Multiple Sclerosis: A Disorder of the Nervous System

Multiple Sclerosis, 1

Multiple Sclerosis: A Disorder of the Nervous

System

Lisa Skiver and Haily VoraTopics in Medicine and Biology

Mr. Wilson KwokSummer Ventures July, 2006


Abstract

Multiple Sclerosis (MS) is a disorder of the nervous system. It is characterized by the

gradual decay of the myelin sheath and axons of the nerves. There are two main types of MS:

Relapsing-remitting MS and Chronic-progressive MS. What factors actually cause multiple

sclerosis are still unknown, but there are many theories derived from extended research by

scientists and doctors. Two of the most supported beliefs among experts for the cause of MS are

genetic factors and infectious agents. People who are susceptible to MS usually start developing

symptoms after the age of 20 and women are twice as likely to acquire the disorder. Even

though the causes are unknown, the accepted theory is that the body’s damaged immune system

is unable to differentiate between a virus and its own myelin, causing autoimmunity, or a self-

attack. To diagnose MS, a brain MRI scan is usually used. The symptoms of multiple sclerosis

differ from person to person and day to day. Weakness, fatigue, pain and bladder difficulties are

just a few symptoms among many. Though there is no cure for multiple sclerosis, most cases

can be treated and cared for with a number of drugs currently on the market. Research is

continuously being done to try and solve the mystery of multiple sclerosis.


Introduction

Multiple Sclerosis is the most common cause of neurological debilitation in young people

around the world. It affects approximately 500,000 people in the United States and occurs in

about 0.1% of all people worldwide. Affecting every 3 in 10,000 people, Northern Europe and

the Northern US have the highest diagnosis rate. No two people have the exact same form of

MS and the course of each patient’s disorder is as unique as the number of hairs on their head.

The advance of the disease, within an individual and a whole population, largely differ in their

timing, severity and location. So, where does this decaying, degenerative disorder emerge from?

The Nervous System

Multiple Sclerosis originates in the central nervous system, and to fully understand this

disorder, one must be familiar with the system. The body’s nerves do not form one single

system, but several which are interrelated. Some of these are physically separate; others are

different in function only. The brain and spinal cord make up the Central Nervous System

(CNS) and the Peripheral Nervous System (PNS) is responsible for the body functions which are

not under conscious control such as the heartbeat or the digestive system. The CNS represents

the largest part of the nervous system. Working with the PNS has the essential role in the control

of behavior and information processing. The CNS stems from the neural plate which forms the

neural tube during embryonic development. This tube will eventually branch off into two major

subdivisions, the spinal cord and the brain. These two vital parts of the body form what is

known as the CNS. Its overall function is to collect information about the external conditions in

relation to the body's internal state, to analyze this data, and to trigger the appropriate response to

satisfy certain needs.


Within the CNS, the brain and spinal cord play a vital role in body communication. The

spinal cord is the crucial link between the whole body and the brain. It emerges from the base of

the skull and continues down the back for 42-45 cm through the vertebral column. There are 31

pairs of spinal nerves, part of the PNS, which stem from the spinal cord. Each one of these

nerves contains a dorsal root and a ventral root. The dorsal roots contain the neurons that carry

messages to the CNS from numerous sensory neurons. The ventral roots contain the axons of

motor neurons. There are also interneurons within the spinal cord. Besides carrying signals to

and from the brain, the spinal cord also regulates reflexes, the simplest response to a stimulus.

Most reflexes never reach the brain due to the immediate response of the sensory and motor

neurons in the spinal cord. Even though the spinal cord does all the work, there would be no

nervous system without the brain. The brain is divided into three main sections: the forebrain,

the midbrain, and the hindbrain. The forebrain is the largest and most complex part of the brain

and contains the cerebrum. The cerebrum contains the information that makes a person;

intelligence, memory, personality, emotion and speech. The outer layer of the cerebrum is called

the cortex. It collects information coming in from the spinal cord from the five senses. The

brain then directs this data to other parts of the nervous system for more processing. The

midbrain is located underneath the middle of the forebrain. It acts as an efficient organizer for

all the messages going in and out of the brain through the spinal cord. The hindbrain sits

underneath the back of the cerebrum and contains the cerebellum, pons and medulla. The

cerebellum is responsible for balance, movement and coordination. Together with the midbrain,

the pons and medulla are often called the brainstream. They take in, send out and coordinate all

of the brain’s messages.


