- What is multiple sclerosis?
- What is multiple sclerosis?
- Multiple sclerosis signs and symptoms
- Clinical progression of multiple sclerosis
- Multiple sclerosis pathophysiology
- Multiple sclerosis risk factors
- Multiple sclerosis diagnosis
- Multiple sclerosis treatment
What is multiple sclerosis?
What is multiple sclerosis?
Sometimes, your body’s defense system can go rogue. Like double agents your immune cells can turn and start causing damage to organs or tissues within your own system. One of the tactics used by these delinquent cells is to cut communications between your brain (HQ) and your organs, muscles and tissues (operations) by destroying parts of your nerves that are essential for efficient and effective transfer of information.
- Multiple sclerosis is an inflammatory disease in which your immune system attacks and damages nerve tissue in your central nervous system (brain and spinal cord).
The central nervous system
Your central nervous system receives information from all parts of your body, processes it and then sends instructions out that activates your tissues and muscles to respond in a specific way. The network of nerves that carry information to and from the central nervous system is called the peripheral nervous system. The nervous system contains millions of nerve cells, called neurons. Information travels along neurons in the form of electrical impulses and between neurons in the form of chemical signals.
How your nerves communicate
Neurons have a unique structure that enables the rapid transfer of information, comprising of:
- a cell body, with dendrites
- this is the receiving end of the neuron; dendrites detect chemicals, called neurotransmitters and transform these signals into electrical impulses.
- an axon
- a long thread-like strand that conducts nerve impulses. Many neurons have axons with an insulating cover, called a myelin sheath. Electrical impulses travel down the axons, “jumping” between nodes of Ranvier, which are gaps in the insulating myelin sheath. This design allows nerve impulses to travel very quickly.
- axon terminals
- the axons terminate in branches with small knobs at the end that are sometimes called terminal buttons. When the nerve impulse reaches the end of the axon, neurotransmitters are released from the terminal buttons. These chemicals are detected by the dendrites of the next neuron, stimulating the nervous impulses to continue along the nerve pathways.
Because nerve impulses travel fastest when they are jumping, the spacing of the nodes of Ranvier in the myelin sheath has to be just right if your neurons are going to work properly. Oligodendrocytes are specialized cells that surround the axons, and create and maintain the myelin sheath.
Labeled diagram of a nerve cell
What happens to nervous tissue when you have multiple sclerosis?
The fluid surrounding the brain and within the spinal column is normally separated from the bloodstream by the blood-brain barrier (a highly selective permeable membrane that prevents immune cells and other unwanted material from entering the central nervous system). Although it is not known why, people with multiple sclerosis often have a leakage in the blood-brain barrier, which allows immune cells through enabling them to invade and attack the nerve tissue inside. This autoimmune attack causes inflammation and destruction of the myelin sheaths of the neurons, disrupting the flow of information along the nerve pathways.
Diagram of myelin on a nerve cell
The name multiple sclerosis refers to the many lesions, or plaques that form in the white matter of the brain or spinal cord as the damage to the nervous tissue becomes more extensive.
Diagram of brain lesions caused by multiple sclerosis
Symptoms and clinical course of multiple sclerosis
Multiple sclerosis produces widely varying signs and symptoms that depend on the extent and location of the nerve damage. In fact this disease can produce almost any neurological symptom. That said, some are more common than others, especially symptoms associated with the autonomic nervous system - which regulates many bodily functions including heart rate, digestion, breathing, urination, widening of the pupils, and sexual arousal - as well as visual, motor, and sensory dysfunctions.
Diagram of the symptoms of multiple sclerosis
Multiple sclerosis is classified into four categories based on the frequency of clinical relapses, time to disease progression, and lesion development:
Relapsing-remitting multiple sclerosis - this form accounts for approximately 85% of cases of multiple sclerosis. Most people experience new symptoms that develop over days or weeks, known as relapses, flare-ups, or attacks that then improve partially or totally, followed by no further problems for months or even years (remissions). Although attacks rarely occur more than twice a year, they are often unpredictable, and occur without warning. It is very common to experience motor or sensory symptoms such as tingling, pins and needles, muscle weakness (often in one side of the body), muscle spasms, loss of vision or double-vision, slurred speech, fatigue, dizziness, and bladder and bowel difficulties.
