Articles on Medical Diseases and Conditions

Month: July 2009

  • Team approach to management

    People with Multiple Sclerosis – and their relatives – often have questions and concerns about who is doing what when they go to see the various health practitioners.
    It is relatively clear that your GP is medically responsible for your routine day-to-day health care. In the first instance you would normally go to your GP for advice about any symptoms, or other issues that concern you, even if they are not symptoms of Multiple Sclerosis. Most GPs will refer you on clinical grounds to support services for people with MS, often in the practice itself, such as nursing, counselling and, possibly, physiotherapy. Some larger general practices are also setting up multidisciplinary support clinics for patients with long-term conditions that, although not specifically targeted to MS, could be of value to people with the disease.
    Once you have been referred to, and then been diagnosed by, a consultant (usually a neurologist), you would automatically become his or her patient as well in several ways:

    • You will have hospital records with notes and records of your condition and, initially, you will be down as being under the care of the neurologist concerned.
    • Most neurologists will want to assess you periodically – traditionally every 6 months – to evaluate how your MS is developing.
    • Many neurologists are involved directly or indirectly in clinical
    trials for new therapies for the disease or its symptoms, and they may invite you to participate in such trials, which will involve further regular monitoring or assessment (see Chapter 18).
    • Particularly with the advent of beta-interferons and glatiramer acetate, possibly with certain other drugs, neurologists now have a special clinical role in dispensing them and monitoring their use.
    • Both for clinical and economic reasons, hospitals are increasingly setting up MS clinics, and/or multidisciplinary support services for people with MS.

    So, in principle, someone with MS could have an embarrassment of services, in both general practice and in a hospital setting! However, this is not usually the case. One of the major problems at present is that services are patchily distributed and relatively ill coordinated, and people with MS are having to take what is available to them. In the light of this unsatisfactory situation, the MS Society and leading neurologists have recently put together a minimum standard of service provision for people with MS, which they hope will lead to more consistent provision (see Appendix 2).
    The situation is confused because, on the one hand, specialist advice and services in relation to your Multiple Sclerosis, i.e. those usually obtained through your neurologist and the hospital, take precedence over your GP’s advice on the disease; on the other hand, your GP is responsible – as we noted earlier – for your day-to-day health care. The problem then becomes what is an MS-related problem, and what is not. Technically the GP and the specialist should be in touch with one another, informing each other of developments in relation to your health. This does not always happen efficiently.
    The best advice to you is to use whichever local services are most convenient and helpful for whatever problems you happen to have, and to press your GP and/or the consultant as necessary for other services that you feel have not been offered. To be frank, what most people with MS have found is that their GP is helpful, supportive and accessible, but is often not particularly knowledgeable about MS, and that the consultant is knowledgeable but not as supportive or as accessible as the GP. The advent of MS clinics with other professional staff, such as nurses, as primary advisers may provide more support in due course.
    The idea of a ‘team approach’ to Multiple Sclerosis has gained considerable ground in recent years and most neurologists and hospitals support it. In the previous (‘non-team’) approach, a doctor, usually the neurologist, might have referred you independently occasionally for separate professional services, e.g. physiotherapy, occupational therapy, speech therapy or
    nursing. People with MS often found this a problem in that each professional dealt with them independently; there seemed to be little communication between the different services, and no single person to whom they could turn for an overall view, apart from the neurologist who was not always accessible. You may be lucky in that you have access to an MS Specialist Nurse – their numbers are rising regularly.
    The team approach, although it may have developed dif ferently in different hospitals, is designed to provide a more coordinated approach to the management of MS. Following your initial assessment, team meetings will be held between the professionals, sometimes involving you and/or your family. These meetings lead to the development of a management strategy of MS. The idea is that this should centre on your problems. Sometimes one professional person is appointed to liaise with you, as the first point of contact. Teams may involve the neurologist, a nurse, a physiotherapist, a speech therapist, an occupational therapist, a counsellor, an Multiple Sclerosis Specialist Nurse and possibly others.
    In general, the move to a team approach has been helpful for people with MS, but problems of coordination between the professions still continue to exist, especially in the community. Sometimes you may be somewhat confused by the large number of professional staff you come into contact with. If you can establish one main person for contact – no matter what their professional discipline – it is very helpful. Note that many hospitals are still underfunded, and the team approach in itself will not lead to a change in that aspect, but they might be used more efficiently. In addition, there are often coordination problems between social services departments and other non-health-based support sources.

