- Brain Science International is pleased to introduce the addition of Dr. J. Lucas Koberda, M.D., Ph.D. to our panel of experts
- By Jason von Stietz, Ph.D.
- April 3, 2018
Brain Science International is pleased to introduce the addition of Dr. J. Lucas Koberda, M.D., Ph.D. to our panel of experts. Dr. Koberda will be reading EEG’s and producing qEEG reports as well as neurofeedback recommendations.
Dr. J. Lucas Koberda, M.D.,Ph.D.
Dr. J. Lucas Koberda is a board certified neurologist and an internationally trained physician who completed his residency in Neurology at the Oregon Health Sciences University in Portland, Oregon. Prior to his neurological training, he received his Ph.D. based on his research in the area of tumor immunology. His research skills were also enhanced by post-doctoral training completed at MD. Anderson Cancer Center in Houston, Tx. Dr. Koberda is currently affiliated with The Florida State University College of Medicine. Dr. Koberda also has founded and became CEO of "Brain Enhancement, Inc." non-for profit organization. This organization focuses on neuromodulation and modern therapy of many neuropsychiatric disorders including Alzheimer's dementia, TBI, depression/anxiety, autistic spectrum/ADHD, epilepsy and chronic pain.
His main interest is in neuro-psychiatry and cognitive enhancement. He uses the newest technology of QEEG and Neurofeedback to successfully diagnose and treat many medical conditions including seizures,
headaches, fibromyalgia chronic pain, anxiety, depression, and prior stroke. Dr. Koberda has also effectively introduced neurofeedback protocols for a cognitive enhancement which may help students and professionals to improve their memory, concentration, verbal function or information processing speed.
Dr. Koberda also has been appointed in August, 2010 by Governor Charlie Christ as a member of the Alzheimer’s Disease Advisory Committee for a 4 years term (The Committee serves as an advising body to the Florida State Government). Dr. Koberda has published multiple publications in different scientific journals and serves as international neuroscience speaker and consultant.
Dr. Koberda has been appointed to the Editorial Board of the "Journal of Neurology and Stroke", "International Journal of Emergency Mental Health and Human Resilience", "Journal of Neurology and Neurobiology" and "Journal of Psychology and Clinical Psychiatry". He also serves as a reviewer-"Clinical EEG and Neuroscience" and the above journals.
Clinical skills and interests: EEG/QEEG/LORETA/Electrical Imaging (Brain Mapping), Neurofeedback, Neurotherapy, Magnetic and Electrical Stimulation, Neuromodulation, Neuropsychiatry, Forensic- neurology, EMG-NCV, Neuro-rehabilitation, IME, Teaching, Consultations, Academic and Research Interest, Clinical Trials, Public Health, Tele-neurology.
Director and Owner- J. Lucas Koberda, MD, PhD, Neurology, PL, Tallahassee Neurobalance Center.
Founder and CEO-Brain Enhancement, Inc.- non-for profit organization-since December, 2014.
Florida State University-Neurologist at FSU Health and Wellness Center-960 Learning Way, Tallahassee,
FL 32306-since November, 2016.
Active and Recent Hospital Privileges:
Neurology Consultant-Florida State Psychiatric Hospital, Chattahoochee, FL-2007-December, 2014. Consulting Neurologist- HealthSouth-Rehabilitation Hospital, Tallahassee, FL.-2007- February, 2015. CRMC Hospital-Tallahassee, FL-community privileges.
Alzheimer Disease Advisory Committee (Florida)-appointed by the Florida Governor- Charlie Christ- August 2010-October 2012.
Licensure - Active: Florida, New York State, Utah, Georgia
2012-Professor of Neurology-Carrick Institute for Graduate Studies, Cape Canaveral, FL.
2007-Clinical Assistant Professor of Neurology-Florida State University-College of Medicine, Tallahassee, FL
2001-Clinical Assistant Professor of Neurology-Albany Medical College, Albany, New York.
Neurology and Geriatrics Elective Teaching Faculty 2010-2011.
Neurology Elective Director-Florida State University-College of Medicine-CRMC hospital-2007-2010.
2013- 2014-Member of the International Board of Quantitative Electrophysiology (IBQE)
International Journal of Emergency Mental Health and Human Resilience-since 2014 Journal of Psychology and Clinical Psychiatry-since 2014,
Journal of Neurology and Stroke-since 2014,
Journal of Neurology and Neurobiology-since 2014,
Valetudinaria-Progress in Clinical and Military Medicine (European medical journal)-2005-2013.
Clinical EEG and Neuroscience-since 2013
Journal of Psychology and Clinical Psychiatry-since 2014.
Journal of Neurology and Stroke-since 2014
International Journal of Emergency Mental health and Human Resilience-since 2014
Foreign languages: English and Polish-Fluently, Russian and German-basic.
Education and Training:
Undergraduate: 1976 - 1980 M. Kopernik School Gdansk, Poland
Graduate: 1980 - 1986 Medical School in Gdansk-graduation-Oct 24, 1986 M. D.
Postgraduate Training and Employment:
Nov 1, 1986- Sep 30, 1989
Internal Medicine Residency A. Hellmann, M.D.-
Director Training, Medical School in Gdansk, Gdansk, Poland
Visiting Scientist Prof. Castoldi, M.D.-Director Department of Hematology- University of Ferrara, Italy
Oct 1, 1989-
Sep 30, 1990
Hematology, J.W. Goethe University, Frankfurt/M., Germany
Postdoctoral Training L. Bergmann, M.D.-Director Department of
Oct 25, 1990- Postdoctoral Training R. Moser, M. D. -Director
Sept 30, 1991 Department of Neurosurgry E.A. Grimm, Ph.D.-Director
And Department of Tumor Biology UT M. D. Anderson Cancer Center, Houston,
Oct 1, 1991- Postdoctoral Training R.E. Champlin, M.D.-Director
April 24, 1994 Dept. of Hematology-BMT Section, UT M. D. Anderson Cancer Center, Houston, TX
Relocation to Pennsylvania
July 1, 1994- June 30, 1995
July 1, 1995- June 30, 1998
Oct. 26, 1995 entitled
Transitional Resident-PGY-1, Easton Hospital, Easton, PA 18042 K.H Wildrick, M.D.-Director
Neurology Resident-Oregon Health Sciences University, Portland R.H. Whitham, M.D.-Director
Ph.D., degree in Immunology and Experimental Tumor Immunotherapy-paper
“Evaluation of oncolytic potential of human lymphocytes activated with low dose of IL-2 and anti-CD3 and
July 1, 1998- July 2006 March, 2004- March 2005
August 1, 2006-
Solo Neurology Practice in Potsdam, NY
Medical Director of Acute Rehabilitation Unit – CHMC-Ogdensburg, NY
present- Neurology practice in Tallahassee, FL
anti-CD28 antibodies.”-Graduated from Medical School in Warsaw-
2007-2010-Capital Regional Medical Center-Co-director of Stroke program and Neurology Elective Director-Florida State University-College of Medicine-CRMC hospital
May, 2000-2020 Board certification-Neurology- by the American Board of Psychiatry and Neurology Society-Organization Memberships:
1996 - American Academy of Neurology, Active Member-Epilepsy and Stroke section
1999-2004- Rotary International
2003-Vice President-St. Lawrence County Medical Society, NY
2004-2006 President - St. Lawrence County Medical Society, NY
2006- Member of Rural and Preventive Medicine Committee –MSSNY
2006-Delegate from St. Lawrence County to House of Delegate meeting in Buffalo, NY
2006-Member of Committee for Governmental Affairs B
2007-2012-Board of Directors-Epilepsy Association of the Big Bend, Tallahassee, FL. 2011-The Society of Applied Neurosciences.
2012-International Society for Neurofeedback and Research
2012-The Biofeedback Society of Florida.
2013-EEG and Clinical Neuroscience Society (ECNS).
