Multiple sclerosis ( MS ) is a demyelinating disease in which the insulating cover of nerve cells in the brain and spinal cord is damaged. This damage impairs the ability of parts of the nervous system to communicate, producing various signs and symptoms, including physical, mental, and sometimes psychiatric problems. Specific symptoms may include double vision, blindness of one eye, muscle weakness, problems with sensations, or problems with coordination. MS takes some form, with new symptoms either occurring in an isolated attack (form of relapse) or building over time (progressive form). Among the attacks, the symptoms may disappear completely; However, permanent neurological problems often persist, especially as the disease progresses.
Although the cause is unclear, the underlying mechanism is thought to be damage by the immune system or the failure of myelin-producing cells. The causes proposed for this include genetics and environmental factors as triggered by viral infections. MS is usually diagnosed based on the signs and symptoms that appear and the results of supporting medical tests.
There is no known cure for multiple sclerosis. Treatment attempts to improve functionality after attacks and prevent new attacks. Drugs used to treat MS, while simple to be effective, can have side effects and are poorly tolerated. Physical therapy can help a person's ability to function. Many people pursue alternative care, despite the lack of evidence. Long-term outcomes are difficult to predict, with good outcomes more often seen in women, those who develop early-onset illnesses, those who experience relapse, and those who initially experience multiple attacks. Life expectancy averages 5 to 10 years lower than the unaffected population.
Multiple sclerosis is the most common immune-mediated disorder that affects the central nervous system. By 2015, approximately 2.3 million people are affected globally with rates that vary widely across different regions and between different populations. That year about 18,900 people died from MS, up from 12,000 in 1990. The disease usually begins between the ages of 20 and 50 and is twice as common in women as in men. MS was first described in 1868 by Jean-Martin Charcot. The name multiple sclerosis refers to many scars (sclerae - better known as plaque or lesion) that develops in the white matter of the brain and spinal cord. A number of new treatments and diagnostic methods are under development. Video Multiple sclerosis
Signs and symptoms
A person with MS can have almost all symptoms or neurological signs, with the most common autonomic, visual, motor, and sensory problems. Specific symptoms are determined by the location of lesions within the nervous system, and may include loss of sensitivity or altered sensations such as tingling, pins and needles or numbness, muscle weakness, blurred vision, very clear reflexes, muscle spasms, or difficulty in moving; difficulties with coordination and balance (ataxia); problems with speech or swallowing, visual problems (nystagmus, optic neuritis or double vision), feeling tired, acute or chronic pain, and difficulty in bladder and bowel, among others. Difficulties of thinking and emotional problems such as depression or an unstable mood are also common. Uhthoff phenomenon, the worsening symptoms due to exposure to higher temperatures than usual, and Lhermitte sign, the electrical sensation that flows behind when bending the neck, especially the characteristics of MS. The primary measure of disability and severity is the scale of extended disability status (EDSS), with other measures such as the multiple sclerosis functional composites increasingly used in the study.
This condition begins in 85% of cases as clinically isolated syndrome (CIS) for several days with 45% of motor or sensory problems, 20% have optic neuritis, and 10% have symptoms related to brainstem dysfunction, while the remaining 25% has more than one difficulty before. The symptom journey occurs on two main patterns initially: either as a sudden episode of deterioration lasting several days to several months (called relapse, exacerbation, attack, attack, or flare-up) followed by repair (85% of cases) or as gradually deteriorates from time to time without a recovery period (10-15% of cases). The combination of both patterns can also occur or people can start with relapse and remission which then becomes progressive in the future. Relaps are usually unpredictable, occurring without warning. Exacerbations rarely occur more frequently than twice per year. Some recurrences, however, are preceded by common triggers and they occur more frequently during spring and summer. Similarly, viral infections like the common cold, influenza, or gastroenteritis increase their risk. Stress can also trigger attacks. Women with pregnant MS experience fewer relaps; However, during the first months after delivery, the risk increases. Overall, pregnancy does not seem to affect long-term disability. Many events have been found not to affect relapse rates including vaccination, breast-feeding, physical trauma, and Uhthoff phenomena.