  • Getting more information on drug therapy

    Side effects of drugs

    Because drugs have powerful effects on a condition, they can also have powerful side (that is, unwanted) effects on other things. It is a good idea to be informed about the possible side effects of the drugs that you are taking; you will be able to assess the balance yourself between the effects and the side effects, and you will be alerted sufficiently to inform your GP, neurologist or MS Specialist Nurse about them, if they are worrying you.
    Your medical practitioner (GP, neurologist or MS Specialist Nurse) should discuss possible side effects with you when your drug(s) are prescribed, including any side effects from combining two or more drugs. If your GP does not, you should ask explicitly about this issue. If you are still unclear or concerned, the pharmacist where you get your prescriptions has expert knowledge about drugs and their effects, and should be willing to answer questions about them. Furthermore, they can inform you about over-the-counter drug therapies that you may purchase, and their potential side effects and interactions with other drugs.
    Several organizations (including the Consumers’ Association and British Medical Association – see Appendix 1) publish excellent family health guides that contain detailed and up-to-date information about drugs and other treatments. It is vital that you use a British edition of any guide, as brand names are frequently changed from country to country. Some titles are included in Appendix 2 at the back of this book.

    Combination therapy

    Beta-interferon or glatiramer acetate and steroids can be taken at the same time but only after careful assessment by your neurologist. Even if you are taking beta-interferon 1b or beta-interferon 1a or glatiramer acetate, you may have a relapse, but probably to a lesser degree than you would have done without the treatment. In this situation, you may well be offered steroids – possibly a combination of methylprednisolone and prednisolone. The objective is to provide an additional means of reducing the inflammation, despite the use of beta-interferons, and reduce your symptoms.

  • Steroids

    Types

    The use of steroid-based drugs for ‘attacks’ or ‘relapses’ of MS has been the standard treatment for MS for some years, and many people may still find that this is the first line of treatment offered to them.
    There are several types of steroid drugs:

    • Adrenocorticosteroids (such as ACTH – AdrenoCorticoTrophic Hormone), used to be one of the most commonly used steroids in MS.
    • Glucocorticosteroids (such as prednisolone, given by mouth; or methylprednisolone, usually given through a drip, intravenously) are used more commonly now.

    Effects of steroids

    There is substantial evidence that both types reduce the inflammation at active disease sites in the CNS and, in particular, reverse disruptions of the blood–brain barrier (see Chapter 1) that may occur when the disease is active. These effects, in turn, should reduce the duration and degree of symptoms. However, most studies suggest that the effects of steroids are relatively short term, perhaps lasting a few weeks, although there have been one or two studies which suggest tantalizingly that there may be far longer positive effects of the combined short-term use of methyl- prednisolone and prednisolone.
    There is also some interesting evidence from a trial on the use of steroids (methylprednisolone and prednisolone) following an initial episode of ‘optic neuritis’ (inflammation of the optic nerve, which makes things seem blurred). This is a significant symptom, which often acts as a forerunner of MS. There is more information on this trial in Chapter 18.
    Overall there is a sense, at the moment, that further definitive trials to assess the most effective steroid, as well as its dose and mode of administration in MS, are now almost a waste of time and resources, as newer drugs – such as the beta-interferons, glatiramer acetate and others – show so much more promise for the control of MS, in relation not only to relapses, but also to the course of the disease.

    How are steroids given?

    ACTH has now been replaced by the use of methylprednisolone and prednisolone, but there is widespread debate amongst neurologists about the most appropriate steroid and mode of administration in MS. People with MS are likely to come across different ways in which steroids are currently given – intravenously administered methylprednisolone (called IVMP for short) normally requires a hospital stay for one to several days, depending on precisely how the drug is administered. There may need to be other hospital stays for assessment purposes.

