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Multiple Sclerosis -
A Guide For Patients & Their Families




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Multiple Sclerosis is the most common cause of Neurological disability that attacks men and women between the ages of 15 and 55. Approximately 90% have their onset in this age range.

After Trauma and Arthritic Disorders, Multiple Sclerosis is the most important cause of moderate to severe disabilty of adult life. Generally MS strikes persons who are healthy, intelligent, and well educated. It cannot be attributed to any known "failing" or cause.

MS is a Chronic Illness that can affect most Motor and Sensory functions of the Nervous System. Pain and Loss Of Mental Faculties are rare.

The disease varies in serverity and allows some to lead full, productive lives, whereas others become severly disabled.

Although the cause of MS is unknown, it is thought to be the result of an abnormal response of the body to persistent infections. Much of the current research is directed along these lines.

Moreover, there is no specific treatment, and nothing alters its unpredictable course. Attacks and remissions come without warning, confusing both patient and their families.

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Multiple Sclerosis is a Chronic, sometimes Disabling disease of the Central Nervous System; it is almost always confusing and frustrating to the patient and their families.

The diagnosis may be learned only after repeated examinations, and the response may be a sense of dread or in many cases one of relief after long periods of uncertainty and concern.

MS is a variable disease in its severity, the milder cases may enjoy a full active life, while the more severe cases will become more disabled over time.


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MS is a disease in which the insulation surrounding Nerve Fibers of the CNS (the Brain and Spinal Cord) is damaged. Tissue outside the CNS is not involved in the disease.

Infections of the Urinary and Respiratory Systems, are simply complications of Multiple Sclerosis. The CNS is characterized by the specialized activities of its component cells.

Actions and reactions of the individual's body depend on "news" of the stimulus being transmitted to the Brain, the Brain's reaction, and "instructions" on how to react to the stimulus then being sent from the Brain back to the original point.

This coordinated transmission of a Nerve Impulse from one Nerve Cell to the next underlies nervous tissue function and is dependent on the connections among the Nerve Cells. These connections are called Nerve Fibers.

The coordination among these Nerve Cells is a result of the integrity and the speed of conduction of an impulse along the Nerve Fibers to the Synapse to the next cell.

Myelin - a fatty substance that surrounds the nerve fibers, forming a sheath - is made and maintained by a cell called the Oligodendrocyte and enhances the velocity with which Nerve Impulses are conducted along the Nerve Fibers (Axons).

The conduction of an impulse along an Axon (the nerve fiber leading to the Synapse) may be viewed as similar to the movement of current in an electric wire.

Myelin provides the insulation around Nerve Fibers and allows only a small portion of the nerve fiber membrane to become Depolarized and the Impulse is transmitted.

The presence of the Myelin sheath markedly reduces any leakage of current. In MS this sheath is damaged, so that the insulation can no longer prevent leakage. As a result transmission may either be delayed or cease completely.

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In either event, a Nervous System activity is diminished or lost because of the delay or block in Impulse Transmisson. The initial lesion in MS that leads to the tissue alterations is still unclear.

However, it is known that Oligodendrocytes are altered or damaged and Myelin breaks down in the presence of cells from the Immune System invading the CNS.

As the Myelin is damaged, certain other cells proliferate and form dense tissue at the site of the damage. This proliferation causes a firmness of the tissue (Sclerosis).

The loss of Myelin, the Sclerosis (Scar Tissue), and the fact that the Lessions (Plaque) occur in many sites throughout the CNS, account for the name Multiple Sclerosis.

The water content of the plaques increses, which permits their detection by MRI's. There are areas of inflammation in MS that are usually characterized by the accumulation of cells.

It is not known how or why they arrive at the site, where they eventually gather and form a lesion. It is known that they both injure the tissue and digest the damaged Myelin. The cells that digest the Myelin are Macrophages.

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Another cell that appears to be related to this inflammatory collection, but which remains within the CNS for a long period of time, is the Plasma Cell. This cell produces ImmunoGlobulin, which is a protein in the Serum that contains AntiBodies.

The Plasma Cells found within Brain tissue of MSers' may produce large amounts of ImmunoGlobulin. Because this material may be detected by laboratory tests, its presence is used to help in the MS diagnosis.

The damage to Myelin in Nerve Cells, which is seen when tissues are examined after death, is usually more extensive than was suggested by the symptoms seen during life.

It appears that there are attacks in patients that have not produced symptoms severe enough to be felt by the patient or seen by the doctor.


The Immune System

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An Immune Response in any individual, with or without a specific disease, simply refers to the body reacting to a foreign agent. Occasionally the body goes haywire and starts to react against its own tissues. This is called an AutoImmune Response.

The host's Immune System may be involved in the onset or perpetuation of MS. Cells of Lymphoid Tissue (Thymus, Spleen, Lymph Nodes, & certain blood cells) generate and control an Immune Response.

In humans, most of the information has been obtained from studies of Lymphocytes (certain blood cells), which are readily accessible for analysis. These Lymphocytes may be subdivided into different types, which have several specialized functions.

Some (B-Cells) produce and secrete AntiBody. Other Lymphocytes (T-Cells) directly attack and destroy an infectious organism; these are "effector" T-Cells. Other T-Cells help promote an Immune Response or suppress it; these are "Regulatory" T-Cells.

Investigation of the general Immune status of MSers has disclosed no consistent abnormality in the blood, although when more specific and sensitive tests are used, regulatory Lymphocytes of the T-Suppressor type sometimes have been found to be reduced in number or actions.