Maps Multiple sclerosis
Cause
The cause of MS is unknown; However, it is believed to occur as a result of some combination of genetic and environmental factors such as infectious agents. The theory of trying to combine the data into possible explanations, but nothing is proven to be certain. Although there are a number of environmental risk factors and although some may be modified, more research is needed to determine whether their elimination can prevent MS.
Geography
MS is more common in people who live farther away from the equator, although there are exceptions. These exceptions include low-risk ethnic groups away from the equator such as Samis, Amerindian, Canadian Hutterite, New Zealand M? Ori, and Canada's Inuit, as well as groups with relatively high risks close to the equator such as Sardinia, the Outback of Sicily, Palestine and Parsi. The cause of this geographical pattern is unclear. While the north-south incidence gradient is declining, in 2010 it still exists.
MS is more common in areas with northern European populations and geographic variations may reflect only the global distribution of this high-risk population. A decrease in sun exposure resulting in a decrease in vitamin D production has also been suggested as an explanation. The relationship between the birth season and MS provides support for this idea, with fewer people born in the northern hemisphere in November compared to May being affected later on. Environmental factors may play a role during childhood, with some studies finding that people who move to other areas of the world before the age of 15 are at risk for new areas for MS. If the migration occurs after the age of 15 years, however, the person still has the risk of their home country. There is some evidence that the effect of displacement may still apply to people older than 15 years.
Genetics
MS is not considered a hereditary disease; However, a number of genetic variations have been shown to increase the risks. Some of these genes appear to have higher levels of expression in microglia cells than would be expected by chance. The probability of developing a disease is higher in the relatives of the affected person, with a greater risk among those more closely related. In identical twins they are affected about 30% of the time, while about 5% for non-identical twins and 2.5% siblings are affected with lower percentage of siblings. If both parents are exposed to risk to their children is 10 times that of the general population. MS is also more common in some ethnic groups than others.
Specific genes that have been associated with MS include differences in human leukocyte antigen (HLA) systems - a group of genes on chromosome 6 that function as a major histocompatibility complex (MHC). Changes in HLA areas related to susceptibility have been known since the 1980s, and besides these same areas have been implicated in the development of other autoimmune diseases such as type I diabetes and systemic lupus erythematosus. The most consistent finding is the relationship between multiple sclerosis and alleles of MHC defined as DR15 and DQ6. Other loci have demonstrated protective effects, such as HLA-C554 and HLA-DRB1 * 11. Overall, it has been estimated that HLA changes between 20 and 60% of genetic predisposition. Modern genetic methods (genome association studies) have found at least twelve other genes outside the HLA loci that simply increase the likelihood of MS.
Contagious agent
Many microbes have been proposed as triggers for MS, but nothing is confirmed. Moving at an early age from one location in the world to another changes the risk of someone else's MS. The explanation for this may be that some types of infections, produced by microbes that spread rather than rarely, are related to disease. Proposed mechanisms include hygiene hypotheses and hypothesis prevalence. The hygiene hypothesis proposes that exposure to certain infectious agents early in life is protective, the disease being a response to late meetings with the agency. The prevalence hypothesis proposes that the disease is caused by a more common infectious agent in areas where MS is common and where in most individuals it causes an ongoing infection without symptoms. Only in some cases and after so many years did not cause demyelination. The hygiene hypothesis has received more support than the prevalence hypothesis.
