Day 1 :
Keynote Forum
Theresa D Hernandez
University of Colorado USA
Keynote: Traumatic Brain Injury: What it is, What it isn’t and What Can be Done about it
Time : 09:00-09:30
Biography:
Hernández, Ph.D. has been studying traumatic brain injury (TBI) using basic and clinical neuroscience models since 1985. Her ongoing, extramurally funded research program assesses the degree to which recovery and functional outcome after TBI can be optimized in a variety of populations (Veterans, civilians, athletes). This includes conducting randomized, placebo-controlled, blinded trials of novel interventions, such as acupressure. This work is accomplished through her appointment as Professor and Chair of the Department of Psychology & Neuroscience at CU Boulder, her appointment as a Senior Investigator and Research Psychologist in the Eastern Colorado Healthcare System, Rocky Mountain MIRECC (Mental Illness, Research, Education & Clinical Center) and through her role as one of the co-Directors of the PAPRR (Promoting Athlete Performance, Recovery and Resilience) Board at CU Boulder. She is also the Director of the CAIRR (Clinical Assessment of Injury, Recovery and Resilience) Neuroscience Laboratory.
Abstract:
Traumatic brain injury (TBI) is highly prevalent. Certain populations appear to be more at risk, even if the functionalrnconsequences are similar. Outcomes from a TBI will be dependent on severity. Though even after a mild TBI, while goodrnoutcomes can be expected for the majority, there are still many for whom symptoms are persistent and problematic. Indeed, onernof the challenges of a TBI is that recovery is typically variable and often incomplete. Gaining an understanding of what relates tornand is predictive of good vs. poor outcome is important. Equally important is taking this information and identifying targets ofrnopportunity for optimizing outcome.
Keynote Forum
Natalie Rasgon
Stanford Health Care, USA
Keynote: 3D Dilemma of this Century
Time : 09:30-10:00
Biography:
Rasgon is a Professor in the Department of Psychiatry and Behavioral Sciences and Obstetrics and Gynecology in the Stanford School of Medicine. Dr. Rasgon has been involved in longitudinal placebo-controlled neuroendocrine studies for over two decades, and she has been involved in neuroendocrine and brain imaging studies of estrogen effects on depressed menopausal women for over 10 years. In addition to her duties as a Professor of Psychiatry and Obstetrics & Gynecology, Dr. Rasgon is also the Director of the Stanford Center for Neuroscience in Women’s Health and Associate Dean of Academic Affairs for the School of Medicine. She has an extensive history of teaching and mentoring, and many of her trainees have secured independent faculty positions in academia.
Abstract:
In the United States, it is estimated that approximately 50% of the population aged 50 years and older have a diagnosis of majorrndepression. 5.3 million Americans of all ages carry a diagnosis of dementia and 29.1 million have diabetes. It is not a coincidencernthen that these three Ds (diabetes, depression, and dementia) are so prevalent in our society. The reciprocal links between thernnervous system and endocrine systems underlie changes in the brain and body in both depressive illness and diabetes. Depressiverndisorder is associated with blunted central serotonin release, which, in turn, has been associated with metabolic dysfunction. Inrnaddition, inflammatory responses are widely implicated in the pathophysiology of diabetes and cardiovascular disease, as well asrnin cognitive impairment. Several other mediators of the reciprocal interaction between the CNS and insulin resistance includernglucocorticoids (cortisol), insulin, serotonin, and glutamate among others. While insulin affects hippocampal structures involvedrnin body weight regulation, it also influences memory processing. It is important to understand that diabetes, depression, andrndementia represent complex psychoneuroendocrine conditions requiring complex multisystem approach to their prevention andrntreatment.
Keynote Forum
Hans von Holst
Royal Institute of Technology, Sweden
Keynote: A new hypothesis to cytotoxic brain tissue edema and its potential treatment in neurosurgery
Time : 10:00-10:30
Biography:
Hans von Holst received his Medical Doctor´s degree in 1976 at Karolinska Institutet and completed his specialist training in Neurosurgery 1982 at Karolinska University Hospital. In 1985 he earned his PhD when he also became Associate Professor in Neurosurgery, Clinical Neuroscience at Karolinska Institutet. Since 1988 he holds a position as Senior Physician in Neurosurgery at Karolinska University Hospital. During 1991-1996 he was appointed as Chairman of the Dept of Neurosurgery and Division Manager of the Neuroclinics at Karolinska University Hospital, respectively. From 1992 to 2006 he was appointed as chairman of the World Health Organization collaborating center for neurotrauma at Karolinska Institutet. Since 2003 he is Professor in Neuroengineering and Head of the Division of Neuroengineering at the Royal Institute of Technology in Stockholm. He has over 120 original research publications, book chapters and books
Abstract:
Brain diseases such as traumatic brain injury often present with cytotoxic brain tissue edema as a secondary consequence\r\nto ischemia. The pathophysiological mechanisms are known to some extent but far from complete. Using an advanced\r\ncomputational simulation model the consequences of kinetic energy transfer following external dynamic impacts were analyzed\r\nincluding the intracranial pressure (ICP), strain level and their potential influences on the non-covalent and covalent bonds in\r\nfolded protein structures. Based on clinical material the simulations showed that the transferred kinetic energy is mainly absorbed\r\nby the skin and three bone layers. Also, a substantial amount of kinetic energy reached the gray and white matter. Thus, the kinetic\r\nenergy from a dynamic impact has the theoretical potential to interfere not only with non-covalent but also covalent bonds when\r\nhigh enough. The induced mechanical strain and pressure may further interfere with the protein structures as well as the energy\r\nrich bonds in nucleotide adenosine-triphosphates. This event causes attraction of increased water molecules into the unfolded\r\nprotein structures and could to some extent explain the etiology to cytotoxic brain tissue edema. Based on the new knowledge\r\nit is realistic to suggest a change the neurosurgical treatment of today by using neuro-engineering simulations already before a\r\nneurosurgical procedure is taking place. Thus, the innovative hypothesis makes it possible to open up for new drug and infusion\r\ntreatments aiming at reducing the severe consequences of cytotoxic brain tissue edema to further improve the prognosis following\r\ntraumatic brain injury.