That is, there may be a decrease or disappearance of these Lymphocytes from the peripheral blood, or a decline in their function at the very time MS exacerbates. The function of these cells returns to normal or above normal when the patient goes into remission.

Whether these cells are destroyed, enter the CNS, or merely alter their circulatory route in the body remains to be determined. The Lymphocytes in MS plaques include B & T-Lymphocytes without a selective T-Cell type (Helper or Suppressor) dominant.

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It is also unclear how an alteration of the number of regulatory T-Lymphocytes would manifest as MS, but the correlation some times noted of the cyclic changes in clinical symptoms and the number of these cells in the bloodstream is intriguing.


CerebroSpinal Fluid

It has been known for more than 35 years that there is usually an increase in the amount of ImmunoGlobulin in the CerebroSpinal Fluid of MSers'.

IgG is the predominant ImmunoGlobulin. CerebroSpinal Fluid normally has up to 45 milligrams of protein per 100 milliliters; IgG constitutes less than 15% of the total amount of Protein present.

As noted, in MSers, the IgG in the CerebroSpinal Fluid is increased, primarily because of the production of IgG by certain cells (Plasma Cells) within the CNS.

These cells appear to arise from blood Lymphocytes, which enter the CNS when the MSer is having bouts of inflammatory Myelin damage.

When examined by suitable techniques, the CerebroSpinal Fluid Proteins of the vast majority (80 to 90%) of MSers show selective increases of certain forms of IgG, but the presence of these forms of IgG in CerebroSpinal Fluid is not specific for MS; they are also found in other diseases as well.

In association with the changes in IgG in the CerebroSpinal Fluid, AntiBodies to a number of Viruses are also found to be increased.

However, neither of these conditions is specific for MS or even precisely parallels the disease's activity. The activity of the major parts of the IgG in CerebroSpinal Fluid is unknown. Attempts to determine this activity are currently being made in many reasearch laboratories.


Viruses And Multiple Sclerosis

Viruses or other infectious agents have been suspected for many years to be the cause of MS. As different infectious organisms have been discovered and identified, they have been examined for a possible linkage to MS.

During the past 20 years, attention to an infectious basis for MS has been directed primarily at Viruses.

Viruses

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Numerous types of Virus exist with an array of features that determine how they infect and alter tissue. The behavior of the Virus is the result of a Virus's own characteristics and the cells to which it is exposed.

A host cell may show a number of reactions in response to a Viral infection, ranging from minimal or no change to malignant transformation to death.

In addition to the changes produced by the usual type of Virus, mutant Viruses may appear that have different characteristics of infectivity or disease induction.

Evidence for Viral involvement in MS or any condition can be sought using several methods. The most convincing is the culture, isolation, and identification of a Virus in tissue taken from areas of damage.

Other methods include recognizing parts of a Virus in tissue and detecting AntiBodies (which would attack that particular Virus) in the blood or CerebroSpinal Fluid of those affected. Finding the AntiBody would indicate that the person had been exposed to the Virus at one time or another.

The Virus that causes Measles has been analyzed extensively as a possible cause of MS. This Measles Virus is known also to cause a chronic Nervous System disease of childhood called Subacute Sclerosing PanenCephalitis.

Beginning in 1962, it was recognized that persons with MS have increased amounts of AntiBody to the Measles Virus in their bloodstream.

Although a number of studies have confirmed this observation and have also shown that some of the AntiBody to Measles is being produced by the CNS, evidence for the Measles Virus also causing MS remains highly circumstantial.


Slow Virus

When attempting to relate enviromental influences from 10 to 20 years before, to the appearance of MS now, a "Slow Virus" must be considered.

In contrast to the usual acute or subacute response to conventual Viruses, "Slow Viruses" cause disease that may evolve over a period of months or years.

One of these Viruses induces an inflammatory CNS disease in sheep, but there is no indication that any one of the known "Slow Viruses" causes MS.

Other Viruses

Several conventional Viruses have been identified as causing a CNS disease in animals that shows some of the same tissue changes as are seen in MS.

Hence, because of the many mechanisms whereby a Virus might inflict CNS damage, a Viral Etiology for MS has by no means been excluded.


The Diagnosis

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Although some helpful diagnostic procedures and tests have been developed, the diagnosis of Multiple Sclerosis is still based on the history and Neurological examination.

The physician must be able to show that there are two or more areas of lesions in the Central Nervous System (CNS) - the Brain and the Spinal Cord.

There must be evidence that the lesions are disseminated not only in space (ie.,in different locations) but in time (symptoms or signs should develop at different times).

The diagnosis remains essentially a clinical one, based on symptoms and signs of the individual's Nervous System malfunction.

A symptom is something that is reported by the patient. A sign is an abnormality detected by the physican while examining the person. At times signs confirm the presence of symptoms.

Some abnormal reflexes or loss of Vibratory Sense may be present without the patient being aware of anything being wrong. Symptoms are subjective complaints, whereas signs are objective observations.

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It must be emphasized that lesions that do not produce any symptom or even signs of malfunction, exist in practically every MSer.

It is important to realize this, so that the appearance of a new symptom does not necessarily signify the formation of a new lesion.

It is difficult to understand how lesions that are discovered at autopsy have not produced symptoms in view of their location and size, but they are seen repeatedly.

Continued In 04-02




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