Source: http://www.mult-sclerosis.org/facts.htmlIn this and later sections, I’d like to explore some of the ways that multiple sclerosis has been observed to affect people. Much of this information is derived from statistical data and, as such, is subject to the vagaries and uncertainties inherent to statistics. In a later section, I shall explore the relationship between MS and statistics.So who does get MS, then?
This would be a much easier question if it were known what causes MS, but since that knowledge remains elusive, we can only look at the distribution of the disease around the globe and at the people who actually have it.
MS is predominately a disease of temperate latitudes and of the western hemisphere. Principally, it is a disease prevalent in Europe, North America, Australia and New Zealand. Although MS is found in Japan, China and some other temperate, eastern countries, it is very much rarer than it is in the West. Regions north of 40 degrees latitude have a markedly higher incidence than those south of this divide. Within Europe, Scandinavia, The British Isles, the Low Countries and Germany have very high rates. Canada, northern USA and New Zealand have an equivalently high prevalence. Within these areas, certain localities such as the border areas of Scotland (203 per 100,000), Crowsnest Pass in Alberta, Canada (217 per 100,000), the northern-most province of Sweden (253 per 100,000) and others have been found to have extremely high incidences of the disease.
So why is MS more common in some areas than others?
Why MS is distributed around the world the way it is is not well understood. There are two main features of the prevalence data for MS that need to be explained. The unequal temperate/tropical distribution of the disease and the much higher rates in Western Hemisphere.
The temperate-tropical divide
Understanding why MS is so rare in tropical climes and so common in temperate ones is a crucial piece of the jigsaw of understanding why people get the disease. Population genetics, which I shall discuss later, provides some of the answers but not the whole picture. There is clearly one or more environmental factors involved in the development of multiple sclerosis and one or more or these has a geographic element. There are several theories as to what this may be.
One theory explains the uneven distribution of MS by focusing on the differences in the pathogens (viruses, bacteria etc.) that affect people in the tropics versus those that affect people in temperate lands. A currently popular theory for autoimmune diseases is called molecular or epitopic mimicy. This suggests that people with MS have previously been infected with a very common pathogen. The immune response that they have developed against that is also reactive against some part of the myelin–oligodendrocyte complex and, as a consequence, they mount an immune attack against themselves in the form of MS. Many pathogens have been examined, including Epstein-Barr virus (EBV), Human Herpes Virus 6 (HHV-6) and various other viruses, although, as with all pathogen work related to MS, it has produced many dead ends.
Sunlight and seasons
Some researchers suggest that multiple sclerosis is common in temperate regions due to the seasonal fluctuations in daylight affecting body chemistry. Research has shown that both disease onset and relapses are more common in the springtime and least common in the winter [Jin et al, 2000]. Levels of vitamin D3, melatonin and other biochemicals have all been shown to vary with the seasons and some of these have been shown to be immunologically or neurologically active [Embry et al, 2000, Timonen TT, 1999; Hayes, 2000, Nelson et al, 2001, Prendergast et al 2001].
If these biochemicals are related to the development of MS, do they also affect its course after onset? If they do, should therapies involving them concentrate on increasing their absolute levels in the body throughout the year or should we attempt to load our levels only at the times of the year when they are at their lowest? Studies in other diseases suggest that this may be a fruitful therapeutic line [Yamashita H, 2001; Guillemant J, 2001; Duhamel JF, 2000; Pawlikowski M et al, 2002 and many others].
Other theroies have addressed dietary habits.
One study has shown that the incidence of MS in coastal regions of Norway is lower than for the rest of the Norwegian population [Larsen et al, 1985]. Some have argued that this is due to the higher levels of fish consumption in coastal regions. The same study also showed a higher incidence of MS in urban areas and a degree of clustering in rural areas leading other commentators to suggest the involvement of an infective agent. Why might a diet rich in fish products be protective against MS? Fish is high in vitamin D3 and omega-3 fish oils, and it is possible that either or both of these might play a part. In any event, there is a lot of unrelated research that implies that a diet rich in fish is protective against a whole variety of diseases. Of course, this provided that you can get hold of fish that has not been polluted by PCBs, dioxins, lindane and other by-products of modern agri-business.
Other studies have found that the incidence of MS is higher in areas of high consumption of dairy produce [Malosse et al, 1993, Malosse et al, 1994, Sepcic et al, 1993, Butcher, 1986 , Butcher, 1992]. Other work has linked dairy proteins to multiple sclerosis at the cellular level [Dosch et al, 2001, Dosch et al, 2001, Stefferl et al, 2001]. Although this work is tantalising, larger studies are needed both to confirm these conclusions and to better explain what is going on. These studies have been cited to support a therapeutic dietary regime called the Paleolithic diet.
