Plenary addresses are open to ALL registered meeting attendees and require no additional fee to attend. Attendees do have the option to pay a separate CE registration fee in order to receive Continuing Education (CE) credit for each plenary they attend in full (please see the CE Program page for complete details).
Plenary speaker abstracts, learning objectives, and bios are listed below in their order of appearance.
Wednesday February 1, 2017
Plenary A — The INS Presidential Address: The Impact of the Past on Current and Future Views of Limb Apraxia
Wednesday February 1, 4:30-5:30 PM in Carondelet (Grand Ballroom)
Kathleen Y. Haaland, PhD, ABPP-CN
Abstract & Learning Objectives: This presentation will explore the impact of single cases on past and current conceptualizations of limb apraxia including the work of Hugo Liepmann and several previous INS presidents (Geschwind, Kaplan, Heilman, and Gonzalez Rothi). Videotapes of classic apraxic syndromes will be presented. A major focus will be on how the views of the cognitive and neuroanatomical correlates of limb apraxia have changed from the 19th to the 21st century leading to the current emphasis on a left hemisphere cortical network with a left parietal node. Unanswered questions, including the differential roles of left parietal, temporal, and frontal regions in limb praxis, will be discussed in the context of future work that utilizes multi-method approaches that integrate lesion studies with functional imaging and stimulation studies.
Upon conclusion of this course, learners will be able to:
- Delineate one way that Liepmann's cases influenced his theory of limb apraxia.
- Discuss one major difference between Geschwind's view and Heilman and Gonzalez Rothi's view of the parietal lobe's role in limb apraxia.
- Specify one function of the left parietal lobe in limb apraxia.
- List two methods that have informed current understanding of the neuroanatomical substrates of limb praxis to emphasize a broad left hemisphere network with critical node in the left parietal lobe.
Speaker Biography: Kathleen Haaland is a Professor of Psychiatry & Behavioral Sciences and Neurology at the University of New Mexico. She is board certified by the American Board of Professional Psychology and the American Board of Clinical Neuropsychology. She has published over 100 papers and chapters largely focused on the cognitive and neuroanatomical correlates of action in stroke, Parkinson's Disease, and Huntington's Disease. Her research has been continuously funded from 1981 to 2014. More recently she has developed an interest in the neuropsychological correlates of PTSD. She has been recognized by the National Academy of Neuropsychology with a Lifetime Career Contribution Award, and she was the previous president of the American Board of Clinical Neuropsychology and the Society of Clinical Neuropsychology of the American Psychological Association. She was the Editor of the Journal of the International Neuropsychological Society from 2004 to 2014, and she is currently the President of the International Neuropsychological Society.
Thursday February 2, 2017
Plenary B: Frontal Cortex and Human Behavior: Evidence from Intracranial Recording
Thursday February 2, 10:45-11:45 AM in Carondelet (Grand Ballroom)
Robert T. Knight, MD
Abstract & Learning Objectives: Neuropsychological evidence has documented the critical role of prefrontal cortex (PFC) in the control of cognitive and social processing with extensive lateral or orbital PFC damage resulting in a profound disintegration of goal-directed behavior. This lecture will first describe novel neural activity linked to cognition recently unveiled by intracranial recordings in humans. Second, these brain signals will be used to link PFC function to cognitive control across a range of tasks. Direct cortical recording (electrocorticography; ECoG) provides unique insights in the role of PFC in cognition and social interaction. Since the discovery of the EEG in the 1920's, neurophysiological dogma stated that the human cortex did not generate reliable rhythms above 50-60 Hz. However, findings over the last decade report neural activity up to 250 Hz in the human cortex. Every cognitive process examined with intracranial recording including language, attention, memory and decision-making generates task-specific high frequency activity in the range of 70-250 Hz (high frequency band; HFB). Importantly, the HFB band has superb spatial localization and task specificity. HFB recording has provided novel insights into the role of Broca's area in language processing, the hierarchical organization of PFC, and the critical role of PFC in contextual processing, decision making and working memory. Importantly, the HFB is phase locked to the trough of slower cortical oscillations with different PFC dependent tasks eliciting unique spatial patterns of HFB-theta coupling. These results provide evidence that transient coupling between low- and high-frequency brain activity provides a mechanism for effective communication in distributed neural networks engaged during PFC dependent cognitive processing. The results obtained from the study of PFC patients and from intracranial recording support the proposal that the devastating human prefrontal syndrome can be viewed as a failure of PFC control of distributed neural networks subserving human behavior.
