Fazekas 1991 [2]
|
2 subjects without and 4 with neurologic disease |
Punctate lesions relate to perivascular damage with lipohyalinosis, atrophic neuropil and rarefaction of myelinated fibers, 2 patients had cortical heterotopia. |
Chimowitz 1992 [3]
|
7 subjects with neurologic disease |
Periventricular rims relate to ependymal loss and subependymal gliosis. |
Periventricular caps relate to myelin pallor. |
Punctate DWMH are widened perivascular spaces. |
Fazekas 1993 [4]
|
11 subjects partly with neurologic disease |
Periventricular rims: Smooth myelin pallor, loose fibers, tortuous venules, no arteriolosclerosis, discontinuity of ependym with mild-moderate gliosis. |
Irregular periventricular lesions have varying fiber loss, gliosis and cavitation with lipohyalinosis |
Deep white matter lesions: Punctate: no ischemic changes; demyelination, atrophic neuropil around lipohyalionotic arterioles and perivenous damage. |
Early confluent: perivascular rarefaction of myelin, mild to moderate fiber loss, varying gliosis. |
Confluent: irregular areas of incomplete parenchymal destruction with focal transitions to true infarcts. |
Munoz 1993 [5]
|
2 Alzheimer cases and 13 controls |
Punctate relates to widened perivascular spaces. |
Extensive white matter lesions are broad areas of loss of myelin, axons, and gliosis. No infarction or vascular wall changes. |
Fernando 2006 [6]
|
99 demented subjects and 108 controls |
Wall thickening, dilated perivascular spaces in WMH, ependym denudation in PVH. |