Periventricular lesion

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). 

Figure 18.1. MRI signal abnormalities in the brain and spinal cord in a 55-year-old woman with multiple sclerosis. (A) FLAIR (Fluid attenuated inversion recovery) image of axial brain image at the level of the lateral ventricles. Arrows point to hyperintense periventricular lesions demonstrating a characteristics MS demyelination pattern (B) T2W image of sagittal view of the spinal cord of the same individual, demonstrating focal bright signal (arrow) representing demyelination in the cervical spinal cord.

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],... 

WM lesions are rated separately in four WM areas periventricular, deep, watershed, and subcortical WM. By definition, periventricular WM foci have to be in contact with the ventricular wall, deep WM foci separated from the ventricles by a strip of normal-appearing WM and located outside watershed regions. Watershed regions are the areas located between the territories of two of the main cerebral arteries, like middle cerebral artery and anterior cerebral artery or middle cerebral artery and posterior cerebral artery. The subcortical... 

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... 

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-... 

Fig. 13.5. T2 -weighted gradient echo images in a patient with biopsy proven cerebral amyloid angiopathy (CAA). Extensive low signal abnormality is noted on the brain surfaces and in the parenchyma indicating the previous hemorrhages. Periventricular high intensity lesions, a common finding in CAA is also noted...

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. 

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. 

The incidence and type of cerebral lesions were studied by ultrasound in 159 preterm infants 76 fetuses were exposed to indometacin used as a tocolytic agent in the other 83 pregnancies, tocolysis was either not started or limited to fenoterol. The incidence of periventricular leu-komalacia was increased in infants exposed to any tocolytic agent cystic lesions occurred more often in those exposed to indometacin (50). 

Crowley WR, Terry LC. Biochemical mapping of somatostatinergic systems in rat brain effects of periventricular hypothalamic and medial basal amygdaloid lesions on somatostatin-like immunoreac-tivity in discrete brain nuclei. Brain Res 1980 200 283-291. 

Metachromatic leukodystrophy is another lysosomal storage disorder caused by a deficiency of arylsulfatase A which leads to the accumulation of 3-0-sulfogalactosylceramide. The defect results in severe demyelination. The disease often takes a presentation of an under- and mis-diagnosed psychiatric affection long before neurological symptoms appear and MRI displays the anatomical lesions. MRI reveals a diffuse demyelination, bilateral and often symmetrical, initially limited to the periventricular areas. 

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

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). 

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