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What is the difference between Mono and Multiple Sclerosis?

While reading the description of Multiple Sclerosis just relate to Mono in the singular events described.

Multiple sclerosis is often described as a 'severe incapacitating progressive disease in which plaques formed in the white matter of the nervous system, with the loss of the insulating white matter'.

It is essential to analyse each aspect, because of the important indications this has for treatment. Even patients who have suffered severe attacks may have complete remission of symptoms and eventually die of an unrelated disease.

However, these patients will have evidence of damage on magnetic resonance imaging. These areas of damage will also be observable at post-mortem examination. The evidence from magnetic resonance imaging of apparently healthy people indicates that, at a single point in time, as many as 40% of the population may have areas affected - UBOs in the brain.

'severe incapacitating progressive disease'

'In which plaques occur'

The term "plaque" is very misleading implying a flat plate of tissue. This is the appearance of the area of damage when the brain is sliced at post-mortem examination. However, the areas are three-dimensional and most often the damage is cylindrical surrounding a vein, that is they are perivenous.

'in the white matter'

It is completely established that lesions also affect the grey matter of the central nervous system and in the spinal cord the grey and white matter may be equally affected.

'In the central nervous system'

There is conclusive evidence that the peripheral nerves may also be involved as may be the autonomic nervous system.

'Insulating myelin sheaths'

The myelin sheaths are necessary to increase the speed of transmission along the fibre, not to insulate or protect. A myelinated fibre may conduct impulses several hundred times faster than a non myelinated fibre of the same size. Many fibres in the nervous system do not have myelin sheaths, and yet they function perfectly well.

It is frequently implied that nerve fibres and nerve cells are preserved but this is not the case and the loss of fibres and cells is responsible for permanent disability. About 20 percent of the nerve fibres are lost in a typical area of damage in multiple sclerosis. In severely affected areas there may be gross destruction of tissue in which nerve fibres and nerve cells disappear leaving a cyst, which is a liquid-filled cavity.

Multiple Sclerosis (MS) is a disease in which certain types of white blood cells called T lymphocytes attack a fatty covering found in the central nervous system. More specifically, most of the individual nerve cells of the brain and spinal chord, which make up the central nervous system, are surrounded by a covering called the myelin sheath. The myelin sheath helps insulate signals from adjacent nerves and increase the speed of signal transmission along the nerve. It is the myelin sheath which is attacked by the lymphocytes. During an attack the lymphocytes destroy the myelin, first causing inflammation followed by the formation of scar tissue.

Normally, lymphocytes do not attack a person's own body. Rather, they are programmed to distinguish between a person's body and foreign, invading substances. Their purpose is to protect the body from invading bacteria and viruses. Occasionally, though, they can develop sensitivity against a person's own cells. This is called an autoimmune disease. Rheumatoid arthritis and lupus are examples of two other autoimmune diseases.

One of the more puzzling aspects of MS is its inconsistency. The attacks typically occur at localized, random sites on a periodic basis. This is opposed to a generalized, continuous attack. Between episodes, a person will typically recover much of the lost function from the attack. The period of time between episodes also varies from individual to individual. Some people have a very slow progress and may not be adversely handicapped decades later and others will have a very rapid progress, culminating in their death within a few years. Within the widespread personal variation, however, is an overall tendency for subsequent attacks to be worse than the first, so that the disease, over time, does tend to worsen. The only thing definite about the disease is its indefiniteness; a person's past history with the disease is not necessarily an indicator of his future history.

Whenever a specific nerve is attacked, the nerve pulses passing through the region of attack tend to weaken and slow down. During remission, that is, the period between attacks, there is typically a certain amount of recovery of the nerve's functionality. Apparently, though, once a site has been attacked it is more likely to be the site of future attacks. Eventually, the scar tissue formed can be so problematic that a nerve cell may die. This, of course, leads to a permanent loss of functionality.

Typical symptoms of MS include sensory problems and muscle control problems, depending on the function of the specific nerve under attack. Thus, a person may feel a numbness or tingling in an arm or leg, or the limb may feel heavy and unresponsive, or any number of other symptoms that could be caused by a nerve not functioning properly.

Short of an autopsy to examine one's brain or spinal chord, so that the scars may be directly observed, there is no specific, definitive test for the disease. Autopsy is an extreme form of diagnosis for those still alive. However, recent advances with magneto-resonance imaging (MRI) scans have shown the scars at the attack sites typically produce characteristic shadows on the scans. These shadows, when coupled with the observed symptoms of MS, tend to be fairly reliable indicators of the disease.

Initially, it was felt that MS was caused by a virus. This was based primarily upon statistical analyses of the medical history of MS patients, who invariably seemed to have had an earlier exposure to a disease such as measles or mumps. However, identification of a virus has eluded many researchers for a long period of time.

Lately, MS is seen as being a disease of the immune system. The cause of the inflammation leading to the depletion of the myelin and the forming of scar tissue has been traced to T4 lymphocytes, certain white blood cells in a person's blood stream. These two viewpoints are not mutually contradictory. Thus, a person may suffer from a viral infection which somehow sensitizes the immune system to attack myelin.

The concept that MS is primarily caused by immune system malfunctions does not explain adequately many observations concerning the disease. For instance, if the disease is primarily caused by an immune system malfunction, why is its behavior so random? One would expect a continuous, universal attack if the nervous system were the sole influence.

Another puzzling phenomenom is that autopsies of the general population have revealed that perhaps as much as two-percent of the population has MS scars in their central nervous system. This is perhaps twenty times larger than one would expect. In general, those who had the scars but did not have any observed symptoms also had very few scars. To me, though, the significant thing is that in order to get any scars at all, these people needed to have an immune system with lymphocytes sensitized to their own myelin. Yet, in these cases, the disease did not seem to progress very rapidly at all. Why?

It is now widely accepted that MS is an autoimmune disorder which means that one's own immune system attacks the myelin in the cells in the Central Nervous System(CNS) but this raises a number of interesting questions. Why? What starts the process? Why are some countries devastated by the condition while the population of others remains largely unaffected? And why are the incidents of the condition generally spread, even within the same country, dependant on distance from the equator - a latitude gradient, in other words.

From published material it is now evident that diet, in conjunction with low levels of natural sunshine(Vitamin D3), is the main cause of the condition in genetically susceptible individuals. It is estimated that around 0.5% of northern Europeans carry the gene that makes them susceptible to the condition and they, and their descendants, are most at risk. As a result, the USA, Canada, NZ and Australia are all high incidence areas.

 

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