Thursday, January 12, 2023
What is Multiple Sclerosis (MS)? | The Johns Hopkins Multiple Sclerosis Center - General Medical Abbreviations
What does m.s. stand for in medical terms - what does m.s. stand for in medical terms:. How to Decode What Your MS Doctor Is Saying
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Apply for Admission M. The Multiple Sclerosis Center. Multiple Sclerosis MS. Between 1 and 2 in every 10 people with the condition start their MS with a gradual worsening of symptoms. In primary progressive MS, symptoms gradually worsen and accumulate over several years, and there are no periods of remission, though people often have periods where their condition appears to stabilise.
MS is an autoimmune condition. This is when something goes wrong with the immune system and it mistakenly attacks a healthy part of the body — in this case, the brain or spinal cord of the nervous system. In MS, the immune system attacks the layer that surrounds and protects the nerves called the myelin sheath. This damages and scars the sheath, and potentially the underlying nerves, meaning that messages travelling along the nerves become slowed or disrupted.
Exactly what causes the immune system to act in this way is unclear, but most experts think a combination of genetic and environmental factors is involved. There's currently no cure for MS, but a number of treatments can help control the condition and ease symptoms. The treatment you need will depend on the specific symptoms and difficulties you have.
Disease-modifying therapies may also help to slow or reduce the overall worsening of disability in people with a type of MS called relapsing remitting MS, and in some people with types called primary and secondary progressive MS, who have relapses. Unfortunately, there's currently no treatment that can slow the progress of primary progressive MS, or secondary progressive MS, where there are no relapses. Many therapies aiming to treat progressive MS are currently being researched.
If you have been diagnosed with MS, it's important to take care of your general health. Read more advice about living with MS. MS can be a challenging condition to live with, but new treatments over the past 20 years have considerably improved the quality of life of people with the condition.
MS itself is rarely fatal, but complications may arise from severe MS, such as chest or bladder infections, or swallowing difficulties. The average life expectancy for people with MS is around 5 to 10 years lower than average, and this gap appears to be getting smaller all the time. These organisations offer useful advice, publications, news items about ongoing research, blogs and chatrooms. They can be very useful if you, or someone you know, has just been diagnosed with MS. There's also the shift.
Environmental factors may play a role during childhood, with several studies finding that people who move to a different region of the world before the age of 15 acquire the new region's risk of MS. If migration takes place after age 15, however, the person retains the risk of their home country. MS is not considered a hereditary disease ; however, a number of genetic variations have been shown to increase the risk. Specific genes that have been linked with MS include differences in the human leukocyte antigen HLA system—a group of genes on chromosome 6 that serves as the major histocompatibility complex MHC.
Many microbes have been proposed as triggers of MS, but none has been confirmed. Only in a few cases and after many years does it cause demyelination. Evidence for a virus as a cause include the presence of oligoclonal bands in the brain and cerebrospinal fluid of most people with MS, the association of several viruses with human demyelinating encephalomyelitis , and the occurrence of demyelination in animals caused by some viral infections. Individuals having never been infected by the Epstein—Barr virus are at a reduced risk of getting MS, whereas those infected as young adults are at a greater risk than those having had it at a younger age.
Smoking may be an independent risk factor for MS. This has led to the theory that uric acid is protective, although its exact importance remains unknown. The three main characteristics of MS are the formation of lesions in the central nervous system also called plaques , inflammation and the destruction of myelin sheaths of neurons. These features interact in a complex and not yet fully understood manner to produce the breakdown of nerve tissue and in turn the signs and symptoms of the disease.
The name multiple sclerosis refers to the scars sclerae — better known as plaques or lesions that form in the nervous system. These lesions most commonly affect the white matter in the optic nerve , brain stem , basal ganglia , and spinal cord , or white matter tracts close to the lateral ventricles.
The peripheral nervous system is rarely involved. To be specific, MS involves the loss of oligodendrocytes , the cells responsible for creating and maintaining a fatty layer—known as the myelin sheath—which helps the neurons carry electrical signals action potentials. When the myelin is lost, a neuron can no longer effectively conduct electrical signals.
