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Multiple Sclerosis (MS)

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Multiple Sclerosis (MS)

Description of Pathology

Multiple sclerosis (MS) is a chronic inflammatory disease affecting primarily the central

nervous system. It leads to clinical symptoms like visual loss or mobility impairment, which may

not always correspond with MRI changes. Often lifelong and rarely severely disabling if

adequately treated and supported by a multidisciplinary team, MS is an autoimmune disease in

which the body's defense system attacks the myelin sheath—a protective covering surrounding

nerve cells in the brain and spinal cord (McGinley et al., 2021). This destructive process causes

these cells to lose function. The relapsing-remitting and primary progressive forms of MS

manifest in cycles of symptoms appearing and improving. Symptoms of multiple sclerosis often

occur together and include double vision, tremors, difficulty walking due to imbalance,

numbness in certain areas of the body, exhaustion, and coordination problems. Long-term

vitamin D insufficiency has been linked to an increased risk of sclerosis and symptom onset,

related to insufficient levels of vitamin D and sun exposure (Baskaran et al., 2023). The rising

number of disease symptoms highlights the need for screening to prevent catastrophic outcomes.

Environmental factors and societal shifts contributes to an increase in the incidence of

multiple sclerosis worldwide. Chronic illness disproportionately affects people of European and

Nordic European descent, which explains the high incidence in European and North American

countries (Baskaran et al., 2023). According to Walton et al. (2020), the prevalence of MS in

North America was 288 cases per 100,000 people, with about 913,925 diagnosed. Situational

data, such as detailed breakdowns by demographics, is not readily available in places like New

Jersey. The state, however, has the highest illness rate in the country, at 377.4 cases per 100,000

people, according to national prevalence data (Wallin et al., 2019).

Normal Anatomy of the Major Body System

The central nervous system (CNS) is the major body system affected by multiple

sclerosis. The CNS is composed of the brain, spinal cord, and optic nerves responsible for

processing sensory information, coordinating movement, and regulating various body functions.

In the CNS, neurons and glial cells form a part of normal anatomy. Neurons which carry the

electric impulses in the body are the most important cells of the body. The cells of the glia or

neuroglia perform an essential function in protecting and insulating the neurons. According to

Calahorra et al. (2022), myelin is a fatty substance produced by oligodendrocytes in the CNS that

creates an insulating sheath that covers the axons of neurons, allowing for rapid nerve impulse

conduction.

In a normal, healthy central nervous system, the myelin sheath enables fast and efficient

conduction of electrical signals between neurons to establish smooth communication with other

parts of our body. The brain is made up of several parts with different functions. The cerebrum

for example is involved in reasoning and memory while the cerebellum is in body movements

and balance. The spinal cord acts as a pathway for signals travelling to and from the brain,

including reflex actions and voluntary movement. The other important feature of the CNS is the

blood-brain barrier (BBB). According to the research done by Schreiner et al. (2022), the blood-

brain barrier is a selective barrier that separates the blood that circulates in one’s body from the

cerebral spinal fluid while only allowing certain substances into the brain. For restoration of the

brain’s microenvironment, the BBB integrity is of utmost importance.

Normal Physiology of the Major Body System

The normal physiology of the central nervous system (CNS) is essential for maintaining

proper functioning and health of the body. The CNS contains the brain, spinal cord and optic

nerves and controls our ability to think, process information through various phenomena like
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memory & cognitive skills, generate emotions as well as coordinate movement by transmission

of both electrical signals (nervous activity) plus chemical neurotransmission. The CNS consists

of a network of nerve cells or neurons that send electrical signals to one another along axons, the

thin projections emerging from each cell body that are covered in slightly fatty wrapping called

myelin. Oligodendrocytes are myelin-producing cells in the central nervous system (CNS),

which increases nerve impulse conduction velocity facilitating rapid communication between

different parts of the nervous system (Calahorra et al., 2022). This communication is important

for muscle coordination, sensory perception, cognitive functions and other body homeostasis etc.

