fields to produce images of nearly any structure of the body. For MOGAD, it is typically used with and without contrast to identify disease activity in the central nervous system. and rather are notable onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. changes in the retina on ophthalmological exam. This reasoning process is applied to each symptom where we try to correlate the symptoms, with changes onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. neurological and objective findings like MRIA noninvasive imaging technique that uses strong magnetic fields to produce images of nearly any structure of the body. For MOGAD, it is typically used with and without contrast to identify disease activity in the central nervous system.. Systemic involvement that is unusual in MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease can also be a clue that there may be two pathologies going onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement..
5. Can MOGAD patients have hormonal or pituitary problems that affect growth, pregnancy and other functions of the brain?
Generally, MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease does not cause damage to the pituitary and endocrinological systems in the body. However, steroidsA type of medication typically given intraveneously or orally. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD) it is used as an immunosuppressant and anti-inflammatory to reduce disease activity and inflammation. In adults, it is sometimes used in high doses for acute attacks. In some adult patients, it may be used for 1-2 months after an acute attack to avoid a rapid onset of relapse. Higher doses (>10mg/day) are not recommended for an extended period of time but lower doses (<=10mg/day) may be used in some patients longer term. In children, it may be used after treatment of an acute attack, but it is not recommended long-term due to the profound effects of chronic steroids on a child’s health. Use of oral prednisone as a maintenance therapy in relapsing pediatric MOGAD patients is discouraged due to side effects in developing children, and other therapies such as monthly immune globulin are suggested. (To understand relapsing during steroid tapering, see Steroid Dependency) used to treat the disease have profound effects onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. these symptoms and some can be long-lasting.
6. Do MOGAD patients experience more hyperthyroidism or hypothyroidism than the general population?
Yes, there does appear to be a higher incidence of thyroid disease in MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. patients than in the general population. However, it is interesting to note that patients with MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease do not appear to have a much higher rate of other autoimmuneA disease in which the immune system incorrectly targets and attacks an individual’s own healthy cells. conditions over and above the general population, compared to, for example, patients with AQP4+ NMOSDA disorder of the central nervous system that primarily affects the nerves of the eye and the spinal cord. Also known as Neuromyelitis Optica (NMO) or Devic’s Disease.
7. Can you describe what causes the mental confusion and forgetfulness that patients casually refer to as MOG fog?
There are several possible explanations for MOG fog. One possibility is that there are small amounts of damage in the brain from MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. attacks that accumulate over time. Another possibility is that inflammationA process of the immune system that involves chemicals released by immune cells (i.e. white blood cells) inducing localized heat, swelling, redness, and pain to an area that occurs when tissue becomes damaged or infected from a pathogen, and usually results in the desctruction and removal of the pathogen and/or healing to the tissue. In the case of myelin oligodendrocyte glycoprotein antibody disease (MOGAD), inflammation is the result of the incorrect targeting of the myelin oligodendrocyte glycoprotein (MOG) by the immune system, resulting in damage to myelin sheaths. in the spinal fluid releases molecules that interfere with normal brain function. Or perhaps there is some sort of systemic inflammationA process of the immune system that involves chemicals released by immune cells (i.e. white blood cells) inducing localized heat, swelling, redness, and pain to an area that occurs when tissue becomes damaged or infected from a pathogen, and usually results in the desctruction and removal of the pathogen and/or healing to the tissue. In the case of myelin oligodendrocyte glycoprotein antibody disease (MOGAD), inflammation is the result of the incorrect targeting of the myelin oligodendrocyte glycoprotein (MOG) by the immune system, resulting in damage to myelin sheaths. occurring in the body that impacts onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. normal brain function. Forgetfulness can also be due to some medications such as those that are used for pain and muscle spasms.
8. What are the challenges of getting these IG-based medicines FDA approved for use in preventing MOGAD?
The challenge is that the company has to complete a human trial with enough statistical rigor to prove scientifically that the medication works. Statistical rigor imposes many challenges including ensuring the data is unbiased and that there are enough patients that the answer is clear. This could take years and millions of dollars. For this type of investment, there has to be a high degree of confidence that the medication will work.
9. For patients who have had transverse myelitis from this disease, is there hope for repairing nerve damage to improve function and reduce pain and spasms?
Transverse myelitis (TM)A disorder caused by inflammation of the spinal cord. It is characterized by symptoms and signs of neurologic dysfunction in motor and sensory tracts on both sides of the spinal cord. The involvement of motor and sensory control pathways frequently produce altered sensation, weakness and sometimes urinary or bowel dysfunction. In relation to MOGAD, the inflammation is caused by the MOG Antibody. from any cause often leads to pain and spasms. Disability can be severe. TMA disorder caused by inflammation of the spinal cord. It is characterized by symptoms and signs of neurologic dysfunction in motor and sensory tracts on both sides of the spinal cord. The involvement of motor and sensory control pathways frequently produce altered sensation, weakness and sometimes urinary or bowel dysfunction. In relation to MOGAD, the inflammation is caused by the MOG Antibody. from MOGAD tends to heal better than TMA disorder caused by inflammation of the spinal cord. It is characterized by symptoms and signs of neurologic dysfunction in motor and sensory tracts on both sides of the spinal cord. The involvement of motor and sensory control pathways frequently produce altered sensation, weakness and sometimes urinary or bowel dysfunction. In relation to MOGAD, the inflammation is caused by the MOG Antibody. from AQP4+ NMOSDA disorder of the central nervous system that primarily affects the nerves of the eye and the spinal cord. Also known as Neuromyelitis Optica (NMO) or Devic’s Disease, for example. For those with persistent symptoms beyond 18 months after the TMA disorder caused by inflammation of the spinal cord. It is characterized by symptoms and signs of neurologic dysfunction in motor and sensory tracts on both sides of the spinal cord. The involvement of motor and sensory control pathways frequently produce altered sensation, weakness and sometimes urinary or bowel dysfunction. In relation to MOGAD, the inflammation is caused by the MOG Antibody. attack, recovery back to normal is rare (but possible!) and the approach should be to find a combination of medical and non-medical therapies that will improve quality of life and allow the person to return to life as normal as possible.
