ISSN 2415-3060 (print), ISSN 2522-4972 (online)
  • 7 of 59
JMBS 2016, 1(1): 37–40

Vascular Dementia: Qualitative Analysis of the Angioarchitectonics of the Cerebral Cortex

Volos L.I.

Dementia is a clinical diagnosis requiring new functional dependence on the basis of progressive cognitive decline. The most common causes of cognitive impairment and dementia are Alzheimer's disease (AD) and vascular brain injury (VBI), either independently, in combination, or in conjunction with other neurodegenerative disorders. The aim of the present study was to investigate the criteria for morphological diagnosis of vascular dementia by identifying specific structural changes in the cerebral cortex of the brain, the hippocampus and cerebellum. Method: We studied case histories of 52 patients with dementia (diagnosis based on DSM-III-R criteria; mean age of 61,4±3,5 years. Autopsy included macroscopic and microscopic study of brain. Investigated fields of the cerebral cortex Brodmann: 10 area – frontopolar prefrontal cortex, 44 and 45 areas - the frontal lobe (Broca's area), 17 area - occipital lobe (visual center), 23/24 area - limbic region, 40 area - supramarginal gyrus, parietal lobe, 41 area - Wernicke's area, temporal lobe, hippocampus, subiculum - old cortex deep hippocampal gyrus, cerebellum. In all 20 zones. As a control group for quantitative morphological studies we have taken pieces of tissue from the respective regions and areas of the brain in six persons killed in accidents and not suffered for the mental life (data collected through case history). Collecting the material carried within 6-8 hours after death. We used modern methods. Histological sections stained by standard methods: hematoxylin and eosin, Nissl staining, Bilshovsky, Cajal's, PAS-reaction. To confirm the presence of vascular amyloidosis, amyloid angiopathy and differential diagnosis of hyalinosis of vessels we used Congo red. We are used Congo red to make a diagnosis of amyloid and state the common opinion that in polarized light, Congo red-stained amyloid shows apple-green birefringence, sometimes called apple-green dichroism. Histological examination was performed with a microscope Hund H500 (Germany). Results: The main signs of macroscopic vascular dementia is overwhelming atrophy fronto-parietal-temporal lobes, which in total amounted to 69.2%. Loss and neurodegenerative changes of neurons, gliosis, spongiosis, forming plaques in brain, the main cause clinical symptoms. In many cases very difficult to morphological differential diagnosis of vascular dementia from Alzheimer's disease, dementia with Lewy bodies. In vascular dementia, lacunar spongiosis and limited perivascular zones microvessels, is a structural basis of the pathogenic mechanisms of its occurrence. In vascular dementia hyperplasia of astrocytes not accompanied by their hypertrophy and is a focal character. Neuronal plaques in the vascular encephalopathy Congo- and PAS-positive, have in polarized light bright birefringence and dichroism, localized mainly in neuropile cortical and subcortical structures of the brain and cerebellum. In vascular dementia, a major component of amyloid plaques are glycosaminoglycans and glycoproteins, which serves one objective differential morphological markers of the disease to other neural degenerative diseases. Conclusions: However, the basic morphological diagnostic criterions of vascular dementia are established which in view of clinical indications can be used in practice department of pathology for statement of the objective diagnosis and differential diagnostics with others neurodegenerative dementive syndromes.

Keywords: vascular dementia, pathomorphological diagnostics

Full text: PDF (Ukr) 88.15K

  1. Volos L.I. DiferentsIalna morfologIchna dIagnostika hvorobi Kreyttsfeldta-Yakoba, Altsgeymera ta sudinnoyi dementsiyi. Vestnik neotlozhnoy i vosstanovitelnoy meditsinyi. 2003; 4 (4): 629-32.
  2. Braekhus A, Engedal K. Vascular dementia: an ill-defined term. Tidsskr Nor Laegeforen. 2004;124 (8): 1097-9.
  3. Butler R, Radhakrishnan R. Dementia. BMJ Clin Evid. 2012, Sep 10. pii: 1001.
  4. Cunningham EL, McGuinness B, Herron B, Passmore A.P. Dementia. Ulster Med J. 2015; 84 (2): 79-87.
  5. Flanagan M, Larson EB, Latimer CS, Brenna Cholerton, Paul K. Crane, Kathleen S. Montine,Lon R. White, C. Dirk Keene, Thomas J. Montine. Clinical-pathologic correlations in vascular cognitive impairment and dementia. Biochim Biophys Acta. 2015 Aug 28. pii: S0925-4439(15)00256-2.
  6. Gold G, Kövari E. Vascular dementia: big effects of small lesions. Rev Med Suisse. 2011; 7 (316-2190): 219-23.
  7. Knopman DS, Parisi JE, Boeve BF, Cha RH, Apaydin H, Salviati A, Edland SD, Rocca WA. Vascular dementia in a population-based autopsy study. Arch Neurol. 2003; 60 (4): 569-75.
  8. O'Brien JT, Thomas A. Vascular dementia. Lancet. 2015;386(10004):1698-706.
  9. Pantoni L, Palumbo V, Sarti C. Pathological lesions in vascular dementia. Ann NY Acad Sci. 2002; 977: 279-91.
  10. Raz L, Knoefel J, Bhaskar K. The neuropathology and cerebrovascular mechanisms of dementia. J Cereb Blood Flow Metab. 2015. Review.
  11. Wu YT, Fratiglioni L, Matthews FE, Lobo A, Breteler MM, Skoog I, Brayne C. Dementia in western Europe: epidemiological evidence and implications for policy making. Lancet Neurol. 2015 Aug 20. pii: S1474-4422(15)00092-7.