    Side effects

    As with all powerful drugs, side effects – that is unwanted effects – can occur. Side effects appear to depend very much on both the type of steroid and how it is administered. When methylprednisolone is given in the usual short-term high intravenous doses, facial flushes, a metallic taste in the mouth during the treatment and sometimes acne occur. Most other reactions are not serious, but occasionally sleep disturbances, stomach upsets and mild mood changes occur. Very occasionally more serious psychological changes are seen.
    With longer term administration of methylprednisolone, often followed by oral prednisolone, a range of unwanted effects may occur. These are very highly dependent on exactly how the steroids are given, for how long and the level of dose. Often signs of some water retention may occur: a ‘moon-shaped face’ and modest swelling (oedema) in several parts of the body. Normally, the cells of the body are bathed inside and outside in water, and this water is regulated by hormones, sodium (salt) levels and the kidneys. Steroids tend to cause the kidneys to retain
    sodium: an increase in sodium levels leads to an increase in water retention in the body, resulting usually in a modest but noticeable swelling – the oedema.
    Steroids can also produce a temporary ‘masculinization’ in women through their hormonal effects, which can include increased body hair, menstrual irregularities, acne and, paradoxically, a loss of scalp hair. Very prolonged administration can produce a range of other effects, some of them very serious.
    There is always a balance to be struck between probable improvement in some MS symptoms following a relapse, and the avoidance of as many of these side effects as possible. It may not be an easy decision for either the clinician or the person with MS. Usually the pressing nature of the symptoms produced by a relapse decides the immediate outcome. Nevertheless, the use of steroids must be very carefully monitored. The objective is to gain the maximum possible beneficial effects following dosage for the shortest possible time. However, longer term administration of steroids is thought on balance to be important in special circumstances, to try to contain the Multiple Sclerosis.

  • The future of DMTs (disease-modifying therapies) in MS

    It is undoubtedly true that we are in a very exciting phase of development of DMTs. Although we cannot yet talk about a cure, we can now consider seriously the possibility of slowing down the course of the disease and not just ameliorating the symptoms of relapses. However, the results of research so far seem to suggest that the earlier the current DMTs (the interferons and glatiramer acetate) are given in the course of the disease, the more effect they are likely to have. One current controversy is how early these drugs should be given. Some believe that
    they should be given at the very earliest sign of MS, others that these drugs should wait upon a full and clear diagnosis on more comprehensive criteria. Their cost is a major issue, particularly in relation to medium- and long-term benefits that have not yet been fully proven, and is a significant factor that has had to be considered by every healthcare system.
    For people whose MS is more advanced, and particularly is progressive in nature, the effects of these DMTs seem to be very substantially less. As such people form the majority of those with MS at any one time, then many people will still feel disappointed that few possibilities exist for them in controlling their disease. However, there is very active research being undertaken at the moment to evaluate whether different combinations of any of the current DMTs could affect the course of Multiple Sclerosis for such people.

  • Glatiramer acetate (Copaxone) and the management of Multiple Sclerosis

    Glatiramer acetate is a synthetic compound made of four amino acids (the building blocks of proteins) that are found in myelin. It has been shown in clinical trials that glatiramer acetate reduces the number and severity of relapses and appears to slow the onset of disability in some people with MS. While the mode of action of glatiramer acetate is not completely understood, it is different from that of the interferons.
    Over the past 15 years, there have been many clinical trials to investigate the efficacy and safety of glatiramer acetate in people with MS. The best results were seen in people with MS who had the lowest levels of neurological disability. Studies have shown that at the end of 2 years there were about 25% fewer relapses in people taking glatiramer acetate compared with those not taking the drug, and more people on the drug tended to improve.

    Administering glatiramer acetate

    The drug is injected subcutaneously (under the skin) every day. People with MS or family members who first receive proper training in aseptic injection techniques can perform the injections without medical supervision.

