Stroke is a focal neurologic deficit of acute onset of presumed vascular origin.
This definition implies a clinical event, with a focal dysfunction of the central nervous
system (CNS), which is likely to be secondary to a disease involving the vessels
and circulation. Stroke can be ischemic or hemorrhagic.
The high sensitivity of the brain to a reduction of blood flow is due to the fact
that the brain covers its energy demands almost exclusively by oxidation of glucose.
A decline of blood oxygen supply below the critical threshold of mitochondrial
respiration causes stimulation of anaerobic glycolysis, the energy yield of which,
however, is minor as compared to oxidative phosphorylation.
Stroke is the third leading cause of death in the United States and the major cause
of adult neurological disability. In 1991, approximately 500,000 Americans had a
stroke and more than 142,000 died from stroke.
The third leading course of death after heart disease and cancer in industrialized
countries is stroke. In Germany, it is estimated that more than 240,000 patients suffer
a first stroke each year.
Stroke is defined as a clinical syndrome of neurological disabilities due to destruction
of brain tissue caused by blockage of a cerebral artery. This blockage can be
due to thrombosis or embolism, stenosis by atherosclerotic plaque, or to hemorrhage
from a ruptured artery (1-4).
Arteriosclerosis is the most common of the chronic pathologic alterations of arterial
blood vessels. The term has been used since the time of Lobstein (1) to denote
sclerosis of the arterial wall.
Cardiovascular disease and stroke resulting from atherosclerosis are the leading
causes of death in all countries where life expectancy is high. The incidence of
atherosclerosis-associated diseases is strongly correlated with age, age being the most
significant risk factor.
The Chinese "yellow" emperor was the first to report that high salt intake makes
the pulse hard (1). Subsequently, in particular in the second half of this century,
numerous studies have examined the dietary sodium intake in relation to hypertension.
The traditional therapeutic goals in the treatment of acute ischemic stroke have
been confined to stabilization of the general medical state, prevention of systemic
medical complications, and efforts to prevent acute recurrence or progression of
The spectrum of heritable disease extends over a wide range from simple Mendelian
traits to very complex genetically determined disorders. In simple Mendelian
traits, the inheritance pattern follows straightforward rules and, in many cases, particularly
in those that are linked to sex chromosomes, the phenotype of the offspring
is readily predictable.
We have studied genetic variation in salt sensitivity in our animal models, the
spontaneously hypertensive rat (SHR) (1,2), and particularly the salt-sensitive substrain,
stroke-prone SHR (SHRSP) (3,4).
The single most important risk factor for stroke is hypertension (1). Therefore,
nutritional factors that reduce hypertension are also beneficial in stroke prevention.
Stroke is the third most common cause of death in Western countries and the
most important cause of adult disability (1). In spite of massive efforts to reduce
the risk of death or disability and to improve outcome in stroke patients, there is
still no effective drug treatment (1-5).
Stroke is a leading cause of disability in the elderly and a significant cause of
disability in younger people as well. Nearly 3 million Americans have some degree
of impairment from strokes, at an estimated annual economic impact of 30 billion
U.S. dollars (1).
Dr. Hennerici: The task of summarizing what everyone has said in a 2-day workshop
is always a little difficult. I shall just remind you that, at the start of this
workshop, some of you may have had no clear-cut idea of what nutrition and stroke
have to do with each other.