After attending this session, learners will be able to demonstrate that they:
- Understand the role of high frequency brain activity in cognition
- Understand the role of low frequency brain oscillations in establishing networks supporting cognition
- Understand the key role of prefrontal cortex in orchestrating neural networks in the service of cognition
Speaker Biography: Dr. Knight received a BS in Physics from the Illinois Institute of Technology, an MD from Northwestern University Medical School, did Neurology training at UC San Diego and Post-Doctoral training at the Salk Institute. He was at UC Davis from 1980-1998 and moved to UC Berkeley in 1998 where he served as Director of the Helen Wills Neuroscience Institute until 2011. Dr. Knight has twice received the Jacob Javits Award from the National Institute of Neurological Disorders and Stroke for distinguished contributions to neurological research, the IBM Cognitive Computing Award, the German Humboldt Prize in Neurobiology and the Distinguished Career Contribution Award from the Cognitive Neuroscience Society. He studies neurological patients with frontal lobe damage and records electrical signals directly from the brain in neurosurgical patients to understand the role of prefrontal cortex in behavior. His laboratory is also engaged in developing a speech prosthesis for use in patients with disabling neurological disorders.
Plenary C — Developmental Amnesia: Memory Formation in the Absence of Remembering
Thursday February 2, 2:45-3:45 PM in Carondelet (Grand Ballroom)
Faraneh Vargha-Khadem, PhD
Abstract & Learning Objectives: Developmental Amnesia, a disorder resulting from early bilateral damage to the hippocampus, is characterized by four dissociations in memory processes, viz: severe impairment of episodic and autobiographical memory, spatial navigation, recall, and recollection, in the presence of spared semantic memory, perception, recognition and familiarity. This lecture will (a) review the history of cognitive memory research in adults and children, (b) examine the evidence for the neural circuits serving different components of memory processes, (c) relate the findings in humans to results of lesion studies in non-human primates, and (d) provide preliminary evidence on new methods of learning and memory retrieval in patients with developmental amnesia. The lecture aims to differentiate between neural systems that support the development of intelligence and knowledge acquisition versus memory and learning.
As a result of attending this lecture, the audience will learn how to (1) diagnose the syndrome of developmental amnesia in children and adolescents, (2) use neuroimaging evidence to determine which components of cognitive processes are compromised, and (3) become familiar with translational research techniques for learning new information in the presence of early damage to the hippocampus.
Speaker Biography: Faraneh Vargha-Khadem is a Professor of Developmental Cognitive Neuroscience, and Head of Section on Cognitive Neuroscience and Neuropsychiatry at the UCL Institute of Child Health. She is also the Clinical-Academic Lead for Neuropsychology at Great Ormond Street Hospital for Children NHS Foundation Trust, and the founding Director of the UCL Centre for Developmental Cognitive Neuroscience (CDCN). The CDCN aims to promote cross faculty and cross disciplinary collaboration to promote a life span approach to clinical translational research. Faraneh conducts research on the effects of brain injury on neural circuits serving memory and learning, speech and language, spatial navigation, and movement organization. Faraneh is the Principal Investigator of two consecutive programme grants from the Medical Research Council. She is a Fellow of the Academy of Medical Sciences, and has received a number of national and international awards including the Distinguished Career Award of the International Neuropsychological Society, the Barbara Wilson Award of the British Neuropsychological Society, and the Jean Louis Signoret Prize for her contributions to understanding the genetics of behaviour.
Plenary D — The Birch Memorial Lecture: Cognitive Neural Prosthetics to Overcome Brain and Spinal Cord Injury
Thursday February 2, 4:00-5:00 PM in Carondelet (Grand Ballroom)
Richard A. Andersen, PhD
Abstract & Learning Objectives: Neural prosthetics are designed to assist patients paralyzed from spinal cord injury, peripheral neuropathies, and stroke. Neural activity is recorded and decoded to determine the subjects' intent, which can then be used to control assistive devices such as robots or computers. Initial proofs of concept can be traced back to studies in animals as early as the late 1950s and early 1960s.
At the turn of this century there have been a handful of clinical studies in humans in which implants of arrays of microelectrodes were made in the motor cortex of tetraplegic participants. On the other hand, posterior parietal cortex (PPC) provides high-order intent signals to motor cortex that are then used by motor cortex to control the muscles. We reasoned that the high-level intent signals of PPC could be easily interpreted by "smart" robotic systems, enhancing the versatility and intuitiveness of brain control.
In the course of PPC recordings with tetraplegic humans we have uncovered remarkable cognitive features that we have used for prosthetic control. Imagined goals and sequences can be decoded extremely rapidly, both sides of the body are represented which promises bilateral control, and complete hand shapes are encoded by single neurons allowing grasp control with very few cells. Individual finger movements are well represented and have even allowed a subject to perform brain controlled typing on a virtual keyboard and playing a simple melody on a virtual piano. Neurons are selective for very high order cognitive features such as both imagined and observed movements, and the representation of numerical quantities and simple mathematical operations. These wide-ranging findings point to future advanced neuroprosthetic applications in which PPC and other cognitive cortical areas are tapped for the unique cognitive variables they represent.
