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. 2012 Nov 15;322(1-2):82–86. doi: 10.1016/j.jns.2012.06.016

Table 1.

The histopathological correlates of different types of white matter lesions.

Study Sample Main findings
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.