Apart from demyelination, the other sign of the disease is inflammation. Fitting with an immunological explanation, the inflammatory process is caused by T cells , a kind of lymphocyte that plays an important role in the body's defenses. The T cells recognize myelin as foreign and attack it, explaining why these cells are also called "autoreactive lymphocytes".
The attack on myelin starts inflammatory processes, which trigger other immune cells and the release of soluble factors like cytokines and antibodies. A further breakdown of the blood-brain barrier, in turn, causes a number of other damaging effects such as swelling , activation of macrophages , and more activation of cytokines and other destructive proteins.
These factors could lead to or enhance the loss of myelin, or they may cause the axon to break down completely. The blood—brain barrier BBB is a part of the capillary system that prevents the entry of T cells into the central nervous system. It may become permeable to these types of cells secondary to an infection by a virus or bacteria. After it repairs itself, typically once the infection has cleared, T cells may remain trapped inside the brain.
Multiple sclerosis is typically diagnosed based on the presenting signs and symptoms, in combination with supporting medical imaging and laboratory testing. The McDonald criteria , which focus on clinical, laboratory, and radiologic evidence of lesions at different times and in different areas, is the most commonly used method of diagnosis [59] with the Schumacher and Poser criteria being of mostly historical significance.
As of [update] , there is no single test including biopsy that can provide a definitive diagnosis. Magnetic resonance imaging MRI of the brain and spine may show areas of demyelination lesions or plaques.
Gadolinium can be administered intravenously as a contrast agent to highlight active plaques and, by elimination, demonstrate the existence of historical lesions not associated with symptoms at the moment of the evaluation.
Central vein signs CVS have been proposed as a good indicator of MS in comparison with other conditions causing white lesions. Brain atrophy is seen as an indicator of MS. Testing of cerebrospinal fluid obtained from a lumbar puncture can provide evidence of chronic inflammation in the central nervous system.
There are several diseases that present similarly to multiple sclerosis. Intractable vomiting, severe optic neuritis, or bilateral optic neuritis raises suspicion for neuromyelitis optica spectrum disorder NMOSD. Several phenotypes commonly termed types , or patterns of progression, have been described. Phenotypes use the past course of the disease in an attempt to predict the future course. They are important not only for prognosis but also for treatment decisions. Relapsing-remitting MS is characterized by unpredictable relapses followed by periods of months to years of relative quiet remission with no new signs of disease activity.
The relapsing-remitting subtype usually begins with a clinically isolated syndrome CIS. In CIS, a person has an attack suggestive of demyelination, but does not fulfill the criteria for multiple sclerosis. It is similar to the age that secondary progressive usually begins in relapsing-remitting MS, around 40 years of age.
Independently of the types published by the MS associations, regulatory agencies like the FDA often consider special courses, trying to reflect some clinical trials results on their approval documents. Also, when deficits always resolve between attacks, this is sometimes referred to as benign MS , [82] although people will still build up some degree of disability in the long term. An international panel has published a standardized definition for the course HAMS.
Atypical variants of MS have been described; these include tumefactive multiple sclerosis , Balo concentric sclerosis , Schilder's diffuse sclerosis , and Marburg multiple sclerosis. There is debate on whether they are MS variants or different diseases. Although there is no known cure for multiple sclerosis, several therapies have proven helpful. Several effective treatments can significantly decrease the number of attacks and the rate of progression. Starting medications is generally recommended in people after the first attack when more than two lesions are seen on MRI.
Older medications used to treat MS were modestly effective, could have side effects, and were poorly tolerated. As with any medical treatment, medications used in the management of MS have several adverse effects.
Alternative treatments are pursued by some people, despite the shortage of supporting evidence of efficacy. During symptomatic attacks, administration of high doses of intravenous corticosteroids , such as methylprednisolone , is the usual therapy, [1] with oral corticosteroids seeming to have a similar efficacy and safety profile.
As of , multiple disease-modifying medications were approved by regulatory agencies for relapsing-remitting multiple sclerosis RRMS. In RRMS they are modestly effective at decreasing the number of attacks.
Treatment of clinically isolated syndrome CIS with interferons decreases the chance of progressing to clinical MS.
The relative effectiveness of different treatments is unclear, as most have only been compared to placebo or a small number of other therapies. As of [update] , only one medication, mitoxantrone, had been approved for secondary progressive MS. As of , review of 9 immunomodulators and immunosuppressants found no evidence of any being effective in preventing disability progression in people with progressive MS.