Medical Advocacy and Advising:
1. May-2004- Neurology on the Hill (Washington DC) - advocacy for development of stroke centers, malpractice reforms, Medicare – organized by American Academy of Neurology (AAN).
2. June-2005- Neurology on the Hill- advocacy for malpractice reforms, Medicare and Medicaid reforms- organized by AAN.
3. Spring 2005 - Albany NY-Advocacy on the State level- Malpractice reforms, access of Medicaid patient to care and services.
4. 2003-2004- Advocacy against obesity in children- resulted in elimination of sodas and “junk” food from local schools
5. 2004-2005-Advocacy in support of “self-pay” patients and insurance coverage.
6. May-2006- Neurology on the Hill- advocacy for fixing Medicare payment formula-organized by AAN.
7. 2006- Health advisory meeting-to Congressman John M. McHugh (23rd. Congressional District of State of New York)-currently 21st United States Secretary of the Army (in the President Obama’s Cabinet).
7. March 2008-Advocacy to restrict trade medication substitution by generic anti-seizure medications without physician’s and patient’s consent-Tallahassee, FL
8. December 22nd, 2008-Host and moderator-Tallahassee Health Care Forum-the community discussion regarding health care reforms.
9. April 16th, 2009-organizer and moderator of the fundraiser to fight high infant mortality rate in Leon County, Tallahassee FL
10. October 8th, 2009-Organizer of fundraising and silent auction to support under-funded Tallahassee institutions including Epilepsy Association of the Big Bend and Neighborhood Health Services, Inc - serving underprivileged population with no health insurance.
Selected and Invited Presentations:
1999-Application of neurophysiologic testing for neurological diagnosis- Clarkson University Health Sciences- Potsdam, NY.
1999- Traumatic Brain Injury- Clarkson University Health Sciences- Potsdam, NY.
2004- New options in the treatment of epilepsy- Claxton-Hepburn Medical Center, Ogdensburg, NY.
2005- Introduction to Neurology- St. Lawrence University, Canton, NY.
2006- Introduction to Neurology- Florida State University, Tallahassee FL
2008-Introduction to diagnosis and treatment of epilepsy, Florida State Psychiatric Hospital, Tallahassee FL
2/2011-Current options in the treatment of epilepsy-hosted by the Epilepsy Association of The Big Bend.
10/2011-Quantitative EEG and Brain Disorders-invited speaker during the Brain Symposium in Tallahassee, FL.
5/25/2012-QEEG and Neurofeedback with Z-score LORETA in neurological practice-multiple-cases presentation-Cancun, Mexico-Z-score Neurofeedback workshop.
6/4/2012-Application of quantitative EEG in epilepsy and other neurological disorders-invited for the Grand Rounds presentation by the Neurology Department (Epilepsy Section) Medical University of Southern Carolina-Charleston, SC.
7/11/2012-QEEG and Neurofeedback in clinical practice-Grand Rounds presentation-Invited by Tallahassee Memorial Hospital in Tallahassee- invited by the residency program director.
7/21/2012—QEEG assessment with Z-score & LORETA neurofeedback in neuro-psychiatric disorders- invited speaker for a workshop presentation during The Biofeedback Society of Florida Meeting in Orlando, FL.
3/26/2013-Electrical Neuroimaging and Neurofeedback-Rotary Club, Tallahassee, FL.
8/8/2013-Electrical Imaging in Neuro-psychiarty-invited by the Tallahassee Memorial Hospital program director of Internal Medicine Residency Training-combined FSU/TMH hospital, Tallahassee, FL.
8/30/2013-The role of LORETA Z-score Neurofeedback in the Treatment of Neuropsychiatric Disorders- invited by Dr. Georges Otte-Medical Director of Neuropsychiatric Hospital-Ghent, Belgium.
9/21/2013-LORETA Z-score Neurofeedback in Neuropsychiatry-ISNR meeting in Dallas, TX-presented during the small group discussion section.
11/2/2013-“Z-score LORETA Neurofeedback in Clinical Practice”-invited speaker lecture during the Southeastern Biofeedback & Clinical Neuroscience Association conference in Lake Junalusca, NC.
1/7/2014-“Application of QEEG (Brain Mapping) in psychiatry-clinical implication for diagnosis and treatment”-TMH-psychiatry department, Tallahassee, FL.
3/20/2014-“Electrical Brain Imaging Cognitive Enhancement with LORETA Z-score Neurofeedback”- Advanced Psychology lecture-L. Chiles High School-Tallahassee, FL.
7/29/2014-“Electrical Brain Imaging LORETA Z-score Neurofeedback”-invited presentation-medical students-FSU.
8/15/2014-“Enhance Your Brain”-invited presentation at Maguire Center-Westminster Oaks, Tallahassee, FL.
2/12/2015-“QEEG/LORETA/Electrical imaging and Z-score LORETA Neurofeedback in neuropsychiatric diagnosis and therapy-presented during “Real-time Functional Imaging and Neurofeedback” international conference organized by University of Florida in Gainesville, FL.
2/21/2015-“Cognitive enhancement using LORETA Z-score Neurofeedback-presented during 30th Annual Alzheimer’s Disease Education and Training Conference-FSU College of Medicine-Tallahassee, FL.
2/2015-“QEEG and neurofeedback in Autistic Spectrum disorders”-invited presentation-by CARDS-FSU Autism Institute-invited by Dr. Amy Whetherby.
12-11-2015-“Neuromodulation Therapy of TBI, Cognitive Problems and Dementia”-Keynote invited speaker during the international conference-International Symposium on Clinical Neuroscience-Orlando, FL.
8/26/2016-Invited keynote speaker-QEEG and LORETA Z-score Neurofeedback application in ADHD- University of North Florida, Jacksonville, FL-Brain Symposium.
9/23/2016-ISNR international meeting in Orlando, FL-LORETA Z-score neurofeedback and electromagnetic stimulation (Neurofield) application in patients with epilepsy.
11/5/2016-invited speaker-Southeast Biofeedback and Clinical Neuroscience Association-Atlanta, GA- LORETA Z-score Neurofeedback and electromagnetic stimulation (Neurofield) application in neuropsychiatric practice.
2/4/2017-Keynote speaker-"Multiple Concussions-Analysis of Former NFL Players-Evidence of Cognitive Impairment and Brain Abnormalities."-presented during the International Symposium on Clinical Neuroscience in Orlando, FL.
Published, submitted or in preparation Articles:
1. Koberda J. Czyz J. Hellmann A. Leukocyte doubling time as a prognostic factor in chronic lymphocytic
leukemia. Acta Haemat Pol 20:195, 1989.
2. Hellmann A, Koberda J. Siekierska-Hellmann M. Use of Cyclosporin A in the treatment of Sezary's Syndrome. Pol Tyg Lek 45:444, 1990.
3. Hellmann, Koberda J. Baran W. Relationship of the duration of the chronic phase in chronic granulocytic leukemia to the total dose of busulphan in the first year of treatment. Acta Haemat Pol 21:60, 1990.
4. Koberda J. Hellmann A. Glutathione S-transferase activity of leukemic cells as a prognostic factor for response to chemotherapy in acute leukemias. Med Oncol & Tumor Pharmacother 21:35, 1991.
5. Koberda J. Bergmann L. Mitrou PS, Hoelzer D. High release of TNF-alpha, INF-gamma, IL-6 by phenotypically T-cell derived adherent lymphokine-activated killer cells. J Cancer Res Clin Oncol 117:425, 1991.
6. Koberda J. Grimm EA, Moser RP. Effect of anti-CD3/anti-CD28/IL-2 stimulation of mononuclear cells on transforming growth factor-beta inhibition of lymphokine-activated killer cells generation. J Cancer Res Clin Oncol 119:131, 1993.
7. Koberda J. Przepiorka D. Moser RP. Grimm EA. Sequential TNF and TGF-beta regulation of expansion and induction of cytotoxicity in long-term cultures of lymphokine-activated killer cells. Lymphokine & Cytokine Res. 13, 2, 1994.