The messages the spinal cord carries from the body to the brain are analyzed and

interpreted and response messages are sent throughout the rest of the body. The cells that carry

these messages are called neurons. The messages they send take the form of electrical signals,

also known as impulses, which only travel in one direction. Neurons can be further classified

into three different types: sensory receptor neurons, motor neurons, and interneurons.

Sensory receptor neurons carry impulses from the sensory organs to the brain and spinal

cord. Receptors sense changes, both internal and external, and send the information to the CNS

through electric signals. They are responsible for converting external stimuli to internal motor

mechanisms and some forms of involuntary behavior. Sensory neurons are commonly located in

the spinal cord and carry sensations such as feelings, impressions and awareness throughout the

body.

Figure 1. Sensory Neuron - Picture adapted from http://www.biotopics.co.uk/humans/recodr.html

Motor neurons, also known as efferent neurons, carry messages to muscles and glands.

They originate in the spinal cord or brain stem and promote muscle contraction. With enough

stimulation, the motor neuron will release a flood of neurotransmitters that will bind to receptors

on muscle fiber and initiate a response. The response of a muscle fiber to a neurotransmitter is

contractile and inhibition of muscle contraction can only occur when the motor neuron itself is

inhibited.


Figure 2. Motor Neuron – picture adapted from http://www.botany.uwc.ac.za/sci_ed/grade10/mammal/nervous.htm

Interneurons connect sensory neurons to motor neurons and carry impulses between the

two. They are found only in the CNS and the brain, alone, contains over 100 billion

interneurons. They only communicate to other neurons and are sometimes called relay neurons.

Interneurons can be used as inhibitors which theoretically help block out boring or irrelevant

input and help focus attention on relevant sensory input.

Figure 3. Interneuron – picture adapted from http://webanatomy.net/anatomy/neuro_notes.htm


All neurons have a cell body, dendrites, and one axon. The cell body is the largest part,

containing the nucleus, most of the cytoplasm and metabolic cell activity. It generates ATP and

synthesizes proteins. The dendrites are short branch extensions that spread out from the cell

body. They receive stimulus and carry impulses from the environment toward the cell body.

The axon of a neuron is a long fiber that carries impulses away from the cell body. The axon

ends with an array of swellings called axon terminals. Neurons can have hundreds of dendrites,

but usually only one axon. These axons are covered with a lipid layer known as a myelin sheath.

Myelin can greatly increase the speed at which an impulse travels along an axon. It is made of

Schwann cells that form an insulated wrap around the axon. Along the axon, there are gaps

between the myelin sheaths called the Nodes of Ranvier. As an impulse moves down an axon, it

jumps between the sheaths instead of traveling straight down the membrane. This jumping from

node to node decreases the time it takes for an impulse to travel. However, sometimes these

crucial myelin sheaths can be destroyed and nerve function becomes impaired, thus, causing

Multiple Sclerosis.

What is it?

So what exactly is MS? The principal characteristic of the disorder is the destruction of

the myelin. The end result of this process is multiple patches of hard, scarred tissue called

plaques. This is called demyelination. Another important feature in the disease is the

destruction of axons, which is now considered to be a major factor in the permanent disability

associated with MS.


Figure 4. Neuron and Myelin – picture adapted from http://www.umm.edu/patiented/articles/what_multiple_sclerosis_000017_1.htm

Types of MS

Relapsing-remitting multiple sclerosis is the most common type of MS and usually

occurs in young people. The most common characteristic of relapsing-remitting MS is the attack

or relapse. It is an attack of MS symptoms such as facial pain or bladder instability that lasts at

least 24 hours and usually for a few days. Most of these attacks are fairly mild and are followed

by a period of remission. The symptoms improve or disappear for about six to eight weeks. To

be considered a remission, there must be 30 days between relapse sessions. Remissions are

almost always followed by a flare-up. Some relapsing-remitting MS patients can go years

without experiencing any progression, although by 25 years, most patients have converted to a

progressive stage.

