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Meet Edith Sullivan, Ph.D.

Edith Sullivan's PhotoWriter Sherry Wasilow interviewed Dr. Sullivan from her office in the Stanford Institute for Neuro-Innovation & Translational Neurosciences at the Stanford School of Medicine.

SW: Do you approach your research with any particular goal in mind?

“When I was with my daughter-in-law in a hospital prenatal care suite, a medical student took her history and, to his credit, asked her how much she drank,” said Sullivan. “After the interview, I asked him what he would do with such information if she had said she had drunk a large amount. Unfortunately, he had no answer. We need to educate the profession not only to ask about hazardous alcohol use, but why it is important to ask, and then what to do about it.”

SW: How did you evolve from your early studies on amnesia to your current focus on alcohol dependence?

ES: Before studying alcoholism and alcoholism-related memory disorders, while I was a researcher at Massachusetts Institute of Technology (MIT), I had the privilege of testing the amnesic patient, H.M., who was not alcoholic but had intractable epilepsy and had undergone surgery to remove brain tissue that was believed to be causing the virtually daily, life-threatening seizures he suffered. image of the brainThe surgery performed to treat his seizures removed an extensive amount of brain tissue in the medial temporal lobes, including nearly all of the hippocampal tissue in both hemispheres of his brain. In addition to reducing the frequency and severity of H.M.'s seizures, this surgery caused his profound memory impairment. Great controversy arose at that time regarding the brain structure that causes of amnesia noted patients with bilateral medial temporal lobe lesions, like H.M. (although his amnesia was perhaps the most dense recognized), compared with amnesia characteristic of patients with diencephalic and thalamic lesions (thought not to have severe hippocampal damage), like those presumed in alcohol-related Korsakoff Syndrome (KS). This early controversy pre-dated high-resolution brain imaging.

In struggling to resolve the controversy, at least within my own conceptualization of amnesia, I became aware of impairments in cognitive and motor functions that non-amnesic alcoholics commonly endure. Placing KS amnesia in the context of additional non-mnemonic (non-memory) impairments served to complicate the KS amnesia picture, which from my perspective needed further exploration.

SW: What is Korsakoff Syndrome?

ES: Korsakoff Syndrome is a neurological disorder characterized by disproportionate memory loss in relation to other cognitive abilities. It is thought to result from a deficiency of thiamine (vitamin B1). In the United States, most cases occur in individuals who abuse alcohol.

Alcoholic KS was one of the primary causes of global amnesia, and these patients helped memory theorists recognize that memory is not a unitary function but is composed of multiple component processes. Some of these processes – most characteristically, those that enable us to remember specific events and new information – are devastated in classical amnesic disorders such as KS and Alzheimer's disease. Yet some other memory processes remain relatively unaffected, such as those involving motor procedural learning (such as riding a bicycle) and visual and verbal priming (such as being unwittingly biased by preceding information that modifies a response).

SW: What came next?

At that time in my career, I was fortunate to become a member of the brain imaging and electrophysiology laboratory of Adolf Pfefferbaum, M.D. in California. Dolf had--and still does have-- an active and highly respected program of research in alcoholism, was publishing seminal work in alcoholism, and had embarked on studies of structural brain imaging using methods for image quantification he had developed. This meant I could use brain imaging to complement my neuropsychology research. Furthermore, Dolf's laboratory had an active alcoholism research program that was working with individuals with alcohol-use disorders (AUDs) and KS from the local Veterans Affairs.

This meant I could pose questions about selective cognitive and motor functions that were spared or impaired in chronic alcoholism, whether or not they were complicated by KS, and at the same time use brain imaging to quantify tissue in brain regions at the center of the memory controversy. Although not all has been resolved, we have discovered through neuroimaging one piece of the puzzle: despite earlier beliefs, KS patients do have hippocampal atrophy, the extent of which correlated with the severity of their amnesia. Thus, we found quantitative evidence that the so-called diencephalic amnesia also had a medial temporal lobe (i.e., hippocampal) source.

SW: Describe your current research activities.

As my years of alcoholism research have evolved, I have become especially interested in nonamnesic alcoholism and the subtler cognitive and motor impairments such individuals sustain. Cognitive functions that are commonly affected in persons in recovery from alcoholism are working memory (especially for nonverbal material, like spatial locations and directions), visuospatial abilities (such as following directions on a map or assembling pieces to make something like a piece of furniture), problem solving, and conflict resolution.

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