A Report On Multiple Sclerosis: Causes, Symptoms, And Treatment

Overview and pathophysiology

Multiple Sclerosis is acquired through the immune-related destruction and normal functioning of the central nervous system. The ailment is associated with myelin and secondary loss of axons. It is similar to a demyelinating disease, but it is different because the myelin is produced through the defective synthesis. Most of the leukodystrophies are genetic, therefore, it is inherited and become symptomatic in childhood. The determined whitish substance plaques the standard wounds in multiple sclerosis found within the optic nerve, (CN II), spinal cord and the brain (Geidl, Gobster, Streber & Pfeifer, 2018). The initial step of formation of a plaque is the penetration into the brain, via the blood-brain barrier, and starts whenever the associated adhesion molecules making circles in lymphocytes are attached to the endothelial receptors. When they enter into the brain, the inflammatory cascades rise with antibody production and cytokine, ingress and immediately there will be activation of more gross autoimmune destruction of the myelin and the inflammatory cells. When the formation of the plague occurs, they are formed in several parts of the central nervous system. Over time, it will form numerous forms of clinical symptoms of multiple sclerosis.

Recovery may vary, depending on the particular plaque; however, it is advisable that the recovery is done at the early stages of the disease. The underlying clinical symptoms may slowly disappear once the inflammation has reduced and only if little destruction of myelin has occurred. Some demyelinated axons sometimes develop certain sodium channels uniformly along a certain surface. These channels will allow it to regain the ability to transmit other possible actions. However, this is not efficient as compared to the salutary conduction of axons in myelin. Cases of significant axonal injury and loss explain a lack of clinical recovery later in the course of MS.

Cause

Much research has been carried out since when it was suggested in 1869 by French neurologist Jean Charcot on the cause of this disorder, but it remains unproven and idiopathic. The treatment is also idiopathic. However, there is much that can be done through the management of the signs and underlying latter signs of the disease. The aspect can be done through the invention of the modified drugs which will slow down the disabilities that come along the disease. However, this has been a challenge because the evidence currently used majorly points towards the interplay of the environmental, epigenetic complex interplay and hereditary factors that trigger the body’s immune system of an individual to produce and release the autoimmune provocative response. Hence, this response can be identified by the short-lived attacks on the cells that compose the myelin. After some time, loss of axons and loss of neurodegeneration and loss of the axons will lead to a person having a disability. The symptoms are experienced during the early stage of the asymptomatic phase. Additionally, the risk factors have evidence to support their impacts. 

Risk Factors

There are several factors that play part in this disease. They include the location of birth, the gender, season of the year in which a person is born, the family risk, the diet in which one consumes and the levels of the available vitamin D in a body. Additionally, recent research shows that smoking UVB exposure may be one of the risk factors associated with multiple sclerosis. The risk can be heightened by migrating influences. The sway is associated with the positive Epstein’s serology; this is specifically followed by premature communicable mononucleosis which is one factor that heightens the risks. The most common explanation is that some infectious environmental agents may gain access to a person's vulnerable genes before adolescents (Petzold, 2018). Evidence supporting this theory states that a person living in some tropical regions rarely develops this disease, however, if the person relocates to a temperate location before the beginning of puberty, they are at risk of acquiring the disease.

Prevalence

Multiple Sclerosis affects around a hundred thousand people worldwide. Thus, this is one of the major causes of several serious physical disabilities recorded in the world among the adult age. The most common pattern associated with the disease is known as the relapsing-remitting disease. It ought to be noted that these are the periods of stability which are referred to as the remission and the relapse and they occur when the symptoms are worse. It ought to be noted that most of the people living with multiple sclerosis experience relapsing-remitting multiple sclerosis at the beginning. Sixty-six percent experience it when the condition gradually develops. The 66% develops secondary progressive multiple sclerosis which causes the disability and gets worse as the time goes. However, this may not be related to the relapses which may experience less frequently and sometimes stop completely. Around 15% of the people living with multiple sclerosis have acute continuous multiple sclerosis. These symptoms grow gradually and may eventually get worst.