    Side effects of the drug

    The drug is generally well tolerated and does not cause any of the ‘flu-like symptoms or increase in depression sometimes associated with the interferon drugs. The most common side effects are injection site reactions, pain upon injection, and a postinjection reaction involving shortness of breath, flushing, palpitations, anxiety and chest pain. This reaction, which occurs in about one in seven people at one time or another resolves itself within 15–20 minutes and does not appear to have any long-term consequences. At the time it can, however, be very frightening.

    Prescribing glatiramer acetate (Copaxone)

    As the effect of glatiramer acetate and its process of development have been broadly similar to that of the interferons, it has also been subject to the same process of assessment by NICE as the interferons (see above). The same judgement was also made in relation to glatiramer acetate, as were also the same risk-sharing arrangements with the company manufacturing the drug. Thus the drug is also available for prescription by neurologists in MS clinics using slightly different criteria. To be prescribed the drug, people must fulfil the following criteria:

    • be able to walk at least 100 metres without assistance
    • have had at least two clinically significant relapses in the last 2 years
    • be 18 years old or older.

  • The beta-interferons and the management of Multiple Sclerosis

    What are beta-interferons?

    Interferons are naturally occurring substances in the body, produced in response to ‘invasion’ by a foreign substance, such as a virus. Two different kinds of beta-interferons have shown a significant effect in MS by reducing the number and severity of its ‘attacks’: beta-interferon 1b (trade name Betaferon) and, more recently, beta-interferon 1a (trade names Avonex and Rebif). They seem to stabilize the immune system but there is conflicting evidence as to whether it also slows disease progression.

    Who is helped by beta-interferons?

    At present, this is not entirely clear. The drugs have been extensively tested on people with specific kinds of relapsing-remitting MS, mainly those in the earlier stages of MS and who can walk (in the jargon, those who were ‘ambulant’). This was because it was easier to demonstrate the effectiveness of the drugs on people who were more mildly affected and who were having relatively regular ‘relapses’. Findings of several trials showed that these people had a (statistically) significantly lower rate of relapses compared to a group of others who did not take the drugs and, furthermore, when they did have a relapse, it was likely to be less severe.
    In the case of secondary progression, as it is preceded by a relapsing- remitting phase, such people may benefit through some of the therapies, which could have some effect on modifying the earlier phase of the disease.
    In primary progressive MS, there is less compelling evidence at present that beta-interferons substantially affect the longer term course of the disease.
    These current findings mean ‘statistically’ that there are still some people who took the drugs and who did not benefit a great deal from them. Beta-interferons may have less effect on people whose disease pro- gression is substantial.
    Nevertheless, at present, drug therapy for primary progressive MS is still mainly to manage any symptoms as they appear. However, given the evidence that beta-interferons can produce some benefits for both relapsing-remitting and secondary progressive MS, research is now increasingly interested in their potential effects in primary progressive MS.

    Effects of beta-interferons

    Expectations of the drugs have been so high that many people have been disappointed that they do not feel much better when they take them, but the drugs do not cure MS nor do they appear to repair existing damage: they just seem to slow down further damage and symptoms in some people, so both the original symptoms and any internal damage to your CNS will still be there. The drugs are working ‘silently’, thus, we anticipate, preventing some future symptoms and damage. You might wonder why you are taking drugs that you may think have no effect on your present symptoms!
    The effect of beta-interferons, as far as we know, is to encourage the immune system to become more ‘placid’. This seems to reduce the number and extent of the periodic ‘inflammations’ that lead to more MS symptoms; however, they do not necessarily eliminate those ‘inflammations’. So relapses may still occur, even if they are fewer in number and less in degree than they would otherwise have been. The problem is that neither the doctor treating you, nor you yourself, know what would
    ‘otherwise have been’. All you may know is that you now have (perhaps a minor) relapse, and are feeling worse. Your relapses might well have been worse without beta-interferon but, of course, you might feel that it was not effective at all.
    Beta-interferons appear to work best when the disease is active, when (although not always) there are recognizable symptoms. The predominant medical opinion at present is that beta-interferons should be given only when there is evidence of recent disease activity, but the increasing research evidence that beta-interferons may slow down the development of symptoms over the medium term (3–5 years) is prompting a serious review of this position. Indeed, there are now scientifically influential voices arguing for the administration of beta- interferons at the earliest possible stage of the disease.

