MOG Project Champions

At 5 years old, my daughter Isabel was a beautiful, bubbly girl with no health problems.  I took her to the Father-Daughter Dance and she became ill 2 days later.  This was the start of what would amount to 3 hospital visits and 5 doctor visits with multiple misdiagnoses.  One week after the Father-Daughter Dance, Isabel was admitted for what would turn out to be a misdiagnosed disease.  At first, she was having seizuresA sudden, temporary disturbance in brain activity that causes changes in behavior, movement, sensation, or consciousness with active vomiting, extreme behavioral changes and her doctors did not know what was going onInflammation of 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. that may be classified as unilateralRefers to disease or attack on a single side. (affecting one eye) or bilateralRefers to disease or attack on two sides. (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement..  They continued to treat her for unrelated illnesses.  Even while in the hospital, the doctors there attempted to discharge her, stating that it was only an infection and that she was fine.  We told the doctors that it was something neurological and that she was in an altered mental state.  They insisted that this was not the case and that we did not know what it was.  By the next day, she was in the Pediatric ICU fighting for her life, paralyzed and unable to speak with absent seizures as well as other neurological problems and altered consciousness. The doctors treating her were concerned and told us she may not make it through the night as her body was shutting down and they were concerned her respiratory function may go next.  In ICU the doctors said they would have to rule out meningitis and would have to do a lumbar puncture without sedation due to how far gone she was.  They requested that we hold her down since there was no sedation.  After the lumbar puncture, they diagnosed her with acuteThe severe and sudden onset of a disease process. disseminated encephalomyelitisAn initial and brief autoimmuneA disease in which the immune system incorrectly targets and attacks an individual's own healthy cells. attack that causes widespread 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. and damage to the brain, spinal cord, and 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., typically in children. This initial attack establishes the basis for diagnosis. The 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. is detectable in a percentage of Acute Disseminated Encephalomyelitis (ADEM)An 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. patients., or ADEMAn initial and brief autoimmuneA disease in which the immune system incorrectly targets and attacks an individual's own healthy cells. attack that causes widespread 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. and damage to the brain, spinal cord, and 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., typically in children. This initial attack establishes the basis for diagnosis. The 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. is detectable in a percentage of Acute Disseminated Encephalomyelitis (ADEM)An 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. patients., and at the time, it was believed to be a “one-time illness”.  After getting high-dose steroidsA type of medication typically given intraveneously or orally. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD)Often referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease   it is used as an immunosuppressant and anti-inflammatory to reduce disease activity and 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 adults, it is sometimes used in high doses for acuteThe severe and sudden onset of a disease process. attacks. In some adult patients, it may be used for 1-2 months after an acuteThe severe and sudden onset of a disease process. attack to avoid a rapid onset 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).. 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 acuteThe severe and sudden onset of a disease process. attack, but it is not recommended long-term due to the profound effects of chronic 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) 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 child’s health. Use of 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) as a maintenance therapy in relapsing pediatric MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease   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 DependencyMay occur for MOGAD patients when tapering to a lower dose of steroids causing recurrance of symptoms and may cause a relapse of new disease activity.) she was able to come home, and it took over a month to get her walking onInflammation of 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. that may be classified as unilateralRefers to disease or attack on a single side. (affecting one eye) or bilateralRefers to disease or attack on two sides. (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. her own and drinking without a straw. The next 18 to 24 months we had her in therapy to help make almost a full recovery with only slight cognitive delay being noted. At the beginning of January and February of 2016, this supposed “one-time illness” attacked again. For 3 weeks we took her to 15 doctor visits with 9 different doctors and 3 hospital visits to be told nothing was wrong and that we were over-reacting.  We continued to fight against these doctors and 3 weeks from the start and almost 2 years to the day of the first attack she had a relapseWhen you present to your doctor or hospital with new or worsening central nervous systemNerve tissue that resides in and composes the brain, spinal cord, and optic nerve symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern 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).. (Also referred to as a flareRefer to Relapse. by the myelinAn insulating layer, or sheath that forms around nerves, including those in the brain and spinal cord. It is made up of protein and fatty substances. This myelin sheath allows electrical impulses to transmit quickly and efficiently along the nerve cells. If myelin is damaged, these impulses slow down. oligodendrocyte glycoproten 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. disease (MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease  ) community). of ADEMAn initial and brief autoimmuneA disease in which the immune system incorrectly targets and attacks an individual's own healthy cells. attack that causes widespread 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. and damage to the brain, spinal cord, and 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., typically in children. This initial attack establishes the basis for diagnosis. The 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. is detectable in a percentage of Acute Disseminated Encephalomyelitis (ADEM)An 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. patients. 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. (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.)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. of 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. that may be classified as unilateralRefers to disease or attack on a single side. (affecting one eye) or bilateralRefers to disease or attack on two sides. (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement..  However this time she was left blind in one eye and for several weeks, continued losing her vision in the other, along with extreme behavioral changes and severe headaches. Doctors then said that we were somewhat right but also wrong in that it was not a relapseWhen you present to your doctor or hospital with new or worsening central nervous systemNerve tissue that resides in and composes the brain, spinal cord, and optic nerve symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern 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).. (Also referred to as a flareRefer to Relapse. by the myelinAn insulating layer, or sheath that forms around nerves, including those in the brain and spinal cord. It is made up of protein and fatty substances. This myelin sheath allows electrical impulses to transmit quickly and efficiently along the nerve cells. If myelin is damaged, these impulses slow down. oligodendrocyte glycoproten 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. disease (MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease  ) community). but what they thought was Multiple SclerosisAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve. (MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve.)An autoimmuneA disease in which the immune system incorrectly targets and attacks an individual's own healthy cells. disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS)Nerve tissue that resides in and composes the brain, spinal cord, and optic nerve leading to neurological symptoms originating from the brain, spinal cord, and/or 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.., a diagnosis