essential stroke

Essential
Neurology
FOURTH EDITION

Iain Wilkinson
BSc, MD, MA, FRCP

Formerly Consultant Neurologist
Addenbrooke’s Hospital
Cambridge
and
Fellow of Wolfson College
and Associate Lecturer
University of Cambridge Medical School

Graham Lennox
BA FRCP

Consultant Neurologist
Addenbrooke’s Hospital
Cambridge
and
West Suffolk Hospital
Bury St Edmunds

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.

cerebrovascular disease 3

Definition of Terms

As discussed below, the term stroke is applied to a sudden focal
neurologic syndrome, specifically the type due to cerebrovascular
disease. The term cerebrovascular disease designates any abnormality
of the brain resulting from a pathologic process of the blood
vessels. Pathologic process is given an inclusive meaning—
namely, occlusion of the lumen by embolus or thrombus, rupture
of a vessel, an altered permeability of the vessel wall, or increased
viscosity or other change in the quality of the blood flowing
through the cerebral vessels. The vascular pathologic process may
be considered not only in its grosser aspects—embolism, thrombosis,
dissection, or rupture of a vessel—but also in terms of the
more basic or primary disorder, i.e., atherosclerosis, hypertensive
arteriosclerotic change, arteritis, aneurysmal dilation, and developmental
malformation. Equal importance attaches to the secondary
parenchymal changes in the brain resulting from the vascular
lesion. These are of two main types—ischemia, with or without
infarction, and hemorrhage—and unless one or the other occurs,
the vascular lesion usually remains silent. The only exceptions to
this statement are the local pressure effects of an aneurysm, vascular
headache (migraine, hypertension, temporal arteritis), multiple small
vessel disease with progressive encephalopathy (as in malignant hypertension
or cerebral arteritis), and increased intracranial pressure
(as occurs in hypertensive encephalopathy and venous sinus thrombosis).
Also, persistent acute hypotension may cause ischemic necrosis
in regions of brain between the vascular territories of cortical
vessels, even without vascular occlusion. The many types of cerebrovascular
diseases are listed in Table 34-1, and the predominant
types during each period of life, in Table 34-2.

cerebrovascular disease 2

Incidence of Cerebrovascular Diseases

Stroke, after heart disease and cancer, is the third most common
cause of death in the United States. Every year there are in this
country approximately 700,000 cases of stroke—roughly 600,000
ischemic lesions and 100,000 hemorrhages, intracerebral or subarachnoid—
with 175,000 fatalities from these causes. Since 1950,
coincident with the introduction of effective treatment for hypertension,
there has been a substantial reduction in the frequency of
stroke. This was most apparent three decades ago, as treatment for
high blood pressure became a public health focus. Among the residents
of Rochester, Minnesota, Broderick and colleagues documented
a reduction of 46 percent in cerebral infarction and hemorrhage
when the period 1975–1979 was compared with 1950–
1954; Nicholls and Johansen reported a 20 percent decline in the
United States between 1968 and 1976. Both sexes shared in the
reduced incidence. During this period, the incidence of coronary
artery disease and malignant hypertension also fell significantly.
By contrast, there has been no change in the frequency of aneurysmal
rupture. Interestingly, despite the continued improvement
in the treatment of hypertension, the incidence rate of stroke for
the period 1980–1984 was 17 percent higher than that for 1975–
1979, a feature attributed by Broderick and coworkers to the widespread
use of computed tomography (CT), which increased the
detection of less severe strokes. In the last decade, according to the
American Heart Association, the mortality rate from stroke has
declined by 12 percent, but the total number of strokes may again
be rising.

cereberovascular disease1

Among all the neurologic diseases of adult life, the cerebrovascular
ones clearly rank first in frequency and importance. At least 50
percent of the neurologic disorders in a general hospital are of this
type. At some time or other, every physician will be required to
examine patients with cerebrovascular disease and should at least
know something of the common types—particularly those in
which there is a reasonable prospect of successful medical or surgical
intervention or the prevention of recurrence. There is another
advantage to be gained from the study of this group of diseases—
namely, that they have traditionally provided one of the most instructive
approaches to neurology. As our colleague C. M. Fisher has aptly
remarked, house officers and students learn neurology literally “stroke
by stroke.” Moreover, the focal ischemic lesion has divulged some of
our most important ideas about the function of the human brain.
It must also be noted that, in the last two decades, new and
extraordinary types of imaging technology have been introduced
that allow the physician to make physiologic distinctions between
normal, ischemic, and infarcted brain tissue. This biopathologic
approach to stroke will likely guide the next generation of treatments
and has already had a pronounced impact on the direction
of research in the field. Salvageable brain tissue to be protected in
the acute phase of stroke can be delineated by these methods. To
identify this ischemic but not yet infarcted tissue virtually defines
the goal of modern stroke treatment. Which of the sophisticated
imaging techniques will contribute to improved clinical outcome
is still to be determined, but certain ones, such as diffusionweighted
imaging, have already proved invaluable in stroke work.
Despite these valuable advances in stroke neurology, three
points should be made. First, all physicians have a role to play in
the prevention of stroke by encouraging the reduction in risk factors
such as hypertension and the identification of signs of potential
stroke, such as transient ischemic attacks, atrial fibrillation, and
carotid artery stenosis. Second, careful bedside clinical evaluation
integrated with the newer testing methods mentioned above still
provide the most promising approach to this category of disease.
Finally, the last decade or two have witnessed a departure from the
methodical clinicopathologic studies that have been the foundation
of our understanding of cerebrovascular disease. Increasingly, randomized
studies involving several hundred and even thousands of
patients and conducted simultaneously in dozens of institutions have
come to dominate investigative activity in this field. These multicenter
trials have yielded highly valuable information about the natural
history of a variety of cerebrovascular disorders, both symptomatic
and asymptomatic. However, this approach suffers from a
number of inherent weaknesses, the most important of which is
that the homogenized data derived from an aggregate of patients
may not be applicable to a specific case at hand. Moreover, many
large studies show only marginal differences between treated and
control groups. Each of these multicenter studies will therefore be
critically appraised at appropriate points in the ensuing discussion.

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