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Multiple Sclerosis (MS) is a neurological disease characterized by multiple areas of damage and scarring (sclerosis) to the nerve fibers of the brain and spinal cord. Although research has brought us closer to understanding the disease process, its cause is not yet fully known, nor is there a cure. What we do know is that MS is not a contagious disease, nor is it considered genetic, although some recent studies suggest a familial predisposition. MS affects an estimated 350,000 to 500,000 Americans, with women nearly twice as likely to contract the disease as men. On average, the age of onset is between 20 to 40 years old, and geographically, the disease occurs more frequently in northern climes. Scientific evidence strongly suggests that MS is an autoimmune disorder in which the body’s immune system ravages its own cells. In MS, the nerve cells are under siege and the resultant fallout affects the entire body. Here’s how it works.
Our nervous system is a “live wire;” a profoundly intricate network that sends signals from our brain to other parts of our body. There is a protective coating of myelin around the nerve fiber, which acts as insulation in the same way that rubber protects the wiring on a lamp cord. In MS, the body’s immune system mistakenly attacks the myelin, eating away at the protective insulation. Because of the damage to the insulation, the “live wire” of our nervous system can become short-circuited in the same way a damaged cord can cause a lamp to malfunction. Depending on the extent of the damage, persons with MS can experience symptoms ranging from mild to very severe. This short-circuiting of the nervous system is the basic nature of MS, and can cause a myriad of difficulties affecting vision, motor skills, speech, balance, and bladder control, to name a few.
To better illustrate this disease process, let’s pretend that you have just run a mile and you are terribly thirsty and want a drink of water. The brain sends the signal to your hand to reach for the glass, which you then raise to your mouth. No problem. In most people, this message travels without incident along the nervous system, and all the essential muscles in the hand and arm easily coordinate to allow the glass to be lifted and the thirst quenched. But in a person with MS, the message can get jumbled and disconnected along the route to its destination. The brain tells the hand to pick up the glass, but the entire message doesn’t get through to the other end. Why? Because the areas in which the myelin is damaged are short-circuited. The result? An uncoordinated movement; a sudden hand tremor; a spilled glass of water.
This short-circuit in MS can cause diverse symptoms that behave in an unpredictable pattern, often causing a series of attacks and remissions. Returning to my earlier lamp cord analogy, consider what happens when you plug the faulty cord into an outlet. The performance of the lamp depends on the amount of damage to the cord. For example, if there’s just a tiny superficial tear in the insulation, the lamp may still perform normally for several months. However, as time wears on and the tear in the cord worsens or more damage occurs, the lamp may initially operate, flicker erratically through the day, then return to normal. Even further down the line, when a serious gouge develops that totally exposes the wire; turning on the lamp may cause a complete blowout or shutdown of function (assuming you don’t electrocute yourself in the process!).
It is this phenomenon that most clearly illustrates the tendency of MS to attack and then remit. A person with MS may experience a sudden onset of symptoms that mysteriously leave after a week or two. Perhaps it’s a bout of double vision or an odd tingling sensation in the legs. Maybe it’s a chronic feeling of excessive fatigue, or extreme hypersensitivity to cold. Possibly, it’s an unexplained clumsiness or an inability to maintain your balance on skates even though you’ve been a champion ice princess since your Sesame Street days.
These series of attacks and remissions make a diagnosis of MS difficult to pin down. Often, early in the disease, a person experiences one or more of these puzzling symptoms but doesn’t bring it to the attention of a physician because it simply goes away on its own. Because the disturbances may last just a week or two–or sometimes a day or two—-many early symptoms are dismissed as signs of stress, or depression, or just a passing curiosity. But make no mistake, just because the disease is “flickering” doesn’t mean that the insulation is intact or that the problem is gone. As more myelin damage occurs, the symptoms will become more pronounced and will recur more often.
People with MS will have one of several different forms of the disease. With progressive disease, the individual will have the gradual progression of worsening symptoms over time. With relapsing forms of the disease, the individual will have attacks of worsened symptoms that either spontaneously get better or respond to treatment and get better for a period of time. The remissions don’t last long, however, and the patient has recurrence of their symptoms. Rarely does the relapsing patient have complete resolution of their symptoms so each exacerbation results in worsened symptoms and some permanent neurological deficits.