Evidence for the virus as a cause includes the presence of oligoclonal bands in the brain and cerebrospinal fluid from most people with MS, association of some viruses with human demyelinephyric encephalomyelitis, and the occurrence of demyelination in animals caused by some viral infections. Human herpes virus is a group of virus candidates. Individuals who have never been infected by the Epstein-Barr virus are at lower risk of acquiring MS, whereas those who are infected as young adults are at greater risk than those who have it at a younger age. Although some people consider this to be contrary to the hygiene hypothesis, since uninfected may have experienced a more hygienic education, others believe that there is no contradiction, since this is the first encounter with the relatively late cause virus in life that is the trigger. for his illness. Other diseases that may be associated include measles, mumps and rubella.
More
Smoking has proven to be an independent risk factor for MS. Stress can be a risk factor although evidence to support this is weak. Associations with occupational exposures and toxins - especially solvents - have been evaluated, but no clear conclusions have been achieved. Vaccination is studied as a causative factor; However, most studies show no relationship. Several other possible risk factors, such as diet and hormone intake, have been seen; However, evidence of their association with the disease is "rare and not persuasive". Gout occurs less than expected and lower uric acid levels have been found in people with MS. This led to the theory that uric acid is protective, although its exact importance remains unknown.
Pathophysiology
The three main characteristics of MS are the formation of lesions of the central nervous system (also called plaque), inflammation, and destruction of the myelin sheath of neurons. These features interact in a complex and yet fully understood way to produce breakdown of nerve tissue and in turn the signs and symptoms of the disease. Cholesterol crystals are believed to damage myelin repair and inflammation of inflammation. In addition, MS is believed to be an immune-mediated disorder that evolves from individual genetic interactions and as an unidentified environmental cause. Damage is believed to be caused, at least in part, by attacks on the nervous system by one's immune system.
Lesions
The name multiple sclerosis refers to a scar (sclerae - better known as plaque or lesion) formed in the nervous system. These lesions most commonly affect white matter in the optic nerve, brain stem, basal ganglia, and spinal cord, or white matter close to the lateral ventricle. The function of white matter cells is to carry signals between the gray matter area, where the processing is done, and the whole body. The peripheral nervous system is rarely involved.
To be more specific, MS involves the loss of oligodendrocytes, the cells responsible for creating and maintaining a layer of fat - known as the myelin sheath - that helps neurons carry electrical signals (action potential). This results in a decreased or total depletion of myelin and, along with the development of the disease, the damage to the axons of neurons. When myelin is lost, neurons can no longer effectively perform electrical signals. The repair process, called remielination, occurs in the early phase of the disease, but oligodendrocytes can not completely rebuild the myelin cell sheath. Repeated attacks cause less effective remyeling streaks, until plaques such as scars form around damaged axons. These scars are the origin of the symptoms and during magnetic resonance imaging (MRI) attacks often show more than ten new plaques. This may indicate that there are a number of lesions below which the brain is able to repair itself without producing any real consequences. Another process involved in the creation of lesions is an abnormal increase in the amount of astrocytes due to damage to nearby neurons. A number of lesion patterns have been described.
Inflammation
Besides demyelination, another sign of the disease is inflammation. In accordance with the immunological explanation, the inflammatory process is caused by T cells, a type of lymphocyte that plays an important role in the body's defenses. T cells can enter the brain through disorders in the blood-brain barrier. T cells recognize mielin as a foreign object and attack it, explaining why these cells are also called "autoreactive lymphocytes".
Myelin attacks begin an inflammatory process, which triggers other immune cells and the release of soluble factors such as cytokines and antibodies. Further damage from the blood-brain barrier in turn causes a number of other damaging effects such as swelling, macrophage activation, and more activation of cytokines and other destructive proteins. Inflammation can potentially reduce the transmission of information between neurons in at least three ways. The soluble factor released can stop neurotransmission by intact neurons. These factors can cause or increase myelin loss, or they can cause a completely damaged axon.