    Longer term effects of beta-interferon

    More studies will be needed to assess ef fects of beta-interferon over
    15–20 years. We have data, at the time of writing this book, only on small groups of people who have had beta-interferons for 8–10 years, and this is not sufficient to make very long-term judgements. However, there are some promising signs. It does appear from current clinical trials that the onset or progression of disability, as measured by a range of tests, is slowed down by the beta-interferons and this slow-down is statistically significant – for at least 4 or 5 years after taking the drug. In addition, disease activity in the CNS as measured by magnetic resonance scans also seems to be reduced, but remember that most of these very positive results were obtained from people with milder forms of MS at an earlier stage of their disease.
    A problem that has arisen in about a third of people being given beta- interferon 1b (Betaferon) is that they have developed ‘antibodies’ to the drug after about a year or so. It appears that their bodies are resisting the ef fects of beta-interferon, attacking beta-interferon as an ‘invader’. In such cases, the positive ef fects of the drug disappear, and rate of relapses and disease progression returns – as far as we can see – to their previous state.
    Another problem is that, at present, there is no test available to ascertain which people will develop these antibodies. It is mainly by the return of increased disease activity and symptoms that these people would recognize this problem. It is not clear whether exactly the same problems will occur with other types of beta-interferon, but the first signs are that they will.

    How is beta-interferon given?

    Beta-interferons may be currently administered in different ways. Beta- interferon 1b (Betaferon) is administered by injection subcutaneously (just below the skin) every other day. Beta-interferon 1a (Avonex) is administered by injection intramuscularly (directly into the muscles) every week. Beta-interferon 1a (Rebif) is administered subcutaneously three times a week. The different types of administration are based on what has proved in clinical trials to be the best way of ensuring the effectiveness of the drug.
    Subcutaneous injections have been given in the past by a doctor or a nurse, not only to check that it is given correctly, but to monitor whether it is given at all – people are sometimes forgetful about administering any drug. However, this is a time-consuming and expensive method and
    some people now self-administer the drug, rather like insulin for people with diabetes. Intramuscular injections have to be given by a doctor (or nurse). Newer modes of administration are now being developed and trials are taking place to test whether these other methods are better and more effective.
    None of the drugs can be taken by mouth (orally) as yet; they are proteins and likely to be broken down by the digestive processes, making them less effective, or possibly even ineffective.

    How long is beta-interferon taken for?

    Decisions will taken by your neurologist based on your personal situation, and taking into account:

    • a longer term reduction in the number and degree of relapses compared to those you had before starting the beta-interferon;
    • no substantial rise in unwanted side effects;
    • no other clinical reason why you should not continue;
    • no better therapies being available;
    • the substantial financial issues involved, i.e. the cost of the drugs.

    Side effects of beta-interferon

    There have been two main side effects noted, mainly with beta-interferon
    1b (Betaferon):

    • There are symptoms best described as ‘flu-like symptoms, which many, perhaps most, people experience in the first few months of treatment. These are generally mild and can be managed with ordinary analgesics (pain relievers), and they disappear in almost everyone after those first few months.
    • Problems at the injection site, such as blotches or pain, which most people experience initially and about half some years later.

    Such reactions are more of an irritation than anything else. Very rarely more serious reactions have been reported – only in a few cases serious enough to warrant stopping treatment.
    As far as beta-interferon 1a drugs (Avonex and Rebif) are concerned, similar types of side effects were experienced, but at a lower rate.
    We do not yet know about any longer term side effects, an important issue in MS where people usually live with their condition for several decades.

