In April, 2022, The MOG Project was joined by Professor Russell Dale, Dr. Sudarshini Ramanathan, and A/Professor Fabienne Brilot from the University of Sydney and Kids Neuroscience Centre, Westmead in a MOGcast series called MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease : Diagnosis, Management and Outcomes. 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 Professor Russell Dale, Dr. Sudarshini Ramanathan, and A/Professor Fabienne Brilot for taking the time to help the community understand the diagnosis, management and outcomes of MOG Antibody DiseaseOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease which 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. in both serum and cerebrospinal fluid (CSF)A 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., the expanding clinical phenotypes of MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , investigations into 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). and all the incredible research that they continue to undertake for this rare neuroimmunological disorder.
You can view the entire MOGCast here.
As promised, we have collected 10 important questions that we did not have time to answer during the podcast which originated from our MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease community. Professor Russell Dale, Dr. Sudarshini Ramanathan, and A/Professor Fabienne Brilot answered these questions for us and we are pleased to provide them below:
Questions and Answers
- How long should a patient be kept 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 steroid taper regimen? What is the recommended time frame?
When a patient first presents with an episode of demyelinationThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. that is consistent with MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , the data suggests that they are often very responsive to treatment with 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), with rapid clinical improvement. This treatment may be in the form of pulsed intravenousA way of giving a drug or other substance through a needle or tube inserted into a vein. 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) for a few days followed by oral prednisoneA 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), or with oral prednisoneA 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) from the start. There is emerging evidence that a slower prednisoneA 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) taper in MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease that lasts at least three months and potentially longer, may reduce the rate of an early 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).. Although it is our practice to consider a cautious steroid taper over a few months, others do not support this. More research is needed to address this.
- What are some triggers for a 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).?
Some patients have features of a viral infection in the week or so prior to the clinical onset of a first presentation or 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). of MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease . This could be in the form of a respiratory tract infection or gastrointestinal infection, for example. There are some reports of presentations being preceded by a vaccine in the week or two prior to clinical onset, although the population health benefits of vaccinations far outweigh the rare occurrence of these events. There is most often no identified trigger for 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)..
- Who should be involved in the clinical care of a patient who has MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease ?
Patients with MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease often come under the care of an ophthalmologistA board-certified medical doctor that specializes in diseases and disorders of the eye. or neurologist depending 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 clinical features they present with (such as 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., transverse myelitisA 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., or brain involvement). Depending 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 clinical scenario, their care may be shared with immunologists as some patients with relapsing disease may require more sustained immunotherapy. Some patients who may struggle with a new diagnosis and the effect of this condition 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. their life may benefit from a team based approach which involves a neuropsychiatrist and/or a psychologist.
- Can children who’ve had ADEM or other presentations of the brain, go 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. to suffer learning difficulties at school?
- Can MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease patients have other comorbidities? (e.g., other diseases and disorders). If so, what are some examples?
- What differentiates paediatric patients from adult patients who have MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease ? Who is likely to have the better outcome?
Children frequently present with ADEMAn initial and brief autoimmune attack that causes widespread inflammation and damage to the brain, spinal cord, and optic nerve, typically in children. This initial attack establishes the basis for diagnosis. The MOG antibody is detectable in a percentage of Acute Disseminated Encephalomyelitis (ADEM) patients., while 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. is common in both children and adults. ADEMAn initial and brief autoimmune attack that causes widespread inflammation and damage to the brain, spinal cord, and optic nerve, typically in children. This initial attack establishes the basis for diagnosis. The MOG antibody is detectable in a percentage of Acute Disseminated Encephalomyelitis (ADEM) patients. is quite rare in adults. Interestingly, apart from ADEMAn initial and brief autoimmune attack that causes widespread inflammation and damage to the brain, spinal cord, and optic nerve, typically in children. This initial attack establishes the basis for diagnosis. The MOG antibody is detectable in a percentage of Acute Disseminated Encephalomyelitis (ADEM) patients., we have noted that the clinical and radiological features of children with 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. and transverse myelitisA 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. are quite similar to those of adults, and that treatment responses are also similar. While children may theoretically do better than adults as they might have fewer comorbidities, this of course still comes down to the severity of the clinical episode, the time to disease recognition and diagnosis, and the timing of appropriate immunotherapy.