Still other commentators suggest that the differences in concentrations of minerals in temperate soils versus tropical ones affect the human intake of these chemicals through the plants we eat and the water that we drink. It is suggested that these variations make people more susceptible to the disease. Copper, iron, vanadium, lead, nickel, selenium, zinc, chromium, molybdenum, cobalt, boron, manganese and chloride, sulfate, nitrate and nitrite salts have all been looked at in this respect but satisfactory explanatory mechanisms are missing.
Different geomagnetic fields across the globe, variations in industrialisation and many other possibilities have all been proffered as potential explanations. Some of these are more worthy of further study than others.
Several studies show that people who migrate from one area of the globe to another at some stage before puberty, take on the incidence of the area to which they migrate. On the other hand, people who move after this point carry with them the incidence of the area from which they migrated. Countries like Israel and South Africa have a much higher incidence than would be expected from their latitude, presumably because they have such high immigration levels of first generation Europeans [Acheson, 1977; Alter M et al, 1966, 1971, 1978; Dean & Kurtzke, 1971; Kurtzke et al 1976 & 1985; Detels R et al 1978; Dean G et al 1997]. Conversely, first generation African, Afro-Caribbean and Indian immigrants to Britain have a much lower incidence of multiple sclerosis than their second generation counterparts [Elian M, 1990].
Contradicting this work is a more recent study of British and Irish born immigrants to Australia. This suggests that the age/geographical risk for developing multiple sclerosis spans a larger timescale than just the first 15 years of life [Hammond SR et al, 2000].
At whatever age the risk factors for multiple sclerosis fall off, if indeed they do, it is clear from other studies that the disease is active sometime before people with MS actually develop clinical symptoms.
This seems to me to be a huge clue towards the understanding of multiple sclerosis. We need to be looking at the earlier lives of PwMS and at the children of families with a high incidence of the disease and who are at a relatively high risk of the disease. Whatever is going on with this disease is starting a while, in my opinion years, before it actually manifests itself.
I am unaware of any studies which examine whether people with multiple sclerosis living in tropical regions have a less severe disease course than those living in temperate regions. If such a study has not been carried out, then it is my opinion that one should be done.
The west-east divide
The explanations for the west-east MS divide are more convincing than those of the tropical-temperate divide. There could, of course, be something different in the soils or diets of oriental peoples than those of occidentals, but by and large, the temperate Western hemisphere has many more similarities to the temperate East than either do to the tropics. The best explanation for why MS is relatively rare in the Orient and relatively common in the Occident is the genetic make up of their peoples.
So what does it matter what racial group a PwMS comes from? In terms of having the disease, treatment, support etc. the answer is nothing – it does not matter. I would like to make it clear that MS is every bit as serious a disease for a person of one genetic make-up as it is for any another. There are people of almost all major racial groups who have MS and I do not wish to downplay what anyone with this disease suffers in any way. In fact, in many ways, PwMS from groups in which it is rare, may find that getting a diagnosis is harder and that the support networks are not as fully developed within their own communities. However are all people with MS and, in the main, we have a awful lot in common with each other. In my opinion we would be much better off politically by emphasising our unity across racial, sexual, religious and national boundaries. I write this only to get a better understanding of the disease.
It is clear that there is a genetic component to the disease but the actual genes themselves remain unidentified. It is likely that there are a number of genes involved working in tandem and it is also possible that more than one combination of genes could result in a predisposition to develop the disease. As already mentioned, identical twin studies show that, when one twin has the disease, the other has only a 30% chance of developing the disease. MRI scans confirm that the identical twins without MS have no lesions. This means that for every person with the disease there are two with the genetic predisposition for the disease who have never contracted it. This makes locating the genes involved extremely difficult because it is virtually impossible to ensure that the control group (those confirmed not to have MS) do not have a genetic predisposition to contract the disease. Many candidate genes have been studied, but as yet, none have been positively identified, although, as is usual with this enigmatic disease, lots of vague correlations have been shown.
Despite the failure to identify which genes are involved, it is still a very reasonable hypothesis to say that a genetic configuration that conveys a predisposition to get MS is more common within some population groups than it is within others. Studies done in Scotland and Canada have shown that MS has a particularly high prevalence within peoples of European descent – British and Scandinavian especially. Within peoples of British descent, it is particularly common in those of Celtic descent. It is unknown within Innuit peoples. It is rare in Japanese and Chinese peoples, and many of those who do get it, get a more aggressive, Asian form, although the European form is known. The descendants of Africans migrating to the US and Britain from Africa are less likely to get MS than the descendants of those migrating from the Caribbean, many of whom have some European ancestry.
