Multiple Sclerosis (“MS”) was first commonly identified in the 19th century during the time in which mercury/silver fillings came into common use. In the early part of the twentieth century,MS was known as the “faker disease.” Unpublished anecdotal evidence indicates that a significant number of, but certainly not all, MS victims who have their mercury/silver fillings removed resolve (spontaneous remission) or improve gradually. By 1993, forty-two MS victims had filed adverse reaction reports with the FDA. Four of these were cured and twenty-nine improved. There is toxicological evidence that mercury poisoning victims (from sources other than fillings) and multiple sclerosis victims share similar symptoms. The Encyclopedia of Occupational Health and Safety discusses the symptoms of chronic mercury poisoning, in part, as follows:
Nervous system involvement may occur with or without gastrointestinal symptoms, and may evolve in line with two main clinical pictures: (a) fine intention tremor reminiscent of that encountered in persons suffering from multiple sclerosis.
The most frequently encountered symptoms resemble those presented by persons with multiple sclerosis except there are no nystagmus and the two conditions have a different serology and different clinical courses.
In 1966 Baasch concluded, based on sometimes severe neuroallergic reactions inacrodynia (pink disease) and his own observations of neurologic patients, that multiple sclerosis was an adult form of acrodynia (pink disease) and a neuroallergic reaction, in most cases, caused by mercury from amalgam fillings. Baasch demonstrated in great detail that facts concerning the geographical and age distribution, pathological development, and symptomatology of MS were all consistent with amalgams being the primary cause of the disease. He reported several specific cases and cited ongoing studies that showed cessation of progression and improvement of resolution of MS after removal of amalgam fillings.
In a very detailed study, Craelius in 1978 showed a strong correlation (P<0.001) between MS death rates and dental caries. The data demonstrated the improbability that this correlation was due to chance. Numerous dietary factors were ruled out as contributing causes.
A hypothesis presented in 1983 by T. H. Ingalls, M.D. proposed that slow, retrograde seepage of mercury from root canals or amalgam fillings may lead to multiple sclerosis in middle age. He proposed a correlation of unilateral multiple sclerosis symptomatology with ipsilateral amalgam-filled teeth. He also re-examined the extensive epidemiological data that show a linear correlation between death rates from MS and numbers of decayed, missing, and filled teeth. Ingalls suggested that investigators studying the causes of MS should carefully examine the patients’ dental histories. Furthermore, Dr. Ingalls’ hypothesis included other environmental exposures to mercury. In 1986, he published data supporting his hypothesis that clearly demonstrate endemic clustering of MS in time and space over a 50-year time span that could be directly correlated to exposure to mercury.  Another study (Ahlrot-Westerlund 1987) found that multiple sclerosis patients had eight (8) times the normal level of mercury in their cerebral spinal fluid as compared to neurologically healthy controls.
In a 1990 study, the University of Aarhus, Denmark, Department of Neurobiology, conducted an experiment in which three vervet monkeys received occlusal amalgam fillings, three others maxillary bone implants of amalgam, and three untreated monkeys served as controls, inorder to trace possible accumulations of mercury. One year later, tissue sections from different organs were subjected to silver amplification by autometallography and analyzed at light andelectron microscopial levels.
It was found that amalgam fillings (total 0.7-1.2g) cause deposition of mercury in the following tissues: spinal ganglia, anterior pituitary, adrenal, medulla, liver,kidneys, lungs, and intestinal lymph glands.
In the monkeys with maxillary silver amalgam implants (total .1-.3g), mercury was found in the same organs with the exception of the liver,lungs, and intestinal lymph glands.
Organs from the three control animals were devoid ofprecipitate. These results strongly support what has been suggested previously– that dental fillings in primates cause absorption of mercury released from amalgam fillings through the lungs and the intestinal tract, and that mercury is distributed to most organs and will eventually be found in the central nervous system. (The present data also show that silver released from the corroding filling is not absorbed.)
In a 1998 study, Dr. Svare and associates analyzed for its mercury content, the expired air of a group of 48 persons, 40 with and eight without dental amalgam restorations, before and after chewing . Expired air samples were collected in polyethylene bags, and a known quantity of each was pumped into the mercury detector for measurement. The results showed that subjects with dental amalgams had higher pre-chewing mercury levels in their expired air than those without amalgams. After chewing, these levels were increased an average of 15.6-fold in the former and remained unchanged in the latter group. It was therefore concluded that in situ dental amalgams can indeed increase the level of mercury in expired air.
A paper written in 1994 by Dr. Siblerud of the Rocky Mountain Research Institute, Inc.,investigated the hypothesis that mercury from silver dental fillings (amalgam) may be related to multiple sclerosis (MS).  It compared blood findings between MS subjects who had their amalgams removed to MS subjects with amalgams. MS subjects with amalgams were found to have significantly lower levels of red blood cells, hemoglobin and hematocrit compared to MS subjects with amalgam removal. Thyroxine levels were also significantly lower in the MS amalgam group and they had significantly lower levels of total T Lymphocytes and T-8 (CD8)suppressor cells. The MS amalgam group had significantly higher blood urea nitrogen and lowerserum IgG. Hair mercury was significantly higher in the MS subjects compared to the non-MS control group. A health questionnaire found that MS subjects with amalgams had significantlymore (33.7%) exacerbations during the past twelve months compared to the MS volunteers withamalgam removal.
An article developed by the MELISA Foundation in March of 2005, noted that MS is caused by the erosion of myelin, a substance which helps the brain send messages to the body. Metal particles entering the body can bind to this myelin. For those who are hypersensitive, thismyelin-metal bond comes under attack from the immune system. In such cases, the progression of MS can be halted by removing the source of the metal. The role of myelin is one of the few factson which those who study MS are able to agree. The MELISA Foundation has developed what they believe is a breakthrough in understanding in MS: the link between metal allergy and the erosion of myelin . They believe that they have also been able to prove that the myelin erosion can be halted if the source of the allergy is removed. Hypersensitive reactions are triggered by metal particles entering the body of a person allergic to the metal in question. These particles then bind to the myelin, slightly changing its protein structure. In hypersensitive people, the newstructure (myelin plus metal particle) is falsely identified as a foreign invader and is attacked; an autoimmune response. Arrows point to the “myelin plaques” in the brain, common in patients with MS. Such plaques can be the result of metal allergy. Already, the MELISA Foundation has seen patients with MS make a partial, and, in some cases, a full recovery by removing the source of metal – often their mercury dental fillings.
Mercury has been documented to accumulate in the very areas of the nervous system from which most dramatic clinical symptoms of MS originate. Specifically, motor neurons accumulate more Hg than sensory neurons, and motor symptoms are seen to predominate over sensory symptoms in MS. Although more research needs to be done in this area, these results suggest dental mercury exposure from amalgams, as well as from any other chronic low-grade mercury exposure, must be given very serious consideration as possibly playing a role in the etiology of MS in such patients and more likely is the major cause of most MS. Genetic variability and individual ability to excrete mercury probably plays a role. 
In conclusion, the causation of MS is probably multi-factorial. Mercury is certainly one cause and probably the major cause of this disease.