Multiple sclerosis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Multiple sclerosis (abbreviated MS, formerly known as disseminated sclerosis or encephalomyelitis disseminata) is a chronic, inflammatory, demyelinating disease that affects the central nervous system (CNS). Disease onset usually occurs in young adults, is more common in women and the disease has a prevalence that ranges between 2 and 150 per 100,000 depending on the country or specific population.[1] MS was first described in 1868 by Jean-Martin Charcot.
MS affects the neurons in the areas of the brain and spinal cord known as the white matter. These cells carry signals in between the grey matter areas, where the processing is done, and between these and the rest of the body. More specifically, MS destroys oligodendrocytes which are the cells responsible for creating and maintaining a fatty layer, known as the myelin sheath, which helps the neurons carry electrical signals. MS results in a thinning or complete loss of myelin and, less frequently, the cutting (transection) of the neuron's extensions or axons. When the myelin is lost, the neurons can no longer effectively conduct their electrical signals. The name multiple sclerosis refers to the scars (scleroses -better known as plaques or lesions) in the white matter. Loss of myelin in these lesions causes some of the symptoms that may vary widely depending upon which signals are interrupted. However, more advanced forms of imaging are now showing that much of the damage happens outside these regions. A consequence of this course of action is that almost any neurological symptom can accompany the disease.
Multiple sclerosis may take several forms, with new symptoms occurring either in discrete attacks (relapsing forms) or slowly accumulating over time (progressive forms). Most people are first diagnosed with relapsing-remitting MS but develop secondary-progressive MS (SPMS) after a number of years. Between attacks, symptoms may resolve completely, but permanent neurological problems often persist, especially as the disease advances.
Although much is known about the mechanisms involved in the disease process, the cause remains elusive. The theory with the most adherents is that it results from attacks to the nervous system by the body's own immune system. Some believe it is a metabolically dependent disease while others think that it might be caused by a virus such as Epstein-Barr. Still other people believe that its virtual absence from the tropics points to a deficiency of vitamin D during childhood.
The disease currently does not have a cure, but several therapies have proven helpful. The aims of treatment are returning function after an attack, preventing new attacks, and preventing disability. As with any treatment, medications have several adverse effects, and many therapies are still under investigation. At the same time different alternative treatments are pursued by many patients, despite the paucity of supporting scientific study.
The prognosis, or expected course of the disease, for a person depends on the subtype of the disease; the characteristics of the individual, the initial symptoms; and the degree of disability the person experiences as time advances. However life expectancy of patients is nearly the same as that of the unaffected population and in many cases a normal life is possible.
Historical Perspective
- [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
- In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
- In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
Classification
Multiple sclerosis may be classified into four groups according to clinical course of the disease.
- Relapsing-remitting
- secondary-progressive
- primary-progressive
- progressive-relapsing[2]
Other variants of Multiple sclerosis include clinically isolated syndrome and radiologically isolated syndrome.
Pathophysiology
- The pathogenesis of [disease name] is characterized by [feature1], [feature2], and [feature3].
- The [gene name] gene/Mutation in [gene name] has been associated with the development of [disease name], involving the [molecular pathway] pathway.
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Causes
- [Disease name] may be caused by either [cause1], [cause2], or [cause3].
- [Disease name] is caused by a mutation in the [gene1], [gene2], or [gene3] gene[s].
- There are no established causes for [disease name].
Differentiating Multiple Sclerosis from other Diseases
The signs and symptoms of MS can be similar to other medical problems, such as neuromyelitis optica, stroke, brain inflammation,infections such as Lyme disease (which can produce identical MRI lesions and CSF abnormalities[3][4][5][6]), tumors, and other autoimmune problems, such as lupus. Additional testing may be needed to help distinguish MS from these other problems.
Epidemiology and Demographics
- The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
- In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].
Age
- Patients of all age groups may develop [disease name].
- [Disease name] is more commonly observed among patients aged [age range] years old.
- [Disease name] is more commonly observed among [elderly patients/young patients/children].
Gender
- [Disease name] affects men and women equally.
- [Gender 1] are more commonly affected with [disease name] than [gender 2].
- The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.
Race
- There is no racial predilection for [disease name].
- [Disease name] usually affects individuals of the [race 1] race.
- [Race 2] individuals are less likely to develop [disease name].
Risk Factors
- Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
Natural History, Complications and Prognosis
- The majority of patients with [disease name] remain asymptomatic for [duration/years].
- Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
- If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
- Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
- Prognosis is generally [excellent/good/poor], and the [1/5/10year mortality/survival rate] of patients with [disease name] is approximately [#%].