Blood-brain barrier
The blood-brain barrier (BBB) ​​is part of the capillary system that prevents the entry of T cells into the central nervous system. This can be permeable for this type of secondary cells due to infection by virus or bacteria. After the repair itself, usually after the infection has healed, T cells may remain trapped inside the brain. Gadolinium can not cross the normal BBB and, therefore, gadolinium-enhanced MRI is used to indicate BBB damage.
Diagnosis
Multiple sclerosis is usually diagnosed based on signs and symptoms that appear, in combination with medical imaging support and laboratory testing. This can be difficult to confirm, especially early on, because the signs and symptoms may be similar to other medical problems. The McDonald's criterion, which focuses on clinical, laboratory, and radiological evidence of lesions at different times and in different areas, is the most commonly used diagnostic method with Schumacher and Poser criteria largely of historical significance.
Clinical data alone may be sufficient for the diagnosis of MS if a person has a separate episode of neurological symptoms that are characteristic of the disease. In those who seek medical attention after only one attack, another test is required for the diagnosis. The most common diagnostic tools used are neuroimaging, cerebrospinal fluid analysis and potential evoking. Magnetic resonance imaging of the brain and spine can show demyelination areas (lesions or plaques). Gadolinium can be administered intravenously as a contrast agent to highlight the active plaque and, by elimination, indicates the presence of a historical lesion unrelated to symptoms at the time of evaluation. Testing of cerebrospinal fluid obtained from lumbar puncture may provide evidence of chronic inflammation of the central nervous system. Cerebrospinal fluid was tested for the oligoclonal IgG band at electrophoresis, which is an inflammatory marker found in 75-85% of people with MS. The nervous system in MS may be less responsive to optic nerve stimulation and sensory nerves due to the demyelination of the pathway. This brain response can be examined using the visual potential and senses.
While the above criteria allows for a non-invasive diagnosis, and although some states are the only definitive evidence is an autopsy or biopsy in which a typical MS lesion is detected, currently, by 2017, no single test (including biopsy) can provide a diagnosis definitive disease.
Type
Some phenotypes (commonly called types ), or patterns of development, have been described. The phenotype uses the path of the past disease in an attempt to predict the future. They are important not only for prognosis but also for treatment decisions. Currently, the National Multiple Sclerosis Society of the United States and the International Federation of Multiple Sclerosis, describes four types of MS (revised in 2013):
- Clinically isolated syndrome (CIS)
- Relapsing-remitting MS (RRMS)
- Primary progressive MS (PPMS)
- secondary progressive MS (SPMS)
MS relapsing is characterized by an unpredictable relapse followed by a period of months to a relatively quiet year (remission) with no new signs of disease activity. Deficits that occur during an attack may resolve or leave a problem, the latter in about 40% of attacks and becoming more common the longer a person has the disease. This explains the initial courses of 80% of individuals with MS. When deficits always resolve between attacks, this is sometimes referred to as benign MS , although people will still build some level of disability in the long run. On the other hand, the term malignant multiple sclerosis is used to describe people with MS after reaching a significant degree of disability in a short time. Relapse-remitting subtypes usually begin with a clinically isolated syndrome (CIS). In CIS, a person has a demylist of demyelinating attacks, but does not meet the criteria for multiple sclerosis. 30 to 70% of people with CIS develop MS.
Progressive primary MS occurs in about 10-20% of individuals, without remission after initial symptoms. It is characterized by the development of disability from the beginning, without, or only occasionally and little, remission and improvement. The usual onset age for primary progressive subtypes is slower than relapse-remitting subtypes. This is similar to the secondary progressive age usually beginning in the arising MS, around the age of 40 years.
Secondary progressive MS occurs in about 65% of those with an early recurrence MS, who eventually progressive progressive neurologic decline between acute attacks without a definite remission period. Occasional relapsing and mild remission may appear. The most common time period between disease onset and conversion from relapsing-remitting to secondary progressive MS is 19 years.