    Controversies over the prescription of beta-interferon

    As you may be aware, there has been great controversy over the availability of the expensive beta-interferons for people with MS on the NHS. An organization called NICE (the National Institute for Clinical Excellence) has been given responsibility by the UK government for the formal cost–benefit assessment of all drugs and medical devices. Only if NICE recommends that a drug or device is indeed sufficiently cost effective can it now be prescribed on the NHS, and even then there may be conditions about the circumstances in which it may be given or who may prescribe it. The issue for NICE, as far as the beta-interferons are concerned, has been what benefits occur, for what costs – remembering that the beta-interferons are very expensive drugs.
    The assessment of beta-interferons was regarded as a priority for NICE because prescribing had already begun by certain neurologists in certain areas – leading to what was considered a ‘postcode lottery’ for people with MS. In fact in a Report issued in February 2002, NICE indicated that it did not believe that there was sufficient evidence at present to prescribe beta-interferons on the NHS. In other words their judgement was that prescription by the NHS was not currently cost effective. However, it indicated that people who had already been prescribed beta- interferons, before its judgment, could continue to receive them. It also indicated that efforts were being made to find ways for the drugs to be supplied on a more cost-effective basis.
    In fact on the same day as the NICE announcement, it was also announced that what was called a ‘risk-sharing agreement’ had been reached with the relevant drug companies and the NHS to provide beta- interferons through neurologists in MS clinics for approximately 9000 people with MS (about 15% of those with the disease) on very specific criteria as follows:

    Relapsing-remitting Multiple Sclerosis
    People with MS must fulfil the following four criteria:

    • be able to walk independently
    • have had at least two clinically significant relapses in the last
    2 years
    • be 18 years old or older
    • have no contraindications.

    Secondary progressive Multiple Sclerosis
    Beta-interferon is only prescribed for people with relapsing secondary
    progressive MS. It is not ef fective in people with a non-relapsing secondary progressive course. People must fulfil the following criteria:

    • be able to walk at least 10 metres with or without assistance
    • have had at least two disabling relapses in the last 2 years
    • have had minimal increase in disability due to slow progression over the last 2 years
    • be 18 years old or older

    In relation to the agreement, a group of people with MS taking the drug will be evaluated over a period of 10 years, and the relationship of any benefits to the costs will be assessed. If the equation between costs and benefits is then considered as positive, the drugs will then be allowed to be prescribed on the NHS.
    Compared to some other countries the proportion of those with MS being prescribed beta-interferons is still relatively low, although it should be said that, in addition to issue of cost, there is still substantial debate amongst neurologists as to the frequency and extent of benefits from the beta-interferons.

  • Approaches to treatment

    There are now two basic approaches to treating MS medically.
    First there are drugs that aim to suppress, minimize or halt the destructive immune response, that is the inflammation and the accompanying symptoms that occur when MS is in an active phase. In this context the overall aim is to move from controlling one or more relapses, to minimizing and ideally halting further disease progression. Steroid drugs have been used for many years to try and control the inflamma- tion attending relapses and lessen symptoms, but they have little effect on the underlying disease. More recently, drugs based on beta-interferon and others based on glatiramer acetate are showing more promise in not only assisting in the control of relapses, but also appearing to modify the disease course in some people, as their effects seem to continue for several years. There are also as many as 50 promising individual therapies undergoing clinical trials at any one time, although few will end up
    being used in clinical practice, and the drugs are often targeted to only very specific types of the disease.
    The second approach is to assess and treat the individual symptoms (e.g. spasticity, continence difficulties, pain or fatigue) that result from the damage to the CNS. In this respect there is no single drug treatment
    – an ‘MS drug’ – for all the symptoms of MS because of the immense variation and different rates of progression in each individual. Fortunately, MS is a condition where many symptoms can, in most cases, be relatively well managed for long periods of time.

  • Treatment rather than cure

    Repairing the damage

    One of the reasons why MS is such a difficult disease to cure is that, once the CNS has been damaged, it would involve major repair of the often severe structural damage. Any further process of damage would have to be prevented as well as the previous structural damage being repaired. However, despite these difficulties, there is considerable interest in experimental work on drugs that may be able to ‘remyelinate’ damaged nerves, and drugs that may slow down or halt the process of further damage.