Through attending this lecture, attendees will:
- Learn how neural prosthetics can help people with paralysis
- Learn what distinguishes a motor prosthetic from a cognitive prosthetic
- Understand how touch sensation is important for manipulation of objects with the hand and how this sensory feedback might be recreated for people with paralysis and loss of somesthesis.
Speaker Biography: Richard Andersen, the James G. Boswell Professor of Neuroscience at Caltech, studies neural mechanisms of sight, hearing, balance, touch, and action, and the development of neural prosthetics. Andersen obtained a Ph.D. from the University of California, San Francisco and completed a postdoctoral fellowship at the Johns Hopkins Medical School. He was a faculty member of the Salk Institute and MIT before coming to Caltech. Andersen is a member of the National Academy of Sciences, the National Academy of Medicine, and the American Academy of Arts and Sciences. He is recipient of a McKnight Foundation Scholars Award, a Sloan Foundation Fellowship, Visiting Professor at the College de France, and the Spencer Award from Columbia University. He has served as Director of the McDonnell/Pew Center for Cognitive Neuroscience at MIT, and the Sloan-Swartz Center for Theoretical Neurobiology at Caltech, as well as being a member or chair of various government advisory committees.
Friday February 3, 2017
Plenary E — Behavioral Clusters and Brain Network Mechanisms of Impairment and Recovery
Friday February 3, 11:00-12:00 PM in Carondelet (Grand Ballroom)
Maurizio Corbetta, MD
Abstract (Learning Objectives Forthcoming): A long-held view is that stroke causes many distinct neurological syndromes due to damage of specialized cortical and subcortical centers. However, in recent studies on a large cohort of first time stroke subjects studied longitudinally at 2 weeks, 3 and 12 months, we showed that a few clusters of behavioral deficits spanning multiple functions explained neurological impairment. These clusters are stable across recovery indicating that they represent a stable solution to describe impairment. It has been also proposed that focal lesions cause remote physiological abnormalities, but the behavioral relevance of these changes vis-a-vis structural damage is unknown. In separate studies we measured resting functional connectivity fMRI (FC), lesion topography, and behavior in multiple domains (attention, visual memory, verbal memory, language, motor, and visual), and used machine-learning models to predict neurological impairment in individual subjects. We found that visual memory and verbal memory were better predicted by FC, whereas visual and motor impairments were better predicted by lesion topography. Attention and language deficits were well predicted by both. These results link key organizational features of brain networks to brain-behavior relationships in stroke.
Speaker Biography: Dr. Maurizio Corbetta is Professor and Chair of Neurology at the University of Padua; Founding Director of the Padua Neuroscience Center; Professor of Neurology, Radiology, Neuroscience, and Bioengineering at Washington University School of Medicine. Dr. Corbetta has pioneered experiments on the neural mechanisms of human attention with Positron Emission Tomography (PET). He has discovered two brain networks dedicated to attention control, the dorsal and ventral attention networks, and developed, in collaboration with Dr. Gordon Shulman, a brain model of attention that has been cited in the literature more than 5,000 times. His clinical work has focused on the physiological correlates of focal injury. He has developed a pathogenetic model of the syndrome of hemispatial neglect. He is currently developing novel methods for studying the functional organization of the brain using functional connectivity MRI, magneto-encephalography (MEG), and electro-corticography (EcoG). He is working on the effects of focal injuries on the network organization of brain systems with an eye to neuromodulation.
Plenary F — Contributions to Understanding the Dynamic Course of Alcoholism: An INS Legacy
Friday February 3, 3:00-4:00 PM in Carondelet (Grand Ballroom)
Edith V. Sullivan, PhD
Abstract & Learning Objectives: Alcohol Use Disorder (AUD) has been a major cause of family, social, and personal strife for centuries, with current prevalence estimates of 14% for 12-month and 29% lifetime AUD. Neuropsychological testing of selective cognitive, sensory, and motor functions complemented with in vivo brain imaging has enabled tracking the consequences of AUD, which follows a dynamic course of development, maintenance, and recovery or relapse. Controlled studies of alcoholism have revealed evidence for disruption of selective functions involving executive, visuospatial, mnemonic, emotional, and balance abilities and brain systems supporting these functions, notably, frontocerebellar, frontostriatal, and frontolimbic circuitry. On a hopeful front, longitudinal study provides convincing evidence for improvement in brain structure and function following sustained sobriety. These discoveries have a strong legacy in INS, starting from its early days when assumptions regarding which brain regions were disrupted relied solely on patterns of functional sparing and impairment deduced from testing. Today's work using refinements in assessment and multi-modal neuroimaging builds on that legacy, moving the field toward examination of compensatory processes to overcome impaired functions.