8. Przepiorka D. Ippoliti C. Koberda J. Chan K.W. Khouri I. Fischer H.E. Huh Y.O. Escudier S. Seong D. Davis M. Gajewski J. Vriesendorp H. Champlin R.E. Short courses interleukin-2, cyclosporine and steroids for prevention of graft-vs-host disease after haploidentical marrow transplantation. Transplantation, 1994.
9. Lackowski D. Koberda J.L. DeLoughery T.G. So Y. Natural Killer cell leukemia as a cause of peripheral neuropathy and meningitis: a case report. Neurology. 1998. Aug; 51 (2): 640-1
10. Koberda J.L. Ischemic stroke prevention and treatment. Valetudinaria.-invited review article-1, 2006.
11. Koberda J.L. Clinical advantages of quantitative electroencephalogram (QEEG)-electrical neuroimaging application in general neurology practice-Clin. EEG Neuroscience-published-March 26, 2013.
12. Koberda J.L. Detection of mild traumatic brain injury (mTBI). Neuroconnection-winter 2011 edition (ISNR). Page- 16-17.
13. Koberda J.L., St. Hillier D., Jones B., Moses A., Koberda L.A. Application of Neurofeedback in General Neurology Practice. Journal of Neurotherapy-3 2012. Page 231-234.
14. Koberda J.L., Moses A., Koberda L, Koberda P. "Cognitive Enhancement Using 19-electrode Z-score Neurofeedback. Journal of Neurotherapy, 3-2012. page 224-230.
15. Koberda J.L. Autistic Spectrum Disorder (ASD) as a Potential Target of Z-score LORETA Neurofeedback. The Neuroconnection- winter 2012 edition (ISNR). Page 24-25.
16. Prichep, L., Surmeli, T., Thatcher, R. W., Koberda, L., Ottes, G. and Berdyugina, A. QEEG AND TRAUMATIC BRAIN INJURY: EVIDENCE BASED MEDICINE ANALYSES. In preparation-2014.
17. Koberda J.L. Koberda L. Koberda P. Moses A. Bienkiewicz A. Alzheimer’s dementia as a potential targer of Z-score LORETA 19-electrode neurofeedback. Neuroconnection, p-30-32, Winter 2013.
18. Koberda J.L., Koberda P, Bienkiewicz A, Moses A, Koberda L. Pain Management Using 19-Electrode Z- Score LORETA Neurofeedback. J. of Neurotherapy- 17:179-190, 2013.
19. Koberda JL, Paula Koberda, Andrew Moses, Jessica Winslow, Andrew Bienkiewicz, Laura
Koberda. "Z-score LORETA Neurofeedback as a potential therapy of ADHD". –summer-Special Edition- Biofeedback Magazine-2014.
20. Koberda JL, Paula Koberda, Andrew Moses, Jessica Winslow, Andrew Bienkiewicz, Laura Koberda. “Z- score LORETA Neurofeedback as a Potential Therapy in Depression and Anxiety”. Spring- Neuroconnection, p-52-55, 2014.
21. Rex L. Cannon, H. E. Pigott, Tanju Surmeli, Deborah R. Simkin, Robert W. Thatcher, Werner Van den Bergh, Gerald Gluck, Joel F. Lubar, Richard Davis, Dale S. Foster, Jonathan Douglas, Atholl T. Malcolm, Donald Bars, Kirk Little, Wes Center, Marvin Berman, Harold Russell, Barbara Hammer, and J. Lucas Koberda. The Journal of Clinical Psychiatry, Volume 75 • March 2014 • Number 3, p. 289. The Problem of Patient Heterogeneity and Lack of Proper Training in a Study of EEG Neurofeedback in Children. Letter to the editor.
21. Koberda JL,. Neuromodulation-An Emerging Therapeutic Modality in Neurology. (2014). J Neurol Stroke 2014, 1 (4) 00027. Editorial.
22. Koberda, JL. Z-score LORETA Neurofeedback as a Potential Rehabilitation Modality in Patients with CVA. (2014) J Neurol Stroke 2014, 1(5) 00029.
23. Koberda, JL. Z-score LORETA Neurofeedback as a Potential Therapy in Cognitive Dysfunction and Dementia. (2014), J Psychol Clin Psychiatry 1 (6): 00037.
24. Koberda, JL. (2015). Application of Z-score LORETA Neurofeedback in therapy of Epilepsy-Editorial- Journal of Neurology Neurology and Neurobiology-Vol. 1.1.
25. Frey LC, Koberda, JL. (2015). LORETA Z-score neurofeedback in patients with medically-refractory epilepsy-Journal of Neurology and Neurobiology-Vol. 1.1.
27. Koberda, JL, Frey LC. (2015). Application of Z-score LORETA Neurofeedback in Therapy of Epilepsy. Journal of Neurology and Neurobiology-Vol. 1.1.
28. Koberda, JL, (2015). Neurofeedback-An Alternative Therapy for Mental Disorders. The Patient Magazine-Q2-2015.
29. Koberda, JL, (2015). Traumatic Brain Injury: Is Neurofeedback the Best Available Therapy?-Editorial- Journal of neurology and Neurobiology-Vol. 1.3.
30. Koberda, JL, (2015). LORETA Z-score Neurofeedback-Effectiveness in Rehabilitation of Patients suffering from Traumatic Brain Injury. Journal of Neurology and Neurobiology-Vol. 1.4-September, 2015.
31. Koberda, JL, Akhmatova N, (2016). Masgutova Neurosensorimotor ReflexIntegration (MNRI) as a New Form of Manual Neuromodulation Technique. Journal of Neurology and Neurobiology-October, 2016, 2 (4).
32. Koberda, JL, Akhmatova N, Akhmatova E, Bienkiewicz A, Nowak, K, Nawrocka H. (2016). Masgutowa Neurosensorimotor Reflex Integration Technique induces Positive Brain Maps (QEEG) changes. Journal of Neurology and Neurobiology-October, 2016, 2 (4).
Published or submitted Abstracts:
1. Koberda J. Bergmann L. Mitrou PS. Hoelzer D. Adherent lymphokine-activated killer (A-LAK) cells-
immunological and functional characterization. Blood 76, 10, 833, Suppl., 1990
2. Koberda J. Grimm EA, Moser RP. Anti-CD3/anti-CD28 stimulation antagonizes TGF-beta suppression of IL-2-activated killer cell generation. Exp Hematol 20, 6, 435, 1992.
3. Koberda J. Przepiorka D. Moser RP. Grimm EA. TNF and TGF-beta involvement in the regulation of proliferation and killing of lymphokine-activated killer (LAK) cells in long-term cultures. Blood 80, 10, 1711, 1992.
4. Koberda J. Przepiorka D. Giralt S. Champlin RE. Characterization of immunological reconstitution of CML patients undergoing allogeneic bone marrow transplantation. Blood 80, 10, 2096, Suppl., 1992.
5. Koberda J. Przepiorka D. Moser RP. Grimm EA. At least two different forms of TGF-beta are involved in the regulation of proliferation and killing of lymphokine-activated killer (LAK) cells in long-term cultures. J Clin Oncol ASCO meeting-1993.
6. Przepiorka D. Huh YO. Mehra R. Geisler D. Koberda J. Champlin RE. Deisseroth AB. Prolonged immunodeficiency in breast cancer patients after sequential high-dose chemotherapy with or without autologous marrow support. Blood 82, 10, 679, Suppl., 1993.
7. Koberda J. Reading C. Mehra R. Champlin RE. The minimal residual disease detection by 9187 monoclonal antibody. Blood 82, 10, 2581, Suppl., 1993.
8. Koberda J. Przepiorka D. Bednarczyk J. Escudier S. Deisseroth AB. McIntyre B. Identification of E- selectin (ELAM-1) on normal human hematopoietic cells. Blood 82, 10, 113, Suppl., 1993.