We can use the relative rarity of MS within certain population groups to attempt to devise better control groups and perhaps get closer to identifying what genes are involved. Isolating the genetic component of MS is likely to be a major step to discovering the cause, better treatments and even ways of preventing the disease.
AN INTERVIEW WITH SARAH CURRENTLY UNDERGOING HSCT TREATMENT
by Beth Prystowsky · November 10th, 2014
When I read about Sarah, an Australian traveling all the way to Chicago for an experimental treatment at Northwestern Memorial Hospital to cure her recently diagnosed multiple sclerosis, I knew that I wanted to interview her. Luckily for me, Sarah is as sweet and generous as can be.
When were you diagnosed with MS?
“I was diagnosed while in the hospital having had my baby boy, Oliver, on 30th January this year. My official diagnosis date is 5th February.”
What were your first symptoms?
“I first got sick August 2012 – I had optic neuritis, leg weakness, extreme fatigue, dizziness and terrible migraines. I had an MRI, but my former neurologist felt it did not indicate MS. At the time I did not even consider MS.”
When did you learn about Hematopoietic stem cell transplantation (HSCT)? (For those that don’t know; HSCT involves the intravenous infusion of autologous or allogeneic stem cells to reestablish hematopoietic function in patients whose bone marrow or immune system is damaged or defective.)
“I learnt about HSCT from seeing the Kristy Cruise story on 60 minutes Australia. At the time, I was still going through denial about my MS. Seeing Kristy, and realising that it was like me on a bad day, snapped me out of denial and into research mode.
Through the DIAD website and Moving Mountains, as well as support from online groups, I started seriously considering non myleoblative HSCT. I enquirered about the only trial available in Australia at St Vincent’s Hospital. I was not a candidate, due to having low disability, and the treatment was myleoblative, which I had decided wasn’t for me.
I encourage anyone who is interested in HSCT to download Kristy Cruise’s book as your starting point. It is easy to understand and gives you all the steps you need for further research.”
How did you know HSCT was right for you?
“I knew it was right for me when I read Dr. Burt’s criteria for his trial and realised that I was a good candidate. Also, when I read his journal from Lancet and the results he was having. I also watched his talk to MSRA, and it made sense to me. The risks I was accepting on drugs seemed a lot worse than HSCT.”
Why travel to Chicago all the way from Australia?
“As I mentioned before, St Vincent’s is the only trial is Australia of HSCT. It is currently myleoblative, and they are only accepting people who have higher disability than me or have failed more drugs.
HSCT should be available to Australians, and I really wish I didn’t have to leave my family, friends, and, in particular, my baby boy, Oliver. However, I am confident that I will receive the best care in the world from Dr Burt and his team.”
What will the treatment involve while you are here?
You can see a complete schedule of October, November and December from Sarah’s website, Hello Sunshine. The grueling months include chemotherapy, injections, antibiotics, stem cell harvest, rest, transplant and more chemo.
I love that you will be home on Christmas Day! That is the best gift ever.
Thank you Sarah for taking the time to speak to me. I am inspired by your determination and fight. Please send Sarah all your well wishes, good vibes and words of encouragement below. I will make sure she sees each and ever.
The Neurological Exam Explained
By Stephanie Butler, RN, MSCN—April 3, 2015
We have all had a thorough once-over by a neurologist, and chances are you see one at least once a year for a check up and exam. Have you ever obediently walked around on your tippy toes, or moved your finger from your nose to your doctors finger over and over wondering what it is they are looking for, or secretly hoping that this isn’t just a trick to make you look ridiculous? All these tests and hoops that your doctors makes you go through give them a good look at how the nervous system is working, but people often ask me what exactly we learn from doing these test. I wanted to take the time today to elaborate a little bit more on each aspect of the exam so you can understand its purpose a little bit better.
Testing the Cranial Nerves
Cranial nerves originate in the brain and control various movements and sensations of the face and neck. There are a total of 12 cranial nerves, and MS can affect them in a variety of ways. Neurologists will sometimes test them one by one, or focus on the nerves that are most pertinent to a specific compliant. Below is a list of each nerve, what it controls, and how we test it:
1. Olfactory Nerve- this controls our sense of smell, we typically do not test this nerve because people can report a change in smell accurately.
2. Optic Nerve- this controls vision, color perception, and visual fields. The optic nerve is commonly damaged by MS, and there are a lot of different ways to test it. Eye charts help detect changes in vision such as blurred or double vision. In people who have MS sometimes colors are less vivid in one eye, and we can test this by holding up a red square and seeing if it looks like the same shade of red in both eyes. To test peripheral vision we hold our hands way out to the sides of the person’s face and ask them to tell us how many fingers we are holding up, or if they can see which fingers are moving. Finally we turn off the lights in the room and look at the back of the eye with a bright light.
