Differentiation of multiple sclerosis plaques, subacute cerebral ischaemic infarcts, focal vasogenic oedema and lesions of subcortical arteriosclerotic encephalopathy using magnetisation transfer measurements

Abstract

Although multiple sclerosis (MS) plaques, subacute cerebral ischaemic infarcts, focal vasogenic brain oedema, and subcortical arteriosclerotic encephalopathy (SAE) often have typical radiological patterns, they are sometimes difficult to distinguish from each other. Our aim was to determine whether they can be differentiated by magnetisation transfer (MT) measurements. We measured MT ratios (MTR) in ten patients with plaques of MS, 11 with subacute ischaemic infarcts, 12 with focal vasogenic oedema, and ten with lesions of SAE and compared the mean MTRs statistically. The MTR of normal white matter was 47.3%; the lowest MTR was found in plaques of MS (mean 26.4%). With the exception of vasogenic oedema and subacute cerebral ischaemic infarcts the mean MTRs were significantly different between all groups. MT measurements can provide additional information for the differentiation of these conditions, but we could not distinguish vasogenic oedema from subacute cerebral ischaemic infarcts.

Brain Edema XIII

“…Smoking cocaine provides the fastest route of entry into the cerebral circulation (6 to 8 seconds) and the intravenous route takes twice as much time; nasal in-su¿ation produces peak levels in 30 to 60 minutes [15,49].…”

“…Brains were frozen in situ using liquid nitrogen 12 hours following onset of local brain cooling (16 hours following hematoma induction) as previously described [39][40][41]49]. Following decapitation, heads were stored at À70 C until sectioned.…”

“…Inflammation and proinflammatory mediators play an essential role in edema development in a variety of neuropathological conditions such as brain trauma, ischemic or hypoxic brain injury, central nervous system (CNS) infection (HIV infection, tuberculosis, or bacterial meningitis), acute attacks of multiple sclerosis, and brain tumors [12,19,21,29,45,49,64]. Brain edema in all of these conditions is mostly classified as vasogenic with extracellular water accumulation resulting from blood-brain barrier (BBB) disruption and massive infiltration of leukocytes.…”

Cerebral MRI lesions and anti-tumor necrosis factor-alpha therapy

“…So far, we understand the occurrence of cerebral lesions as a potential side-effect of anti-TNF-α treatment with adalimumab. The existence of microangiopathic cerebrovascular disease due to metabolic syndrome covering arterial hypertension, diabetes, hyperlipoproteinemia and adipositas should be discussed as well [12,24].…”

A magnetization transfer study of mild and advanced Parkinson’s disease

“…A decrease in MT ratio (MTR) values can result from an increase in the mobile proton pool, occurring as a result of inflammation and oedema, or a decrease in the semi‐solid proton pool, associated with damage to myelin and other cellular components [9]. In fact, abnormal MTR have been measured in a variety of white matter diseases with no visible abnormality on T2‐weighted images [10].…”