Early Signs of a Rare Disease
Now that I have been diagnosed with Myelin Oligodendrocyte GlycoproteinA type of protein involved in cell adhesion. Present throughout myelin sheaths. Antibody DiseaseOften referred to as MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , Anti-MOG, MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Ab+, MOG Antibody DiseaseOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Associated 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, MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. positive disease , or MOG-ADOften referred to as MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , Anti-MOG, MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Ab+, MOG Antibody DiseaseOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Associated 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, MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. positive disease , I have met others who are afflicted and have listened to their stories. They all start similarly, with an acuteThe severe and sudden onset of a disease process. attack, out of the blue, and always marking the start of an unexpected turn in health. My story is different. I experienced unexplained chronic fatigue and a slight dimming of vision: a little peek of what was to come. Almost 19 years ago at the point of writing this story, I was a young mother, with a wonderful husband and 2 beautiful little girls. By all rights I was in the happiest part of motherhood. I had a good life with my family and I had plenty of energy. I don’t really remember how or exactly when it came 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., but I started to notice that I was feeling very fatigued, shaky and weak, especially when exerting myself. I had labored breathing at times and I felt like my legs weighed a million pounds. It is hard to describe, but it seemed like if I stopped struggling to breath, my body would just stop breathing naturally. A typical day for me started with normal energy, which only lasted about 2 hours. After that I could barely walk, I had labored breathing and I felt like if I did not lie down, I would fall down. Frankly, it was frightening. If I took a nap for about an hour, I was fine again and the whole cycle would repeat. That feeling, while waxing and waning, did not leave me for two years. I prayed and a few times, there were tears. Because of the support of my husband and family though, I never gave up hope even though life was over as I knew it. Early in this two-year battle, I remember noticing one day that our normally bright kitchen seemed dimmer than usual. I asked my husband what he thought and he said it didn’t seem darker to him. It was very subtle and only lasted a week. Also during this time, I remember many trips to the doctor to try to figure out what was wrong. The repeated visits were frustrating for my doctor, who just told me that he had no idea what was wrong with me as my blood tests were perfect. His staff stopped returning my calls. Frustrated myself, I found a new doctor. I was told the same thing by this new doctor as well and my visits, I could tell, were an annoyance to him. Despite asking for more tests, I never saw a neurologist or was given an MRIA noninvasive imaging technique that uses strong magnetic fields to produce images of nearly any structure of the body. For MOGADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , it is typically used with and without contrast to identify disease activity in the central nervous systemNerve tissue that resides in and composes the brain, spinal cord, and optic nerve.. I look back and wonder if they would have seen something. My doctor did, however, send me to a psychiatrist because he suspected that my fatigue was caused by depression. Despite being adamant that I was not depressed, he insisted, so I went. After talking with the psychiatrist, he said the funniest thing I’ve ever heard one doctor say about another. I won’t repeat it here. Needless to say, he did not diagnose me with depression. He instead said that he did not know what was wrong with me, but he did know that I needed a new doctor. After those two years of chronic fatigue, I slowly got better, always wondering if that terrible fatigue would return. I wondered if I would die from this mysterious illness and thought about never seeing our girls get married or meeting our grandchildren. It was a scary time. I did pretty well for the next four years until I got Lyme Disease. At the time, I was very sick and I noticed again that the dimming vision occurred. Again, it was very slight and this time I brushed it off because it had happened before and it didn’t seem to be a problem because it went away. Little did I know, that was a clue to unlocking the mystery. Fast forward to April of 2014. After a terrible cold, I started having intense stabbing pain around my eye sockets, especially while rolling them around. I was treated with antibiotics assuming it was a sinus infection, but the treatment did not work and the pain only got worse. It wasn’t long before I started going blind. I raced to the eye doctor who immediately got me in touch with an optic neurologist, Dr. Shalom Kelman in Baltimore. By the time I saw him, I was almost blind. He confirmed that I had Optic NeuritisInflammation 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. and I he treated me with a round of high-dose SolumedrolA 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