Demyelinating diseases

Abstract

A diagnosis of demyelination carries important therapeutic and prognostic implications. In most cases the diagnosis is made clinically, and involvement of the histopathologist is largely confined to postmortem confirmation and clinicopathological correlation. However, every now and then, accurate diagnosis of the presence or cause of demyelination before death hinges on the histopathological assessment. Recognition of demyelination depends on an awareness of this as a diagnostic possibility, and on the use of appropriate tinctorial and immunohistochemical stains to identify myelin, axons and inflammatory cells. In biopsy specimens, the critical distinction is usually from ischaemic or neoplastic disease, and the types of demyelinating disease most likely to be encountered are multiple sclerosis, acute-disseminated encephalomyelitis, progressive multifocal leucoencephalopathy and extrapontine myelinolysis. Interpretation of the pathology has to be made in the context of the clinical, radiological and biochemical findings. Freezing of a small amount of fresh tissue allows for later virological studies, and electron microscopy is occasionally helpful for demonstration of viral particles.

Skin-derived neural precursors competitively generate functional myelin in adult demyelinated mice

“…Adult white-matter tracts in the CNS are highly vulnerable to various types of damages from hypoxic-ischemic, metabolic, or traumatic forms of demyelination to inflammatory and immunemediated insults (20). Remyelination of adult axons in various neuropathological conditions is known to rescue the lost function and protect neurons from subsequent axonal degeneration.…”

Tumefactive acute disseminated encephalomyelitis complicating human swine influenza (H1N1)

“…5,6 It is one of the many syndromes that can develop after vaccination or a microbial infection, and has a 2-to 30-day latency period. 3,7 The typical MRI appearance is of demyelinating lesions preferentially affecting white matter tracts in a periventricular distribution. Diagnostic difficulty occurs whenever these demyelinating lesions appear to be solitary, large, or tumefactive.…”

Iatrogenic Central Pontine Myelinolysis: A Case Report

“…The mechanism of myelinolysis is characterized by intramyelinitic splitting, vacuolization, and rupture of myelin sheaths presumably because of osmotic effects. Macrophages with cytoplasm filled by myelin debris appear after several days [9]. Pathologically, (ODS) is characterized by sparing of axons and neurons, sparse or absent infiltration by lymphocytes, and degeneration or loss of oligodendrocytes [2,10].…”