9. Przepiorka D. Ippoliti C. Koberda J. Chan KW. Khouri I. Huh YO. Escudier S. Seong D. Gajewski J. Vriesendrop H. Champlin RE. Short-coures interleukin-2, cyclosporine and steroids for prevention of
graft-vs-host disease after haploidentical marrow transplantation. J. Cell. Biochem. Keystone Symposia - Jan, 1994.
10. Koberda J. Przepiorka D. Bednarczyk J. Escudier S. Champlin RE, Deisseroth AB, McIntyre BW. Identification of hyperglycosylated E-selectin (ELAM-1) expression on normal and leukemic hematopoietic cells. Exp. Hematol. Suppl., 1994.
11. Koberda J.L. Clark W. Letsup H. Nesbit G. Successful clinical recovery and reversal of mid-basilar occlusion in clinically brain dead patient with intra-arterial urokinase. Neurology. 48, Suppl. PO3.004, March, 1997.
12. Lackowski D. Koberda J.L. Natural killer cell proliferation as a cause of peripheral neuropathy. Blood. 90, 10: Suppl. 2964, November 15, 1997.
13. Koberda J.L. Clinical advantages of quantitative electroencephalogram (QEEG) application in general neurology practice-presented during the Society of Applied Neuroscience meeting-Abstract published in Neuroscience Letters, Vol. 500, Suppl. 1, July 2011, p-32.
14. Koberda J.L., Moses A. Application of quantitative electroencephalogram (QEEG) and neurofeedback in general neurology practice-presented-ISNR meeting-September, 2011.
15. Koberda J.L. Application of Quantitative EEG and LORETA in general neurology practice for detection and localization in epilepsy. Presented during the American Academy of Neurology (AAN) meeting (April 23, 2012) Neurology suppl.
16. Koberda J.L, Moses A, Koberda P, Koberda L. Comparison of the Effectiveness of Z-Score Surface/LORETA 19-Electrodes Neurofeedback to Standard 1-Electrode Neurofeedback. J. of Neurotherapy, 4, p-302, 2012.
17. Koberda J.L. Bienkiewicz A., Koberda L., Koberda P. Moses A. Electrical Imaging and Z-score LORETA Neurofeedback-New paradigm to Neuro-Psychiatric Diagnosis and Treatment. Presented during the First International Conference on Basic and Clinical Multimodal Imaging-Geneva, Switzerland-September 5-8, 2013.
18. Koberda J.L., Bienkiewicz A., Koberda L., Koberda P. Moses A. LORETA Z-score Neurofeedback as a Potential Application in Epilepsy.-presented during the ISNR meeting in Dallas-September 20, 2013- abstract expected to be published in J. of Neurotherapy, 4, 2013.
19. Koberda J.L., Bienkiewicz A., Koberda L., Koberda P. Moses A. LORETA Z-score Neurofeedback as a Potential Application in Depression.-presented during the ISNR meeting in Dallas-September 22, 2013- abstract expected to be published in J. of Neurotherapy, 4, 2013.
20. Koberda J.L., Bienkiewicz A., Koberda L., Koberda P. Moses A. High Effectiveness of LORETA Z-score Neurofeedback in the treatment of Headaches-presented during the ISNR meeting in Dallas, TX- September 19, 2013-abstract expected to be published in J. of Neurotherapy, 4, 2013.
21. Koberda J.L. Andrew Moses; Paula Koberda; Jessica Winslow
“Cognitive Enhancement with LORETA Z-score Neurofeedback”-presented during the AAPB meeting in
Savannah, GA-March, 2014.
22. Koberda, JL. Bienkiewicz A., Koberda L., Koberda P. Moses A, Winslow J. Accelerated Recovery from Traumatic Brain Injury (TBI) with Z-score Neurofeedback Therapy-presented during the ISNR meeting- San Diego, CA-October 16, 2014-published in NeuroRegulation-Vol. 1(3-4):273-316 2014.
23. Koberda, JL. QEEG/LORETA Electrical Imaging in Neuropsychiatric Disorders-Clinical Applications- ISNR meeting San Diego, CA-October 19, 2014
Published Newspaper Articles and Press Releases:
Reforming health care: Where do we go next? Tallahassee Democrat. Feb 7th, 2009
Forum focuses on the need for health-care reforms. Tallahassee Democrat. Chronicle. Feb 4th.
3. Community-health forum provides input to Obama’s transition team. Tallahassee Democrat. Jan 10th, 2009.
We can’t support defensive medicine. Tallahassee Democrat. Dec 13th. 2008.
Should we limit president’s age? Tallahassee Democrat. Oct 28th, 2008.
Health center needs community support. Tallahassee Democrat. March 31st, 2009.
Improve safety on Tallahassee roads. Tallahassee Democrat. May 9th, 2009.
Policy is shaped by right and wrong. Tallahassee Democrat. September 30th, 2009.
Computer is good for everything. Invited article in the Riviera-European newspaper in July 2012.
Dr. J. Lucas Koberda using neurofeedback to treat brain-related illnesses. Tallahassee Democrat.
March 6, 2013.
11. “Neuroscience Advances Bring Modern Therapy”-Tallahassee Democrat, December 8, 2014.
“The Migraine Revolution”-by Martin Brink-Koberda JL-contributor of neurofeedback cases-
published by Body Mind and Brain-Queensland, Australia-December 2012.
“Clinical Methods of Neurotherapy: Techniques and Treatment Applications”. Editors David Cantor and Jim Evans-author of chapter 5-Koberda, JL,“Defining Developing Evidence-Based Medicine Databases Proving Treatment Efficacy”-published-November, 2013.p-127-138. Academic Press-Elsevier.
“Advances in Neuroimaging Research”-Editor-Victoria Asher-Hansley-chapter2-Koberda,
JL. “QEEG/LORETA Electrical Imaging in Neuropsychiatry-Diagnosis and treatment Implications”- published in September, 2014. P-121-146. Nova Biomedical Publishing.
"Z Score Neurofeedback: Clinical Applications". Editor-Robert Thatcher-Koberda, JL, author of three chapters-including:
Chapter 5-“Z-score LORETA Neurofeedback as a Potential Therapy in Depression/Anxiety and Cognitive Dysfunction”.
Chapter 6-“LORETA Z-score Neurofeedback in Chronic Pain and Headaches”.
Chapter 10-“Therapy of Seizures and Epilepsy with Z-score LORETA Neurofeedback- October 2014-Academic Press-Elsevier.
Asperger Syndrome: Risk Factors, Cognitive-Behavioral Characteristics and Management Strategies-Editor-Michael Shaughnessy-chapter by Koberda, JL. “QEEG/LORETA Electrical Imaging and Z-score LORETA Neurofeedback-New Approach to Diagnosis and Therapy of Autistic Spectrum Disorders (ASD)”- published March, 2015.
Handbook of Clinical QEEG and Neurotherapy-Edited by Tom Collura and Jon Frederick-Koberda JL-book chapter-“LORETA Z-score Neurofeedback in Neuropsychiatric Practice”-published- December, 2016.
Updated on 2/4/2017
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- Holding Hands With a Loved One Synchronized Heart Rate And Brainwaves, Decreases Pain
- By Jason von Stietz, Ph.D.
- March 25, 2018
Why does holding hands with a loved one seem to comfort us? Researchers at the University of Colorado, Boulder and the University of Haifa examined the relationship between holding hands with a spouse or partner and the experience of physical pain. Findings showed that when couples held hands their brainwaves and respiration synchronized and their experience of pain from a mild burn decreased. The study was discussed in a recent article in Neuroscience News:
“We have developed a lot of ways to communicate in the modern world and we have fewer physical interactions,” said lead author Pavel Goldstein, a postdoctoral pain researcher in the Cognitive and Affective Neuroscience Lab at CU Boulder. “This paper illustrates the power and importance of human touch.”
