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Multiple Sclerosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. Associate Editor(s)-in-Chief: Shivam Singla M.B.B.S.

Overview

Multiple Sclerosis ( MS) is a demyelinating disease of brain and spinal cord affecting mostly peoples in the age of 20-40, Although it affects the children also. The term multiple sclerosis refers to the numerous glial scars (or sclerae – essentially plaques or lesions) that develop on the white matter of the brain and spinal cord. The disease course of MS varies from mild to to moderate in severity with the presence of disabilities as disease progresses over time. Its hard to predict the course disease for any individual who has been recently diagnosed with M.S. The more is still to learn regarding the course of disease, its progression and the newer therapies used these days to treat and slow the progression of M.S. Even after years of research and medical advancement still there is no cure and no clear ways to prevent MS from developing.

Historical Perspective

In 1868 : The French neurologist "Jean-Martin Charcot" first recognize multiple sclerosis as a distinct disease and the diagnostic criteria was first introduced - named as "Charcot's Triad"- 1) Nystagmus 2) Intention tremor 3) Telegraphic speech (scanning speech)
In 1965 Schumacher gave the standarized criteria that included the Dissemination of lesions in time (DIT) and Dissemination of lessions in space (DIS) along with the fact that the signs and symptoms failed to be explained by any other disease process.
In 20th Centuary: Various theories about the cause and Pathogenesis of disease were introduced.
1990's: Treatments begin to appear.
In 2010: new version of Poser criteria and McDonald criteria.
In 2013: Revision of the "Phenotypes for the disease course" that included consideration of CIS as one of the phenotype of MS.

Classification[edit | edit source]

Disease is mainly categorized into 4 groups:
- Relapsing–remitting MS: It is the most common form, affecting about 85% of MS patients, marked by flare up and remission of symptoms.
- Secondary progressive MS: This disease course continue to worsen irrespective of remission of symptoms.
- Primary progressive MS: 10% of MS patients. Symptoms keep on worsening right from the beginning.
- Progressive-relapsing MS: A rare form, affecting less than 5% of patients.This disease course mainly involves the progressive severity with flare ups in between without any of remission episodes.

Pathophysiology[edit | edit source]

MS is characterized by demyelination of neurons, inflammation and formation of lesions called "plaques" in CNS.

The disease is thought to develop from the interaction of environmental factors and individuals genetics.

The another name for multiple sclerosis is the "Scars formed in CNS". The lesions affects the white matter in brain, spinal cord, optic nerve and the white matter close to lateral ventricles. 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. PNS is rarely involved in disease pathophysiology.

Myelin sheath ( play major role in carrying action potentials by neurons) is mainly composed of Fatty layer that is formed by oligodendrocytes. As the disease progress there is complete loss of myelin along with the destruction of neurons, resulting in non conduction of the action potential. remyelination shown little bit effectiveness in early phase of disease but unable to completely build the myelin sheath. Repeated attacks leads to remyelination until a scar like plaque is formed the site of injury on the axons. Marked increase in no of astrocytes also play minor role in the pathophysiology of M.S.

Along with demyelination Inflamation also plays important role. This is mediated by T cells. T cells after entering crossing Blood- Brain barrier recognize the myelin as a foreign body and attack it, justifying their name as autoreactive lymphocytes.

Clinical Features[edit | edit source]

Differentiating [disease name] from other Diseases[edit | edit source]

[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:

[Differential dx1]
[Differential dx2]
[Differential dx3]

Epidemiology and Demographics[edit | edit source]

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[edit | edit source]

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[edit | edit source]

[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[edit | edit source]

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[edit | edit source]

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[edit | edit source]

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[edit | edit source]

Diagnostic Criteria[edit | edit source]

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[edit | edit source]

[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[edit | edit source]

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[edit | edit source]

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[edit | edit source]

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[edit | edit source]

[Disease name] may also be diagnosed using [diagnostic study name].
Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].

Treatment[edit | edit source]

Medical Therapy[edit | edit source]

There is no treatment for [disease name]; the mainstay of therapy is supportive care.

The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
[Medical therapy 1] acts by [mechanism of action 1].
Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].

Surgery[edit | edit source]

Surgery is the mainstay of therapy for [disease name].
[Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
[Surgical procedure] can only be performed for patients with [disease stage] [disease name].

Prevention[edit | edit source]

There are no primary preventive measures available for [disease name].

Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].

Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].

References[edit | edit source]

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Introduction

@@ Line 29: / Line 29: @@
 <br />
 == Pathophysiology[edit | edit source] ==
+[[File:Multiple sclerosis.png|thumb|382.986x382.986px]]
-==== MS is characterized by demyelination of neurons, inflammation and formation of lesions called "plaques" in CNS. ====
+==== MS is characterized by demyelination of neurons, inflammation and formation of lesions called "[[Plaque|plaques]]" in CNS. ====
 ==== The disease is thought to develop from the interaction of environmental factors and individuals genetics. ====
@@ Line 36: / Line 37: @@
 * The another name for ''multiple sclerosis'' is the "Scars formed in CNS". The lesions affects the white matter in brain, spinal cord, optic nerve and the white matter close to lateral ventricles. 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. PNS is rarely involved in disease pathophysiology.
-* Myelin sheath ( play major role in carrying action potentials by neurons) is mainly composed of Fatty layer that is formed by oligodendrocytes. As the disease progress there is complete loss of myelin alon with the destruction of neurons, resulting in non conduction of the action potential. remyelination shown little bit effectiveness in early phase of disease but unable to completely build the myelin sheath. Repeated attacks leads to remyelination until a scar like plaque is formed the site of injury on the axons. Marked increase in no of astrocytes also play minor role in the pathophysiology of M.S
+* Myelin sheath ( play major role in carrying action potentials by neurons) is mainly composed of Fatty layer that is formed by oligodendrocytes. As the disease progress there is complete loss of myelin along with the destruction of neurons, resulting in non conduction of the action potential. remyelination shown little bit effectiveness in early phase of disease but unable to completely build the myelin sheath. Repeated attacks leads to remyelination until a scar like plaque is formed the site of injury on the axons. Marked increase in no of astrocytes also play minor role in the pathophysiology of M.S.
-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. T cells gain entry into the brain via disruptions in the blood–brain barrier. The T cells recognize myelin as foreign and attack it, explaining why these cells are also called "autoreactive lymphocytes".
+*Along with demyelination Inflamation also plays important role. This is mediated by T cells. T cells after entering crossing Blood- Brain barrier recognize the myelin as a foreign body and attack it, justifying their name as autoreactive lymphocytes.
-The attack of myelin starts inflammatory processes, which triggers 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. Inflammation can potentially reduce transmission of information between neurons in at least three ways. The soluble factors released might stop neurotransmission by intact neurons. These factors could lead to or enhance the loss of myelin, or they may cause the axon to break down completely.
-=== Blood–brain barrier ===
-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. Gadolinium cannot cross a normal BBB and, therefore, gadolinium-enhanced MRI is used to show BBB breakdowns.
+<br />
 == Clinical Features[edit | edit source] ==