The Neuropsychoimaging Group studies human brain function related to behavior, cognition, and emotion. Special emphasis is given to drug addiction (crack/cocaine, methamphetamine, alcohol), and other problem behaviors (aggression, intermittent explosive disorder). Comorbid psychopathology (depression, post traumatic stress disorder, antisocial personality) is also of interest.
Our research specifically incorporates the cutting-edge imaging technologies available for Medical Research at Brookhaven National Laboratory (BNL); we harvest the benefits of developing cross-modality imaging (e.g., simultaneous ERP-fMRI recordings) and sensitive behavioral and neuropsychological assays, thus creating the translational capabilities that are the cornerstone of neuropsychoimaging research.
Our unique toolset includes BNL's 4-Tesla MRI and PET facilities, Magstim non-invasive magnetic stimulation system, tailored neuropsychological batteries, Compumedics NeuroSCAN event-related potentials and EEG analyses, and NeuroSCAN STIM and e-Prime experiment presentation software. All stimulation and assessment systems include specialized modules for examining inhibitory control and reward processing.
The organization of our neuropsychoimaging research is represented by the pyramid above, with its foundation based on cognitive and behavioral measures. The complementary nature of the interrelationships between the various approaches to studying the behaving human brain is emphasized by the left-sided bi-directional arrow.
Level I encompasses a broad range of both computerized and paper-and-pencil measures of cognition (attention, memory, inhibitory control, decision-making), emotion and personality (anger, harm avoidance, depression), and behavioral tendencies (e.g., aggression). This broad foundation of tests and measures is selected based on a-priori hypotheses about underlying neural pathways.
Level II provides a platform to test common neuropsychological questions (see below). Here we develop and test new behavioral assays to non-invasively target specific neural networks implicated in the core characteristics of drug addiction and other problem behaviors.
Level III provides more direct, although still correlational, studies of the interplay between behavioral measures (e.g., inhibition of prepotent response tendencies as measured by the Stroop effect, see Goldstein et al., 2001; harm avoidance/fear as measured by MPQ, see Goldstein et al., 2002; and anger as measured by the MMPI, see Goldstein et al., 2005) and their putative neurobiological substrates (e.g., glucose metabolism in the orbitofrontal cortex as measured by PET FDG).
Level IV provides experimental testing of a-priori hypotheses: a well-controlled study (including a control group and a control intervention/condition) is designed for the fMRI, PET, or ERP environment.
At each level the neuropsychoimaging method can serve both exploratory and confirmatory purposes (e.g., fMRI/PET SPM voxel-by-voxel analyses vs. ROI analyses), depending on the design of the study and data analysis. Also note that feed-forward and feedback loops between all four levels are essential for our comprehensive research, where we advance the dynamic psychobiological study of human behavior.
Basic Neuropsychological Questions
- Does drug addiction impair cognitive function? See Goldstein et al., 2004 for documentation of the level of cognitive impairment in drug addiction and Woicik et al., 2009 for modulation by recent drug use.
- Are there associated personality-emotional changes? If so, to what extent?
- What are the cognitive-behavioral impairments and emotional changes most characteristic of drug (particularly psychostimulant) addiction? See recent focus on impairments in insight/self-awareness (Moeller et al., 2009 , Moeller et al., 2010, and Goldstein et al., 2009).
- Are there differences between the various classes of drugs of addiction in their effects on psychological functioning?
- What are the similarities with other non-drug forms of addiction (e.g., gambling, obesity)?
- What is the neurobiological basis of each of these changes? Are there parallel changes in the underlying neural networks that can be mapped/imaged using fMRI, PET, or ERP?
Is there a genetic contribution? See recent study showing the MAO A contributes to low grey matter in the orbitofrontal
cortex in cocaine addicted individuals.
- Can these dysfunctions be normalized in addiction and what would be the impact on longer-term treatment outcome? See recent study showing effect of oral methylphenidate on reducing impulsivity and improving prefrontal cortical function in cocaine addicted individuals.
We have designed an extensive neuropsychological battery which is administered to all subjects that participate in our fMRI, ERP, and PET studies (e.g., drug addicted subjects, individuals at-risk for developing drug addiction, healthy controls) to allow for both between- and within-group comparisons. This battery of tests includes:
(1) paper-and-pencil or computerized cognitive-behavioral tasks that assess attention, memory, emotional processing, motor speed, and executive functions (inhibitory control, shifting, planning, reasoning);
(3) newly developed computerized tasks that target drug-related choice, self-awareness, and other behaviors (e.g., sensitivity to reward, predisposition to aggression) associated with the mesolimbic and mesocortical pathways. See Drug Addiction.
(4) neuroimaging tasks (cognitive-behavioral tasks) conducted simultaneously during fMRI, ERP, PET are described under the links in the left-hand frame.