In March the FDA approved ocrelizumab as a treatment for primary progressive MS in adults, the first drug to gain that approval, [] [] [] with requirements for several Phase IV clinical trials. In , siponimod and cladribine were approved in the United States for the treatment of secondary progressive multiple sclerosis.
The disease-modifying treatments have several adverse effects. Fingolimod may give rise to hypertension and slowed heart rate , macular edema , elevated liver enzymes, or a reduction in lymphocyte levels. Both medications and neurorehabilitation have been shown to improve some symptoms, though neither changes the course of the disease.
A multidisciplinary approach is important for improving quality of life; however, it is difficult to specify a 'core team' as many health services may be needed at different points in time. There is some evidence that aquatic therapy is a beneficial intervention. The spasticity associated with MS can be difficult to manage because of the progressive and fluctuating course of the disease.
Physical therapy including vibration interventions, electrical stimulation, exercise therapy, standing therapy, and radial shock wave therapy RSWT , were beneficial for limiting spasticity, helping limit excitability, or increasing range of motion. The availability of treatments that modify the course of multiple sclerosis beginning in the s, known as disease-modifying therapies DMTs , has improved prognosis.
These treatments can reduce relapses and slow progression, but as of there is no cure. The prognosis of MS depends on the subtype of the disease, and there is also great individual variation in the progression of the disease.
A cohort study found that after a median of However, "silent progression" of the disease still occurs. Most treatments have been approved for use in relapsing MS; there are limited effective treatments for progressive forms of MS, and treatments aren't as effective. After diagnosis of MS, characteristics that predict a worse course are male sex, older age, and greater disability at the time of diagnosis. Female sex, though, is associated with a higher relapse rate. MS is the most common autoimmune disorder of the central nervous system.
Increasing rates of MS may be explained simply by better diagnosis. MS usually appears in adults in their late twenties or early thirties but it can rarely start in childhood and after 50 years of age. Robert Carswell — , a British professor of pathology , and Jean Cruveilhier — , a French professor of pathologic anatomy, described and illustrated many of the disease's clinical details, but did not identify it as a separate disease. The French neurologist Jean-Martin Charcot — was the first person to recognize multiple sclerosis as a distinct disease in The first attempt to establish a set of diagnostic criteria was also due to Charcot in He published what now is known as the "Charcot Triad", consisting in nystagmus , intention tremor , and telegraphic speech scanning speech.
Diagnosis was based on Charcot triad and clinical observation until Schumacher made the first attempt to standardize criteria in by introducing some fundamental requirements: Dissemination of the lesions in time DIT and space DIS , and that "signs and symptoms cannot be explained better by another disease process".
During the 20th century, theories about the cause and pathogenesis were developed and effective treatments began to appear in the s. In this first version they provided standardized definitions for four MS clinical courses: relapsing-remitting RR , secondary progressive SP , primary progressive PP , and progressive relapsing PR.
There are several historical accounts of people who probably had MS and lived before or shortly after the disease was described by Charcot. A young woman called Halldora who lived in Iceland around suddenly lost her vision and mobility but recovered them seven days after.
Saint Lidwina of Schiedam — , a Dutch nun , may be one of the first clearly identifiable people with MS. From the age of 16 until her death at 53, she had intermittent pain, weakness of the legs and vision loss: symptoms typical of MS. D'Este left a detailed diary describing his 22 years living with the disease. His diary began in and ended in , although it remained unknown until His symptoms began at age 28 with a sudden transient visual loss amaurosis fugax after the funeral of a friend.
During his disease, he developed weakness of the legs, clumsiness of the hands, numbness, dizziness, bladder disturbance and erectile dysfunction. In , he began to use a wheelchair. Despite his illness, he kept an optimistic view of life.
Barbellion , pen name of Bruce Frederick Cummings — , who maintained a detailed log of his diagnosis and struggle. It did not find an increased risk after infection with other viruses, including the similarly transmitted cytomegalovirus.
Medications that influence voltage-gated sodium ion channels are under investigation as a potential neuroprotective strategy because of hypothesized role of sodium in the pathological process leading to axonal injury and accumulating disability.
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