No one knows the exact cause of multiple sclerosis; however, it is known to be an autoimmune disease of the central nervous system. This means that the individual’s own immune cells make antibodies against myelin or the cells that make myelin, resulting in a loss of the myelin sheath and nerve cell dysfunction. As to the cause of the autoimmune dysfunction, the underlying cause may be related to genetics/heredity as well as environmental factors, including the possibility that a viral infection triggers the autoimmune dysfunction.
LOOKING BACK- HISTORY OF MS
Multiple sclerosis was first identified as a unique disease in 1868 by French neurologist and professor of anatomical pathology, Jean-Martin Charcot. It was called multiple sclerosis because of the finding of multiple plaques or scars found in the white matter of the brain and spinal cord. It is considered the most common central nervous system autoimmune disease. Worldwide, there are about 2.5 million individuals affected by the disorder, although the rate of the disorder varies from geographic region to geographic region throughout the world. While there are millions of people who have the disorder, only about 18,000 individuals die from the disease each year.
The commonly-affected patient is 20-50 years at the time of diagnosis. As mentioned earlier about two times as many females are affected when compared to males. The incidence is about 30 people out of 100,000, although the incidence is highly variable. For example, only about 0.5 out of 100,000 individuals is affected by multiple sclerosis in Africa, while 80 out of 100,000 individuals are affected in Europe. In parts of Northern Europe, the incidence of MS is as high as 200 individuals out of 100,000 in the population.
Multiple sclerosis most often affects the person in their late twenties to early thirties. The rare patient will develop multiple sclerosis in childhood or after the age of fifty, when it often results in the primary progressive subtype. As an autoimmune disorder, it behaves much like other immune-related disorders, affecting women much more commonly than men. In fact, twice as many women have the disease as men, except when it affects older individuals. In such cases, there are equal numbers of men and women affected by the disease.
SIGNS AND SYMPTOMS OF MS
There are numerous signs and symptoms of multiple sclerosis, making it a “copycat” neurological disorder with symptoms that can mimic other diseases. Central symptoms include cognitive impairment, fatigue, mood lability, depression, and anxiety. Visual symptoms are common and include optic neuritis, diplopia, and nystagmus. Speech and the oral muscles can be impaired with dysarthria and dysphagia.
Musculoskeletal symptoms/motor symptoms include weakness of various muscles, muscle spasms, and cerebellar ataxia. Sensory symptoms include pain in the nerves, paresthesias, and decreased sensation. Bowel problems can include constipation, diarrhea, and bowel incontinence. Urinary frequency, urinary retention, and urinary incontinence are also possible. In fact, nearly any autonomic, motor, sensory, or visual problem can affect the patient with MS.
Because this can affect the peripheral muscles, the reflexes can be diminished. Because it can affect the central nerves, the reflexes can be hyperactive. The muscles can be spasmodic with difficulty moving the muscles, coordination difficulties, and ataxia (balance problems). Optic neuritis is a common phenomenon in multiple sclerosis, although others can have double vision or nystagmus (lateral movement of the eyes). Chronic pain is common as well as acute pain during exacerbations. Patients with the disease often feel tired all the time with sensory problems like pins and needles, numbness of parts of the body, or other changes in sensation.
Emotional and mood symptoms may be subtle or obvious. These patients often have anxiety and depression, instability of mood, and thought disturbances. The symptoms tend to be worse in warm ambient temperatures—a phenomenon called Uhthoff’s phenomenon. There is a characteristic and common neurological sign in MS called the Lhermitte’s sign, which is a sharp, electrical sensation that runs up and down the back when the neck is bent forward.
Patients have varying degrees of disability with their multiple sclerosis symptoms. The EDSS or expanded disability scale measures the degree of disability the patient has. The EDSS measures the degree of disability in eight functional systems in multiple sclerosis and allows doctors to assign a Functional System Score (FSS) in each of these systems. Another disability score (the Multiple Sclerosis Functional Composite) is being increasingly used by researchers studying multiple sclerosis.
