Dement Neurocogn Disord.  2012 Sep;11(3):79-86. 10.12779/dnd.2012.11.3.79.

Micro-vascular Diseases of White Matter

Affiliations
  • 1Department of Neurology, The Catholic University of Korea, College of Medicine, Seoul, Korea. neuroman@catholic.ac.kr

Abstract

White matter hyperintensity (WMH) is commonly observed on the brain MRI of elderly subjects. It has been considered as an important biomarker for the micro-vascular damages of white matter of the brain. Aging, hypertension, diabetes mellitus, and hyperhomocysteinemia have been associated with WMH development. WMH is an important risk factor for the vascular dementia (VD), however it also considered as one of risk factors for conversion of mild cognitive impairment to dementia and progression of Alzheimer's disease (AD). WMH has impact on gait, bladder control, and fine motor coordination. It also has negative effects on memory retrieval, mental flexibility, mental processing speed, and executive function by disconnecting nerve fibers that convey signals for normal cognition. Control of vascular risk factors can delay progression of WMH and this may be beneficial for VD as well as AD with ischemic changes, especially in the early state of diseases. In this paper, we will review clinical significance of WMH and three important diseases, subcortical vascular dementia, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, and cerebral amyloid angiopathy that associated with cerebral micro-vascular damages.

Keyword

White matter hyperintensity; Vascular dementia; Micro-vascular damage; Alzheimer's disease

MeSH Terms

Aged
Aging
Alzheimer Disease
Brain
CADASIL
Cerebral Amyloid Angiopathy
Cognition
Dementia
Dementia, Vascular
Diabetes Mellitus
Executive Function
Gait
Humans
Hyperhomocysteinemia
Hypertension
Memory
Mild Cognitive Impairment
Nerve Fibers
Pliability
Risk Factors
Urinary Bladder
Cerebral Amyloid Angiopathy

Figure

  • Fig. 1 (A) Blood supply of cerebral white matter (WM) by (a) medullary artery (b) lenticulostriate artery and (c) choroidal artery. Dark circle represents a pneumbra zone of three arteries. (B) Area (a) is the most frequently affected WM regions of the subcortical vascular dementia patients.

  • Fig. 2 Microvascular changes of the brain in patients with subcortical vascular ischemic dementia. Toruous and elongated (A) and stenotic (B) changes of arterioles cause complete or incomplete infarcts in the white matter with two different mechanisms of ischemia.

  • Fig. 3 Visual rating scale of the white matter hyperintensities (WMH). Severity of WMH can be measured in the (a) periventricular area around the fontal and occipital horns of lateral ventricle (b) periventicular area long the lateral ventricle (c) deep white matter area.

  • Fig. 4 MRI and histopathologic features of the 72-year-old female with dementia and recurrent lobar hemorrhages. FLAIR axial MRI shows periventricular white matter hyperintensity and cortical lobar hemorrhage in the right frontal area (A). On gradient echo MRI, there are numerous microbleedings mostly on the cortex (B). Thickened homogeneous pink material is noted in the H&E stain (C). Apple-green birefringence of amyloid deposits is proved under the polarized light on Congo red stain (D).


