eMedicine Specialties > Neurology > Inflammatory and Demyelinating Diseases

Multiple Sclerosis: Multimedia

Author: Fernando Dangond, MD, Senior Director of Medical Affairs, Neurology, EMD Serono, Inc
Contributor Information and Disclosures

Updated: Sep 11, 2009

Multimedia

The mechanism of demyelination in multiple sclero...Media file 1: The mechanism of demyelination in multiple sclerosis may be activation of myelin-reactive T cells in the periphery, which then express adhesion molecules, allowing their entry through the blood-brain barrier (BBB). T cells are activated following antigen presentation by antigen-presenting cells such as macrophages and microglia, or B cells. Perivascular T cells can secrete proinflammatory cytokines, including interferon gamma and tumor necrosis factor alpha. Antibodies against myelin also may be generated in the periphery or intrathecally.

Ongoing inflammation leads to epitope spread and recruitment of other inflammatory cells (ie, bystander activation). The T cell receptor recognizes antigen in the context of human leukocyte antigen molecule presentation and also requires a second event (ie, co-stimulatory signal via the B7-CD28 pathway, not shown) for T cell activation to occur. Activated microglia may release free radicals, nitric oxide, and proteases that may contribute to tissue damage.
The mechanism of demyelination in multiple sclero...

The mechanism of demyelination in multiple sclerosis may be activation of myelin-reactive T cells in the periphery, which then express adhesion molecules, allowing their entry through the blood-brain barrier (BBB). T cells are activated following antigen presentation by antigen-presenting cells such as macrophages and microglia, or B cells. Perivascular T cells can secrete proinflammatory cytokines, including interferon gamma and tumor necrosis factor alpha. Antibodies against myelin also may be generated in the periphery or intrathecally.

Ongoing inflammation leads to epitope spread and recruitment of other inflammatory cells (ie, bystander activation). The T cell receptor recognizes antigen in the context of human leukocyte antigen molecule presentation and also requires a second event (ie, co-stimulatory signal via the B7-CD28 pathway, not shown) for T cell activation to occur. Activated microglia may release free radicals, nitric oxide, and proteases that may contribute to tissue damage.

MRI of the head of a 35-year-old man with relapsi...Media file 2: MRI of the head of a 35-year-old man with relapsing remitting multiple sclerosis. MRI reveals multiple lesions with high T2 signal intensity and one large white matter lesion. These demyelinating lesions may sometimes mimic brain tumors because of the associated edema and inflammation.
MRI of the head of a 35-year-old man with relapsi...

MRI of the head of a 35-year-old man with relapsing remitting multiple sclerosis. MRI reveals multiple lesions with high T2 signal intensity and one large white matter lesion. These demyelinating lesions may sometimes mimic brain tumors because of the associated edema and inflammation.

MRI of the head of a 35-year-old man with relapsi...Media file 3: MRI of the head of a 35-year-old man with relapsing remitting multiple sclerosis. This MRI, performed 3 months after the one shown in Media file 2, shows a dramatic decrease in the size of lesions.
MRI of the head of a 35-year-old man with relapsi...

MRI of the head of a 35-year-old man with relapsing remitting multiple sclerosis. This MRI, performed 3 months after the one shown in Media file 2, shows a dramatic decrease in the size of lesions.

Inflammation in multiple sclerosis. Hematoxylin a...Media file 4: Inflammation in multiple sclerosis. Hematoxylin and eosin (H&E) stain shows perivascular infiltration of inflammatory cells. These infiltrates are composed of activated T cells, B cells, and macrophages.
Inflammation in multiple sclerosis. Hematoxylin a...

Inflammation in multiple sclerosis. Hematoxylin and eosin (H&E) stain shows perivascular infiltration of inflammatory cells. These infiltrates are composed of activated T cells, B cells, and macrophages.

Demyelination in multiple sclerosis. Luxol fast b...Media file 5: Demyelination in multiple sclerosis. Luxol fast blue (LFB)/periodic acid-Schiff (PAS) stain confers an intense blue to myelin. Loss of myelin is demonstrated in this chronic plaque. Note that absence of inflammation may be demonstrated at the edge of chronic lesions.
Demyelination in multiple sclerosis. Luxol fast b...

Demyelination in multiple sclerosis. Luxol fast blue (LFB)/periodic acid-Schiff (PAS) stain confers an intense blue to myelin. Loss of myelin is demonstrated in this chronic plaque. Note that absence of inflammation may be demonstrated at the edge of chronic lesions.

More on Multiple Sclerosis

Overview: Multiple Sclerosis
Differential Diagnoses & Workup: Multiple Sclerosis
Treatment & Medication: Multiple Sclerosis
Follow-up: Multiple Sclerosis
Multimedia: Multiple Sclerosis
References

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Further Reading

Keywords

multiple sclerosis, MS, multiple sclerosis treatment, multiple sclerosis symptoms, MS symptoms, MS treatment, multiple sclerosis diagnosis, myelin, inflammatory disease of central nervous system, demyelinating disease, sclerosis in plaques, CNS disease, disseminated sclerosis, focal sclerosis, insular sclerosis, elevated immunoglobulin G, interleukin-12, IL-12, B7-1, relapsing remitting MS, RRMS

secondary progressive MS, SPMS, primary progressive MS, PPMS, relapsing progressive MS, RPMS, brain atrophy, spinal cord atrophy, short-term memory problems, difficulty executing sequential tasks, visuospatial disturbances, benign MS, cognitive dysfunction, mental slowing, cognitive slowing, lack of sleep, optic nerve dysfunction, Uhthoff phenomenon, Marburg variant of MS

necrotizing myelopathy, neuromyelitis optica, Devic disease, acute disseminated encephalomyelitis, ADEM, Schilder disease, Baló concentric sclerosis, ataxia, hemiparesis, paraparesis, depression, bipolar disorder, dementia, optic neuritis, orbital pain, patchy loss of vision, cecocentral scotoma, afferent pupillary defect

facial palsies, trigeminal neuralgia, facial myokymia, nystagmus, internuclear ophthalmoplegia, painful limb syndromes, central vertigo, diplopia, dysarthria, pseudobulbar affect, social disinhibition, chronic inflammatory demyelinating polyradiculopathy, CIDP, conversion reactions, la belle indifference, urinary retention

urinary incontinence, sexual dysfunction, Kurtzke Expanded Disability Status Scale, immune dysfunction, HLA-DR2 allele, pro-demyelinative tumor necrosis factor alpha molecule, pro-inflammatory interferon gamma, proinflammatory interferon gamma

Contributor Information and Disclosures

Author

Fernando Dangond, MD, Senior Director of Medical Affairs, Neurology, EMD Serono, Inc
Fernando Dangond, MD is a member of the following medical societies: American Academy of Neurology and American Medical Association
Disclosure: EMD Serono, Inc. Salary Employment

Medical Editor

William J Nowack, MD, Associate Professor, Epilepsy Center, Department of Neurology, University of Kansas Medical Center
William J Nowack, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Electroencephalographic Association, American Medical Informatics Association, and Biomedical Engineering Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis Society
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

B Mark Keegan, MD, FRCPC, Assistant Professor of Neurology, College of Medicine, Mayo Clinic; Master's Faculty, Mayo Graduate School; Consultant, Department of Neurology, Mayo Clinic, Rochester
B Mark Keegan, MD, FRCPC is a member of the following medical societies: American Academy of Neurology, American Medical Association, and Minnesota Medical Association
Disclosure: Nothing to disclose.

 
 
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