Other unusual MS types have been described; these include Devic's disease, Concentric Bald sclerosis, Schilder's diffuse sclerosis, and Marburg multiple sclerosis. There is debate whether they are MS variants or different diseases. Multiple sclerosis behaves differently in children, taking more time to reach progressive stages. Nevertheless, they still achieve it at an average age lower than the usual adult.
Management
Although there is no known cure for multiple sclerosis, some therapies have proven to be beneficial. The main purpose of therapy is to restore function after attack, prevent new attacks, and prevent disability. Starting treatment is generally recommended in people after the first attack when more than two lesions are seen on MRI.
As with any medical treatment, drugs used in MS management have some side effects. Alternative treatments are performed by several people, despite lack of supporting evidence.
Acute attacks
During symptomatic attacks, high-dose intravenous corticosteroids, such as methylprednisolone, are a common therapy, with oral corticosteroids that appear to have similar efficacy and safety profiles. Although, in general, effective in the short term to relieve symptoms, corticosteroid treatment does not seem to have a significant impact on long-term recovery. The consequences of severe attacks that do not respond to corticosteroids may be treated with plasmapheresis.
Treatments that modify the disease
Relapseing with multiple sclerosis remissions
By 2017, ten drugs that change the disease are approved by the regulatory body for relapse-remitting multiple sclerosis (RRMS). They are interferon beta-1a, interferon beta-1b, glatiramer acetate, mitoxantrone, natalizumab, fingolimod, teriflunomide, dimethyl fumarate, alemtuzumab, and ocrelizumab.
Their cost effectiveness in 2012 is unclear. In March 2017 the FDA approved ocrelizumab, a humane anti-CD20 monoclonal antibody, as a treatment for RRMS, with requirements for some Phase IV clinical trials.
In RRMS they are very effective in reducing the number of attacks. Interferon and glatiramer acetate are first-line treatments and roughly equivalent, reducing relapse by about 30%. Long-term start-up therapy is safe and improves results. Natalizumab reduces the recurrence rate over first-line agents; However, because of the side effect problem is a second-line agent provided for those who do not respond to other treatments or with severe illness. Mitoxantrone, whose use is limited by severe side effects, is a third-line option for those who do not respond to other drugs. Clinically isolated syndrome treatment (CIS) with interferon decreases the likelihood of developing a clinical MS. The efficacy of interferon and glatiramer acetate in children has been estimated to be approximately equal to that of adults. The roles of some new agents such as fingolimod, teriflunomide, and dimethyl fumarate, in 2011, are not yet fully clear.
In 2017, rituximab is widely used off-label to treat RRMS.
Multiple progressive sclerosis
By 2017, rituximab has been used extensively beyond labels to treat progressive primary MS. In March 2017 the FDA approved ocrelizumab, as a treatment for primary progressive MS, the first drug approved, with requirements for some Phase IV clinical trials.
In 2011, only one drug, mitoxantrone, was approved for secondary MS progressive. In this population the tentative evidence supporting mitoxantrone has been slowing the progression of the disease and reducing the relapse rate for two years.
Adverse effects
Disease-modifying treatments have several side effects. One of the most common is irritation at the injection site for glatiramer acetate and interferon (up to 90% with subcutaneous injection and 33% with intramuscular injection). Over time, dents are visible at the injection site, because the local destruction of fatty tissue, known as lipoatrophy, can develop. Interferon can produce flu-like symptoms; some people taking glatiramer experience post-injection reactions with flushing, chest tightness, palpitations, and anxiety, which usually lasts less than thirty minutes. More harmful but less common are liver damage from interferon, systolic dysfunction (12%), infertility, and acute myeloid leukemia (0.8%) of mitoxantrone, and progressive multifocal leukoencephalopathy occurring with natalizumab (occurring in 1 in 600 treated individuals ).
