~Stroke and Cerebrovascular Disease

~Stroke and Cerebrovascular Disease
Reprinted with permission of Life Extension®.

Cerebrovascular disease, including stroke, is the third-leading cause of death in the United States and a leading cause of disability among older Americans. Cerebrovascular disease occurs when the blood vessels supplying the brain with oxygenated blood are damaged or their function is compromised. If the blood flow is severely restricted, depriving the brain of adequate oxygen even briefly, a stroke can occur. It has been estimated that every 45 seconds, another American suffers from a stroke, often with debilitating consequences or even death. One in four men and one in five women over the age of 45 will suffer a stroke.

There are two main kinds of stroke. The most common, an ischemic stroke, occurs when an artery in the brain is blocked by a blood clot, usually because of atherosclerosis (the deposition of plaque on the inside of artery walls). Alternatively, a hemorrhagic stroke can occur when a portion of the arterial wall weakens and bursts. A stroke is a serious medical emergency that requires immediate medical attention. Time is a critical factor in stroke management: some experts now refer to strokes as “brain attacks” to stress the need for emergency treatment.

Researchers have conducted thousands of clinical trials searching for better ways to prevent and treat stroke victims. As a result, we have a robust knowledge of cerebrovascular disease, and we are learning more every day. As with atherosclerosis in the coronary arteries (coronary artery disease), the underlying cause of ischemic stroke can often be traced back decades, to early insults to the inner lining (endothelium) of the arteries that set a deadly chain reaction into motion. Now that they have identified endothelial dysfunction as a fundamental process of cardiovascular and cerebrovascular disease, along with the prime risk factors for endothelial dysfunction, such as high blood pressure and smoking, researchers are pursuing new therapies aimed at preventing strokes by improving the health of our arteries.

Stroke is primarily a condition of the elderly, mostly because of the cumulative effects of endothelial dysfunction, which can take decades to reach a crisis point. Nearly three quarters of all strokes occur in people who are over the age of 65, and the risk of stroke more than doubles every decade beyond the age of 55 (NINDS 2005).

Stroke is an insidious condition because of the nature of the anatomy of the brain. Heart disease is often preceded by a characteristic pain in the chest or arm (angina) or shortness of breath. These symptoms occur when the blood supply to the heart is temporarily reduced. The brain, however, lacks pain receptors, so temporary episodes of ischemia don’t cause pain. Although there may be warning signs, the first signal of atherosclerosis in the brain is often a stroke.

When blood flow to the brain is briefly disrupted, causing what is called a ministroke, the symptoms are similar to those of a stroke (vision and speech difficulty, limited paralysis) but not as severe, and they usually subside within 24 hours. In the past, physicians viewed ministrokes as relatively benign events, or “near misses.” Today, we understand that not only are they damaging in their own right because of the deprivation of blood to the brain, but the presence of ministrokes is a major warning signal. Any person suffering from suspected cerebrovascular disease should seek immediate medical supervision and comprehensive diagnostic testing to assess the likelihood of a stroke and take active steps to reduce the risk.

Kinds of Stroke

Strokes are caused either by an arterial blockage that reduces blood flow to the brain (ischemic stroke) or by a rupture in an artery that allows blood to spill into the surrounding area (hemorrhagic stroke). It is extremely important that the kind of stroke be identified as quickly as possible because each is treated differently. For example, if the stroke is caused by a blood clot (an ischemic stroke), drugs should be administered to help dissolve the clot. If, however, these drugs were administered to a person suffering from a bleeding stroke, the damage could be intensified because of increased bleeding (NINDS 2005).

Ischemic stroke. Ischemic stroke is responsible for 80 percent of all strokes (NINDS 2005). There are two kinds of ischemic stroke. The first, a thrombotic stroke, results from a blood clot (thrombus) forming in a vessel inside the brain and cutting off the blood supply to the tissues served by that vessel.