Reference

1. de Leeuw FE, de Groot JC, Achten E, Oudkerk M, Ramos LM, Heijboer R, et al. Prevalence of cerebral white matter lesions in elderly people: a population based magnetic resonance imaging study. The Rotterdam Scan Study. J Neurol Neurosurg Psychiatry. 2001. 70:9–14.
Article
2. Jeerakathil T, Wolf PA, Beiser A, Massaro J, Seshadri S, D'Agostino RB, et al. Stroke risk profile predicts white matter hyperintensity volume: the Framingham Study. Stroke. 2004. 35:1857–1861.
Article
3. Schmahmann JD, Smith EE, Eichler FS, Filley CM. Cerebral white matter: neuroanatomy, clinical neurology, and neurobehavioral correlates. Ann N Y Acad Sci. 2008. 1142:266–309.
4. Schmidt R, Fazekas F, Kapeller P, Schmidt H, Hartung HP. MRI white matter hyperintensities: three-year follow-up of the Austrian Stroke Prevention Study. Neurology. 1999. 53:132–139.
Article
5. Fernando MS, Simpson JE, Matthews F, Brayne C, Lewis CE, Barber R, et al. MRC Cognitive Function and Ageing Neuropathology Study Group. White matter lesions in an unselected cohort of the elderly: molecular pathology suggests origin from chronic hypoperfusion injury. Stroke. 2006. 37:1391–1398.
Article
6. Roman GC. Brain hypoperfusion: a critical factor in vascular dementia. Neurol Res. 2004. 26:454–458.
Article
7. Kapeller P, Barber R, Vermeulen RJ, Ader H, Scheltens P, Freidl W, et al. Visual rating of age-related white matter changes on magnetic resonance imaging: scale comparison, interrater agreement, and correlations with quantitative measurements. Stroke. 2003. 34:441–445.
Article
8. Erkinjuntti T. Subcortical ischemic vascular disease and dementia. Int Psychogeriatr. 2003. 15:Suppl 1. 23–26.
Article
9. Fazekas F, Chawluk JB, Alavi A, Hurtig HI, Zimmerman RA. MR signal abnormalities at 1.5 T in Alzheimer's dementia and normal aging. AJR Am J Roentgenol. 1987. 149:351–356.
Article
10. Scheltens P, Barkhof F, Leys D, Pruvo JP, Nauta JJ, Vermersch P, et al. A semiquantative rating scale for the assessment of signal hyperintensities on magnetic resonance imaging. J Neurol Sci. 1993. 114:7–12.
Article
11. Pantoni L, Poggesi A, Inzitari D. Cognitive decline and dementia related to cerebrovascular diseases: some evidence and concepts. Cerebrovasc Dis. 2009. 27:Suppl 1. 191–196.
Article
12. Prasad K, Wiryasaputra L, Ng A, Kandiah N. White matter disease independently predicts progression from mild cognitive impairment to Alzheimer's disease in a clinic cohort. Dement Geriatr Cogn Disord. 2011. 31(6):431–434.
Article
13. Longstreth WT Jr, Arnold AM, Beauchamp NJ Jr, Manolio TA, Lefkowitz D, Jungreis C, et al. Incidence, manifestations, and predictors of worsening white matter on serial cranial magnetic resonance imaging in the elderly: the Cardiovascular Health Study. Stroke. 2005. 36:56–61.
Article
14. van den Heuvel DM, ten Dam VH, de Craen AJ, Admiraal-Behloul F, Olofsen H, Bollen EL, et al. Increase in periventricular white matter hyperintensities parallels decline in mental processing speed in a non-demented elderly population. J Neurol Neurosurg Psychiatry. 2006. 77:149–153.
Article
15. Richard E, Gouw AA, Scheltens P, van Gool WA. Vascular care in patients with Alzheimer disease with cerebrovascular lesions slows progression of white matter lesions on MRI: the evaluation of vascular care in Alzheimer's disease (EVA) study. Stroke. 2010. 41:554–556.
Article
16. Jellinger KA. Alzheimer disease and cerebrovascular pathology: an update. J Neural Transm. 2002. 109:813–836.
Article
17. Jellinger KA. Morphologic diagnosis of "vascular dementia" - a critical update. J Neurol Sci. 2008. 270:1–12.
Article
18. De Groot JC, De Leeuw FE, Oudkerk M, Van Gijn J, Hofman A, Jolles J, et al. Periventricular cerebral white matter lesions predict rate of cognitive decline. Ann Neurol. 2002. 52:335–341.