Fingolimod may cause hypertension and slow heart rate, macular edema, elevated liver enzymes or decreased lymphocyte levels. Temporary evidence supports the short term safety of teriflunomide, with common side effects including: headache, fatigue, nausea, hair loss, and leg pain. There are also reports of liver failure and PML with its use and it is dangerous for fetal development. The most common side effects of dimethyl fumarate are flushing and gastrointestinal problems. While dimethyl fumarate may cause a decrease in the number of white blood cells no cases of opportunistic infections are reported during the trial.
Related symptoms
Both drugs and neurorehabilitation have been shown to improve some of the symptoms, although they do not change the course of the disease. Some symptoms have a good response to medications, such as bladder and unstable spasticity, while others are slightly altered. For neurological problems, a multidisciplinary approach is essential to improving quality of life; However, it is difficult to define the 'core team' as many health services may be required at different time points. Multidisciplinary rehabilitation programs increase the activity and participation of people with MS but do not affect the level of disturbance. There is limited evidence for the overall efficacy of individual therapeutic disciplines, although there is good evidence that specific approaches, such as exercise, and psychological therapy, especially effective cognitive behavioral approaches.
Alternative care
Over 50% of people with MS may use complementary and alternative medicine, although the percentage varies depending on how alternative treatments are defined. Evidence of effectiveness for such treatment in many cases is weak or non-existent. Treatments of the unproven benefits used by people with MS include dietary supplements and regimens, vitamin D, relaxation techniques such as yoga, herbal remedies (including medical marijuana), hyperbaric oxygen therapy, self infections with hookworm, reflexology, acupuncture, and awareness. Regarding user characteristics, they are more often women, have MS for longer periods, tend to be more disabled and have lower satisfaction levels with conventional health care.
Prognosis
The expected future journey of the disease depends on the subtype of the disease; gender, age, and individual early symptoms; and the degree of disability the person has. Female sex, subtype remap, optic neuritis or sensory symptoms at onset, some attacks in early years and especially early age at onset, are associated with better travel.
The average life expectancy is 30 years from the onset of the disease, ie 5 to 10 years less than the unaffected person. Nearly 40% of people with MS reach the seventh decade of life. However, two-thirds of deaths are directly related to disease consequences. Suicide is more common, whereas infections and other complications are very dangerous for those with more disabilities. Although most people lose the ability to walk before death, 90% are able to walk independently at 10 years from the beginning, and 75% at 15 years.
Epidemiology
MS is the most common autoimmune disorder of the central nervous system. In 2010, the number of people with MS was 2-2.5 million (about 30 per 100,000) globally, with numbers varying in different regions. It is estimated to have resulted in 18,000 deaths that year. In Africa, the tariff is less than 0.5 per 100,000, while it is 2.8 per 100,000 in Southeast Asia, 8.3 per 100,000 in America, and 80 per 100,000 in Europe. Prices surpass 200 per 100,000 in certain populations of North European descent. The number of new cases developing per year is about 2.5 per 100,000.
MS rates seem to increase; This, however, can be explained only with a better diagnosis. The study of population and geographical patterns has been common and has led to a number of theories about the causes.
MS usually appear in adults in their late twenties or early thirties but rarely start in childhood and after 50 years. The primary progressive subtype is more common in people in their fifties. Similar to many autoimmune disorders, the disease is more common in women, and the trend may increase. In 2008, globally it was about twice as common in women as compared to men. In children, it's even more common in women than men, while in people over fifty, it affects men and women almost the same.
History
Medical discovery
Robert Carswell (1793-1857), a professor of English pathology, and Jean Cruveilhier (1791-1873), a professor of French pathological anatomy, described and illustrated many of the clinical details of the disease, but did not identify it as a separate disease. In particular, Carswell described the injury he found as "an extraordinary lesion of the spinal cord accompanied by atrophy". Under the microscope, Swiss pathologist Georg Eduard Rindfleisch (1836-1908) noted in 1863 that inflammation-related lesions were distributed around the blood vessels.