    Symptom remission

    Most claims for a cure for MS have been made on the basis that the symptoms seem to have disappeared, temporarily at least, but not that the structural damage of MS has been repaired. The problem is that symptoms of MS can be dormant for many years, or dramatic remissions in symptoms have occurred, but the damage to the CNS has not necessarily been repaired. Symptoms can reappear, and there is a significant
    possibility that they will do so, but without evidence that the underlying demyelination has been repaired, the disappearance of symptoms appears to be a temporary, although happy, coincidence; it is probably due to the absorption of fluid caused by the inflammatory response to demyelination. A number of newer drugs, particularly the beta-interferons and glatiramer acetate, may have some effects on modifying the disease process.
    At present therefore, treatment mainly consists of:

    • ameliorating a symptom or its effects;
    • preventing or lessening the degree or length of time of a ‘relapse’;
    • encouraging the early arrival of a ‘remission’;
    • changing various aspects of your lifestyle that will make life with the symptoms of MS easier to manage;
    • seeking to slow down the rate of progression of the disease.

    In many cases, up until recently, the treatment of MS has been on the basis of symptoms as they occur. Now, in addition to attempts to reduce the number of relapses in MS, there are increasingly promising efforts to alter the course of MS itself. There are some drugs that offer the promise of lower rates of disease progression for some people, although for how many people and for how long is a subject of major controversy. Indeed the acronym DMT is now being used quite widely in discussions of MS, but we are still not talking about a cure, just a possibility of slower pro- gression of the MS.

  • Diagnosing MS

    The diagnosis of MS has previously been a long, slow and complicated process, since there was no definitive laboratory test for MS. The newer and sophisticated brain scanning techniques that are now used, such as magnetic resonance imaging (MRI) can locate lesions or patchy scarring (scleroses) in the nervous system, but require very careful interpretation by a skilled doctor. Although many people in the early stages of MS do not exhibit the ‘classic’ symptoms considered to be the ‘textbook’ features of the disease, MRI can be the definitive test as it shows lesions in the white matter which contains myelinated fibres. Finally, many other conditions may produce symptoms almost indistinguishable from MS symptoms. Thus the difficulty in diagnosing MS lies in establishing sufficient evidence to exclude other possibilities. There is more about diagnosing MS in Multiple Sclerosis – the ‘at your fingertips’ guide.

  • The causes of Multiple Sclerosis

    The cause or causes of Multiple Sclerosis are still unknown. Although there are significant geographical variations in the distribution of people with MS throughout the world, a great deal of research has failed to uncover any tangible evidence that there are specific avoidable risk factors associated with the onset of the disease.

    Genetic versus environmental causes

    At present, the most likely cause appears to be a combination of genetic and environmental factors. Studies of identical twins, where one or both has MS, of fer what might be called the ‘purest’ way in which to investigate this theory: it appears that genetic factors contribute between
    30 and 35% and environmental factors about 65–70% of the total contribution to the cause. These two figures suggest that further research needs to be undertaken on both issues. There does not seem to be one simple gene linked to MS, but we do know, for example, that first- degree blood relatives of someone with Multiple Sclerosis, such as children and siblings (brothers and sisters), are at slightly enhanced risk of the disease.
    Amongst many other theories about the causes of MS, there has been a particular interest in the role of ‘heavy metals’. It is certainly true that an excess of some heavy metals in the body, such as lead, mercury and cadmium, may result in serious neurological damage. Lead in particular is a potential cause of neurological damage, although, with the reduction of lead in petrol, it is gradually being reduced in our environment, but at present there is no evidence that excess lead causes MS. Excess mercury can also produce neurological damage, and there has been much discussion about the possible problems with mercury-based dental fillings. However, a large proportion of the adult population will have had at least some mercury fillings in their lifetimes, and yet only a fraction of those people have MS. Dental amalgam does contain mercury which can erode over time and be absorbed into the bloodstream, but this is a very small contribution to the amount of mercury ingested by most people
    (deep-sea fish is a much greater source). The exposure to dental amalgam is well within the safety limits currently recommended for mercury.