Secondary progressive multiple sclerosis - most people with relapsing-remitting multiple sclerosis will eventually develop a steady progression of symptoms, with more frequent relapses and less complete recovery with each shortening remission. Eventually the disease may become essentially continuous, with increasingly serious symptoms. The rate of disease progression varies widely between individuals.
Primary progressive multiple sclerosis - 10 to 15% of people with multiple sclerosis have this form of the disease. It is characterized by a gradual onset and steady worsening of neurological functioning with no relapses or remissions. The rate of progression varies from person to person. Because primary progressive multiple sclerosis mainly affects nerves in the spinal cord, symptoms are often related to leg muscle weakness and stiffness, which upsets walking and balance.
Progressive-relapsing multiple sclerosis - this is the least common of the four types of disease, occurring in around 5% of cases. Progressive-relapsing multiple sclerosis causes attacks of symptoms, and steadily worsening neurological functioning. Unlike the other relapsing forms, there are no remissions; i.e., times when there are few or no symptoms, instead, the disease continues to slowly get worse.
Graph of increasing disability as a function of time for different forms of multiple sclerosis.
What are the risk factors for multiple sclerosis?
The reason why the immune system starts its attack on the myelin coating of neurons in the central nervous system is not yet known. However, it is clear that accumulating nerve tissue damage due to this autoimmune response is responsible for disease progression. Although multiple sclerosis is not directly inherited, clustering in families indicates genetics do play a role. There are likely multiple genes involved and some scientists propose that the combination of genetic make-up and specific environmental factors may trigger the autoimmune response. Possible environmental factors suggested so far include where you live - multiple sclerosis tends to be more common in countries further from the equator, vitamin D deficiency, viral infections, and smoking. Other factors that are associated with a higher risk of developing multiple sclerosis include: age and gender - it is most often diagnosed in young people, between the ages of 15 and 40, and affects twice as many women as men. You are also at higher risk for this disease if you have certain other autoimmune diseases including thyroid disease, type 1 diabetes, or inflammatory bowel disease.
How common is multiple sclerosis?
Multiple sclerosis is found in every region of the world, and is the leading cause of disability in young and middle-aged people in the developed world. The number of people with multiple sclerosis has increased from 2.1 million in 2008 to 2.3 million in 2013.
Prevalence map of MS by country
Can multiple sclerosis be prevented?
At this point, there is no known way to prevent multiple sclerosis or its attacks. However, some people may benefit from medications that reduce the frequency of relapses and reduce disability.
Diagnosis and treatment of multiple sclerosis
Diagnosing multiple sclerosis can be very difficult, as there is no specific test. Instead, your healthcare provider will first try to rule out other conditions that could produce similar symptoms. After taking a medical history and performing a physical exam, you will likely need to give a blood sample, and/or have lumbar puncture to collect a sample of cerebrospinal fluid. Tests on these samples can help rule out infections and other inflammatory diseases. Your doctor may recommend magnetic resonance imaging, which can reveal lesions in the brain or spinal cord, and electrical tests, called evoked potential tests that measure how quickly nervous impulses travel along nerves.
Diagnostic criteria typically include:
- Age - multiple sclerosis is usually diagnosed between the ages of 15 and 40.
- Symptoms and signs, or other evidence of brain or spinal cord disease.
- Two or more lesions on a magnetic resonance imaging scan.
- One episode of MS symptoms and changes on magnetic resonance image.
- No other explanation for the symptoms.
There are various medications available that help speed recovery from attacks, slow disease progression, and help you manage symptoms.