The symptoms of multiple sclerosis can start as a clinically isolated syndrome evolving over several days—seen in 85 percent of cases. About 45 percent of sufferers will have isolated motor or sensory deficits; 20 percent will present with optic neuritis; and 10 percent will have brainstem deficits, which can be serious and life-threatening. About 15 percent won’t have an isolated syndrome but will have symptoms spanning several neurological areas.
There are two major patterns of disease. The patient may have episodic exacerbations of symptoms that are interspersed with remissions. These exacerbations are referred to as relapses or flare-ups, with the natural course of the disease being resolution of the symptoms. This is the course of the disease seen in 85 percent of cases. The remaining 15 percent will have a progressive disease that gradually worsens over time with few remissions in symptomatology. Some patients will have a combined “relapsing/remitting course” that ultimately becomes “progressive” in nature—without recovery between exacerbations.
Patients with relapsing disease cannot predict when they will have an exacerbation. They may occur just 1-2 times per year or more often than that. Spring and summer appear to be particular times of relapses in the healthy person with MS. Patients who suffer from a common viral infection of the GI tract or respiratory tract may have an exacerbation because of the infection. Even things like psychological stress can trigger a relapse. Pregnancy interestingly decreases the relapse rate; however, there will often be more relapses during the postpartum period. Fortunately, pregnancy does not make the disease worse. The things that do make it worse, on the other hand, include increased ambient temperature, physical trauma, becoming vaccinated, and breastfeeding an infant.
CAUSES OF MULTIPLE SCLEROSIS
The only known fact about multiple sclerosis is that it is an autoimmune disease. The exact underlying cause of the disease is not completely clear. There have been many theories as to what triggers this autoimmune disease, including genetic factors, infectious diseases, and other environmental factors. There has been no unifying theory that explains the onset of multiple sclerosis in every patient. Even so, doctors and researchers have determined many of the risk factors behind the disease state’s onset as well as those things that lead to an exacerbation.
Geography seems to be one of the risk factors. The further away a person lives from the equator, the greater is the likelihood that the patient will have the disease. There are, however, exceptions to this rule. People indigenous to one of the areas of the world that is far from the equator (such as the Inuit people of Canada) have a low risk of the disease. In addition, people who normally are indigenous to areas near the equator (like people from Palestine, Sardinia, and Sicily) have a high risk for the disorder, even though they live near the equator.
Northern Europe appears to be a “hot spot” for multiple sclerosis. These people experience less sunlight when compared to those living near the equator and have decreased vitamin D production. While low vitamin D has been linked to multiple sclerosis, the connection hasn’t been completely established. The environment in these areas seems to be partly responsible for the changes in the incidence of MS because people who move away from a high-risk area to a low-risk area prior to the age of fifteen will take on the risk of the area they move to. Moving after the age of fifteen doesn’t confer a risk related to the place they move to but instead results in retaining the risk of the place they were born in.
While multiple sclerosis is not hereditary in the usual sense, there are some specific genetic findings that have been found to increase a person’s chance of getting the disease. The genetic defects seem to be upregulated (seen to a greater degree) in the microglial cells of affected patients with MS. In addition, people with a first-degree relative will have a greater than average risk of having the disease themselves. The twin-twin concordance rate is the chance that identical twins will have the disease together. This is about 30 percent—much higher than can be expected by chance alone. About 5 percent of non-identical twins and 2.5 percent of brothers and sisters will have the disease together in their lifetime. Two affected patients who have children will have a child that has a ten-fold greater risk of developing the disease themselves. Certain ethnicities appear to have a greater than average risk of having multiple sclerosis.
Infectious agents have long been believed to be behind the development of multiple sclerosis; however, there haven’t been any particular findings of specific infections that are known to trigger the disease. It is believed that exposure to a variety of infectious diseases as a young child will protect the child against the development of getting the infection during a key later time in their lifetime—leading to MS. This is called the “hygiene hypothesis”. It is also believed that the infection causing MS happens many years prior to the development of the actual autoimmune disease. It may be that just a few susceptible people are at a risk of getting MS from the infectious agent.
