Research: Cognitive neuroscience, learning and memory, functional neuroimaging and computational modeling

My research is aimed at determining the neural mechanisms that underlie memory. Functional magnetic resonance imaging (fMRI) plays a dominant role in both my current and future research plans. However, I will begin by briefly describing the amnesic syndrome. The pattern of impairments found in amnesia provides an insight into the neural underpinnings of memory that not only sparked my initial interest in memory, but also serves to motivate and elucidate the questions that are at the core of my present and future research.

The amnesic syndrome, resulting from damage to the medial temporal lobe, is characterized by a strikingly selective deficit. Amnesic patients are impaired at learning new facts or events. In the most severe cases, such as patients H.M. and E.P., the impairment of "declarative" memory can be complete, such that no new facts or events can be learned after the onset of amnesia. For example, when E.P. is given a simple recognition memory task in which he is asked to decide which of two words was studied five minutes earlier, his performance is at chance. Despite numerous attempts to improve his accuracy, he does no better than flipping a coin (e.g., 49.9% over five experiments). Yet, amnesic patients' IQ, language, and immediate or working memory are normal, as are remote memories like childhood memories. Importantly, a large class of "nondeclarative" or "implicit" learning and memory tasks are normal as well. For example, when shown the first three letters of a word and asked to complete it with the first word that comes to mind, E.P., like healthy controls, is approximately 25% more likely to generate a word if he has recently seen it (a phenomenon called repetition priming). Yet, even immediately after E.P. responds with the "primed" word as the first word that comes to mind that completes the three-letter stem, he still has no ability to tell you whether or not the word was on the studied list (E.P. data from Stark & Squire, Behavioral Neuroscience, 2000).

Why? How is the brain constructed in such a way that one form of the memory for a word can be completely eliminated while leaving the other form completely intact? If there are two separate systems, why? How does each work? How are they similar? How are they different? How do they interact to both affect behavior or to affect each other? Studies of amnesic patients have allowed us to glimpse inside "the box" and given us some of our first insights to answering these questions. My research plan will make extensive use of fMRI to look further inside, aiming at elucidating the central question: What are the neural mechanisms of memory and how do they operate?

Stark Lab

224 Ames Hall
Department of Psychological and Brain Sciences
Johns Hopkins University
3400 North Charles Street
Baltimore, MD 21218
Phone: 410-516-6577
Fax: 410-516-4478