Article
19. van den Heuvel DM, ten Dam VH, de Craen AJ, Admiraal-Behloul F, Olofsen H, Bollen EL, et al. Increase in periventricular white matter hyperintensities parallels decline in mental processing speed in a non-demented elderly population. J Neurol Neurosurg Psychiatry. 2006. 77:149–153.
Article
20. Park KH, Lee JY, Na DL, Kim SY, Cheong HK, Moon SY, et al. Different associations of periventricular and deep white matter lesions with cognition, neuropsychiatric symptoms, and daily activities in dementia. J Geriatr Psychiatry Neurol. 2011. 24:84–90.
Article
21. Herrmann LL, Le Masurier M, Ebmeier KP. White matter hyperintensities in late life depression: a systematic review. J Neurol Neurosurg Psychiatry. 2008. 79:619–624.
Article
22. Seo SW, Lee JM, Im K, Park JS, Kim SH, Kim ST, et al. Cortical thinning related to periventricular and deep white matter hyperintensities. Neurobiol Aging. 2012. 33:1156–1167.
Article
23. Wen W, Sachdev PS, Chen X, Anstey K. Gray matter reduction is correlated with white matter hyperintensity volume: a voxel-based morphometric study in a large epidemiological sample. Neuroimage. 2006. 29:1031–1039.
Article
24. Selden NR, Gitelman DR, Salamon-Murayama N, Parrish TB, Mesulam MM. Trajectories of cholinergic pathways within the cerebral hemispheres of the human brain. Brain. 1998. 121(Pt 12):2249–2257.
Article
25. Bocti C, Swartz RH, Gao FQ, Sahlas DJ, Behl P, Black SE. A new visual rating scale to assess strategic white matter hyperintensities within cholinergic pathways in dementia. Stroke. 2005. 36:2126–2131.
Article
26. Reed BR, Eberling JL, Mungas D, Weiner M, Kramer JH, Jagust WJ. Effects of white matter lesions and lacunes on cortical function. Arch Neurol. 2004. 61:1545–1550.
Article
27. Schmidt R, Fazekas F, Kapeller P, Schmidt H, Hartung HP. MRI white matter hyperintensities: three-year follow-up of the Austrian Stroke Prevention Study. Neurology. 1999. 53:132–139.
Article
28. van der Flier WM, van Straaten EC, Barkhof F, Ferro JM, Pantoni L, Basile AM, et al. Medial temporal lobe atrophy and white matter hyper-intensities are associated with mild cognitive deficits in non-disabled elderly people: the LADIS study. J Neurol Neurosurg Psychiatry. 2005. 76:1497–1500.
Article
29. Gold G, Kovari E, Herrmann FR, Canuto A, Hof PR, Michel JP, et al. Cognitive consequences of thalamic, basal ganglia, and deep white matter lacunes in brain aging and dementia. Stroke. 2005. 36:1184–1188.
Article
30. van Den Boom R, Lesnik Oberstein SA, van Duinen SG, Bornebroek M, Ferrari MD, Haan J, et al. Subcortical lacunar lesions: an MR imaging finding in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. Radiology. 2002. 224:791–796.
Article
31. Viitanen M, Kalimo H. CADASIL: hereditary arteriopathy leading to multiple brain infarcts and dementia. Ann N Y Acad Sci. 2000. 903:273–284.
Article
32. Smith EE, Greenberg SM. Beta-amyloid, blood vessels, and brain function. Stroke. 2009. 40:2601–2606.
33. Weller RO, Nicoll JA. Cerebral amyloid angiopathy: pathogenesis and effects on the ageing and Alzheimer brain. Neurol Res. 2003. 25:611–616.
Article
34. McCarron MO, Nicoll JA. Apolipoprotein E genotype and cerebral amyloid angiopathy-related hemorrhage. Ann N Y Acad Sci. 2000. 903:176–179.
Article
35. Chen YW, Gurol ME, Rosand J, Viswanathan A, Rakich SM, Groover TR, et al. Progression of white matter lesions and hemorrhages in cerebral amyloid angiopathy. Neurology. 2006. 67:83–87.
Article
Full Text Links
  • DND
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
Copyright © 2024 by Korean Association of Medical Journal Editors. All rights reserved.     E-mail: koreamed@kamje.or.kr