cerebrovascular disease 4

More than any other organ, the brain depends from moment
to moment on an adequate supply of oxygenated blood. Constancy
of the cerebral circulation is assured by a series of baroreceptors
and vasomotor reflexes under the control of centers in the lower
brainstem. In Stokes-Adams attacks, for example, unconsciousness
occurs within 10 s of the beginning of asystole. In animal experiments
and probably in humans, the complete stoppage of blood
flow for longer than 5 min produces irreversible damage. Brain
tissue deprived of blood undergoes ischemic necrosis or infarction
(also referred to as a zone of softening or encephalomalacia). Obstruction
of an artery by thrombus or embolus is the usual cause of
focal ischemic damage, but failure of the circulation and hypotension
from cardiac decompensation or shock, if severe and prolonged
enough, can produce focal as well as diffuse ischemic changes.
Cerebral infarcts vary greatly in the amount of congestion and
hemorrhage found within the softened tissue. Some infarcts are
devoid of blood and therefore pallid ( pale infarction); others show
mild congestion (dilatation of blood vessels and escape of red blood
cells), especially at their margins; still others show an extensive
extravasation of blood from many small vessels all through the
infarcted tissue (red or hemorrhagic infarction). Some infarcts are
all of one type, either pale or hemorrhagic; many are mixed. The
reason for the occurrence of hemorrhagic infarction—almost always,
occurring in cases of cerebral embolism—is not fully
understood. The explanation most consistent with our observations is
that embolic material, after occluding an artery and causing ischemic
necrosis of brain tissue, then fragments and migrates distally
from its original site. This allows partial restoration of the circulation
to the infarcted zone, and blood seeps through the damaged
small vessels (Fisher and Adams). In such cases, one often cannot
find the embolus by arteriography or postmortem examination, or
one finds only a few fragments proximal to the pale ischemic zones.
Cerebral hemorrhage is one of two types. In the intracerebral
variety, blood leaks from the vessel (usually a small artery) directly
into the brain, forming a hematoma in the brain substance and
sometimes spreading into the ventricles and then to the subarachnoid
space. Once the leakage is arrested, the blood slowly disintegrates
and is absorbed over a period of weeks and months. The
mass of clotted blood causes physical disruption of the tissue and
pressure on the surrounding brain. The second type of bleeding
originates from an aneurysmal dilation at branching points of the
large arteries of the circle of Willis; the bleeding is almost exclusively
contained within the subarachnoid spaces and therefore,
causes little immediate focal effect on the brain. In this way, subarachnoid
hemorrhage differs from other stroke syndromes. However,
blood within the subarachnoid space, if large in quantity, may
cause a delayed cerebral ischemia through a mechanism of constriction
of the vessels of the circle of Willis and their primary
branches (vasospasm). In addition to these two main types of hemorrhage,
a bland infarction in many instances has areas of leakage
of blood into the brain, so-called hemorrhagic infarction.