The second, an embolic stroke, occurs when a clot forms somewhere else in the body, breaks off, and travels to the brain. The clot can originate in a peripheral artery, in the heart itself, or in the arteries in the neck or brain. Among people with an abnormal heart rhythm called atrial fibrillation, clots can arise in the left atrium and travel through the left side of the heart and the aorta and into the brain. When the clot becomes lodged in the artery, the tissue beyond the blockage is starved of oxygen and begins to die.

Hemorrhagic stroke. The second category of stroke, hemorrhagic stroke, occurs when a vessel in or near the brain ruptures and leaks blood into the brain or surrounding tissues. In this case, the blood pushes against otherwise healthy brain tissue and compresses it. The increased pressure reduces blood flow into the area, and if the pressure becomes high enough, it can cause damage to brain cells. There are two primary kinds of hemorrhagic strokes, named according to the location of the bleeding (Stanford Stroke Center 2005):

  • Subarachnoid hemorrhage occurs when blood floods the space between the brain and the skull.
  • Intracerebral hemorrhage happens when an artery inside the brain ruptures, spilling blood into the surrounding brain tissue.

Hemorrhagic strokes are often caused by aneurysms, or weakened portions of the artery wall. An aneurysm may have no symptoms and go unnoticed for years. In many cases, the first sign of an aneurysm is a stroke.

Effects of Stroke

Strokes are so feared because of their debilitating effects. Even ministrokes have been shown to reduce cognitive function (Mosley TH Jr. et al 2005), and large strokes can have serious, life-altering and life-threatening consequences. Common effects from stroke include the following:

  • Paralysis or weakness. Paralysis, weakness, and tiredness are the most common effects from stroke. These effects may involve one side of the body or just the face or an arm or leg. A survivor also may lose the ability to recognize the need to urinate or to control bladder or bowel muscles, which can result in not getting to the toilet in time. Constipation can also occur. Incontinence problems are usually temporary, but they can be emotionally distressing.
  • Aphasia. At least 25 percent of all stroke survivors lose the ability to speak, write, or understand spoken or written language. This condition can improve with therapy.
  • Spatial perception, thinking, and memory. Stroke can damage areas of the brain that control memory, spatial relationships, learning, and awareness. Survivors may have significantly shortened attention spans or find short-term memory problematic. They may lose the ability to learn new tasks, follow a set of instructions, make plans, or carry out actions in sequential steps.
  • Mental health changes. Depression, personality changes, and trouble controlling emotions are common after stroke because of the debilitating emotional effect of the trauma. Strokes can also damage the frontal cortex and other parts of the brain involved with emotion. Poststroke depression usually responds well to antidepressant medications and psychological counseling (NINDS 2005).

Endothelial Dysfunction and Stroke Risk

Most strokes are caused by blood clots that form as a result of atherosclerosis (Gorelick PB 2002). Once known as “hardening of the arteries,” atherosclerosis occurs when the arteries become clogged with plaque deposits and the structure and function of the inner arterial wall (the endothelium) are compromised. If atherosclerotic plaque deposits become brittle and rupture, blood clots can form that lead to stroke. Scientists have spent decades unraveling the complicated biological processes that lead to atherosclerosis. We now understand atherosclerosis as a long-term disease, one that accelerates as we age, raising the risk of heart attack and stroke.

For many years, conventional science has depicted the arteries as pipes, often using plumbing analogies to describe procedures such as balloon angioplasty or endarterectomy, an operation in which plaque is stripped away from the linings of arteries. The problem with the plumbing analogy, however, is that the arteries are actually muscular, complex organs that play an active role in regulating blood pressure and other biological functions.

Arteries are composed of three layers. The outer layer is mostly connective tissue and provides structure to the layers beneath. The middle layer is smooth muscle and contracts and dilates to help blood flow and maintain blood pressure. And the inner layer is a thin layer of endothelial cells and provides a smooth, protective surface. Endothelial cells prevent toxic, blood-borne substances from penetrating the smooth muscle of the artery. They also respond to changes in blood pressure and release substances into the cells of the smooth muscle that help change the tone of the artery. Furthermore, endothelial cells secrete chemicals that provoke a protective response in the artery after an injury.

