Progressive multifocal leukoencephalopathy pathophysiology

Jump to navigation Jump to search


Progressive multifocal leukoencephalopathy Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Progressive multifocal leukoencephalopathy from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Progressive multifocal leukoencephalopathy pathophysiology On the Web

Most recent articles

cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Progressive multifocal leukoencephalopathy pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Progressive multifocal leukoencephalopathy pathophysiology

CDC on Progressive multifocal leukoencephalopathy pathophysiology

Progressive multifocal leukoencephalopathy pathophysiology in the news

Blogs on Progressive multifocal leukoencephalopathy pathophysiology

Progressive multifocal leukoencephalopathy

Risk calculators and risk factors for Progressive multifocal leukoencephalopathy pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

PML is a demyelinating disease, in which the myelin sheath covering the axons of nerve cells is gradually destroyed, impairing the transmission of nerve impulses. It affects the white matter, which is mostly composed of axons from the outermost parts of the brain (cortex). Symptoms include weakness or paralysis, vision loss, impaired speech, and cognitive deterioration. PML is similar to another demyelinating disease, multiple sclerosis, but since it destroys the cells that produce myelin (unlike MS, in which myelin itself is attacked but can be replaced), it progresses much more quickly. Most patients die within four months of onset. PML destroys oligodendrocytes and produces intranuclear inclusions.

References


Template:WH Template:WS