    Infections and other diseases

    Research has not shown Multiple Sclerosis to be caused by any particular bacterial or viral infection, but it is possible that the timing of a relapse may coincide with an infection. This could be due to a change in immune activity that allows the infection to gain hold: the bacterial infection can trigger an immune response, or both the relapse and the infection may occur in response to some unknown third factor.

    Candida
    At present there is a widespread interest, particularly amongst many involved in alternative or complementary medicine, in Candida albicans (thrush). Although candida can be associated with many symptoms, as well as having a low-level but debilitating ef fect on health, there is almost no formal evidence that it is associated with relapses of MS in itself. Candida infection may be a result rather than a cause of a weakened immune system, and it is also known to be more common as a side effect of some anti-inflammatory drugs used in Multiple Sclerosis. Of course, any infection with potentially problematic symptoms should be treated with antibiotics.

    Herpes
    Amongst viruses that have prompted scientific interest in relation to MS, the herpes virus HHV-6 is one of a number currently being researched. However, as with other viral candidates for a cause of MS, this line of enquiry is controversial and much debated.

    Lyme disease
    There is no evidence that this disease, which is spread by tics living on a range of animal species in the countryside, can cause MS, although its symptoms may mimic those of MS.

    ’Flu jabs and other injections
    Many people with MS naturally look for a preceding event, such as a ‘flu jab, to explain why their symptoms have worsened, or why they have had an ‘attack’ or ‘relapse’. Research studies have failed to demonstrate any link between injections (vaccinations or inoculations) and any subsequent worsening of the MS.

    Links between MS and other conditions including cancer
    Many people with MS can point to symptoms and illnesses that seem to have preceded its onset. There is no clear definitive link that been established between the prior effects of diseases and the onset of MS. Of course as MS progresses, it may itself give rise, in ef fect, to other conditions, through a weakened immune system or just by ageing, for example.
    There is no known link between cancer of any type and MS, but it is to be expected that some people with MS will develop cancer, but no more frequently than people who do not have MS.

    Autoimmune diseases
    There are strong similarities between some aspects of other autoimmune diseases, where the immune system is triggered into mistakenly attacking normal tissues in the body, and some aspects of MS. At present these conditions are still thought to be completely separate disease entities, although it is possible that there may be some very general biological processes underlying these conditions. These processes are the object of considerable recent research.

    Stress
    Fatigue, and possibly what we call ‘stress’, could have had some effect, not as a cause of MS, but perhaps as an exacerbating factor on some symptoms. However, although most people with MS probably feel that undue stress in their lives may bring on a relapse, scientifically this issue is still being argued over. Even so, many people have their own ideas about things that they feel are linked with their Multiple Sclerosis symptoms, and try to avoid them.

    Accidents and injuries
    Studies have compared accident and injury rates in people with MS who have had relapses and those who have not. Almost all have concluded that there is no significant dif ference in rates, or evidence to support trauma as causing or worsening MS. A more general issue is whether head injuries may have broken what is called the blood–brain barrier so that some parts of the CNS may themselves become contaminated and thus be damaged by the various blood products that are released. However, the relationship of any breach of the blood–brain barrier and the onset of MS is disputed.

    Diet
    There has also been extensive scientific research on MS and diet which may have some bearing in the medium and longer term on health in general.
    There is substantial research indicating that what are called
    ‘unsaturated fatty acids’ – essential building blocks of the brain and nervous system – may be deficient in people with Multiple Sclerosis, which is why supplements containing these fatty acids have become popular. However, there is little evidence that taking supplements with the fatty acids has any major effect on MS. More generally, there is also little evidence that any particular diet has major effects on the course of MS, although some evidence suggests that a low-saturated fat diet may be beneficial as regards relapses.
    Finally, there is little or no evidence that poor diet in itself causes MS – if this were so, the geographic and social distribution of MS would be very different.