While the infectious agent could be anything, there is more support for this being a viral phenomenon rather than a bacterial, fungal, or parasitic infectious disease. There are DNA changes in the brain and spinal cord of patients with multiple sclerosis that are specifically related to having had a viral infection. Certain animal studies have shown demyelinating disease states after a viral infection. While Epstein-Barr viral infections (EBV) haven’t been tightly linked to MS, it is known that people who have never had an EBV infection have a decreased chance of developing MS in their lifetime and people who have an EBV infection as a young adult have a greater risk for multiple sclerosis when compared to children who had an EBV infection as a young child. Measles, mumps, and rubella infections also seem to increase the risk of multiple sclerosis.
Other risk factors linked to multiple sclerosis include being a smoker. There is limited evidence to support increased stress as a trigger for MS. No particular association has been found between developing MS and exposure to vaccinations or solvents. The same is true of changes in dietary habits and hormone intake when it comes to the risk of getting multiple sclerosis. The levels of uric acid in the bloodstream are inversely proportional to the incidence of multiple sclerosis for reasons that are not completely known.
LOOKING EVEN CLOSER- PATHOPHYSIOLOGY OF MULTIPLE SCLEROSIS
When it comes to the pathophysiology of multiple sclerosis, it should be known that there are three aspects to the disease. 1) There are plaques in the white matter that ultimately become areas of demyelination of nerves; 2) there is inflammation of the nerve tissue; and 3) there is classical destruction of the myelin sheath surrounding the nerve axons. No one knows exactly how these three things interact to make the symptoms typical of multiple sclerosis.
MS is an immune-mediated autoimmune disease, in which the patient’s own immune system attacks part of the nerves. The exact mechanism behind why the immune system decides to attack part of the body’s tissues is not clear. As with all autoimmune diseases, the causation is complex, with genetic factors strongly participating with the environment to create autoantibodies that destroy nerve function.
As the name implies, multiple sclerosis involves several plaques or lesions of the nervous system that are evident almost exclusively in the white matter. There is white matter in the brain, spinal cord, brainstem, basal ganglia, and in the optic nerve in the nervous system. These are the areas most greatly associated with plaque formation, which actually represent areas where demyelination has occurred. While there can be involvement of peripheral nerves, this is much less common than the lesions seen in the central nervous system.
Pathophysiologically, the finding in multiple sclerosis is the loss of oligodendrocytes, which are the primary cells responsible for making the myelin sheath surrounding nerve axons. The myelin sheath helps improve the speed of transmission of the action potentials (nerve signals) of the long nerve axons. This loss of myelin greatly reduces the speed of the nerve, leading to symptoms commonly seen when the nerve doesn’t transmit a signal well.
There is a repair process, known as remyelination, that can happen early in the course of the disease; however, the oligodendrocytes responsible for doing this cannot do it as effectively as in normal people, leading to scar tissue and plaques in the axons that continually get demyelinated and remyelinated. The MRI usually shows more than ten plaques in the CNS. These are lesions that have been repaired multiple times and represent the areas where there hasn’t been the presence of the regular repair process. Astrocytes increase in number near the plaques as a sign of the inflammation going on in these areas.
The autoimmune process involves ongoing inflammation of areas of the CNS. This is in keeping with the immune-mediated etiology behind the disease process. The inflammatory process starts with autoantibodies getting made by B cells and activation of cytotoxic T cells that cross the blood-brain barrier, leading to CNS cell attack by the activated T cells. The T cells see myelin as a foreign substance and direct an immune response against it. The T cells that perform this function are called “autoreactive T lymphocytes”.
Other immune cells participate in the inflammatory process besides autoreactive T cells. The entire immune system gets activated, releasing inflammatory cytokines and forming more antibodies. The blood-brain barrier becomes compromised and there is local inflammatory swelling, activation of cytokines, and the development of activated macrophages. The inflammation alone can reduce the nerve cell transmission by otherwise healthy neurons. The axon can get destroyed completely by the inflammatory process or can simply get demyelinated.
Normally, the blood-brain barrier exists in order to protect the brain and spinal cord from the influx of inflammatory cells and inflammatory mediators. In multiple sclerosis, there is a process that increases the permeability of the blood-brain barrier, leading to T cell influx and an increase in CNS inflammatory processes. One way to assess the permeability of the blood-brain barrier is to do a Gadolinium scan, which shows an influx of Gadolinium in patients who have multiple sclerosis. In normal people, Gadolinium won’t even cross the blood-brain barrier.
