Arteriovenous Malformation (cont.)
How do AVMs Damage the Brain and Spinal Cord?
AVMs become symptomatic only when the damage they cause
to the brain or spinal cord reaches a critical level. This is one of the reasons
why a relatively small fraction of people with these lesions experiences
significant health problems related to the condition. AVMs damage the brain or
spinal cord through three basic mechanisms: by reducing the amount of oxygen
reaching
neurological tissues; by causing bleeding (hemorrhage) into surrounding tissues;
and by compressing or displacing parts of the brain or spinal cord.
AVMs compromise oxygen delivery to the brain or spinal cord by altering
normal patterns of blood flow. Arteries and veins are normally interconnected by
a series of progressively smaller blood vessels that control and slow the rate
of blood flow. Oxygen delivery to surrounding tissues takes place through the
thin, porous walls of the smallest of these interconnecting vessels, known as
capillaries, where the blood flows most slowly. The arteries and veins that make
up AVMs, however, lack this intervening capillary network. Instead, arteries
dump blood directly into veins through a passageway called a fistula. The flow
rate is uncontrolled and extremely rapid-too rapid to allow oxygen to be
dispersed to surrounding tissues. When starved of normal amounts of oxygen, the
cells that make up these tissues begin to deteriorate, sometimes dying off
completely.
This abnormally rapid rate of blood flow frequently
causes blood pressure inside the vessels located in the central portion of an
AVM directly adjacent to
the fistula-an area doctors refer to as the nidus, from the Latin
word for nest-to rise to dangerously high levels. The arteries feeding blood
into the AVM often become swollen and distorted; the veins that drain blood away from it
often become abnormally constricted (a condition called stenosis). Moreover, the
walls of the involved arteries and veins are often abnormally thin and weak.
Aneurysms-balloon-like bulges in blood vessel walls that are susceptible to
rupture-may develop in association with approximately half of all neurological
AVMs due to this structural weakness.
Bleeding can result from this combination of high internal pressure and
vessel wall weakness. Such hemorrhages are often microscopic in size,
causing limited damage and few significant symptoms. Even many nonsymptomatic
AVMs show evidence of past bleeding. But massive hemorrhages can occur if the
physical stresses caused by extremely high blood pressure, rapid blood flow
rates, and vessel wall weakness are great enough. If a large enough volume of
blood escapes from a ruptured AVM into the surrounding brain, the result can be
a catastrophic stroke. AVMs account for approximately 2 percent of all
hemorrhagic strokes that
occur each year.
Even in the absence of bleeding or significant oxygen
depletion, large AVMs can damage the brain or spinal cord simply by their
presence. They can range in size from a fraction of an inch to more than 2.5
inches in diameter, depending on the number and size of the blood vessels making
up the lesion. The larger the lesion, the greater the amount of pressure it
exerts on surrounding brain or spinal cord structures. The largest lesions may
compress several inches of the
spinal cord or distort the shape of an entire hemisphere of the brain. Such
massive AVMs can constrict the flow of cerebrospinal fluid-a clear liquid that
normally nourishes and protects the brain and spinal cord-by distorting or
closing the passageways and open chambers (ventricles) inside the brain that
allow this fluid to circulate freely. As cerebrospinal fluid accumulates,
hydrocephalus results. This fluid buildup further increases the amount of
pressure on fragile neurological structures, adding to the damage caused by the
AVM itself.
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