Chronic-progressive multiple sclerosis is a type of MS where the patient has no periods

of remission and their symptoms continue to worsen slowly. Most patients who develop MS

after the age of 45 are afflicted with the chronic-progressive type of MS without first developing

relapsing-remitting MS. Chronic-progressive MS has a wide spectrum of severity and is

categorized into three groups: Primary-Progressive MS (PPMS), Secondary-Progressive MS

(SPMS), Progressive-Relapsing MS (PRMS). PPMS progresses gradually with no remission but

can occasionally level off and even have minor improvement. SPMS occurs after the relapsing-

remitting phase in about half of MS patients within 10 years and almost all after 25 years. It’s an

evolving course of nerve and muscle decay with intermittent flare-ups, remissions and plateaus.

PRMS is progressive from the beginning with intense symptoms and continued disintegration

between relapses. It is the least common type of MS, occurring in only 5% of patients.

Causes


Despite the great progress that has been made in trying to find a cute for MS, the cause for this

degenerative disorder is still unknown. Genetics most probably play a role in MS, but no single

gene is responsible for the disorder. Currently, the most popular theory is that the disease occurs

in people with a genetic susceptibility who were exposed to some environmental attack (a virus

or a toxin) that disrupts the blood-brain barrier. Immune factors gather in the nerve cells and

cause inflammation and an autoimmune attack on myelin and axons. Still, some experts believe

that MS may prove not just be a single disorder, but may represent several diseases with several

different causes.

Genetic factors may make a person more vulnerable to MS, but the risk for someone

inheriting the disorder is less than 5%. Close relatives of a patient with MS are more likely to

develop it themselves. Some researchers believe that there is more than one gene that increases

susceptibility. Other scientists believe that MS develops because a person is born with a

genetically lower tolerance to some environmental agents, and instead of a normal response, the

exposure triggers an autoimmune response. However, as technology improves, techniques are

being developed to identify genes that are most likely responsible for MS.

Infectious agents, viruses in particular, are most likely the cause of an autoimmune

response in people genetically susceptible to MS. Much research and experimentation has been

done to support this belief:

Geographical Distribution – MS is a disease of temperate climates. The number

of MS cases increases the further one gets from the equator in either direction.

Multiple Sclerosis is very rare in traditional culture, but it increases in

industrialized Western nations.


MS Clusters – Four separate clusters of MS outbreaks occurred between 1943 and

1989 in the Faroe Islands (located between Iceland and Scandinavia). During

WWII, the area was occupied by British troops and the number of patients with

MS increased each year for 20 years, following the war. Some researchers think

that the troops could have brought the disease causing agent with them.

Sexually Transmitted Infection – The disease clusters in the Faroe Islands could

be related to high sexual activity between the troops and the native women. High

diagnosis rates are found in countries with a high degree of sexual

permissiveness.

Viral Similarity – Some viruses are extremely similar to myelin protein and could

therefore confuse the immune system, causing the T-cells to attack their own

protein instead of the virus.

HIV-6 – Herpesvirus 6 is known to cause encephalitis, or brain inflammation in

patients with damaged immune systems. Many studies have shown that some MS

patients have higher rates of HHV-6 infection than normal. Some scientists and

doctors believe this may be important to discovering the cause of MS, while

others argue that nearly everyone harbors this virus and there is not a strong

enough relationship between MS and HHV-6.

Chlamydia Pneumoniae – This bacterium has been associated with persistent

inflamed small vessels. A few studies have shown that patients with MS have a

significantly higher rate of previous Chlamydia infection. Many experts disagree,

but it is possible that the infection, which widely spreads inflammation, could

play an early role in the course of MS.


Epstein-Barr virus (EBV) – Almost all people with MS have evidence of EBV

infection, the cause of mononucleosis. However, EBV is very common in people

who will never develop mono.

Other viruses have been explored such as the measles virus, adenovirus,

polyomavirus, and the retroviruses (HIV, HTLV-I, HTLV-II).

Figure 5. Environmental Theory – picture adapted from http://mscenter.ucsf.edu/faq.htm

Who is most likely to get MS?

Women are twice as likely to get MS as men. Most people start developing symptoms

between the ages of 20 and 40. People from Northern Europe, the United States and Canada are

more likely to develop MS than Asian people, Eskimos and American Indians. It is an inherited

disease in the sense that a child or sibling of someone with MS is about 10 times more likely to

get MS than someone in the population at large.