10. If a MOGAD patient has a high titer level, are they at risk for a relapsing form of MOG Antibody Disease? What is considered a high titer level?
We don’t yet know if titers are a reliable marker of relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community). but in one study, those with persistent positive MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. titers – 6-12 months since the first positive test had the highest risk of relapse. More work is required to confirm the prognostic and therapeutic implications of MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. titers.
11. For patients who have only had one attack, how many years do you feel is sufficient to diagnose a patient as having monophasic disease?
The average relapse rate is 1 attack per year for MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease . If you go three years without medication and you don’t relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community)., chances are fairly good that you have a monophasicA disease characterized by only one phase or attack. disease. Of course, there are no guarantees.
Key Takeaways
- Some MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease patients who have relapsing optic neuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. tend to have attacks intermittently with periods of disease activity and then stability. However, some patients are steroid dependent and follow a chronic relapsing inflammatory optic neuropathy (CRION)A disease where the optic nerve is the target of two or more demyelinating attacks separated by at least 30 days, resulting in visual deficits and may or may not be accompanied by pain on eye movement. CRION patients may or may not be MOG antibody positive. category where worsening of optic neuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. or recurrence occurs due to a steroid taper or cessation of steroidsA type of medication typically given intraveneously or orally. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD) it is used as an immunosuppressant and anti-inflammatory to reduce disease activity and inflammation. In adults, it is sometimes used in high doses for acute attacks. In some adult patients, it may be used for 1-2 months after an acute attack to avoid a rapid onset of relapse. Higher doses (>10mg/day) are not recommended for an extended period of time but lower doses (<=10mg/day) may be used in some patients longer term. In children, it may be used after treatment of an acute attack, but it is not recommended long-term due to the profound effects of chronic steroids on a child’s health. Use of oral prednisone as a maintenance therapy in relapsing pediatric MOGAD patients is discouraged due to side effects in developing children, and other therapies such as monthly immune globulin are suggested. (To understand relapsing during steroid tapering, see Steroid Dependency).
- The MOG antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. test SHOULD NOT be taken in cerebrospinal fluidA clear, colorless liquid found throughout the cavities of the central nervous system that helps protect the brain and spinal cord by acting like a cushion against sudden impact or injury, and provides a medium for the transport of nutrients and the removal of waste products for proper functioning. alone, but rather simultaneously with serum onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. a live cell-based assayA laboratory test used to: • Measure the presence or amount of a specific substance: in a sample, such as blood, urine, or tissue.
• Determine the potency or activity: of a drug or other substance.
• Analyze the purity: of a chemical compound.
• Identify and quantify: biomarkers related to a disease or condition.
and the most accurate test is onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. the first attack prior to treatment.
- There are NO individual biomarkers that are predictive of a future relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community)..
- Mental health problems such as depression and anxiety are often pre-existing in a patient or often reactive to their new diagnosis, losing neurological function or response to needing long-term treatment in relapsing patients. This needs to be recognized, diagnosed and managed proactively as it impacts quality of life.
- Patients who have MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease reported more sleeping difficulties and fatigue, based onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. a study done by The MOG Project in collaboration with Johns Hopkins Medicine, compared to their household controls. This was highly evident in those who suffered from bilateralRefers to disease or attack on two sides. optic neuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement.. https://journals.sagepub.com/doi/10.1177/20552173221131235
- Phenotypes tend to change according to age and transition to puberty. A lot of work needs to be done around understanding the role of sex hormones, including the role of estrogen.
- Pain onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. eye movement and a sudden decline in vision over a few days points to a possible optic neuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community)., compared to a more slow and gradual decline in vision loss which is more likely attributed to a cataract or a retinal detachment. Either way, both need to be investigated immediately.
- For challenging MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease cases who are not responding to therapeutic approaches, it is important to go back and review their scans, examinations and blood work to ensure that they indeed have MOG antibody diseaseOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease . Once it is confirmed that they do indeed have MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , try and find the right combination therapy for them, a different treatment option such as tocilizumabAn immunosuppressive drug that blocks the inflammatory protein IL-6. This may improve symptoms caused by inflammation. The common brand for this drug is Actemra. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), this medication is used to suppress the immune system to reduce disease activity. May be given intraveneously or by subcutaneous injection. or enroll them in one of the the new clinical trials for new drugs such as rozanolixzumab or satralizumab.
- IVIGA human blood donor product made up of immunoglobulins (IgG and IgM antibodies) derived from plasma that can be administered intravenously (IVIG) or subcutaneously (SCIG). For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), it is used as an immunomodulator to reduce disease activity. Sometimes used for acute attacks or as an ongoing preventative treatment. is effective in reducing relapsesWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community). in adults, one study shows, as long as they are onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. an adequately high dose. The study data showed best efficacy in those higher doses as compared to those who were onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. a lower and less frequent dose. https://jamanetwork.com/journals/jamaneurology/article-abstract/2790493