Signs and symptoms / Clinical Features

It’s usually a disease of the young adults, between ages 20-40; however, if suspected in older adults, a careful and thorough neurological examination may be done and can reveal milder symptoms of the illness. 80% of patients may have a relapsing and remitting course, consisting of episodic signs and symptoms with minimal up to no residual neurologic deficit (Leahy, Elseed & Counihan, 2017). After many years, the recovery from recurrent episodes tends to be incomplete or absent in about half of the patients and neurological deficits arise as part of the secondary progressive phase of the disease. The other 20% of diagnosed MS patients have a serious progressive neurological disorder referred to as primary progressive MS. Hence, this has a different progression and does not respond effectively to immunomodulating therapy.

The most common early signs of multiple sclerosis are experienced in the Optic Nerve (CN II) or the motor and the sensory deficits in the lower limbs since the elongated white substance tracts in the Central Nerves System is functionally related to the lower limbs and are likely to develop plaques. Blurry vision and diplopia are common as a result of internuclear ophthalmoplegia or Medial Longitudinal Fasciculus (MLF) syndrome. The patient may experience the Paroxysmal jabs of pain on one part of his or her face due to Trigeminal Neuralgia. The patient may report a tingling sensation and an electric shock down the spine into the arms or legs provoked by neck flexion –Lhermitte’s sign. The aspect is associated with the short-circuiting in the subsequent parts of the cervical spinal cord due to the local destruction of myelin from MS plaques or vitamin B12 deficiency or compression of the spinal cord. There may be also bowel and bladder dysfunction and cognitive impairment.

Diagnosis

Clinical Diagnosis of this disease is majorly based on the sign of lesions that are separated in space and time. They include the sending and relapsing signs which affect more than two distinct areas in the spinal cords and brain. Multiple sclerosis can be difficult to recognize because there are no tests or any clinical signs that are associated with the disease. Additionally, some other underlying causes may be eradicated and therefore the diagnosis and results may take longer. Recently, there are three major investigations carried but none of the investigations is one hundred percent inclusive. These three major investigations are an investigation of cerebrospinal fluid (CSF), Magnetic resonance imaging (MRI), and neurophysiological tests which may help in diagnosis in the near future. These methods are used to aid in diagnosis and much research has been conducted on them recently.

Treatment of Multiple Sclerosis

There’s no current treatment of MS, however, new neurological symptoms may be triggered by an infection such as cystitis which resolves once the infection is treated. Moreover, fever control is vital in MS patients, since patients who recovered well from previous MS attacks may have the symptoms resurfaced if their core body temperature is increased during fever or physical exertions in hot conditions. Episodes of blindness or paralysis may resolve faster if treated with a few days of intravenous high dosage of corticosteroids.

Moreover, other drugs such as Copaxone (Glatiramer acetate) may be given subcutaneously daily, Beta –interferon, synthesized by recombinant DNA technology and is available in different forms. They include Betaseron – Beta 1b drug, injected subcutaneously daily, Avonex –Beta 1a drug injected intramuscularly weekly, Rebif –Beta 1a injected subcutaneously twice a week. Medications to relieve limb spasticity, pain, paresthesia, fatigue are also given to reduce the effect of the symptoms. Bladder, bowel and skincare hygiene is vital also to reduce the risk of infection.

References

• Geidl, W., Gobster, C., Streber, R., & Pfeifer, K. (2018). A systematic critical review of physical activity aspects in clinical guidelines for multiple sclerosis. Multiple Sclerosis and Related Disorders, 25, 200-207. doi: 10.1016/j.msard.2018.07.039
• Leahy, T., Elseed, M., & Counihan, T. (2017). Clinically isolated syndromes or clinically isolated patients? A patient and clinician perspective on the utility of CIS as a diagnosis. Multiple Sclerosis and Related Disorders, 17, 249-255. doi: 10.1016/j.msard.2017.08.015
• Luczynski, P., Laule, C., Hsiung, G., Moore, G., & Tremlett, H. (2019). Coexistence of Multiple Sclerosis and Alzheimer's disease: A review. Multiple Sclerosis and Related Disorders, 27, 232-238. doi: 10.1016/j.msard.2018.10.109
• Petzold, A. (2018). Applying the 2017 McDonald diagnostic criteria for multiple sclerosis. The Lancet Neurology, 17(6), 496-497. doi: 10.1016/s1474-4422(18)30159-5
• Tremlett, H., & Waubant, E. (2018). Gut microbiome and pediatric multiple sclerosis. Multiple Sclerosis Journal, 24(1), 64-68. doi: 10.1177/1352458517737369