Process


Although the causes are unknown, research has led scientists to better understand what

exactly happens within an MS patient’s body. The common and accepted theory for the

development of MS is that a damaged immune system is unable to differentiate a virus protein

and the body’s own myelin. It generates antibodies to attack and basically becomes allergic to

itself, causing autoimmunity. In the case of MS, the body attacks the myelin tissues.

In MS, an unknown trigger activates helper T-cells whose antigen specific receptors

recognize central nervous system myelin as an antigen. Once triggered, the activated T-cells

reproduce clones that have the same myelin-specific activation. All of the activated T-cells then

release cytokines and adhesion molecules that enable the T-cells to adhere to and cross over the

blood-brain barrier, which normally prohibits the flow of substances into the brain. The greatly

weakened barrier becomes easily permeable, allowing additional immune system cells, such as

B-cells and cytotoxic T-cells to cross over. Once through the barrier, B-cells produce antibodies

which bind to the oligodendracytes (the cells of the CNS which create myelin) and the myelin

itself. Associated macrophages proceed to destroy the myelin and may also damage the

oligodendracytes.

As the body starts to attack itself, the myelin sheath is destroyed, marking the climax of

multiple sclerosis. The nodes in the sheath house channels for sodium ions that boost the

electrical charge required to pass nerve signals. As the myelin insulation is being destroyed,

signals transmitted from nerve to nerve throughout the CNS are disrupted. The destruction of

axons is now well established as a major feature of MS. Research shows that axons are severed

early on in the process and as the disease progresses, the exposed axons decay even further. This

is most likely the major reason for MS irreversibility.


The body does seem to have some sort of defense against MS though. Studies show that

the body increases the density of sodium ions that carry electric charges. By increasing these

ions, the nerves can continue to communicate despite the lack of myelin. It has also been shown

that the body can retain some remyelinate, used to restore the insulating myelin. These processes

are most likely responsible for the remission that some MS patients experience. However, the

disease is too powerful and eventually outpaces the body’s attempt to correct itself.

Diagnosis

The diagnosis of MS is based on the presence of central nervous system (CNS) lesions

that occur in different parts of the CNS at least three months apart, with no better explanation for

the disease process. No single test is totally reliable in identifying MS and other conditions of the

CNS can occur that are very similar to the disease. CNS infections such as Lyme disease,

syphilis, human immunodeficiency virus infection and human T-lymphotrophic virus type I

mimic MS. Also, CNS inflammatory conditions such as sarcoidosis and systemic lupus

erythematosus and genetic disorders such as leukodystrophy, hereditary myelopathy and

mitochondrial disease can be very similar in nature to MS.

The International Panel on MS Diagnosis has made several changes to the older

diagnostic criteria in 2001 referring to the newer criteria as the McDonald criteria. They have

incorporated specific MRI (magnetic resonance imaging) findings into the diagnostic scheme.

The major advantage of the proposed criteria is that an early diagnosis of MS can be made if an

MRI scan performed three months after a clinically isolated attack demonstrates formation of a

new lesion. The proposed diagnostic criteria also define MRI lesion characteristics that increase

the likelihood of MS. This includes

number of lesions: nine or more


location of lesions position abutting the ventricles: juxtacortical, infratentorial, or spinal

position

lesion enhancement with the use of contrast medium.

The MRI lesion characteristics that suggest multiple sclerosis consist of brain lesions and spinal

cord lesions. These characteristics are shown in Table 1. Table adapted by

http://www.aafp.org/afp/20041115/1935.html.

TABLE 1MRI Lesion Characteristics Suggestive of Multiple Sclerosis

Brain lesionsHigh signal on T2-weighted and FLAIR MRI sequences (more than nine lesions)When actively inflamed, often enhanced with gadolinium contrastPosition abutting ventricles (often perpendicular)Juxtacortical position (gray-white junction)Involvement of brainstem, cerebellum, or corpus callosumSpinal cord lesionsOne or two vertebral segments in lengthIncomplete cross-sectional involvement (dorsolateral common)Less likely to enhance with gadolinium contrastNo cord swellingBetter seen with STIR MRI sequences

MRI = magnetic resonance imaging; FLAIR = fluid attenuation inversion recovery; STIR = short tau inversion recovery.