DIAGNOSING THE DISEASE
Because of the many possible symptoms seen in multiple sclerosis, it can be difficult to diagnose the disorder. The signs and symptoms can point to the diagnosis of MS along with certain imaging studies and laboratory testing. Doctors can use the McDonald criteria to make the diagnosis of multiple sclerosis. These criteria are based on the numbers of attacks, laboratory testing, and the lesions seen on the MRI of the brain. There are other criteria that have been used in the past; however, the McDonald criteria are used most commonly today.
Some patients are diagnosed based on the clinical picture alone. Any patient with suspicious symptoms of MS that come in exacerbations and remissions will have a high likelihood of having multiple sclerosis. If the patient has had just one attack of symptoms, further testing may be indicated. The major diagnostic tests used in identifying MS include a cerebrospinal fluid (CSF) analysis, neuroimaging studies, and an evaluation of the patient’s evoked potentials. MRI of the brain and spinal cord may show areas of plaques or lesions suspicious for demyelination.
Gadolinium scanning can be done to show leakage of the blood-brain barrier. Gadolinium will normally not cross the blood-brain barrier. In MS, the gadolinium will highlight any active plaques in the central nervous system. It will show past lesions as well. The CSF testing (gotten from a lumbar puncture) will show evidence of ongoing inflammation of the CNS. The CSF is tested in order to identify oligoclonal bands of IgG on an electrophoresis test. This test will be positive for oligoclonal bands in 75-85 percent of patients who have multiple sclerosis. Stimulation of the optic nerve and sensory nerves will show less activity because of the demyelination of these nerves. Visual and sensory-evoked potentials will be decreased in MS.
While these criteria will strongly point to multiple sclerosis, they won’t absolutely prove the diagnosis of multiple sclerosis because there is no test besides a nerve biopsy or autopsy evaluation that can prove the presence of MS lesions. These tests aren’t practical in life and, for the most part, aren’t necessary to make the diagnosis of MS in the typical patient.
WHAT ARE THE DIFFERENT TYPES OF MULTIPLE SCLEROSIS?
There are different subtypes of multiple sclerosis, based on the different patterns of disease progression. All subtypes represent MS but are different in their clinical course and can predict the patient’s future course. The different subtypes are treated differently so that, when a specific subtype is identified, the treatment is based on the diagnostic classification.
The different subtypes include clinically isolated syndrome, relapsing-remitting multiple sclerosis, primary progressive multiple sclerosis, and secondary progressive multiple sclerosis. A common type is the relapsing-remitting MS. This is seen by having unpredictable relapses followed by periods of many months or years between exacerbations. The deficits seen in a relapse have a 60 percent chance of resolving completely and a 40 percent chance of leaving behind some residual disease. Relapsing-remitting MS makes up 80 percent of MS cases—at least in the first several years of the disease process.
Some patients won’t have benign disease but will instead have malignant multiple sclerosis. This defines the MS patient having progressive disease over a short period of time. These patients are rapidly disabled, with no period of remission. Patients who have CIS (clinically isolated syndrome) have a single episode suggestive of MS but don’t have relapses and remissions, making it not exactly fitting the criteria for multiple sclerosis. Only 30-70 percent of people with CIS actually develop MS later in life with ongoing symptomatology.
Primary progressive multiple sclerosis happens in up to 20 percent of MS patients without any remission after the onset of initial symptoms. There may be minor improvements in symptomatology over time; however, they aren’t significant enough to make the diagnosis of a remission. These patients have later onset of initial disease at around 40 years of age.
Secondary progressive MS happens in about 65 percent of patients that start with relapsing-remitting MS and who ultimately go on to having progressive disease. Occasional relapses and minor states of remission may be seen in the beginning of the disease but eventually, there is only progression of symptoms. The time period between the onset of MS and conversion to the secondary progressive type of the disease is about 19 years.
There are no drugs or treatments that can cure multiple sclerosis. The treatments that are available will improve function after an attack and will prevent recurrences of symptoms. The downside of medications for MS is that, while they are effective, they have side effects that are difficult to deal with. Some patients instead have physical therapy to help regain physical functioning or use alternative therapies, which may or may not be helpful in managing symptoms.