Intact myelin sheath and functional synapses (at which neurons communicate with each

other) are indispensable for the normal physiology of CNS. In a healthy CNS, nerve impulses

hop along the myelinated axons from one node of Ranvier (gaps in the myelin sheath) to another,

this action is known as saltatory conduction (Calahorra et al., 2022). This speed of signal

propagation in a manner well suited to conducting signals over long distances, such as within the

nervous system or from one side of the body to the other is necessary for voluntary muscle

control, particularly fine skills requiring high temporal precision and support low error rates.

Moreover, synapses also allow the release of neurotransmitters by one neuron which are relayed

to another thereby providing a basis for higher-order function processing supporting cognitive

and motor behaviors. Another crucial normal physiological component of the CNS is the blood-

brain barrier (BBB), which shields the brain from toxic substances allowing only essential

nutrients to pass through. The BBB is necessary to keep the synaptic environment stable which

maintains proper neuronal function (Schreiner et al., 2022).

Mechanism of Pathophysiology
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The pathophysiology of multiple sclerosis involves the central nervous system and is

characterized by inflammation and neurodegenerative changes. According to Tobore (2020), this

results in white matter lesions or plaques within the central nervous system from inflammation

caused by immune cells attacking myelin and damaging axons. This causes nerves to transmit

signals more slowly (since the Myelin helps increase electric velocity) thus impairing normal

nerve signaling; a condition called Demyelination. Multiple sclerosis leads to injury and loss of

neurons, which result from chronic inflammation and demyelination (Tobore, 2020). An

individual with a normal, healthy immune system usually produces proteins (immunoglobulins,

Ig or antibodies) and cells that help protect the body from invaders but are kept from

overreacting against itself. But in MS, this balance goes awry when genetic susceptibility

combines with environmental factors (like a viral infection or vitamin D deficiency) to set off an

autoimmune response. According to Van Langelaar et al. (2020), it is a type of response that

occurs when T cells —a set of white blood cells that too, aim to keep a person healthy by

recognizing and destroying potentially harmful invaders— become active. In MS, these T cells

wrongfully perceive the myelin sheath — a fatty insulation layer surrounding nerve fibers in the

CNS — as an alien antigen.

After activation, these autoreactive T cells are attracted to travel through the blood-brain

barrier (BBB) — a key feature designed to keep harmful components from getting into the CNS.

The breakage of the BBB in MS results in an influx of anti-myelin T cells through (i) producing

pro-inflammatory cytokines that recruit other immune effector populations including B cells and

macrophages to inflammatory sites within CNS. B cells manufacture antibodies that target

myelin, prompting an even stronger immune assault. Macrophages, the cells that normally engulf

and destroy pathogens then begin to assault and degrade the myelin sheath (Van Langelaar et al.,
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2020). This loss of myelin, also referred to as demyelination, impedes the ability of neurons to

effectively carry electrical signals leading directly to the different forms of neurological

disability observed that exemplify MS: muscle weakness; visual disruptions and coordination

problems.

With time, the continuous inflammation and demyelination with attempted repair

contribute to plaque or scar formation in the CNS, mainly seen within the white matter of the

brain/spine. These patches are where the myelin has been stripped away and replaced with scar

tissue, which makes it even more difficult for nerves to send signals. Moreover, the continuing

immune-mediated assault can damage axons beneath neurons or possibly as well, resulting in

permanent neuronal loss and driving gradual disability of MS patients (Haki et al., 2024). These

features of demyelination, axonal injury and sclerotic plaque are the pathological hallmarks of

MS obviating major disruption to normal CNS anatomy and physiology leading ultimately to

illness.

Prevention

Disease prevention is the main goal of primary-level intervention, which must be

consistent with environmental factors contributing to multiple sclerosis's onset. Given the fact

that the majority of individuals do not know about its early signs or can otherwise misinterpret

initial symptoms to those related to other diseases, this patient education program may

tentatively serve as a feasible approach to controlling prevalence across the national level (Haki

et al., 2024). Unfortunately, multiple sclerosis cannot be prevented as it is linked to certain non-

modifiable risk factors such as age, sex, and family history. Research done by Baskaran et al.

(2023) however, shows that changing diet and lifestyle may reduce the risk of developing MS.