The study is the latest in a growing body of research exploring a phenomenon known as “interpersonal synchronization,” in which people physiologically mirror the people they are with. It is the first to look at brain wave synchronization in the context of pain, and offers new insight into the role brain-to-brain coupling may play in touch-induced analgesia, or healing touch.
Goldstein came up with the experiment after, during the delivery of his daughter, he discovered that when he held his wife’s hand, it eased her pain.
“I wanted to test it out in the lab: Can one really decrease pain with touch, and if so, how?”
He and his colleagues at University of Haifa recruited 22 heterosexual couples, age 23 to 32 who had been together for at least one year and put them through several two-minute scenarios as electroencephalography (EEG) caps measured their brainwave activity. The scenarios included sitting together not touching; sitting together holding hands; and sitting in separate rooms. Then they repeated the scenarios as the woman was subjected to mild heat pain on her arm.
Merely being in each other’s presence, with or without touch, was associated with some brain wave synchronicity in the alpha mu band, a wavelength associated with focused attention. If they held hands while she was in pain, the coupling increased the most.
Researchers also found that when she was in pain and he couldn’t touch her, the coupling of their brain waves diminished. This matched the findings from a previously published paper from the same experiment which found that heart rate and respiratory synchronization disappeared when the male study participant couldn’t hold her hand to ease her pain.
“It appears that pain totally interrupts this interpersonal synchronization between couples and touch brings it back,” says Goldstein.
Subsequent tests of the male partner’s level of empathy revealed that the more empathetic he was to her pain the more their brain activity synced. The more synchronized their brains, the more her pain subsided.
How exactly could coupling of brain activity with an empathetic partner kill pain?
More studies are needed to find out, stressed Goldstein. But he and his co-authors offer a few possible explanations. Empathetic touch can make a person feel understood, which in turn – according to previous studies – could activate pain-killing reward mechanisms in the brain.
“Interpersonal touch may blur the borders between self and other,” the researchers wrote.
The study did not explore whether the same effect would occur with same-sex couples, or what happens in other kinds of relationships. The takeaway for now, Pavel said: Don’t underestimate the power of a hand-hold.
“You may express empathy for a partner’s pain, but without touch it may not be fully communicated,” he said.
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- Key Difference in the Brains of Super-Agers
- By Jason von Stietz, M.A.
- March 9, 2018
Why do some people in their 90’s seem mentally sharp when others do not? Researchers at Northwestern University examined the brains and cognitive abilities of “super-agers.” Findings from autopsies showed that the brains of super-agers had a significantly thicker cortex than those of their average peers. The study was discussed in a recent article in MedicalXpress:
It's pretty extraordinary for people in their 80s and 90s to keep the same sharp memory as someone several decades younger, and now scientists are peeking into the brains of these "superagers" to uncover their secret.
The work is the flip side of the disappointing hunt for new drugs to fight or prevent Alzheimer's disease.
Instead, "why don't we figure out what it is we might need to do to maximize our memory?" said neuroscientist Emily Rogalski, who leads the SuperAging study at Northwestern University in Chicago.
Parts of the brain shrink with age, one of the reasons why most people experience a gradual slowing of at least some types of memory late in life, even if they avoid diseases like Alzheimer's.
But it turns out that superagers' brains aren't shrinking nearly as fast as their peers'. And autopsies of the first superagers to die during the study show they harbor a lot more of a special kind of nerve cell in a deep brain region that's important for attention, Rogalski told a recent meeting of the American Association for the Advancement of Science.
These elite elders are "more than just an oddity or a rarity," said neuroscientist Molly Wagster of the National Institute on Aging, which helps fund the research. "There's the potential for learning an enormous amount and applying it to the rest of us, and even to those who may be on a trajectory for some type of neurodegenerative disease."
What does it take to be a superager? A youthful brain in the body of someone 80 or older. Rogalski's team has given a battery of tests to more than 1,000 people who thought they'd qualify, and only about 5 percent pass. The key memory challenge: Listen to 15 unrelated words, and a half-hour later recall at least nine. That's the norm for 50-year-olds, but the average 80-year-old recalls five. Some superagers remember them all.
"It doesn't mean you're any smarter," stressed superager William "Bill" Gurolnick, who turns 87 next month and joined the study two years ago.
Nor can he credit protective genes: Gurolnick's father developed Alzheimer's in his 50s. He thinks his own stellar memory is bolstered by keeping busy. He bikes, and plays tennis and water volleyball. He stays social through regular lunches and meetings with a men's group he co-founded.
"Absolutely that's a critical factor about keeping your wits about you," exclaimed Gurolnick, fresh off his monthly gin game.
Rogalski's superagers tend to be extroverts and report strong social networks, but otherwise they come from all walks of life, making it hard to find a common trait for brain health. Some went to college, some didn't. Some have high IQs, some are average. She's studied people who've experienced enormous trauma, including a Holocaust survivor; fitness buffs and smokers; teetotalers and those who tout a nightly martini.
But deep in their brains is where she's finding compelling hints that somehow, superagers are more resilient against the ravages of time.
Early on, brain scans showed that a superager's cortex—an outer brain layer critical for memory and other key functions—is much thicker than normal for their age. It looks more like the cortex of healthy 50- and 60-year-olds.
It's not clear if they were born that way. But Rogalski's team found another possible explanation: A superager's cortex doesn't shrink as fast. Over 18 months, average 80-somethings experienced more than twice the rate of loss.
Another clue: Deeper in the brain, that attention region is larger in superagers, too. And inside, autopsies showed that brain region was packed with unusual large, spindly neurons—a special and little understood type called von Economo neurons thought to play a role in social processing and awareness.
The superagers had four to five times more of those neurons than the typical octogenarian, Rogalski said—more even than the average young adult.
The Northwestern study isn't the only attempt at unraveling long-lasting memory. At the University of California, Irvine, Dr. Claudia Kawas studies the oldest-old, people 90 and above. Some have Alzheimer's. Some have maintained excellent memory and some are in between.
About 40 percent of the oldest-old who showed no symptoms of dementia in life nonetheless have full-fledged signs of Alzheimer's disease in their brains at death, Kawas told the AAAS meeting.
Rogalski also found varying amounts of amyloid and tau, hallmark Alzheimer's proteins, in the brains of some superagers.
Now scientists are exploring how these people deflect damage. Maybe superagers have different pathways to brain health.
"They are living long and living well," Rogalski said. "Are there modifiable things we can think about today, in our everyday lives" to do the same?
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- Why Some People Cannot See Pictures in Their Mind
- By Jason von Stietz, M.A.
- February 9, 2018
Some people are able to clearly visualize objects in their “mind’s eye” while others are unable to visualize objects at all. The inability to picture something in your mind is called Aphantasia. Recently researcher from the University of New South Wales investigated this phenomenon. The findings were discussed in a recent article in Neuroscience News:
One of the creators of the Firefox internet browser, Blake Ross, realised his experience of visual imagery was vastly different from most people when he read about a man who lost his ability to imagine after surgery. In a Facebook post, Ross said:
“What do you mean ‘lost’ his ability? […] Shouldn’t we be amazed he ever had that ability?”
We’ve heard from many people who have experienced a similar epiphany to Ross. They too were astonished to discover that their complete lack of ability to picture visual imagery was different from the norm.
Visual imagery is involved in many everyday tasks, such as remembering the past, navigation and facial recognition, to name a few. Anecdotal reports from our aphantasic participants indicate that while they are able to remember things from their past, they don’t experience these memories in the same way as someone with strong imagery. They often describe them as a conceptual list of things that occurred rather than a movie reel playing in their mind.
As Ross describes it, he can ruminate on the “concept” of a beach. He knows there’s sand and water and other facts about beaches. But he can’t conjure up beaches he’s visited in his mind, nor does he have any capacity to create a mental image of a beach.
