By Jeffrey C. Friedman

Paul Cox is a man of quiet reserve who in casual conversation gives the impression of a business executive just entering his peak earning years, rather than the hard working carpenter he was in his youth. But today, at 43, Paul has no career—unless you count the prison job he toils at each day in the New York penitentiary where he is serving double life for the 1988 murders of a couple he had never met. On the night before New Years Eve in 1988, in an alcohol-induced blackout, Paul stabbed them to death.

You might remember the case of Paul Cox, but not for the fact that he had committed an unspeakably brutal crime while in an alcoholic blackout—crimes committed in alcohol-fueled blackouts are way too common to make the front pages of newspapers. His case made headlines for an entirely different reason. Paul was arrested and charged with two counts of second-degree murder four long years after the night of the stabbings because he had disclosed his involvement in the crimes to members of Alcoholics Anonymous.

At his trial, Paul’s freedom depended on his lawyers’ assertion of two key points: One, that his blackout on the night of the crimes constituted a state of temporary insanity that prevented him from appreciating the wrongness of his actions. And two, that, since Paul’s confession was made to A.A. members, his statements should be considered privileged in the same way a disclosure to a priest or psychiatrist is. Because communication within an Alcoholics Anonymous meeting was privileged, his lawyers argued, any utterances Paul made to other members of A. A. were inadmissible in court.

It was bad news for Paul when the trial judge ruled against him on both of these points. The even worse news was that the state’s attorney’s case against Paul was of the slam-dunk variety.

Strange state of oblivion. At trial, the story told by the prosecutor about Paul’s actions on that night in December 1988 is one guaranteed to send a chill down the spine of anyone who has ever suffered an alcoholic blackout. After an evening of heavy drinking at a Larchmont, New York, bar, Paul was driving home with two drinking buddies. His last memory of that night was trying to negotiate a tight curve and one of his friends warning, “You’re not going to make it.” Then nothing.

The alcohol Paul had consumed that night had triggered a biological reaction deep within his forebrain that temporarily but effectively prevented it from forming new memories. Not even knowing it, Paul had entered the strange oblivion of an alcoholic blackout.

But somehow he made it home that night, and too early the next morning a bleary-eyed and befuddled Paul was roused by a phone call from the local police, who were pointedly interested in why they had found his damaged but drivable car abandoned along a Westchester County highway. Paul stammered through a weak and implausible explanation, but in reality he had no clue. In fact, prior to hearing from the police, he had assumed the car was parked in its usual spot in his driveway. Eventually, one of his drinking buddies told Paul that he had hit a guardrail, and, even though the car was still operable, he had abandoned it and his bewildered friends and calmly walked off down the road.

The same morning he spoke to the police, Paul first heard an ominous buzz circulating in the neighborhood about a husband and wife, both prominent local doctors, who had been stabbed to death the night before while asleep in their Dutch colonial home at 36 Lincoln St.—the same house in which the Coxes had lived when Paul was a child.

Detectives mounted a vigorous investigation of the murders, but before long, despite the money and man-hours they put into the case, they hit a dead end. They hadn’t found any viable suspects, they had no promising leads, and they lacked even a plausible motive for the crime. At the same time that the Larchmont police were scratching their heads over the murders, Paul began to feel a haunting unease and an inexplicable but increasingly intense sense of guilt whenever anyone talked about the crime. He also began to experience fragmented but persistent dream-like recollections of stabbing his own parents in their old family home.

These frightful quasi-memories combined with other alcohol-related life problems, and eventually Paul sought recovery in Alcoholics Anonymous. Two years after joining A. A., and in the clarity of sobriety, Paul was beginning to connect the dots of that horrible night. Ultimately he shared his fears and recollections about the stabbings with A.A. members. One of them informed the police about what he had disclosed, and detectives soon matched Paul’s fingerprints with those left in the victims’ blood all over the crime scene. Short months later, Paul was looking at the world through the bars of the upstate New York prison where he will likely spend the rest of his life.

Anatomy of a blackout. Paul Cox’s journey to prison began in an alcoholic blackout—a phenomenon known to anyone with a working knowledge of alcohol and alcoholism. Actually, an alcoholic blackout is a peculiar form of anterograde amnesia caused by the presence of a sufficient amount of alcohol in a drinker’s bloodstream. The term “anterograde amnesia” refers to memory loss in which the affected person is unable to form new memories after an actuating event (in this case, alcohol intoxication) but can remember everything, including procedural or how-to memory, known before the onset of the amnesia.

Anterograde amnesia is distinct from another kind of memory loss called retrograde amnesia. In retrograde amnesia, a person can remember present and ongoing events but cannot recall anything that happened prior to the actuating event (typically a traumatic brain injury) that triggered the amnesia.

Alcohol can produce measurable impairments in memory after only 2-3 drinks. A drinker who is in the netherworld of an alcoholic blackout can appear fairly normal; they are usually able to carry on conversations and even negotiate their way through difficult or complex tasks. There are even documented cases of pilots flying airplanes, surgeons performing complex operations and lawyers trying cases—all while in full-blown alcoholic blackouts. Both men and women drinkers seem to experience blackouts in about equal numbers and, surprisingly, blackouts are as common among social drinkers as they are in alcoholics.

Some drinkers, particularly those with a history of blackouts, are at a higher risk for blacking out whenever they drink heavily. There might also be a link between prenatal exposure to alcohol and a vulnerability toward blackouts. Some researchers believe there may even be a specific genetic predisposition to having blackouts.

