G35 - G37Demyelinating diseases of the central nervous system G35Multiple Sclerosis G35._0Relapsing remiting MS G35._1Primary progressive MS G35._2Secondary proressive MS G35._8Other symptomatic form of MS G36Other acute disseminated demyelination G36.0Neuromyelitis optica(Devic)Demyelination in optic neuritis G36.1Acute and subacute haemorrhagic leukoencephalitis(Hurst G36.8Other specified acute disseminated demyelination G36.9Acute disseminated demyelination,unspecified G37Other demyelinating diseases of central nervous system G37.0Diffuse sclerosisPeriaxial encephalitis,Schilder's disease G37.1Central demyelination of corpus callosum G37.2Central pontine myelinolysis G37.3Acute transverse myelitis in demyelinating disease of cAcute transverse myelitis NOS G37.4Subacute necrotizing myelitis G37.5Concentric sclerosis(Balo) G37.8Other specified demyelinating diseases of central nervo G37.9Demyelinating disease of central nervous system,unspeci
Caps over the anterior horns of the lateral ventricles or diffuse halo surrounding the lateral ventricle Periventricular T2 and PD hyperintensites of variable thickness often become evident after 40y and seen in 40% of elderly. They have no impact on cognitive function but indicates underlying disorders of fluid dynamics. They are more prominent in Alzheimer disease. The pathologic correlates of the periventricular caps and bands is a spongiform zone separated from the ventricular lumen by a rim of subependymal gliosis. There is demyelination in the spongiform zone. Discontinuities within the adjacent ependymal lining are common. Theses changes are likely the result of chronically elevated quantities of interstitial periventricular fluid. There is no evidence for microscopic infarction within these lesions and thus vascular disease presumably does not play a role in the pathophysiology. Because the brain has no lymphatics, extracellular fluid circulates through the ependyma and into ventricles (extrachoroidal CSF production). Processes that increases the extracellular fluid volume (such as ischemia or infarction) or impaired subependymal fluid resorption (such as increased intracranial pressure associated with hydrocephalus) may result in a backup of fluid in the periventricular space. The tip of the anterior horns have a particularly rich venous plexus, and large veins pass along the ventricular walls making these regions especially vulnerable to venous transudation (as may occur when the central venous pressure is increased in congestive heart failure). Additionally, the discontinuities in the ependymal lining may promote leakage of CSF into the periventricular tissue. The demyelination, gliosis and, to some extent the increased extracellular fluid results in the T2 hyperintensities surrounding the lateral ventricles. If the periventricular hyperintensities are irregular or extend into the central white matter, a pathologic vascular cause is much more likely. Diffuse periventricular hyperintensities may occur in multiple sclerosis, lymphoma, CSF seeding of intracranial malignant disease, or periventricular infections such as CMV, HIV, or Lyme neuroborreliosis. Contrast enhancement occurs with most of the malignant, infectious, and inflammatory causes, making the differentiation easy.
Punctate high-signal T2 and PD lesions within the subcortical and periventricular white matter. These hyperintensities are present in 30-80% of people over 40years old and increase in frequency and size with increasing age, chronic, hypertension, other vascular risk factors, past stroke or transient ischemic attack. Although the frequency of scattered punctate UBOs is higher in older age They may be the result of an inadequate supply of nutrients necessary to sustain and replace normally catabolized myelin, with the loss of myelin leading to reactive gliosis. Atrophic periventricular demyelination appears as high signal on T2 and PD images. Some, if not most, UBOs are part of continuum of vascular disease, which is the most extreme form present in multi-infarct dementia. As the bulk of white matter diseases increases, decreased attention and speed of mental impairment develops.
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