The idea some people are born wholly unable to imagine is not new. In the late 1800s, British scientist Sir Francis Galton conducted research asking colleagues and the general population to describe the quality of their internal imagery. These studies, however, relied on self-reports, which are subjective in nature. They depend on a person’s ability to assess their own mental processes – called introspection.
But how can I know that what you see in your mind is different to what I see? Perhaps we see the same thing but describe it differently. Perhaps we see different things but describe them the same.
Some researchers have suggested aphantasia may actually be a case of poor introspection; that aphantasics are in fact creating the same images in their mind as perhaps you and I, but it is their description of them that differs. Another idea is that aphantasics create internal images just like everyone else, but are not conscious of them. This means it’s not that their minds are blind, but they lack an internal consciousness of such images.
In a recent study we set out to investigate whether aphantasics are really “blind in the mind” or if they have difficulty introspecting reliably.
To assess visual imagery objectively, without having to rely on someone’s ability to describe what they imagine, we used a technique known as binocular rivalry – where perception alternates between different images presented one to each eye. To induce this, participants wear 3D red-green glasses, where one eye sees a red image and the other eye a green one. When images are superimposed onto the glasses, we can’t see both images at once, so our brain is constantly switching from the green to the red image.
But we can influence which of the coloured images someone will see in the binocular rivalry display. One way is by getting them to imagine one of the two images beforehand. For example, if I asked you to imagine a green image, you will be more likely to see the green image once you’ve put on 3D glasses. And the stronger your imagery is the more frequently you will see the image you imagine.
We use how often a person sees the image they imagine as a measure of objective visual imagery. Because we’re not relying on the participant rating the vividness of the image in their mind, but on what they physically see in the binocular rivalry display, it removes the need for subjective introspection.
In our study, we asked self-described aphantasics to imagine either a red circle with horizontal lines or a green circle with vertical lines for six seconds before being presented with a binocular rivalry display while wearing the glasses. They then indicated which image they saw. They repeated this for close to 100 trials.
We found that when the aphantasics tried to form a mental image, their attempted imagined picture had no effect on what they saw in the binocular rivalry illusion. This suggests they don’t have a problem with introspection, but appear to have no visual imagery.
Why some people are mind blind
Research in the general population shows that visual imagery involves a network of brain activity spanning from the frontal cortex all the way to the visual areas at the back of the brain.
Current theories propose that when we imagine something, we try to reactivate the same pattern of activity in our brain as when we saw the image before. And the better we are able to do this, the stronger our visual imagery is. It might be that aphantasic individuals are not able to reactivate these traces enough to experience visual imagery, or that they use a completely different network when they try to complete tasks that involve visual imagery.
But there may be a silver lining to not being able to imagine visually. Overactive visual imagery is thought to play a role in addiction and cravings, as well as the development of anxiety disorders such as PTSD. It may be that the inability to visualise might anchor people in the present and allow them to live more fully in the moment.
Understanding why some people are unable to create these images in mind might allow us to increase their ability to imagine, and also possibly help us to tone down imagery in those for whom it has become overactive.
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- Exercise Recommended in Treatment of Mild Cognitive Impairment
- By Jason von Stietz, MA
- January 11, 2018
According to the American Academy of Neurology, 6 percent of individuals in their 60’s suffer from mild cognitive impairment. Clinicians from the Mayo Clinic suggest that regular physical exercise totaling 150 minutes a week should be part of treatment to address symptoms related to mild cognitive impairment. This new guideline was discussed in recent article in Medical Xpress:
The recommendation is part of an updated guideline for mild cognitive impairment published in the Dec. 27 online issue of Neurology, the medical journal of the American Academy of Neurology.
"Regular physical exercise has long been shown to have heart health benefits, and now we can say exercise also may help improve memory for people with mild cognitive impairment," says Ronald Petersen, M.D., Ph.D., lead author, director of the Alzheimer's Disease Research Center, Mayo Clinic, and the Mayo Clinic Study of Aging. "What's good for your heart can be good for your brain." Dr. Petersen is the Cora Kanow Professor of Alzheimer's Disease Research.
Mild cognitive impairment is an intermediate stage between the expected cognitive decline of normal aging and the more serious decline of dementia. Symptoms can involve problems with memory, language, thinking and judgment that are greater than normal age-related changes.
Generally, these changes aren't severe enough to significantly interfere with day-to-day life and usual activities. However, mild cognitive impairment may increase the risk of later progressing to dementia caused by Alzheimer's disease or other neurological conditions. But some people with mild cognitive impairment never get worse, and a few eventually get better.
The academy's guideline authors developed the updated recommendations on mild cognitive impairment after reviewing all available studies. Six-month studies showed twice-weekly workouts may help people with mild cognitive impairment as part of an overall approach to managing their symptoms.
Dr. Petersen encourages people to do aerobic exercise: Walk briskly, jog, whatever you like to do, for 150 minutes a week—30 minutes, five times or 50 minutes, three times. The level of exertion should be enough to work up a bit of a sweat but doesn't need to be so rigorous that you can't hold a conversation. "Exercising might slow down the rate at which you would progress from mild cognitive impairment to dementia," he says.
Another guideline update says clinicians may recommend cognitive training for people with mild cognitive impairment. Cognitive training uses repetitive memory and reasoning exercises that may be computer-assisted or done in person individually or in small groups. There is weak evidence that cognitive training may improve measures of cognitive function, the guideline notes.
The guideline did not recommend dietary changes or medications. There are no drugs for mild cognitive impairment approved by the U.S. Food and Drug Administration.
More than 6 percent of people in their 60s have mild cognitive impairment across the globe, and the condition becomes more common with age, according to the American Academy of Neurology. More than 37 percent of people 85 and older have it.
With such prevalence, finding lifestyle factors that may slow down the rate of cognitive impairment can make a big difference to individuals and society, Dr. Petersen notes.
"We need not look at aging as a passive process; we can do something about the course of our aging," he says. "So if I'm destined to become cognitively impaired at age 72, I can exercise and push that back to 75 or 78. That's a big deal."
The guideline, endorsed by the Alzheimer's Association, updates a 2001 academy recommendation on mild cognitive impairment. Dr. Petersen was involved in the development of the first clinical trial for mild cognitive impairment and continues as a worldwide leader researching this stage of disease when symptoms possibly could be stopped or reversed.
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- Callous Unemotional Traits Related to Brain Structure in Boys
- By Jason von Stietz, MA
- December 28, 2017
Researcher at the University of Basel have discovered a structure in the brains of boys, that when larger, is related to callous-unemotional traits. Utilizing magnetic resonance imaging, researchers found that the anterior insula, a structure in the brain related to emotion and empathy, is larger in boys. However, this relationship was not found in girls. The study was discussed in a recent article in Neuroscience News:
Callous-unemotional traits have been linked to deficits in development of the conscience and of empathy. Children and adolescents react less to negative stimuli; they often prefer risky activities and show less caution or fear. In recent years, researchers and doctors have given these personality traits increased attention, since they have been associated with the development of more serious and persistent antisocial behavior.
However, until now, most research in this area has focused on studying callous-unemotional traits in populations with a psychiatric diagnosis, especially conduct disorder. This meant that it was unclear whether associations between callous-unemotional traits and brain structure were only present in clinical populations with increased aggression, or whether the antisocial behavior and aggression explained the brain differences.
Using magnetic resonance imaging, the researchers were able to take a closer look at the brain development of typically-developing teenagers to find out whether callous-unemotional traits are linked to differences in brain structure. The researchers were particularly interested to find out if the relationship between callous-unemotional traits and brain structure differs between boys and girls.
Only boys show differences in brain structure
The findings show that in typically-developing boys, the volume of the anterior insula – a brain region implicated in recognizing emotions in others and empathy – is larger in those with higher levels of callous-unemotional traits. This variation in brain structure was only seen in boys, but not in girls with the same personality traits.
