Alcohol, stroke, and the cerebral circulation

Alcohol Health & Research World,  Summer, 1990  by Burton M. Altura,  Bella T. Altura

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The idea that continued ingestion of alcohol can produce adverse effects on brain tissue is no surprise, particularly to the physician treating alcoholic patients or the social worker caring for alcoholic clients. Scientific documentation appears as early as 1725, when Sedgewick wrote that alcohol may compromise the cerebral circulation. Lawson (1878) described delirious states that could lead to general cerebral decline and deterioration of recent memory in chronic alcoholic patients. In 1804, Trotter stated that alcohol could precipitate cerebrovascular disease.

Despite early studies and Biblical accounts, however, the connection between alcohol and circulation in the brain was unexplored until about 35 years ago, when Pakkenberg (1954) reported that one-third of young male patients presenting with cerebral infarction (1) were heavy drinkers. Many years later, case reports appeared in the literature that supported this association (Bengesser and Weiser 1974; Hillbom and Kaste 1978; Lee 1979).

At about the same time, large-scale epidemiologic studies (reviewed by Ashley 1982) revealed that the risk of developing cerebrovascular diseases, such as stroke, increases with increasing alcohol consumption. However, Ashley (1982) took a step forward by differentiating between ischemic and hemorrhagic strokes.

Ischemia occurs when the blood supply to a tissue (or organ) is insufficient to meet its metabolic needs. More than most organs in the body, the metabolic needs of the brain are very high. Although it contributes only about 2 percent of the total body weight, the brain requires approximately 20 percent of the total cardiac output and 20 percent of the body's oxygen. A fall in the blood supply of only 10 percent to 15 percent can have disastrous effects on cerebral function and will result in permanent brain damage. Further reduction leads to loss of sight or other senses; blackouts; intellectual impairment; impaired motor performance; paralysis of the limbs, digits, and respiratory muscles; and, ultimately, to coma and death.

TYPES OF STROKES AND

ALCOHOL-INDUCED STROKES

In today's hospital population, patients who have vascular disorders of the nervous system are among the most numerous, making up more than one-half of all admissions for neurological disorders. Included among disorders of the cerebral vasculature are occlusions or obstructions by emboli (typically blood clots or fat droplets), ruptures of cerebral blood vessels, collapse of cerebral vessel lumina (openings), and increased permeability of blood vessel walls. Whatever the exact process, one of the following results:

* Transient brain ischemia, known as transient ischemic attack (TIA)

* Ischemic stroke syndrome (ISS)

* Hemorrhagic stroke syndrome (HSS).

Whenever possible, hemorrhagic strokes are subdivided further into intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH), depending on the area of the brain affected. An intracerebral hemorrhage usually refers to a bleed deep within the brain. A subarachnoid hemorrhage usually refers to ruptured blood vessels in the subarachnoid space, the area between the pia mater and the dura mater (protective membranes encasing the brain and lying directly below the skull).

Over the past few decades, researchers have focused increasing attention on what was once termed minor or little strokes, now termed transient ischemic attacks. This type of stroke is described as a focal neurologic deficit of sudden onset and very short duration (lasting seconds to a few minutes); it tends to recur frequently in patients with underlying cerebrovascular disease.

Neurologic deficits that last less than 24 hours are arbitrarily classified as resulting from transient ischemic attacks; in practice, the deficits usually last a matter of minutes. In contrast, a stroke in evolution connotes a stepwise, progressive worsening of a neurologic deficit, which parallels an ongoing ischemia that usually is completed within 24 hours. A third type of ischemic stroke, a completed stroke, results in a neurologic deficit that is both stable and persistent. Ischemia of the brain, although often spontaneously reversible, if allowed to continue for too long (as little as 3 to 8 minutes, depending on the region of the brain), will result in cerebral infarction and permanent brain damage. It is important to note that 30 percent to 40 percent of all patients who experience more than one transient ischemic attack will experience a cerebral infarction during the following 5 years. The mortality rate from cerebral infarctions subsequent to the first attack is 40 percent to 50 percent (Fisher 1989).

Stroke of all types is a major contributor to disability and, when severe, its treatment usually fails to restore the patient to he prestroke state. Thus, prevention would appear to be the most realistic approach to reducing stroke-related disease (or illness) and death.

Germane to this discussion is a growing body of evidence suggesting that even moderate alcohol consumption (15 ounces (2) to 39 ounces of alchol per month), addition to excessive consumption (more than 40 ounces per monyh) and "binge" drinking (more than 80 grams ingested in less than 24 hours), predisposes humans to strokes and sudden death.