Table 1. MRI Lesion Characteristics Suggestive of MS – table adapted from http://www.aafp.org/afp/20041115/1935.html

Types of testing

A brain MRI scan is the most useful test for confirming the diagnosis of MS. MRI is a

test that produces very clear pictures of the human body without the use of X-rays. It uses a large

magnet, radio waves and a computer to produce these images. Disease-related changes in the

brain or spinal cord are detected by MRI in more than 90% of people suspected of having MS.


MRI scanning is useful for detecting structural pathology in regions that can be difficult to see

through computer images, such as the posterior fossa, craniocervical junction, and cervical cord.

Figures 6 and 7. MS Brains – pictures adapted from http://www.aafp.org/afp/20041115/1935.html

In the image above to the right, the arrows show the multiple high-signal white lesions,

showing suggestive characteristics of MS. In the image to the left, a fluid attenuation inversion

recovery (FLAIR) image of a slice of the brain is shown.

A lumbar puncture, or a spinal tap, where a sample of cerebrospinal fluid is taken by

inserting a needle between two vertebrae of the spine can be performed to diagnose MS. A spinal

tap that reveals a large number of immunoglobulins as well as oligoclonal bands or certain

proteins that are the breakdown products of myelin is suggestive of MS. These findings indicate

an abnormal autoimmune response within the brain and spinal cord, meaning that the body is

attacking itself. Over 90% of people with MS have oligoclonal bands in their CSF. While

increased immunoglobulin in the CSF and oligoclonal bands are seen in many other brain and

spinal cord conditions, their presence is often useful in helping to establish a diagnosis of MS.

Sensory evoked potential testing may also be used in finding MS in the human body.

Evoked potential tests measure electrical activity in certain areas of the brain in response to

stimulation of certain groups of nerves. These tests are often used to assist in the diagnosis of MS


because they can indicate problems along the pathways of certain nerves that are too small to be

noticed or found on a physician’s exam. Direst results of the disease are problems along the

nerve pathways. The demyelination causes the nerve impulses to be slowed or stopped

altogether. The three main types of evoked potential tests are visual, brainstem auditory, and

sensory. In visual evoked potentials, or VEP, the patient looks at a screen on which an

alternating checkerboard pattern is displayed. In brainstem auditory evoked potentials, or BAEP,

the patient hears a series of clicks in each ear. And, in sensory evoked potentials, or SEP, short

electrical impulses are sent to a patient’s arm or leg.

Symptoms

The symptoms of MS obviously vary from person to person and even from day to

day. There are many common symptoms, though, to indicate a potential case of MS. These

are the common possible symptoms of MS:

Weakness Bladder and Bowel Dysfunction Cognitive dysfunction Dizziness and Vertigo Sexual Dysfunction Depression and other emotional changes

Pain Fatigue Difficulty in walking (gait) Numbness Spasticity Vision Problems

Table 2. MS Symptoms – table adapted from http://www.nationalmssociety.org/Symptoms.asp

When caused by MS, weakness is a result of damaged nerve impulse flow, preventing

instructions from reaching the extremities. This type of weakness does not result from any type

of loss in muscle strength.

About 75% of MS patients experience bladder difficulties at some time. The most

common symptoms are frequency (the urge to urinate often) and urgency (the urge to urinate

immediately and the inability to hold the urine once the urge is felt).


For a patient with MS, having bowel dysfunctions means having constipation.

Constipation is more apparent in those with MS than the general population and can be regulated

when Timing, fluid intake, diet and physical activity are taken into consideration.

Approximately 50% of people with MS will develop some degree of cognitive

dysfunction, affecting the ability to think, reason, concentrate or remember. The memory is the

cognitive function most likely to be affected. Other cognitive functions frequently affected in MS

include speed of information processing, executive functions (planning and prioritizing),

visuospatial functions (impairment in visual perception and constructional abilities), abstract

reasoning and problem-solving, and attention and concentration. One of the reasons MS may

affect cognitive function for several reasons is because MS damages both myelin and the nerve

cells within the brain, thereby compromising a variety of functions handled by the brain.

Dizziness is a common symptom of MS. Those with MS may feel off balance or

lightheaded. Much less often, they have the sensation that they or their surroundings are spinning

—a condition known as vertigo. These symptoms are due to lesions, or damaged areas, in the

complex pathways that coordinate visual, spatial, and other input to the brain needed to produce

and maintain equilibrium.

