Arteriovenous Malformation (cont.)
What causes vascular lesions?
Although the cause of these vascular anomalies of the
central nervous system is not yet well understood, scientists believe that they
most often result from mistakes that occur during embryonic or fetal
development. These mistakes may be linked to genetic mutations in some cases. A
few types of vascular malformations are known to be hereditary and thus are
known to have a genetic basis. Some evidence also suggests that at least some of
these lesions are acquired later in
life as a result of injury to the central nervous system.
During fetal development, new blood vessels continuously form and then
disappear as the human body changes and grows. These changes in the body's
vascular map continue after birth and are controlled by angiogenic factors,
chemicals produced by the body that stimulate new blood vessel formation and
growth. Researchers have recently identified changes in the chemical structures
of various angiogenic factors in some people who have AVMs or other vascular
abnormalities of the central nervous system. However, it is not yet clear how
these chemical changes actually cause changes in blood vessel structure.
By studying patterns of familial occurrence, researchers have established
that one type of cavernous malformation involving multiple lesion formation is
caused by a genetic mutation in chromosome 7. This genetic mutation appears in
many ethnic groups, but it is especially frequent in a large population of
Hispanic Americans living in the Southwest; these individuals share a common
ancestor in whom the genetic change occurred. Some other types of vascular
defects of the central nervous system are part of larger medical syndromes known
to be hereditary. They include hereditary hemorrhagic telangiectasia
(also known as Osler-Weber-Rendu
disease), Sturge-Weber syndrome,
Klippel-Trenaunay syndrome, Parkes-Weber syndrome, and
Wyburn-Mason syndrome.
Next: How are arteriovenous malformations and other vascular lesions detected? »
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