Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease - Causes, Symptoms, and Treatments

Introduction

Immune cells are intended to attack and resist external agents and disease-causing microbes. However, immune cells occasionally behave indifferently and exhibit resistance against bodily cells, which is reflected in autoimmune diseases. Myelin oligodendrocyte glycoprotein antibody-associated disease is one such disorder with broad manifestations.

What Is Meant by Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease?

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is quite a rare condition arising from an indifferent immune response towards a particular body protein present in the myelin sheath of nerves. It exhibits manifestations as a result of the nerves involved. Studies revealed that MOGAD does not exist in parallel with other autoimmune conditions.

What Is the Cause of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease?

The exact cause that triggers MOGAD is still not clear. Research is going on over the unanswered queries. However, the widely accepted hypothesis concerning MOGAD suggests its autoimmune origin.MOGAD is an immune-mediated condition wherein the immune system exhibits troubles. Immune cells wrongly recognize a specific protein in the myelin sheath medically known by the name myelin oligodendrocyte glycoprotein (MOG) as an invading substance and produce antibodies specifically against MOG protein molecules. Myelin oligodendrocyte glycoproteins are flagged on the surface of the myelin sheath. Antibodies aimed at MOG attack them and induce damage. It targets the myelinated nerve cells and exerts its impact on the central nervous system. This particular disease condition severely affects nerve cells forming the brain's backbone, optic nerves, and spinal cord. Any form of trauma to the nerve cells greatly influences its functions and reflects as disturbed and interrupted impulse conduction.

What Are the Symptoms Associated With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease?

MOGAD exhibits wide-ranging manifestations involving the optic nerve, spinal cord, brain, and brain stem. However, clinical findings are more pronounced with optic nerve involvement than other central nervous areas. Widely encountered manifestations of MOGAD include the following:

• Visual Disturbances: Optic nerve involvement reflects in the form of optic neuritis, which is responsible for significant changes in eyesight. Visual disturbances range from blurred vision to complete vision loss in one or both eyes. Certain patients manifested challenges with color vision as well.

• Aching Eyes: Eye pain is frequently encountered in MOGAD, resulting from inflammation (swelling and pain) in the optic nerve. Pain aggravates upon eye movements.

• Motor Functional Deficit: MOGAD often elicits in the form of compromised motor functions, especially in the limbs. Frequently, it is associated with failing limbs with general weakness. In severe cases, it could even result in the paralysis of the entire limb.

• Urinary and Bowel Issues: Patients exhibit challenges in urine control. Often, urination becomes involuntary and uncontrollable, impacting the patient's quality of life. Apart from urination, bowel movements are also influenced by MOGAD. At times, the patient elicits challenges in urinating fully. Some amount of urine tends to be retained in the bladder.

• Paresthesia: Certain bodily parts exhibit poor sensations.

• Altered Tonicity: Muscle strength and elasticity will significantly change. Muscles exhibit more firmness and rigidness.

• Neck Pain: Occasionally unbearable and troublesome pain will be felt in and around the neck region. Apart from neck pain, it may also elicit pain in the abdominal area.

• Sexual Dysfunction: MOGAD may significantly impact the sexual lives of men by eliciting trouble with penile erection.

• Acute Disseminated Encephalomyelitis: In younger age groups, MOGAD may lead to a medical condition called acute disseminated encephalomyelitis (ADEM). It is manifested with diverse symptoms, including confusion, disorientation, fever, challenges in vision and balance, nausea, headache, and vomiting. Paresthesia (altered sensation) is also encountered in MOGAD with ADEM.

• Cerebral Cortical Encephalitis: Epileptic seizures are elicited in MOGAD due to associated cortical encephalitis. Other prominent manifestations associated with cerebral cortical encephalitis include nystagmus (constant and speedy eye movement), dysphagia (strained swallowing), diplopia (doubling of vision), and dysarthria (speaking difficulty).

How Is Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Diagnosed?

• Diagnosis initiates with a detailed medical history and clinical findings. Blood tests to detect serum myelin oligodendrocyte glycoprotein antibody guide to final diagnosis as it is a reliable and confirmatory test for MOGAD.

• Neurological evaluation determines compromised neurological functions like coordination, vision, balance, etc. Visual tests and other diagnostic tests also facilitate the detection of visual loss.

• Magnetic resonance imaging (MRI) of the brain and brain stem are advised to get a clearer picture of the area, which helps to point out areas of irregularities and impairment.

• Evaluation and assessment of the cerebrospinal fluid also aid in diagnosing the disease condition. The lumbar puncture technique is advised for gathering cerebrospinal sap.

• Eye scans are proposed to determine the extent and type of damage in the optic nerve, which helps understand the diagnosis.

• Optic neuritis can be graded more accurately by optical coherence tomography, which provides an idea about the intensity of nerve damage.

What Are the Treatment Interventions Available for Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease?

As the MOGAD condition is marked by inflammation in the central nervous system, it can be tackled with the help of medicines that deal with the inflammation and thereby check the symptoms. Some of the regularly preferred treatment strategies include the following:

• Steroids: Corticosteroids are preferred for dealing with the symptoms. Methylprednisolone is the chiefly advised steroid, typically in high doses, and is administered into the veins (intravenously).

• Plasma Exchange (PLEX): It is a specialized treatment intervention in which the plasma is exchanged to reduce the antibody concentration against the MOG protein in the blood.

• Intravenous Immunoglobulin (IVIG): It helps to cope with inflammation. In this technique, antibodies are administered into the veins. Frequent IVIG transfusions are preferred for long-standing MOGAD patients.

• Immunosuppressives: They are a specific class of medicines that suppress and conceal immune reactions. As MOGAD is greatly immune-mediated, immunosuppressives are advised when other drugs do not seem fruitful. Azathioprine is an extensively prescribed immunosuppressive drug for MOGAD.

• Rehabilitative Therapies: In case of complications like limb paralysis and vision loss, rehabilitative therapies are advised to manage the impairment.

Conclusion

Myelin oligodendrocyte glycoprotein antibody-associated disease is projected as an immune-mediated illness or condition that results in demyelination. The treatment strategies are primarily based on the severity of the symptoms.