Sexual problems are often experienced by people with MS. Sexual arousal begins in the

central nervous system, as the brain sends messages to the sexual organs along nerves running

through the spinal cord. If MS damages these nerve pathways, sexual response—including

arousal and orgasm—can be directly affected. Sexual problems also stem from MS symptoms

such as fatigue or spasticity, as well as from psychological factors relating to self-esteem and

mood changes. In both men and women, symptoms of sexual dysfunction include difficulty

achieving orgasm and loss of libido.


Depression may be the result of difficult life situations or stresses. It is easy to understand

how a diagnosis of multiple sclerosis, a chronic condition with the potential for progressing to

permanent disability, can bring on depression. It may also be a result of the MS disease process

itself, since MS damages the myelin and nerve fibers deep within the brain. If MS damages areas

of the brain that are involved in emotional expression and control, a variety of behavioral

changes can result, including depression. Also, some of the emotional changes observed in MS

include major depressive episodes as well as less severe depressive symptoms, grieving for

losses related to the disease, stress and reactions to stressful situations, generalized distress and

anxiety and emotional lability or mood swings.

Another symptom a person with MS might experience is pain. When experiencing acute

pain, one has cases of trigeminal neuralgia, Lhermitte's sign and burning or aching around the

body. In trigeminal neuralgia is a stabbing pain in the face which is neuropathic, or caused by

damage to the trigeminal nerve. It can occur as an initial symptom of MS. Lhermitte's sign is a

brief, stabbing, electric-shock-like sensation that runs from the back of the head down the spine,

brought on by bending the neck forward. Burning and aching around the body are all

neurological symptoms. The technical name for them is dysesthesias. Acute symptoms of pain

are milder than chronic symptoms. Chronic pain includes burning, aching or prickling, pain of

spasticity and back and other musculoskeletal pain. Burning, aching or prickling can be a chronic

form of the acute symptoms. Pain of spasticity has two categories. Muscle spasms or cramps,

called flexor spasms, may occur. Tightness and aching in joints is another type of spasticity.

Fatigue is one of the most common symptoms of MS, occurring in about 80% of people. It is

a debilitating kind of overall weariness, which is not predictable and unrelated to your

activity level. Increase in body temperature will temporarily worsen fatigue. It can


significantly interfere with a person's ability to function at home and at work, and may be the

most prominent symptom in a person who otherwise has minimal activity limitations. MS

fatigue is unique in that it:

Generally occurs on a daily basis May occur early in the morning, even after a restful night's sleep Tends to worsen as the day progresses Tends to be aggravated by heat and humidity Comes on more easily and suddenly Is generally more severe than normal fatigue Is more likely to interfere with daily responsibilities

Table 2. MS fatigue characteristics - Table adapted by http://www.nationalmssociety.org/Sourcebook-Fatigue.asp

Problems with gait (difficulty in walking) are among the most common mobility

limitations in MS. Gait problems are usually related to several factors including weakness,

spasticity, loss of balance, sensory deficit and fatigue.

Numbness of the face, body, or extremities (arms and legs) is another one of the most

common symptoms of MS, and is many times the first symptom experienced by those eventually

diagnosed with MS. The numbness may be mild or so severe that it interferes with the ability to

use the affected body part. Numb hands may prevent writing, dressing, or holding objects safely.

Many people with MS have problems with spasticity, a condition that primarily affects

the lower limbs. Spasticity refers to feelings of stiffness and a wide range of involuntary muscle

spasms. It may be as mild as the feeling of tightness of muscles or may be so severe as to

produce painful, uncontrollable spasms of extreme levels, usually of the legs. Spasticity may also

produce feelings of pain or tightness in and around joints, and can cause low back pain. Two

types of severe MS-related spasticity are flexor spasticity and extensor spasticity. Flexor

spasticity, involving the hamstrings and hip flexors, refers to bent hips and knees that are

difficult to straighten. Extensor spasticity, on the other hang, involves the quadriceps and


adductors. Here, the hips and knees remain straight with the legs very close together or crossed

over at the ankles.