- The literature seems to be mixed about 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. Why do some patients still have high 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 but have never relapsed (monophasicA disease characterized by only one phase or attack. course) and others are becoming negative and still relapsing?
This is an interesting topic which still needs work. There is evidence that looking at longitudinal 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. titres/end point dilutions/binding levels in a single patient shows that they often have more 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. binding at clinical onset or during 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). compared to when they are in disease remission. But some patients have prolonged intervals between 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)., with either sustained positive titres or they become seronegative for a period and then become seropositiveA laboratory test result that shows the presence of a specific marker, usually an antibody, in the blood. For MOGAD, seropositive means that you have tested positive for the MOG antibody. at the next 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).. It would be unusual for a relapsing patient to be seronegative, and if this was the case, the timing of sample collection and its proximity to the 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)., the type of diagnostic 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.
used to detect 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. in serum, and the type of concomitant immunotherapy that the patient 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., should all be taken into account
- When should a patient present to the emergency department or call their neurologist in terms of exhibiting signs of a 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).?
Patients should always come to get medical attention if they notice clinical deterioration or signs consistent with a relapse such as loss of vision, weakness or sensory changes, bladder dysfunction, or other concerning features. Clinicians would always want to investigate and act 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. new neurological deficits as early intervention reduces the extent of residual disability.
- If a patient is positive for the MOG 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., and goes 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. to have multiple 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). that are typical clinical presentations of MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease but their blood work is persistently negative, would you still classify them as having MOG-AD?
As mentioned in question 7, it is unusual for a patient to 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). persistently with ongoing seronegative results. So, in such a case, the timing of sample collection and its proximity to the 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)., the type of diagnostic 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.
used to detect the MOG 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. in serum, and the type of concomitant immunotherapy that the patient 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., should all be taken into account. And it is certainly important to keep an open mind with differential diagnoses as a patient can have more than one medical condition.
- How important is the doctor-patient relationship for the management and care of a MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease patient considering it is a relatively new disease?
In any medical condition, the doctor-patient relationship is of critical importance. Good communication and developing a partnership is critical to ensure the patient understands the condition, their options, and implications of different pathways.
Key Takeaways from the MOGCast and questions answered in this blog
- A positive serum test 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.
is vital for an accurate diagnosis of MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , as long as it fits the typical clinical picture and/or radiological findings are consistent with MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease .
- Early research is being undertaken to understand if 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. positivity in both serum and CSFA 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. is more commonly associated with a more severe and/or relapsing form of MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease .
- The data suggests that patients who present with a demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. episode consistent with MOG-AD are often very steroid responsive with rapid clinical improvement. Emerging evidence supports a slow 3 months or potentially longer taper reduces the risk of early 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).. However, more research is needed to clarify this.
- It is unusual for a patient to relapse on a negative 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. result, however still possible. Things that need to be taken into consideration for a patient relapsing 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 negative result include: timing of the sample collected, the 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.
that was used and treatment/s 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.. However, clinical judgement remains the key for these relapsing presentations.
- According to international and national data, patients who are relapsing tend to do better 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. treatment than no treatment.
- A clinical evaluation and an expedited 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. is vital during a suspected 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 not always accessible. It’s up to the clinician to make a clinical judgement 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. symptom onset and disability in a timely manner so that more damage is not accumulated.
- Yes, it’s time for MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease to have its OWN international criteria. A manuscript is in revision internationally and will help with the diagnosis, clinical trials and better care of patients who have MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease .
By Jenny Khazen, Australian Ambassador & Medical Professional Outreach Specialist
With contributions from Dr. Sudarshini Ramanathan, A/Prof. Fabienne Brilot and Prof. Russel Dale.
