Alcohol, Memory Blackouts and the Brain

How Does Alcohol Impair Memory?
by National Institute of Health

(Page 4 of 6)

Are Some People More Likely Than Others to Experience Blackouts?

In classic studies of hospitalized alcoholics by Goodwin and colleagues, 36 out of the 100 patients interviewed indicated that they had never experienced a blackout. In some ways, the patients who did not experience blackouts are as interesting as the patients who did. What was it about these 36 patients that kept them from blacking out, despite the fact that their alcoholism was so severe that it required hospitalization? Although they may actually have experienced blackouts but simply were unaware of them, there may have been something fundamentally different about these patients that diminished their likelihood of experiencing memory impairments while drinking.

In support of this possibility, a recent study by Hartzler and Fromme suggests that people with a history of blackouts are more vulnerable to the effects of alcohol on memory than those without a history of blackouts. These authors recruited 108 college students, half of whom had experienced at least one fragmentary blackout in the previous year. While sober, members of the two groups performed comparably in memory tasks. However, when they were mildly intoxicated those with a history of fragmentary blackouts performed worse than those without such a history. There are two possible interpretations for these data, both of which support the hypothesis that some people are more susceptible to blackouts than others. One plausible interpretation is that subjects in the fragmentary blackout group always have been more vulnerable to alcohol-induced memory impairments, which is why they performed poorly during testing under alcohol, and why they are members of the blackout group in the first place. A second interpretation is that subjects in the blackout group performed poorly during testing as a result of drinking enough in the past to experience alcohol-induced memory impairments. In other words, perhaps their prior exposure to alcohol damaged the brain in a way that predisposed them to experiencing future memory impairments. This latter possibility is made more likely by recent evidence that students who engage in repeated episodes of heavy, or binge, drinking are more likely than other students to exhibit memory impairments when they are intoxicated. Similar results have been observed in animal studies.

The argument for an inherent vulnerability to alcohol-induced memory impairments, including blackouts, is strengthened by two recent studies. In an impressive longitudinal study, Baer and colleagues examined the drinking habits of pregnant women in 1974 and 1975, and then studied alcohol use and related problems in their offspring at seven different time points during the following 21 years. These authors observed that prenatal alcohol exposure was associated with increased rates of experiencing alcohol-related consequences, including blackouts, even after controlling for the offsprings' general drinking habits. In addition, a recent report by Nelson and colleagues suggests that there might actually be a genetic contribution to the susceptibility to blackouts, indicating that some people simply are built in a way that makes them more vulnerable to alcohol-induced amnesia.

As discussed in the section below on the potential brain mechanisms underlying alcohol-induced amnesia, it is easy to imagine that the impact of alcohol on brain circuitry could vary from person to person, rendering some people more sensitive than others to the memory-impairing effects of the drug.

How Does Alcohol Impair Memory?

During the first half of the 20th century, two theoretical hurdles hampered progress toward an understanding of the mechanisms underlying the effects of alcohol on memory. More recent research has cleared away these hurdles, allowing for tremendous gains in the area during the past 50 years.

The first hurdle concerned scientists' understanding of the functional neuroanatomy of memory. In the 1950s, following observations of an amnesic patient known as H.M., it became clear that different brain regions are involved in the formation, storage, and retrieval of different types of memory. In 1953, large portions of H.M.'s medial temporal lobes, including most of his hippocampus, were removed in an effort to control intractable seizures. Although the frequency and severity of H.M.'s seizures were significantly reduced by the surgery, it soon became clear that H.M. suffered from a dramatic syndrome of memory impairments. He still was able to learn basic motor skills, keep information active in short-term memory for a few seconds or more if left undistracted, and remember episodes of his life from long ago, but he was unable to form new long-term memories for facts and events. The pattern of H.M.'s impairments also forced a re-examination of models of long-term memory storage. Specifically, although H.M. was able to retrieve long-term memories formed roughly a year or more before his surgery, he could not recall events that transpired within the year preceding his surgery. This strongly suggests that the transfer of information into long-term storage actually takes place over several years, with the hippocampus being necessary for its retrieval for the first year or so.

Subsequent research with other patients confirmed that the hippocampus, an irregularly shaped structure deep in the forebrain, is critically involved in the formation of memories for events. Patient R.B. lost a significant amount of blood as a result of heart surgery. He survived but showed memory impairments similar to those exhibited by H.M. Upon his death, histology revealed that the loss of blood to R.B.'s brain damaged a small region of the hippocampus called hippocampal area CA1, which contains neurons known as pyramidal cells because of the triangular shape of their cell bodies. Hippocampal CA1 pyramidal cells assist the hippocampus in communicating with other areas of the brain. The hippocampus receives information from a wide variety of brain regions, many of them located in the tissue, called the neocortex, that blankets the brain and surrounds other brain structures. (Neocortex literally means "new bark" or "new covering." When one looks at a picture of the human brain, most of what is visible is neocortex.) The hippocampus somehow ties information from other brain regions together to form new autobiographical memories, and CA1 pyramidal cells send the results of this processing back out to the neocortex. As is clear from patient R.B., removing CA1 pyramidal cells from the circuitry prevents the hippocampal memory system from doing its job.

The second barrier to understanding the mechanisms underlying alcohol's effects on memory was an incomplete understanding of how alcohol affects brain function at a cellular level. Until recently, alcohol was assumed to affect the brain in a general way, simply shutting down the activity of all cells with which it came in contact. The pervasiveness of this assumption is reflected in numerous writings during the early 20th century. For instance, Fleming wrote, "The prophetic generalization of Schmiedeberg in 1833 that the pharmacological action of alcohol on the cerebrum is purely depressant has been found, most pharmacologists will agree, to characterize its action in general on all tissues". During the 1970s, researchers hypothesized that alcohol depressed neural activity by altering the movement of key molecules (in particular, lipids) in nerve cell membranes. This change then led to alterations in the activity of proteins, including those that influence communication between neurons by controlling the passage of positively or negatively charged atoms (ions) through cell membranes. This view persisted into the late 1980s, at which time the consensus began to shift as evidence mounted that alcohol has selective effects on the brain's nerve-cell communication (neurotransmitter) systems, altering activity in some types of receptors but not others. Substantial evidence now indicates that alcohol selectively alters the activity of specific complexes of proteins embedded in the membranes of cells (receptors) that bind neurotransmitters such as gamma-aminobutyric acid, glutamate, serotonin, acetylcholine, and glycine. In some cases, only a few amino acids appear to distinguish receptors that are sensitive to alcohol from those that are not. It remains unclear exactly how alcohol interacts with receptors to alter their activity.

About the Author

NIH is the nation's medical research agency - making important medical discoveries that improve health and save lives. The National Institutes of Health (NIH), a part of the U.S. Department of Health and Human Services, is the primary Federal agency for conducting and supporting medical research.