In the event an artery is injured, the endothelium signals smooth muscle cells to gather at the site of the injury. Endothelial cells also signal white blood cells to congregate on the injured vessel wall, provoking an immune response. As we age, however, the endothelium becomes leaky, allowing lipids and toxins to penetrate the endothelial layer into the smooth muscle cells. As a result, smooth muscle cells gather at the site of the injury, and the artery in turn loses some flexibility. In response, the endothelium signals white blood cells to congregate along the cell wall. The endothelium is further weakened by the pro-inflammatory immune response, in which leukotrienes and prostaglandins contribute to inflammation, which aggravates the abnormal smooth muscle tone of the arterial wall (Touyz RM 2005). Toxins soon begin to penetrate into the arterial wall. Inside the artery, lipids such as low-density lipoprotein (LDL) cholesterol and triglycerides accumulate and gradually become oxidized.

At this point, the atherosclerotic process has begun in earnest. In response to the oxidized lipids, the body mounts an immune response that causes more white blood cells to attack the fats, producing more inflammation within the arterial wall. In an attempt to heal the injury, smooth muscle cells begin to produce collagen to form a cap over the injury site. The mixture of oxidized lipids, white blood cells, and smooth muscle cells forms a plaque deposit. Over time, calcium accumulates on the deposit and forms a brittle cap. If this calcified plaque ruptures, a blood clot can form.

All the processes described above, in which the arterial wall is damaged and normal endothelial function is compromised, are collectively referred to as endothelial dysfunction. Risk factors that aggravate endothelial dysfunction include high blood pressure, smoking, elevated LDL and triglycerides, low levels of high-density lipoprotein (HDL) cholesterol, diabetes, elevated insulin levels, obesity, lack of exercise, and several recently identified risk factors, such as elevated levels of homocysteine and C-reactive protein. Each of these contributes to endothelial dysfunction of cerebral arteries and the subsequent increased risk of stroke.

High blood pressure, for example, is very strongly associated with stroke; in fact, high blood pressure is associated with about half of ischemic strokes. It is known that high blood pressure contributes to endothelial dysfunction. Cigarette smoke is another major risk factor because the smoke contains many toxins that contribute to endothelial injury, while homocysteine has been shown to cause the initial injury to the endothelium that begins the atherosclerotic process (Sainani GS et al 2002). Similarly, a Physician’s Health Study found that men in the highest quartile of levels of C-reactive protein (an inflammatory marker that signals inflammation somewhere in the body) had twice the risk of ischemic stroke of those in the bottom quartile (Ridker PM et al 1997). Other studies have found that C-reactive protein is a strong independent predictor of a reduced survival rate after ischemic stroke (Di Napoli M et al 2001).

If researchers can identify drugs or supplements that support healthy endothelial function, it may be possible to slow the relentless advance of atherosclerosis and reduce the risk of the most common kind of stroke. One common therapeutic focus is nitric oxide, which causes arteries to dilate and improves blood flow. A nutrient or drug that improves the production of nitric oxide may have the potential to reduce the risk of stroke or other atherosclerotic insults.

It also makes sense to modify as many other risk factors as possible, including high blood pressure, cholesterol, and even infection. Studies have linked certain common infections to increased stroke risk, including Chlamydia pneumonia, Helicobacter pylori, cytomegalovirus, and C Pneumonia (Winkelstein JA et al 2001; Meier CR et al 1999; Nieto FJ et al 1999). The first National Health and Nutrition Examination Survey (NHANES) found that periodontal disease, though treatable, is a risk factor (Wu T et al 2000). Other studies indicate that patients hospitalized with bacterial and viral infections had increased risk of stroke within one week of the infection, highlighting the importance of infection, even in younger people (Grau AJ et al 1995, 1998, 1999).

Continued . . .

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