3. Oculomotor Nerve- this nerve constricts the pupils, opens the eyelids, and controls the movement of the eye (extraocular movements). We test this by shining a light in the eyes to see if the pupils constrict properly, and by having the person follow our finger as we move it up, down, and side to side.
4. Trochlear Nerve- this nerve also moves the eye, and is specifically responsible for moving the eye down and inwards. This is also tested by having the person follow our finger with their eyes.
5. Trigeminal Nerve- this nerve moves the jaw, and processes sensory information from the face. Facial pain, called trigeminal neuralgia, is a common MS symptom. To test this nerve we have the person clench the jaw and look to see if it is symmetrical. We can also test sensation by touching each side of the face to see if sensation is the same on each side.
6. Abducens Nerve- this is responsible for moving the eyes to the side (away from the nose). Again, we test this by having people follow our fingers with their eyes.
7. Facial Nerve- this nerve controls movement of the face and our sense of taste. To test it we have people make facial expressions like smiling, squeezing their eyes shut, puffing their cheeks, and raising their eyebrows to see if both sides of the face are symmetrical.
8. Acoustic/Vestibulocochlear Nerve- this nerve is responsible for hearing and for balance. To test this nerve we can either test the hearing by seeing if the person can hear a soft sound such as whispering in each ear, or by using a tuning fork. A tuning fork is a metal fork-like instrument. When it is struck it produces audible vibrations, and we can see if one ear hears the vibrations better then the other ear. These are called the Weber and Rinne tests.
9. Glossopharyngeal Nerve- this nerve also plays a role in our sense of taste, the movement of the soft palate, and it also controls the gag reflex. It is tested by watching the palate rise with the person’s mouth open. Luckily we don’t force you to gag to test this one!
10. Vagus Nerve- movement of the palate and throat. To assess this nerve we have the person say “ahhh” and watch the movement of the uvula to ensure that it is in the middle, and not deviated to the side.
11. Spinal Accessory Nerve- this nerve moves the neck muscles. To test it’s function we have the person move their head from side to side, and shrug their shoulders against resistance (meaning we place our hands on the face and shoulders, and the person has to overcome the resistance of our hand to complete the motion).
12. Hypoglossal Nerve- this nerve controls the movement of the tongue. To test it we have the person stick out their tongue and look to see if it is in the middle. We also look to see if there are any signs of muscle weakness in the tongue. Most people love the opportunity to stick their tongue out at their doctor!
Testing the Brain and the Spinal Cord
There are several ways that we test the brain and spinal cord. These tests provide us with a lot of information about how the nervous system is functioning overall, and whether there are any disruptions in communication.
Walking: the way a person walks (or their gait) tells us a lot about how well the nervous system is working. We look for muscle weakness, foot drop, imbalance, and speed. We will also have a person walk on their toes, heels, and in a straight line (heel to toe) to check their balance and the strength of different muscle groups.
Reflexes: these are involuntary movements controlled by the spinal cord. Absent, unequal, or weak reflexes indicate a lesion on the spinal cord. Exaggerated reflexes or clonus (rhythmic muscle movements/oscillations) can also be a result of spinal cord lesions.
Balance: one of the most common ways of assessing balance is to have the person stand up straight and close their eyes. If they lose their balance with their eyes closed this is usually a sign of a spinal cord lesion.
Sensation: sensory nerves travel from the spinal cord to the brain, and can be tested by seeing if a person can tell the difference between a sharp and dull, cold and hot, and if they can feel vibration.
Coordination: to test coordination we check to see how well a person can do fine movements, such as tapping their fingers together, rapidly moving their hand, and by moving their finger back and forth from their nose to the doctor’s finger. Another way to assess coordination is to have the person run the heel of their right foot up and down their left shin, and vice versa. These coordination tests tell us how well a part of the brain called the cerebellum is functioning.
Strength: we will have the person move their arms and legs against resistance to see how strong they are, and if both sides of the body are equally strong. To do this we have the person push and pull our hands with their arms and legs, and squeeze our fingers.
Range of Motion: If the person has spasticity of the muscles it will limit how much movement they have in their joints. Moving the joints of the legs and arms helps us to determine how severe muscle spasticity is.
I hope this helps you understand what it is your doctor is looking for every time you go in for your check ups! Have you ever had any other exam done that left you wondering “what on earth are they looking for”? Let me know in the comments below!
Stephanie is a nurse, fitness enthusiast, science nerd, and eternal optimist. After being diagnosed with RRMS she realized that she could use her experiences as a patient to make a difference in the lives of others. Six months after she was diagnosed she became a Multiple Sclerosis Certified Nurse and began working in an MS center where she is a patient.
This website is certified by Health On the Net Foundation. Click to verify. This site complies with the HONcode standard for trustworthy health information: verify here.