MOGAD is caused by a specific protein in the blood called the MOG antibody (Myelin Oligodendrocyte Glycoprotein antibody), which is produced by our white blood cells. Sometimes MOGAD is a self-limiting illness, which means it can resolve itself without treatment. The attacks caused by MOGAD can be more severe and may leave permanent damage, compared to those seen in MS, which are usually followed by good recovery. Some patients may suffer from seizures or stroke-like episodes. The most common symptoms are vision loss due to inflammation of the optic nerve (optic neuritis), or a weakness of the arms and legs, due to inflammation of the spinal cord (transverse myelitis).
MOGAD is a disorder that may appear identical to NMO and MS. Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease (MOGAD) What is Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease (MOGAD)? All these medications may require blood monitoring. Commonly used oral medications include prednisone, azathioprine, and mycophenolate mofetil. The drugs proven to be most effective include rituximab, inebilizumab, eculizumab, satralizumab, and tocilizumab. These drugs are different to the ones given to MS patients. In order to prevent further attacks, many drugs can be given which suppress the immune system. A plasma exchange (a treatment like dialysis that cleans the blood of antibodies) can also be given to prevent further damage and speed up recovery. A high-dose steroid is given which suppresses the immune system. There is no cure for NMO, but a relapse or attack can be treated with medication. However, one third of patients may not have the antibody despite otherwise being typical for NMO, so if other symptoms are present and diagnostic tests have ruled out other possible causes, a diagnosis of seronegative NMO can be made. Blood is tested for NMO antibodies and if present, confirms the disease. If a patient presents with loss of sight or weakness, an MRI scan is usually performed first, sometimes with spinal fluid tests. It is more common in women, and occurs all over the world, with African, Asian, and Native American populations being more at risk. While we understand the mechanisms that cause NMO (specifically the NMO antibody), just like in MS, we do not know what causes NMO. This means that if we can prevent the relapses, then patients can remain stable. This is not the case with NMO as it is a relapsing-remitting disease and there is no progressive phase. MS has a secondary progressive stage, which means that the condition worsens gradually over time – often years – after a long period of relapsing disease if left untreated. The immune attacks in NMO are typically more severe and may leave permanent damage, compared to MS attacks which are often associated with a better recovery. It is not known why the white blood cells of the immune system mistakenly attack the nervous system. This antibody attacks parts of the nervous system and is a specific marker for the disease. Most cases of NMO are caused by a specific protein in the blood called NMO antibody (anti-aquaporin-4 antibody), which is produced by the white blood cells. Other symptoms can include nerve pain, spasms, and stiffness, as we as bladder, bowel and sexual problems. Some patients may experience severe episodes of nausea and vomiting for no apparent reason.
The main symptoms are loss of sight due to inflammation of the optic nerve (optic neuritis) or weakness of the arms and legs due to inflammation of the spinal cord (transverse myelitis). Neuromyelitis Optica Spectrum Disorder (NMOSD) or Neuromyelitis Optica (NMO), is a disease that resembles MS. Neuromyelitis Optica Spectrum Disorder (NMO) What is Neuromyelitis Optica Spectrum Disorder?
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