Abstract
Cerebral small vessel disease (CSVD) is a chronically proceeding pathology of small
brain vessels associated with white matter lesions, lacunar infarcts, brain atrophy
and microbleeds. CSVD leads to slowly increasing cognitive and functional deficits
but may also cause stroke-like symptoms, if vessels in critical brain areas are affected.
Spontaneously hypertensive stroke-prone rats (SHRSP) exhibit several vascular risk
factors, develop infarcts and hemorrhages and therefore represent a relevant model
for the study of CSVD. Using this animal model, we recently demonstrated that intravasal
accumulations of erythrocytes, we interpreted as stases, stand at the beginning of
a pathological vascular cascade. After stases microbleeds occur, which are followed
by reactive microthromboses. Bleeds and thromboses finally cause hemorrhagic infarcts.
Immunohistochemical stainings show, that plasma proteins like IgG are deposited in
the walls of vessels affected by stases. Further, we found small clots and thread-shaped
aggregations of thrombocytes as well as thread-shaped structures of von Willebrand-Factor
within stases. Thus, we conclude that blood–brain barrier damages occur in the neighborhood
of stases and stases seem to be associated with a restricted activation of blood coagulation
without formation of obstructive thromboses. Finally, we demonstrate that small vessel
damage rarely appears in the cerebellum. Even animals with multiple cerebral infarcts
may be free of any cerebellar vascular pathology.
Keywords
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Article info
Publication history
Published online: July 25, 2012
Accepted:
June 25,
2012
Received in revised form:
June 4,
2012
Received:
December 22,
2011
Identification
Copyright
© 2012 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
