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White periventricular

MS lesions or plaques can be identified grossly at autopsy (Fig. 38-1) and are sharply demarcated from the surrounding tissue. Plaques occur throughout the white matter, but areas of predilection such as the periventricular white matter are well known. Microscopic examination characteristically shows loss of myelin with preservation of axons (primary demyelination). However, although the most prominent pathology in MS is demye-lination, there are recent indications also for axonal and cortical pathology. Now techniques of confocal microscopy and immunocytochemistry have clearly demonstrated that transected axons are common in MS lesions [9],... [Pg.642]

Fig. 9.6a-f. Periventricular white matter changes (FLAIR images), a Small caps around the frontal horns of lateral ventricles, b Large caps, c Extending caps, d Thin lining along the bodies of the lateral ventricles, e Smooth halo, f Irregular halo... [Pg.154]

Fig. 9.7a-f. White matter changes in regions other than the periventricular area (FLAIR images), a Multiple small focal lesions, b Multiple large focal lesions, c Multiple focal confluent lesions, d Diffusely confluent lesions irregular in shape. e,f Extensive... [Pg.155]

Hyperintensities in the Regions Other Than Periventricular White Matter (HI)... [Pg.155]

In normal elderly controls, non-specific periventricular and subcortical T2-hyperintense lesions of the brain are a common finding and are reported in 27%-92% of the elderly population (Breteler et al. 1994 de Leeuw et al. 2001). In asymptomatic individuals over 50 years of age, changes in the white matter on T2-weighted, proton density and FLAIR images are frequently found, varying from a few scattered lesions in the centrum semiovale or peri-... [Pg.200]

It should be noted that the abnormalities on brain imaging described above are not exclusive to or diagnostic of vascular cognitive impairment deep white matter lesions and periventricular lesions have been shown in 50% and 90%, respectively, of patients with Alzheimer s disease and are also often present in patients with Lewy body disease (Barber et al. 1999). [Pg.374]

Smith CD, Snowdon DA, Wang H et al. (2000). White matter volumes and periventricular white matter hyperintensities in aging and dementia. Neurology 54 838-842 Stebbins GT, Nyenhuis DL, Wang C et al. (2008). Gray matter atrophy in patients with ischemic stroke with cognitive impairment. Stroke 39 785-793... [Pg.379]

Interstitial edema is seen in the periventricular regions in patients with hydrocephalus (Fig. 9). The widened extracellular space is the site of transependymal flow of CSF. The movement of ISF into the frontal white matter leads to difficulty walking and incontinence in the syndrome of normal pressure hydrocephalus. [Pg.152]

On MRI multiple periventricular and discrete cerebral hemisphere white-matter lesions (plaques measuring at least 3 mm in diameter) are seen as bright areas. The 10-year ONTT results showed that an MRI obtained at baseline (new optic neuritis attack) can predict the risk of a patient developing MS. Patients with at least one brain lesion on MRI at the time of the optic neuritis episode have a 56% risk of developing MS within 10 years, whereas those with no brain lesions have only a 22% risk. There appears to be no increased risk of developing MS with a higher number of baseline lesions. [Pg.370]

Figure 3.4. Cellular components of the central nervous system. (A) Neurons impregnated with Golgi silver satin, (C) Calbindin immunoreactive intemeurons in the neocortex, (G) astrocytes immunoreactive with an antibody against GFAP, (H) peri-vascular astrocytes components of the BBB, (I) oligodendrocytes and white matter tracts stained with luxol fast blue, (F) ependimal cells around the periventricular zone. Figure 3.4. Cellular components of the central nervous system. (A) Neurons impregnated with Golgi silver satin, (C) Calbindin immunoreactive intemeurons in the neocortex, (G) astrocytes immunoreactive with an antibody against GFAP, (H) peri-vascular astrocytes components of the BBB, (I) oligodendrocytes and white matter tracts stained with luxol fast blue, (F) ependimal cells around the periventricular zone.
A 40-year-old man, who had taken stavudine 30 mg bd, lamivudine 150 mg bd, and indinavir 800 mg qds, developed an occipital headache, nausea, and vomiting. His blood pressure was 220/140 mmHg and he had bilateral papilledema. His blood pressure was controlled and his symptoms disappeared. An MRI scan of the brain showed lesions in the periventricular white matter the nuclei semiovale and occipital asta were most severely affected. Indinavir was withdrawn and replaced by nel-finavir his blood pressure returned to normal and the MRI white matter lesions disappeared. [Pg.1735]

Corpus callosum, periventricular white matter, and hippocampus... [Pg.270]

Rezaie, P. Dean, A. (2002). Periventricular leukomalacia, inflammation and white matter lesions within the developing nervous system. Neuropathol. 22 106—132. [Pg.363]

In the tissue of the CNS, under normal conditions, fluid flows within the gray matter are negligible flows can be significant within white matter. For example, flows of 10 fj,m/ min were measured in white matter, but not gray matter, in the periventricular tissue of cats [17]. This extracellular fluid (ECF) flow, which moves towards the ventricular surface, is presumably the result of fluid leakage from the capillaries that moves predominantly through white matter tracts. [Pg.171]

Fig. 7.10 Periventricular nonspecific white matter changes vs. acute infarction. Sixty-one-year-old female with hypertension. FLAIR-weighted images demonstrate multiple hypeiintense white matter foci of unclear chronicity. Diffusion-weighted images demonstrate that lesions in the left external capsule and left temporal subcortical white matter (white arrvws) are acute... Fig. 7.10 Periventricular nonspecific white matter changes vs. acute infarction. Sixty-one-year-old female with hypertension. FLAIR-weighted images demonstrate multiple hypeiintense white matter foci of unclear chronicity. Diffusion-weighted images demonstrate that lesions in the left external capsule and left temporal subcortical white matter (white arrvws) are acute...
Structural manifestations of phenylalanine neurotoxicity include dysmyelination in the white matter of the brain, revealed with MRl as intense lesions and cortico-subcortical atrophy on T2-weighted images with specifically high-signal intensity in periventricular white matter. White matter abnormaUties may be explained by cytotoxic edema and dysmyelination changes with increase in free water trapped in myeUn sheaths [44]. The size and distribution of WMA vary between patients with locahzation in the white matter of temporal and occipital lobes as the most common areas affected [42] (Figs. 9.5 and 9.6). [Pg.96]


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