After attending this session, learners will be able to:
- Recognize that alcohol dependence disrupts selective brain structures and functions
- Appreciate that alcoholism-related functional brain changes are a form of neuroadaptation that may underlie dysfunction, making alcoholism a self-perpetuating disorder
- Learn that sustained sobriety can result in improvement in brain structure and function, indicative of damage reversal or compensatory mechanisms that can be identified with formal neuropsychological testing and longitudinal, quantitative structural and functional brain imaging
Disclosed support: AA010723, AA012388, AA013521-INIA, AA017168, AA021697-NCANDA
Speaker's Biography: My commitment to research on human alcoholism began nearly 30 years ago when I joined the Neuroimaging Group at Stanford. I brought to this research collaboration my background as an experimental neuropsychologist and gained from the collaboration experience and expertise as a brain imaging scientist, thus providing complementary understanding about the potential of establishing brain structure-function relations for the first time in alcoholism. This background led to the development of my program of study in alcoholism, focusing on faulty frontocerebellar circuitry as underlying a selective subset of cognitive and motor dysfunctions commonly expressed in alcoholism. In addition to my R01 grant of two decades and now a MERIT Award, I am a recipient of an U01 award for international studies on alcoholism with two INSERM sites in France. In addition, over the past 10 years, I have sought neural mechanisms of alcohol's untoward effect on brain structure and function using rodent models of chronic exposure to high levels of alcohol. My current work focuses on neural mechanisms of structural and functional connectivity underlying cognitive and motor process and interhemispheric communication in human alcoholism and how comorbidities of HIV infection, hepatitis C infection along with normal aging compound the throes of alcoholism on brain structure, function, and neural circuitry. Most recently, I have embarked on a multi-site consortium study aimed at determining the developmental trajectories of brain, neuropsychological, and emotional development of adolescents and to track deviations from normal trajectories in adolescents who initiate excessive alcohol drinking and measure recovery in those who stop drinking. Coupled with my NIAAA K05 Senior Mentor Award, this integrated research program provides a rich environment for mentoring promising young investigators, who will be the next generation of scientists dedicated to the field of alcohol research.
Saturday February 4, 2017
Plenary G — The 1st Annual Edith Kaplan Memorial Lecture: Language and the Brain: From Past Studies to Future Aspirations
Saturday February 4, 12:00-1:00 PM in Carondelet (Grand Ballroom)
Nina Dronkers, PhD
Abstract & Learning Objectives: Past approaches to the study of language and the brain have focused largely on the contributions of Broca's and Wernicke's areas. By using advanced neuroimaging techniques with individuals who have aphasia, we have now learned that language is an extraordinarily complex system that requires an extensive and interactive network of brain regions to sustain it. We have also learned that an intricate system of fiber pathways connect these regions together and has been underestimated in terms of its importance in supporting language. This information has advanced our understanding of how the brain processes language in important ways, while inviting future investigations to embrace novel approaches to the study of brain-behavior relationships.
This lecture is intended to help the listener: 1) compare past versus present methods of assessing brain-language relationships, and 2) incorporate localizationist models of language and cognition with a network perspective to better understand the neural mechanisms of language and cognition.
Speaker Biography: Nina F. Dronkers is a VA Research Career Scientist and Director of the Center for Aphasia and Related Disorders with the Department of Veterans Affairs Northern California Health Care System. She is also an Adjunct Professor at the University of California, Davis in the Department of Neurology. She received her interdisciplinary Ph.D. degree in Neuropsychology from the University of California, Berkeley in 1985, as well as earlier degrees in Linguistics and Educational Psychology from UC Berkeley. Dr. Dronkers' research and clinical interests have always focused on understanding the speech, language, and cognitive disorders that occur after injury to the brain as determined by structural neuroimaging. She and her colleagues have worked extensively with individuals who have aphasia to understand the relationship between areas of the brain affected by injury and the speech and language disorders that ensue. Using numerous methodologies, including their voxel-based lesion symptom mapping (VLSM) technique, Dr. Dronkers and her colleagues have isolated numerous brain regions that play critical roles in the processing of speech and language, as well as how these relate to other cognitive skills. Her latest work involves analyzing the structural and functional connections that contribute to language and cognitive processing through advanced work with diffusion and resting state functional neuroimaging.