French neurologist Jean-Martin Charcot (1825-1893) was the first to recognize multiple sclerosis as a different disease in 1868. Summarizing previous reports and adding his own clinical and pathological observations, Charcot is called sclerose en plaques >.
Diagnosis
The first attempt to establish a set of diagnostic criteria was also due to Charcot in 1868. He published what is now known as the "Charcot Triad", consisting of nystagmus, intentional tremor, and telegraph speech (scanning talk). Charcot also observed cognitive changes. , describes his patient as a "marked memory extension" and a "slowly formed conception".
The diagnosis was based on Charcot triads and clinical observations until Schumacher made the first attempt to standardize the criteria in 1965 by introducing some basic requirements: The spread of lesions in time (DIT) and space (DIS), and that "signs and symptoms could not be explained. with other disease processes ". Both requirements are then inherited by Poser criteria and McDonald's criteria, which the 2010 version is in use.
During the 20th century, theories about causes and pathogenesis developed and effective treatments began to emerge in the 1990s. Since the beginning of the 21st century, the perfection of concepts has taken place. The 2010 revision of McDonald's criteria allowed for the diagnosis of MS with only one proven lesion (CIS). Furthermore, three years later, the 2013 revision of the "phenotype for travel disease" was forced to consider the CIS as one of the MS phenotypes, creating some obsolete expressions such as "conversion from CIS to MS".
Historical case
There are some historical records of people who may have MS and live before or shortly after the illness is described by Charcot.
A young woman named Halldora who lived in Iceland around 1200 suddenly lost her vision and mobility but, after praying to the saints, restored them seven days later. Saint Lidwina of Schiedam (1380-1433), a Dutch nun, is probably one of the first to be clearly identified with MS. From the age of 16 to his death at 53, he experienced intermittent pain, leg weakness, and vision loss - typical symptoms of MS. Both cases have led to the hypothesis proposed "Viking genes" for the spread of the disease.
Augustus Frederick d'Este (1794-1848), the son of Prince Augustus Frederick, Duke of Sussex and Lady Augusta Murray and the grandson of George III of the United Kingdom, almost certainly have MS. D'Este left a diary explaining about 22 years of his life with the disease. His diary began in 1822 and ended in 1846, although it remained unknown until 1948. The symptoms began at age 28 with sudden sudden sight loss (amaurosis fugax) after a friend's funeral. During his illness, he develops leg weakness, clumsiness, numbness, dizziness, bladder disturbances, and erectile dysfunction. In 1844, he began to use a wheelchair. Regardless of his illness, he still has an optimistic outlook on life. Other early MS notes were kept by English author W. N. P. Barbellion, nom-de-plume of Bruce Frederick Cummings (1889-1919), who kept detailed records of his diagnosis and struggle. His diary was published in 1919 as The Journal of a Disappointed Man .
Research
Drugs
There is ongoing research looking for more effective, convenient, and tolerable treatments for recurrent MS; the creation of therapy for progressive subtypes; strategy of neuroprotection; and effective symptomatic treatment.
During the 2000s and 2010s, there was approval of some oral drugs that were expected to gain popularity and frequency of use. Several other oral medications are being investigated, including ozanimod, laquinimod, and estriol. Laquinimod was announced in August 2012 and in third phase III trials after mixed results on the previous one. Similarly, studies aimed at improving the efficacy and ease of use of existing therapies occur. This includes the use of new preparations such as the interferon - 1 - 1a PEG version, which is expected to be administered at less frequent doses with similar effects. Estriol, a female sex hormone found at high concentrations during late pregnancy, has been identified as candidate therapy for women with recurrent MS and has progressed through Phase II trials. Approval requests peginterferon beta-1a are expected during 2013.