Treatments for acute attacks - corticosteroids such as prednisolone or methylprednisolone may be used to treat sudden, severe attacks. These medications shorten the attack by reducing inflammation, but do not alter the course of the disease. If the attacks are particularly severe, you may be offered plasma exchange (plasmapheresis), which is a process that reduces the autoimmune response by removing immune cells and other immune factors from your bloodstream.
Immunomodulatory therapy - also known as disease modifying agents, these medications are immunosuppressants that reduce the severity and frequency of attacks, and the accumulation of lesions within the brain and spinal cord, slowing the progression of the disease. Disease modifying therapies include: beta-interferons, glatiramer acetate, natalizumab, fingolimod, teriflunomide, dimethyl fumarate, alemtuzumab, and mitoxantrone. They are used to treat relapsing forms of multiple sclerosis. Unfortunately, there is currently no medication that slows the progression of primary-progressive multiple sclerosis.
Beta-interferons and glatiramer acetate are commonly used as first-line therapies for the treatment of relapsing-remitting multiple sclerosis. These treatments are usually given by self-injection, and typically reduce the rate of relapses by about one-third, as well as slowing the development of brain lesions.
Natalizumab is a monoclonal antibody that is given intravenously every four weeks. It reduces relapse rates by about two-thirds, but sometimes causes a serious brain infection, which means patients taking natalizumab must be carefully monitored. Due to this risk, natalizumab is generally only used when all other options have failed.
There are three oral disease modifying therapies that treat relapsing forms of multiple sclerosis, fingolimod, teriflunomide, and dimethyl fumarate. They all effectively reduce relapse rates by around 50%, but also cause a variety of side effects. For example, fingolimod can’t be taken by people with a heart condition, teriflunomide causes multiple troublesome side effects at the higher, more effective dosage, and dimethyl fumarate commonly causes gastrointestinal upsets. As a result, the safety profile of the medications strongly influences whether or not they are suitable for a patient to take.
Alemtuzumab is another monoclonal antibody that effectively reduces relapse rates, disability, and disease activity. It is administered by intravenous infusion, which sometimes causes side effects such as hypotension, rigors, fever and shortness of breath. Its use has also been associated with serious respiratory and cardiac side effects, as well as the triggering of other autoimmune diseases.
Mitoxantrone is administered by injection, and is used to treat several forms of worsening multiple sclerosis including secondary progressive, progressive relapsing, and advanced relapsing-remitting forms of the disease. Unfortunately, it is very cardiotoxic and over time causes heart muscle damage. As a result, it can only be used for two to three years.
Treatments for signs and symptoms - as many of the symptoms are related to loss of motor function, there are interventions available that may help. These include physical or occupational therapy, which may help you maintain muscle strength, and make it easier to perform every-day tasks. Muscle relaxants can be used to treat muscle stiffness, and other medications are available that may help with fatigue, depression, pain, and bladder and bowel dysfunction.
Consider the following
A combination of genetic and environmental factors are thought to influence whether or not a person will get multiple sclerosis. Among these, the potential link between Vitamin D deficiency and the risk of developing multiple sclerosis is a very active area of interest. The rationale for this is based on observations that the prevalence of multiple sclerosis tends to be higher in countries that are further away from the equator. In addition, the risk for this disease decreases for people who immigrate from countries further from the equator to countries that are closer to the equator. As countries far from the equator have less sunshine, the people living there tend to have lower levels of vitamin D, leading to the hypothesis that the lack of vitamin D may play a role in the development of multiple sclerosis. More direct evidence that vitamin D may be a protective factor has come from a recent study showing that people with early stage multiple sclerosis, with higher blood levels of vitamin D, had fewer new active lesions, a slower increase in brain lesion volume, lower loss of brain volume, and less disability. Several randomized controlled trials are now underway to better establish whether or not identifying and correcting vitamin D deficiency should become routine practice for newly diagnosed multiple sclerosis patients.
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