Diagnosis
Diagnostic Criteria
- The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
- [criterion 1]
- [criterion 2]
- [criterion 3]
- [criterion 4]
Symptoms
- [Disease name] is usually asymptomatic.
- Symptoms of [disease name] may include the following:
- [symptom 1]
- [symptom 2]
- [symptom 3]
- [symptom 4]
- [symptom 5]
- [symptom 6]
Physical Examination
- Patients with [disease name] usually appear [general appearance].
- Physical examination may be remarkable for:
- [finding 1]
- [finding 2]
- [finding 3]
- [finding 4]
- [finding 5]
- [finding 6]
Laboratory Findings
- There are no specific laboratory findings associated with [disease name].
- A [positive/negative] [test name] is diagnostic of [disease name].
- An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
- Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
Imaging Findings
- There are no [imaging study] findings associated with [disease name].
- [Imaging study 1] is the imaging modality of choice for [disease name].
- On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
- [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
Prevention
Secondary Prevention
A physiotherapist can help to reduce spasticity and avoid the development of contractures with techniques such as passive stretching.[7]
Alternative Therapies
Different alternative treatments are pursued by many patients, despite the paucity of supporting, comparable, replicated scientific study. Examples are dietary regimens,[8], herbal medicine, including the use of marijuana to help alleviate symptoms,[9][10] or hyperbaric oxygenation.[11] On the other hand the therapeutic practice of martial arts such as tai chi, relaxation disciplines such as yoga, or general exercise, seem to mitigate fatigue and improve quality of life.[12]
References
- ↑ Rosati G (2001). "The prevalence of multiple sclerosis in the world: an update". Neurol. Sci. 22 (2): 117–39. PMID 11603614.
- ↑ Lublin FD; Reingold SC. Defining the clinical course of multiple sclerosis: results of an international survey. National Multiple Sclerosis Society (USA) Advisory Committee on Clinical Trials of New Agents in Multiple Sclerosis. Neurology 1996 Apr;46(4):907-11. PMID 8780061
- ↑ Garcia-Monco JC; Miro Jornet J; Fernandez Villar B; Benach JL; Guerrero Espejo A; Berciano JA. [Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion] Med Clin (Barc) 1990 May 12;94(18):685-8.PMID 2388492
- ↑ Hansen K; Cruz M; Link H. Oligoclonal Borrelia burgdorferi-specific IgG antibodies in cerebrospinal fluid in Lyme neuroborreliosis. J Infect Dis 1990 Jun;161(6):1194-202. PMID 2345300
- ↑ Schluesener HJ; Martin R; Sticht-Groh V.Autoimmunity in Lyme disease: molecular cloning of antigens recognized by antibodies in the cerebrospinal fluid. Autoimmunity 1989 2(4):323-30. PMID 2491615
- ↑ Kohler J; Kern U; Kasper J; Rhese-Kupper B; Thoden U. Chronic central nervous system involvement in Lyme borreliosis Neurology 1988 Jun;38(6):863-7. PMID 3368066
- ↑ Cardini RG, Crippa AC, Cattaneo D (2000). "Update on multiple sclerosis rehabilitation". J. Neurovirol. 6 Suppl 2: S179–85. PMID 10871810.
- ↑ Farinotti M, Simi S, Di Pietrantonj C; et al. (2007). "Dietary interventions for multiple sclerosis". Cochrane database of systematic reviews (Online) (1): CD004192. doi:10.1002/14651858.CD004192.pub2. PMID 17253500.
- ↑ Chong MS, Wolff K, Wise K, Tanton C, Winstock A, Silber E (2006). "Cannabis use in patients with multiple sclerosis". Mult. Scler. 12 (5): 646–51. PMID 17086912.
- ↑ Zajicek JP, Sanders HP, Wright DE, Vickery PJ, Ingram WM, Reilly SM, Nunn AJ, Teare LJ, Fox PJ, Thompson AJ (2005). "Cannabinoids in multiple sclerosis (CAMS) study: safety and efficacy data for 12 months follow up". J. Neurol. Neurosurg. Psychiatr. 76 (12): 1664–9. doi:10.1136/jnnp.2005.070136. PMID 16291891.
- ↑ Bennett M, Heard R (2004). "Hyperbaric oxygen therapy for multiple sclerosis". Cochrane database of systematic reviews (Online) (1): CD003057. doi:10.1002/14651858.CD003057.pub2. PMID 14974004.
- ↑ Oken BS, Kishiyama S, Zajdel D; et al. (2004). "Randomized controlled trial of yoga and exercise in multiple sclerosis". Neurology. 62 (11): 2058–64. PMID 15184614.