And, while the alcoholic blackout is something that has long been recognized by medical science, the neurobiological process by which alcohol robs the brain of its ability to remember has only more recently been discovered.

Marker for alcoholism. The noted alcoholism researcher E. M. Jellinek studied alcoholic blackouts in the 1940s by surveying recovering members of Alcoholics Anonymous. Because of the high prevalence of blackouts in the drinking histories of A. A. members, Jellinek concluded that alcohol-induced blackouts, especially blackouts occurring early in one’s drinking career, were an accurate biological marker of alcoholism.

In 1969, based on interviews with 100 hospitalized alcoholics, Goodwin and his colleagues concluded that there were two distinct forms of alcoholic blackout: en bloc and fragmentary. According to Goodwin, an en bloc blackout is a complete loss of memory, characterized by an inability — despite all efforts by the drinker or others to cue recall — to remember any events that occurred while intoxicated. Fragmentary blackouts, as the term implies, involve only a partial inability to remember events. In fragmentary blackouts, forgotten events can sometimes be recalled with persistent cueing.

These data and their clinical implications were the result of careful observations of blackout drinkers. Alcoholism researchers had to be content with this kind of observed clinical data, because they lacked the kind of neuroimaging technology that would allow them to look deeply into the brains of blacked-out subjects. In the late 1960s though, innovative neuroimaging systems allowed a new generation of brain scientists to unravel the neurobiological intricacies of the alcoholic blackout.

The neurobiology of a blackout. To make sense of how alcohol can disrupt the brain’s ability to make memories, researchers first had to identify a model of memory formation that could be used as a contextual reference for the process of remembering, and also one that was adaptable to the rigors of neuroscientific investigation. A number of the early studies into the neurobiology of alcoholic blackouts used a paradigm of memory formation first described by Atkinson and Shiffrin and called the Modal Model of Memory.

In the Modal Model of Memory the formation of memories involves a number of distinct but coordinated actions that begin with sensory input forming an immediate, or sensory, memory (the kind of memory that lasts only a few seconds). If a person attends to the sensory memory and if information encoded in the sensory memory is important enough or if the information related to the memory is rehearsed, the immediate memory may then proceed to long-term storage—a place where it can be retrieved whenever it is needed.

Each of these processes is handled by a different part of the brain; the most critical of which is the hippocampus, a chili pepper shaped structure deep in the forebrain. The job of the hippocampus is to coordinate the process of memory formation by routing raw sensory data from a variety of sites in the neocortex (the outer, wrinkled surface layer of the brain) and sorting this often-jumbled information into a coherent autobiographical memory.  The hippocampus then sends the memory on—via tiny structures on its surface called pyramidal cells—to the brain’s frontal cortex, where it can be used to reason, plan and guide behavior.

In sufficient amounts, alcohol can prevent memory formation by disrupting the normal function of the hippocampus and paralyzing the pyramidal cells. When affected by alcohol the hippocampus loses its ability to sort the random sensory data sent to it by various areas of the neocortex. Hippocampal impairment is then compounded by alcohol-soaked pyramidal cells that are now incapable of sending memories, jumbled or otherwise, to the frontal cortex. By causing a dysfunction in the hippocampus and pyramidal cells, alcohol ensures that the drinker’s brain cannot form new usable memories. A person in an alcoholic blackout lives only in the present, lacking any kind of immediate or recent memory to guide their speech or actions. Memory loss is why intoxicated people often repeat themselves in conversation—going over the same conversational ground again and again.

Some drinking behaviors can increase the risk of triggering an alcohol-induced blackout. There is persuasive data that suggests that gulping drinks can heighten one’s risk of blacking out. Drinkers who suffer alcoholic blackouts often drink too much and too quickly. The rapidity of rise in blood alcohol level (BAL) may be as important in triggering a blackout as a high BAL itself . Alcohol can also interact with other drugs, several of which even when taken alone, are capable of producing dysregulation in hippocampal function similar to that produced by alcohol.

Benzodiazepines, like Valium® and Xanax® can cause memory impairment even when taken alone and in amounts only minimally higher than a large therapeutic dose. And when alcohol and benzodiazepines are taken in combination, the effect is almost guaranteed to result in a blackout. Recent data clearly show that using alcohol and marijuana together results in greater memory impairment than would result if either drug were taken alone.

Over the past twenty years tremendous advances have been made in our understanding of alcohol-related memory loss. In the near future, a new generation of electrophysiological recording devices—instruments that will allow scientists to gather data from many parts of the brain simultaneously–will likely yield new and more detailed information and possibly a more nuanced understanding of how alcohol can impact a wide range of brain functioning, including memory formation. But these new insights may end up being of more interest to the neuroscientific community than to the typical problem drinker.

Most problem drinkers are already familiar with a much more cogent reality: Horrible things can happen to people when alcohol shuts down their brain’s ability to remember. Just ask Paul Cox.

Jeffrey C. Friedman is a licensed substance abuse therapist at Cottonwood Tucson, a behavioral health treatment center in Tucson, Arizona. His work includes treating chemically dependent and disordered gambling patients, lecturing on the neurobiology of addictive and mood disorders, and presenting workshops on behavioral health issues at conferences throughout the U.S., Europe and Asia. For more information: www.cottonwoodtucson.com. Email Jeff at jfriedman@Cottonwoodtucson.com.