Vision problems can also be a symptom of MS but very rarely does it result in vision

loss. The problems with vision include optic neuritis, uncontrolled eye movement and double

vision. Optic neuritis is an inflammation of the optic nerve, the nerve that transmits light and

visual images from the retina to the brain. The condition is also known as retrobulbar neuritis

because the nerve is located behind the globe of the eye. Optic neuritis is generally experienced

as an acute blurring, graying, or loss of vision, almost always in one eye. Nystagmus, or

uncontrolled horizontal or vertical eye movements, is another common symptom. It may be mild,

only occurring when the person looks to the side or it may be severe enough to impair vision.

Diplopia, or double vision, happens when muscles controlling eye movement are not perfectly

coordinated due to weakness in one or both pairs of muscles. When the images are not properly

synched, a false double image occurs. Double vision may increase with fatigue or overuse of the

eyes. Patching one eye can be done until regular eyesight returns.

Treatment

A cure has not been found for multiple sclerosis. Diagnosed early, most cases of MS can

be cared for. Studies indicate that early treatment delays disability, presumably by decreasing the

injury to the nervous system caused by the disease. Generally, treatment of the disease falls into

two categories: treatments that address symptom management, and treatments that change the

course of the disease by modifying the number and severity of attacks and the progression of

disability. Five different products have been approved by the FDA as disease modifying

treatments for MS since 1993. These included three interferon-beta products (Betaseron®,

Avonex®, and Rebif®) and two unrelated products (Copaxone®, Novantrone®).


Betaseron® was the first beta interferon to be approved by the FDA and marketed in the

United States. The product shuts down the inflammation of MS lesions through various

mechanisms including repairing the blood brain barrier and reducing the inflammatory process in

the lesions. Betaseron® decreases relapse rate, increases time between attacks, decreases the

severity of attacks, while decreasing the amount of accumulated lesions seen on MRI.

Betaseron® is to be taken every other day through an injection under the skin. This product

provides the highest dose of interferon-beta available for treatment of MS. Marketed by Berlex

Laboratories, Inc.

Avonex® is known to slow the rate of progression of disability in relapsing-remitting

MS. It has been demonstrated to decrease the relapse rate and the amount of accumulated

damage seen on MRI, but to a lesser extent than other available agents. Avonex® is given every

week through an intramuscular injection. Avonex® treats the relapsing-remitting type of MS.

Marketed by Biogen, Inc.

Rebif® is identical in chemical structure to Avonex®. The difference is that Rebif® is

given just under the skin rather than in the muscle in higher and more frequent doses. Rebif is

effective in reducing the number and severity of relapses, delaying the progression of disability,

and reducing the number of new and accumulated lesions seen on MRI. It is approved for use in

relapsing-remitting MS. Marketed by Serono, Inc.

Copaxone® is different from beta interferon in chemical structure and mechanisms of

action. It consists of a group of amino acids that looks something like myelin itself. It acts by

suppressing the immune system's attack on myelin and possibly other mechanisms. It decreases

the frequency and severity of attacks to the same extent as Betaseron and Rebif, but with slightly


less effect on MRI lesions. Copaxone® is taken daily through an injection just underneath the

skin and is used for relapsing-remitting MS.

Novantrone® another chemotherapy agent that slows disease progression in MS and

lessens the number of relapses through its ability to suppress the activity of T cells and B cells.

These white blood cells attack the myelin that protects nerve cells, and by doing so causes the

scarring associated with MS. It is approved for MS that is getting worse and worse including

secondary progressive and relapsing-remitting forms of the disease. Novantrone is typically

administered through an injection into the vein once every three months for two years. Marketed

by Immunex Corporation.

For acute exacerbations, steroids have been reported to shorten the duration of acute

attacks by lessening the swelling and inflammation in MS lesions. However they do not alter the

frequency of exacerbations or the progression of the MS, and long term use should be avoided

except in selected patients.

Conclusion

Though multiple sclerosis is not a fatal disease, it has been known to shorten the lifespan

of those who have been diagnosed with MS by about six years. Understanding MS and its origins

are often difficult to understand because of the complexity of the part of our body we call the

nervous system. Scientists and medical doctors everywhere are trying to understand the nervous

system and therefore understand the diseases that come from it. Doing this takes them one step

closer to finding a cure. Those with MS can lead their daily lives with little complication, but

they know that they will be living with the disease forever. To find a cure would be a dream

come true. With the technology of today, this dream is just around the corner.


Bibliography

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Multiple Sclerosis: A Disorder of the Nervous System

Health & Medicine

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