Monoclonal antibodies also heighten high interest. In 2012 alemtuzumab, daclizumab and CD20 monoclonal antibodies such as rituximab, ocrelizumab and ofatumumab all show some benefits and are being studied as potential treatments, and the FDA approved ocrelizumab for recurrence and primary MS in March 2017. Their use was also accompanied by the emergence of dangerous side effects , the most important is the opportunistic infection. Associated with this investigation is the development of tests for JC virus antibodies, which may help to determine who is at greater risk of developing progressive multifocal leukoencephalopathy while taking natalizumab. While monoclonal antibodies may have a role in the treatment of future illnesses, it is believed that it will be small due to the risks associated with them.
Another research strategy is to evaluate the combined effectiveness of two or more drugs. The main reason for using some drugs in MS is that the treatments involved target different mechanisms and, therefore, their use is not always exclusive. Synergy, in which one drug enhances other effects is also possible, but there can also be disadvantages such as blocking other actions or adverse side effects. There have been several experimental combinations of therapy, but none have shown positive enough results to be considered a useful treatment for MS.
Research on neuroprotection and regenerative care, such as stem cell therapy, while very important, is at an early stage. Likewise, there is no effective treatment for this progressive variant of the disease. Many of the newest drugs as well as those being developed may be evaluated as therapy for PPMS or SPMS.
Biomata disease
While diagnostic criteria are not expected to change in the near future, work to develop biomarkers that help diagnose and predict disease progression is ongoing. New diagnostic methods under investigation include working with anti-myelin antibodies, and studies with serum and cerebrospinal fluids, but none of them have produced reliable positive results.
At this time, no laboratory investigation can predict prognosis. Several promising approaches have been proposed including: interleukin-6, nitric oxide and nitric oxide synthase, osteopontin, and fetuin-A. Because disease progression is the result of neuron degeneration, the role of proteins that indicate the loss of neural tissue such as neurofilament, tau, and N-acetylpartate is under investigation. Other effects include finding biomarkers that differentiate between those who will and will not respond to drugs.
Improved neuroimaging techniques such as positron emission tomography (PET) or magnetic resonance imaging (MRI) carry promise for better diagnosis and predicting prognosis, although the effects of such improvements in daily medical practice may take decades. Regarding MRI, there are several techniques that have demonstrated some usefulness in the research setting and can be introduced into clinical practice, such as double inversion recovery sequence, magnetization transfer, diffusion tensor, and functional magnetic resonance imaging. These techniques are more specific to the disease than they already are, but still lack some standardization of the acquisition protocol and the creation of normative values. There are other techniques under development that include contrast agents capable of measuring the level of peripheral macrophages, inflammation, or neuronal dysfunction, and techniques that measure iron deposition that can serve to determine the role of this feature in MS, or cerebral perfusion. Similarly, new PET radiotracers may serve as markers of altered processes such as brain inflammation, cortical pathology, apoptosis, or remylienation. Antibiodies against the Kir4.1 potassium canal may be associated with MS.
Chronic cerebrospinal venous insufficiency
In 2008, vascular surgeon Paolo Zamboni suggested that MS involves constriction of blood vessels that drain the brain, which he calls chronic cerebrospinal venous insufficiency (CCSVI). He found CCSVI in all patients with MS in his studies, performed surgical procedures, then called the media "clearance procedure" to fix it, and claimed that 73% of the participants increased. This theory received significant attention in the media and between them with MS, especially in Canada. Concern has arisen with Zamboni research because it is neither blind nor controlled, and assumptions about the causes of the disease are not supported by known data. Furthermore, further research does not find a similar or found relation that is less powerful, raising serious objections to the hypothesis. The "liberation procedure" has been criticized for causing serious complications and death with unproven benefits. Therefore, in 2013 is not recommended for MS treatment. Additional research investigating the CCSVI hypothesis is ongoing.
See also
- List of multiple sclerosis organizations
- List of people with multiple sclerosis
References
External links
- Multiple sclerosis in Curlie (based on DMOZ)
- A database for the analysis and comparison of global data on MS epidemiology
Source of the article : Wikipedia
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