“Our findings demonstrate that callous-unemotional traits are related to differences in brain structure in typically-developing boys without a clinical diagnosis,” explains lead author Nora Maria Raschle from the University and the Psychiatric Hospital of the University of Basel in Switzerland. “In a next step, we want to find out what kind of trigger leads some of these children to develop mental health problems later in life while others never develop problems.”
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- Brain Implant Boosts Short-Term and Working Memory
- By Jason von Stietz, MA
- November 30, 2017
Researchers from University of Southern California have used a brain implant to help the brain’s of study participants function more effectively. Electrodes were implanted into the brain’s of participants. Once the pattern of activity associated with optimal memory performance was determined, the electrode was used to stimulate the brain reinforcing the optimal pattern. Findings indicated the short-term memory was improved by 15% and working memory was improved by 25%. The study was discussed in a recent article in Futurism:
With everyone from Elon Musk to MIT to the U.S. Department of Defense researching brain implants, it seems only a matter of time before such devices are ready to help humans extend their natural capabilities. Now, a professor from the University of Southern California (USC) has demonstrated the use of a brain implant to improve the human memory, and the device could have major implications for the treatment of one of the U.S.’s deadliest diseases.
Dong Song is a research associate professor of biomedical engineering at USC, and he recently presented his findings on a “memory prosthesis” during a meeting of the Society for Neuroscience in Washington D.C. According to a New Scientist report, the device is the first to effectively improve the human memory.
To test his device, Song’s team enlisted the help of 20 volunteers who were having brain electrodes implanted for the treatment of epilepsy.
Once implanted in the volunteers, Song’s device could collect data on their brain activity during tests designed to stimulate either short-term memory or working memory. The researchers then determined the pattern associated with optimal memory performance and used the device’s electrodes to stimulate the brain following that pattern during later tests.
Based on their research, such stimulation improved short-term memory by roughly 15 percent and working memory by about 25 percent. When the researchers stimulated the brain randomly, performance worsened.
As Song told New Scientist, “We are writing the neural code to enhance memory function. This has never been done before.”
A GROWING PROBLEM
While a better memory could be useful for students cramming for tests or those of us with trouble remembering names, it could be absolutely life-changing for people affected by dementia and Alzheimer’s.
As Bill Gates noted when announcing plans to invest $100 million of his own money into dementia and Alzheimer’s research, the disease is a multi-level problem that’s positioned to get even worse.
Age is the greatest risk factor for Alzheimer’s, according to the Alzheimer’s Association, with the vast majority of sufferers over the age of 65. With advances in medicine and healthcare continuously increasing how long we live, that segment of the population is growing dramatically, and by 2030, 20 percent of U.S. citizens are expected to be older than 65.
This increase in the number of potential dementia sufferers can be costly in both a financial and emotional sense. In 2016, the total cost of healthcare and long-term care for those suffering from dementia and Alzheimer’s disease was an estimated $236 billion, and according to the Alzheimer’s Association, the more severe a person’s cognitive impairment, the higher the rates of depression in their familial caregivers.
Of course, further testing is required before Song’s device could be approved as a treatment for dementia or Alzheimer’s, but if it is able to help those patients regain even part of their lost memory function, the impact would be felt not only by the patients themselves, but their families and even the economy at large.
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- Neural Signatures of Suicidal Thoughts Detected by fMRI
- By Jason von Stietz, MA
- November 26, 2017
Can suicidal thoughts be detected by a machine? Researchers from Carnegie Mellon University among other institutions investigated the use of fMRI brain scans and machine-learning, the ability of a machine to learn without it being explicitly programmed, in the detection of neural signals related to suicidal thoughts. The researchers were able to identify individuals who had attempted suicide with 94% accuracy. The study was discussed in a recent article in MedicalXpress:
Suicidal risk is notoriously difficult to assess and predict, and suicide is the second-leading cause of death among young adults in the United States. Published in Nature Human Behaviour, the study offers a new approach to assessing psychiatric disorders.
"Our latest work is unique insofar as it identifies concept alterations that are associated with suicidal ideation and behavior, using machine-learning algorithms to assess the neural representation of specific concepts related to suicide. This gives us a window into the brain and mind, shedding light on how suicidal individuals think about suicide and emotion related concepts. What is central to this new study is that we can tell whether someone is considering suicide by the way that they are thinking about the death-related topics," said Just, the D.O. Hebb University Professor of Psychology in CMU's Dietrich College of Humanities and Social Sciences.
For the study, Just and Brent, who holds an endowed chair in suicide studies and is a professor of psychiatry, pediatrics, epidemiology and clinical and translational science at Pitt, presented a list of 10 death-related words, 10 words relating to positive concepts (e.g. carefree) and 10 words related to negative ideas (e.g. trouble) to two groups of 17 people with known suicidal tendencies and 17 neurotypical individuals.
They applied the machine-learning algorithm to six word-concepts that best discriminated between the two groups as the participants thought about each one while in the brain scanner. These were death, cruelty, trouble, carefree, good and praise. Based on the brain representations of these six concepts, their program was able to identify with 91 percent accuracy whether a participant was from the control or suicidal group.
Then, focusing on the suicidal ideators, they used a similar approach to see if the algorithm could identify participants who had made a previous suicide attempt from those who only thought about it. The program was able to accurately distinguish the nine who had attempted to take their lives with 94 percent accuracy.
"Further testing of this approach in a larger sample will determine its generality and its ability to predict future suicidal behavior, and could give clinicians in the future a way to identify, monitor and perhaps intervene with the altered and often distorted thinking that so often characterizes seriously suicidal individuals," said Brent.
To further understand what caused the suicidal and non-suicidal participants to have different brain activation patterns for specific thoughts, Just and Brent used an archive of neural signatures for emotions (particularly sadness, shame, anger and pride) to measure the amount of each emotion that was evoked in a participant's brain by each of the six discriminating concepts. The machine-learning program was able to accurately predict which group the participant belonged to with 85 percent accuracy based on the differences in the emotion signatures of the concepts.
"The benefit of this latter approach, sometimes called explainable artificial intelligence, is more revealing of what discriminates the two groups, namely the types of emotions that the discriminating words evoke," Just said. "People with suicidal thoughts experience different emotions when they think about some of the test concepts. For example, the concept of 'death' evoked more shame and more sadness in the group that thought about suicide. This extra bit of understanding may suggest an avenue to treatment that attempts to change the emotional response to certain concepts."
Just and Brent are hopeful that the findings from this basic cognitive neuroscience research can be used to save lives.
"The most immediate need is to apply these findings to a much larger sample and then use it to predict future suicide attempts," said Brent.
Just and his CMU colleague Tom Mitchell first pioneered this application of machine learning to brain imaging that identifies concepts from their brain activation signatures. Since then, the research has been extended to identify emotions and multi-concept thoughts from their neural signatures and also to uncover how complex scientific concepts are coded as they are being learned.
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- Chronic Alcohol Consumption Kills Brain Stem Cells
- By Jason von Stietz, MA
- November 19, 2017
Chronic alcohol abuse gone untreated can lead to severe brain damage. Researchers at The University of Texas Medical Branch at Galveston recently investigated the impact of alcohol consumption on stem cells in the brains of mice. Findings indicated that chronic alcohol consumption killed brain stem cells, reduced the production of new nerve cells, and affected females significantly worse than males. The study was discussed in a recent article in MedicalXpress:
Because the brain stems cells create new nerve cells and are important to maintaining normal cognitive function, this study possibly opens a door to combating chronic alcoholism.
The researchers also found that brain stem cells in key brain regions of adult mice respond differently to alcohol exposure, and they show for the first time that these changes are different for females and males. The findings are available in Stem Cell Reports.
Chronic alcohol abuse can cause severe brain damage and neurodegeneration. Scientists once believed that the number of nerve cells in the adult brain was fixed early in life and the best way to treat alcohol-induced brain damage was to protect the remaining nerve cells.