Additionally, avoiding smoking, maintaining normal body weight and getting enough vitamin D
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either from diet or sun exposure can help reduce the risk. Furthermore, being physically active,

reducing stress and eating a well-balanced diet can be helpful (Baskaran et al., 2023).

Treatment

While there currently exists no cure for multiple sclerosis (MS), treatments available

today seek to prevent future damage, mitigate symptoms and avoid any complications. For

people with relapsing-remitting MS, the first line of treatment from a doctor can often be

disease-modifying drugs. These therapies slow the progression of multiple sclerosis and reduce

exacerbations. These drugs curb the immune system, which is the main defense against germs to

stop it from attacking myelin (the nerve coating) and so neither type of open-label trial shows if

the treatment works better than no treatment at all (McGinley et al., 2021). As such, the primary

strategy is disease-modifying therapies (DMTs), which target relapses and associated

inflammation, prevent disability progression over time to a lesser degree than in reducing

annualized relapse rates as studied by animal models of human MS but not yet proven clinically

or through pathologic correlates. Corticosteroids such as methylpred-nisolone are often used to

treat acute MS relapses by suppressing inflammation and aiding recovery in addition to DMTs

(McGinley et al., 2021). Another important aspect is symptomatic treatments (treatments that

ameliorate specific symptoms, e.g. muscle spasticity, fatigue, pain and bladder/bowel

dysfunction). Physical and occupational therapy can help patients with mobility, strength or

independence.

Conclusion

Conclusively, multiple sclerosis is a chronic inflammatory disease affecting primarily the

central nervous system and has a complex clinical progression with neurological dysfunction.

This disease affects the neuron's capacity for signal transmission. As a result, the brain's ability
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to function normally is compromised. This leads to common complications such as loss of

sensations, inability to walk and talk. With the complexities of its pathophysiology and variety in

presentation, over time progress has been made in understanding MS characteristics as well that

eventually, more directed treatments to slow down disease progression or symptom management

have come about although no cure is available. Changing diet and lifestyle, avoiding smoking,

maintaining normal body weight and getting enough vitamin D may help reduce the risk of

getting MS.

References
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Baskaran, A. B., Grebenciucova, E., Shoemaker, T., & Graham, E. L. (2023). Current updates on

the diagnosis and management of multiple sclerosis for the general neurologist. Journal

of Clinical Neurology (Seoul, Korea), 19(3), 217.

Calahorra, L., Camacho-Toledano, C., Serrano-Regal, M. P., Ortega, M. C., & Clemente, D.

(2022). Regulatory cells in multiple sclerosis: From blood to brain. Biomedicines, 10(2),

335.

Haki, M., Al-Biati, H. A., Al-Tameemi, Z. S., Ali, I. S., & Al-Hussaniy, H. A. (2024). Review of

multiple sclerosis: Epidemiology, etiology, pathophysiology, and

treatment. Medicine, 103(8), e37297.

McGinley, M. P., Goldschmidt, C. H., & Rae-Grant, A. D. (2021). Diagnosis and treatment of

multiple sclerosis: a review. Jama, 325(8), 765-779.

Schreiner, T. G., Romanescu, C., & Popescu, B. O. (2022). The blood-brain barrier—A key

player in multiple sclerosis disease mechanisms. Biomolecules, 12(4), 538.

Tobore, T. O. (2020). Towards a comprehensive etiopathogenetic and pathophysiological theory

of multiple sclerosis. International journal of neuroscience, 130(3), 279-300.

Van Langelaar, J., Rijvers, L., Smolders, J., & Van Luijn, M. M. (2020). B and T cells driving

multiple sclerosis: identity, mechanisms and potential triggers. Frontiers in

immunology, 11, 760.

Walton, C., King, R., Rechtman, L., Kaye, W., Leray, E., Marrie, R. A., & Baneke, P. (2020).

Rising prevalence of multiple sclerosis worldwide: Insights from the Atlas of

MS. Multiple Sclerosis Journal, 26(14), 1816-1821.

Wallin, M. T., Culpepper, W. J., Campbell, J. D., Nelson, L. M., Langer-Gould, A., Marrie, R.

A., ... & LaRocca, N. G. (2019). The prevalence of MS in the United States: a

population-based estimate using health claims data. Neurology, 92(10), e1029-e1040.