Patients who respond the best to treatment are people who have early-onset disease states, people with few exacerbations of the disease, those with remitting-relapsing disease, and women. Patients have a decreased life expectancy when compared to normal individuals, even with treatment, of about 5-10 years on average.
The goal of therapy for MS is to shorten the length of time the person is having an exacerbation, prevent exacerbations from occurring, and decrease the degree of overall disability. The side effects of medications for MS can be so severe that patients often aren’t able or willing to take the drugs but have a tendency to stop them early or to take alternative medications instead.
The main treatment of acute attacks of MS is to give high doses of intravenous corticosteroid medications, such as methylprednisolone (although oral steroid drugs often work just as well). The corticosteroids will help control symptoms early in the disease but don’t seem to have a major impact on the patient’s long-term prognosis. Another treatment is plasmapheresis, which involves a removal of autoantibodies from the bloodstream in a plasma exchange treatment. This is reserved for very severe attacks of MS.
There are a few disease-modifying treatments that seem to be effective particularly in relapsing-remitting multiple sclerosis. These are interferon beta-1b, interferon beta-1a, certain monoclonal antibody treatments, and other uncommonly used drugs. The biggest problem with using these drugs is that they are very costly and are not particularly effective in treating MS cases. These drugs have gone through clinical trials for safety and efficacy but don’t work on everyone; they are specifically directed toward certain types of MS and work better for relapsing-remitting disease. Even so, they seem to be only modestly effective in reducing the number of attacks of MS. Many of the disease-modifying drugs will decrease the number of attacks by 30 percent when started early in the course of the disease.
The drug natalizumab has been approved for relapsing-remitting MS and will decrease the number of relapses. The major downside of this treatment is that it doesn’t do anything for active MS symptoms and has a lot of adverse side effects. The same is true of mitoxantrone, which has too many side effects to take for the long-term. Interferons are particularly helpful in the management of CIS (clinically isolated syndrome) because it decreases the chances of this syndrome progressing to full-blown multiple sclerosis. It can be used in both adults and children with MS. There are some off-label drugs that have been tried for relapsing-remitting multiple sclerosis.
There are much fewer drugs available to treat progressive multiple sclerosis. Rituximab is entirely off-label for this disease but it has been used by some neurologists. Other drugs that are FDA approved include ocrelizumab (a monoclonal antibody drug) for primary progressive MS and mitoxantrone (which is used for secondary progressive MS). It is modestly effective in decreasing and slowing the progression of the disease process—also decreasing the relapse rate.
All disease-modifying drugs have side effects that preclude their use in some people. A common side effect with these types of drugs is irritation at the injection site (seen in interferon administration and glatiramer acetate), which his seen in up to 90 percent of cases where the drugs are given subcutaneously and 30 percent of cases where the drugs are given IM. There can be a permanent indentation at the injection site secondary to lipoatrophy (or breakdown of fat cells) at the site of the injection. The interferon drugs are well known to cause patients to have influenza-like symptoms after injection. Glatiramer will have frequent episodes of anxiety, palpitations of the heart, tightness of the chest, and skin flushing after taking the drug.
Less commonly, the interferon drugs can result in liver damage; mitoxantrone can cause infertility, acute myeloid leukemia, and systolic heart dysfunction. Natalizumab can cause progressive multifocal leukoencephalopathy. Fingolimod will cause high blood pressure, macular edema of the eye, liver damage, lymphocyte cell reduction numbers, and decreased heart rate. While these aren’t seen in everyone, the side effects are clearly severe and can be life-threatening when given in therapeutic doses. Dimethyl fumarate can lead to a decreased WBC count but won’t adversely affect the tendency to get opportunistic infections. Many of these drugs cannot be given in pregnancy because of teratogenic effects; fortunately, MS tends not to be very severe in pregnancy so they are less commonly used during this time in a woman’s life.
Medications for multiple sclerosis are best used in situations where rehabilitation and physical therapy can be used at the same time. Together these will positively affect a few of he MS symptoms but won’t change the natural history of the disease. What should be emphasized is the fact that MS treatment involves a multidisciplinary treatment model, with therapy just as helpful as medications. There needs to be a team of professionals, including a neurologist, social worker, psychologists, and different types of therapists who together work to define the best treatment protocols and to improve the patient’s quality of life while living with multiple sclerosis. Nothing can be done to alter the disease course but there are things that can be done to make life easier for the MS sufferer.
Because of side effects, more than half of all patients with multiple sclerosis will turn to alternative medical therapy for their symptoms. There is no evidence that any of these treatments are helpful for the disease but some people have subjective improvement. The major alternative therapies tried for MS include yoga, acupuncture, vitamin D supplementation, herbal medical therapies, cannabis treatment, hyperbaric oxygen treatments, reflexology, mindfulness therapy, and becoming purposely infected with hookworms. Women try these therapies more often than men, and patients who’ve had MS for many years with ongoing disability tend to turn to alternative therapies, being discouraged by treatments offered by conventional medicine.
PROGNOSIS OF MS AND WHAT TO EXPECT
The actual prognosis of multiple sclerosis depends on the subtype of MS the person has. Patients with malignant MS have a worsened prognosis when compared to people who have relapsing-remitting MS. Patients who are disabled have more complications and a reduced lifespan when compared to patients who have lesser degrees of disability. Statistically, women, those with optic neuritis only, those with fewer attacks over the first few years, and those with relapsing-remitting MS will have better outcomes overall.
Once the person has been diagnosed with MS, the average lifespan is around thirty years, which tends to be about five to ten years less than the average person. While most patients live into their sixties, they live with a great deal of disability that affects their everyday life. Two-thirds of patients will die from the disease itself (and its complications). Sadly, suicide is a common way to die from multiple sclerosis as there is a great deal of depression and disability associated with the disease. Most people ultimately become wheelchair-bound by the time they die from the disease, although this often takes 10-20 years before this happens. Infections are another cause of death from the disease as these patients are sedentary and get infections more easily.
MULTIPLE SCLEROSIS WEBSITES
What is MS?-This site starts with the basics of what MS is all about and progresses to telling you where you can find an MS provider and how you can get involve in MS research and fundraising activities. This is a website that has the backing of the National MS Society.
Multiple Sclerosis (MS)- This is a more advanced site that talks about what MS really is and about where the latest research on MS currently stands—all written out in layman’s terms. This is a good site for the MS patient who wants to be informed about the latest research.
Where to Find MS Support Online– Someone went to the trouble of finding the top support groups online for MS patients and has it nicely laid out for the MS patient. Look here first for an MS support group; you’ll find a listing of them as well as the pros and cons of each group.
Multiple Sclerosis Health Center-This is a good site for anyone who doesn’t know anything about multiple sclerosis and wants to know the basics about multiple sclerosis in simple-to-understand terms. This site is chock full of the usual and unusual information about MS.
Drugs used to Treat MS– This is a site that knows the medications used to treat a variety of diseases, including multiple sclerosis. For a list of specific drugs that might be used to treat the different manifestations of MS and their side effects, this is the site you’ll want to turn to.
Multiple Sclerosis– This site isn’t for everyone but is the best scientific information on multiple sclerosis. It’s intended for health professionals but it is a good site for the well-informed layperson to get the latest in research, statistics, and treatment of multiple sclerosis.
16 Early Symptoms of Multiple Sclerosis– For people who are worried they might have multiple sclerosis, the site provides the reader with the top sixteen early signs that a person might have the disease. It’s fairly detailed and provides other information on the disorder.
Multiple Sclerosis Foundation-This is a national site that gives practical information on how MS patients can get the care they need for things like emergency assistance, assistive devices, and homecare assistance.
Multiple Sclerosis (MS)– This site has information for sufferers in the US and elsewhere in the world. It offers brain training brains for MS sufferers and a listing of the top resources for patients dealing with MS.
The Difference a Balance Dog Makes for Multiple Sclerosis- This is a site most people with multiple sclerosis may not have thought of. It explains how people with MS can get a therapy dog to help them with everyday tasks. There are a number of sites like this but this site has a nice list of organizations you can connect with to start the process of getting a therapy dog.