"The discovery that the adult brain produces stem cells that create new nerve cells provides a new way of approaching the problem of alcohol-related changes in the brain," said Dr. Ping Wu, UTMB professor in the department of neuroscience and cell biology. "However, before the new approaches can be developed, we need to understand how alcohol impacts the brain stem cells at different stages in their growth, in different brain regions and in the brains of both males and females."
In the study, Wu and her colleagues used a cutting-edge technique that allows them to tag brain stem cells and observe how they migrate and develop into specialized nerve cells over time to study the impact of long-term alcohol consumption on them.
Wu said that chronic alcohol drinking killed most brain stem cells and reduced the production and development of new nerve cells.
The researchers found that the effects of repeated alcohol consumption differed across brain regions. The brain region most susceptible to the effects of alcohol was one of two brain regions where new brain cells are created in adults.
They also noted that female mice showed more severe deficits than males. The females displayed more severe intoxication behaviors and more greatly reduced the pool of stem cells in the subventricular zone.
Using this model, scientists expect to learn more about how alcohol interacts with brain stem cells, which will ultimately lead to a clearer understanding of how best to treat and cure alcoholism.
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- Should Schizophrenia Be Reconceptualized?
- By Jason von Stietz, MA
- October 26, 2017
People commonly view schizophrenia as a chronic and hopeless brain disease. However, researchers and clinicians are beginning to believe that this is not the case. Rather, some believe that what we now know as schizophrenia is the most severe end of the spectrum or of psychosis. They believe that what we call schizophrenia is actually many different diseases and disorders that we currently lump together. Sciencr discussed this new conceptualization in a recent article:
Today, having a diagnosis of schizophrenia is associated with a life-expectancy reduction of nearly two decades. By some criteria, only one in seven people recover. Despite heralded advances in treatments, staggeringly, the proportion of people who recover hasn’t increased over time. Something is profoundly wrong.
Part of the problem turns out to be the concept of schizophrenia itself.
Arguments that schizophrenia is a distinct disease have been “fatally undermined”. Just as we now have the concept of autism spectrum disorder, psychosis (typically characterised by distressing hallucinations, delusions, and confused thoughts) is also argued to exist along a continuum and in degrees. Schizophrenia is the severe end of a spectrum or continuum of experiences.
Jim van Os, a professor of psychiatry at Maastricht University, has argued that we cannot shift to this new way of thinking without changing our language. As such, he proposes the term schizophrenia “should be abolished”. In its place, he suggests the concept of a psychosis spectrum disorder.
Another problem is that schizophrenia is portrayed as a “hopeless chronic brain disease”. As a result, some people given this diagnosis, and some parents, have been told cancer would have been preferable, as it would be easier to cure. Yet this view of schizophrenia is only possible by excluding people who do have positive outcomes. For example, some who recover are effectively told that “it mustn’t have been schizophrenia after all”.
Schizophrenia, when understood as a discrete, hopeless and deteriorating brain disease, argues van Os, “does not exist”.
BREAKING DOWN BREAKDOWNS
Schizophrenia may instead turn out to be many different things. The eminent psychiatrist Sir Robin Murray describes how:
I expect to see the end of the concept of schizophrenia soon … the syndrome is already beginning to breakdown, for example, into those cases caused by copy number [genetic] variations, drug abuse, social adversity, etc. Presumably this process will accelerate, and the term schizophrenia will be confined to history, like “dropsy”.
Research is now exploring the different ways people may end up with many of the experiences deemed characteristic of schizophrenia: hallucinations, delusions, disorganised thinking and behaviour, apathy and flat emotion.
Indeed, one past error has been to mistake a path for the path or, more commonly, to mistake a back road for a motorway. For example, based on their work on the parasite Toxoplasma gondii, which is transmitted to humans via cats, researchers E. Fuller Torrey and Robert Yolken have argued that “the most important etiological agent [cause of schizophrenia] may turn out to be a contagious cat”. It will not.
Evidence does suggest that exposure to Toxoplasma gondii when young can increase the odds of someone being diagnosed with schizophrenia. However, the size of this effect involves less than a twofold increase in the odds of someone being diagnosed with schizophrenia. This is, at best, comparable to other risk factors, and probably much lower.
For example, suffering childhood adversity, using cannabis, and having childhood viral infections of the central nervous system, all increase the odds of someone being diagnosed with a psychotic disorder (such as schizophrenia) by around two to threefold. More nuanced analyses reveal much higher numbers.
Compared with non-cannabis users, the daily use of high-potency, skunk-like cannabis is associated with a fivefold increase in the odds of someone developing psychosis. Compared with someone who has not suffered trauma, those who have suffered five different types of trauma (including sexual and physical abuse) see their odds of developing psychosis increase more than fiftyfold.
Other routes to “schizophrenia” are also being identified. Around 1% of cases appear to stem from the deletion of a small stretch of DNA on chromosome 22, referred to as 22q11.2 deletion syndrome. It is also possible that a low single digit percentage of people with a schizophrenia diagnosis may have their experiences grounded in inflammation of the brain caused by autoimmune disorders, such as anti-NMDA receptor encephalitis, although this remains controversial.
All the factors above could lead to similar experiences, which we in our infancy have put into a bucket called schizophrenia. One person’s experiences may result from a brain disorder with a strong genetic basis, potentially driven by an exaggeration of the normal process of pruning connections between brain cells that happens during adolescence. Another person’s experiences may be due to a complex post-traumatic reaction. Such internal and external factors could also work in combination.
Either way, it turns out that the two extreme camps in the schizophrenia wars – those who view it as a genetically-based neurodevelopmental disorder and those who view it as a response to psychosocial factors, such as adversity – both had parts of the puzzle. The idea that schizophrenia was a single thing, reached by a single route, contributed to this conflict.
IMPLICATIONS FOR TREATMENT
Many medical conditions, such as diabetes and hypertension, can be reached by multiple routes that nevertheless impact the same biological pathways and respond to the same treatment. Schizophrenia could be like this. Indeed, it has been argued that the many different causes of schizophrenia discussed above may all have a common final effect: increased levels of dopamine.
If so, the debate about breaking schizophrenia down by factors that lead to it would be somewhat academic, as it would not guide treatment. However, there is emerging evidence that different routes to experiences currently deemed indicative of schizophrenia may need different treatments.
Preliminary evidence suggests that people with a history of childhood trauma who are diagnosed with schizophrenia are less likely to be helped by antipsychotic drugs. However, more research into this is needed and, of course, anyone taking antipsychotics should not stop taking them without medical advice. It has also been suggested that if some cases of schizophrenia are actually a form of autoimmune encephalitis, then the most effective treatment could be immunotherapy (such as corticosteroids) and plasma exchange (washing of the blood).
Yet the emerging picture here is unclear. Some new interventions, such as the family-therapy based Open Dialogue approach, show promise for a wide range of people with schizophrenia diagnoses. Both general interventions and specific ones, tailored to someone’s personal route to the experiences associated with schizophrenia, may be needed. This makes it critical to test for and ask people about all potentially relevant causes. This includes childhood abuse, which is still not being routinely asked about and identified.
The potential for different treatments to work for different people further explains the schizophrenia wars. The psychiatrist, patient or family who see dramatic beneficial effects of antipsychotic drugs naturally evangelically advocate for this approach. The psychiatrist, patient or family who see drugs not working, but alternative approaches appearing to help, laud these. Each group sees the other as denying an approach that they have experienced to work. Such passionate advocacy is to be applauded, up to the point where people are denied an approach that may work for them.
WHAT COMES NEXT?
None of this is to say the concept of schizophrenia has no use. Many psychiatrists still see it as a useful clinical syndrome that helps define a group of people with clear health needs. Here it is viewed as defining a biology that is not yet understood but which shares a common and substantial genetic basis across many patients.
Some people who receive a diagnosis of schizophrenia will find it helpful. It can help them access treatment. It can enhance support from family and friends. It can give a name to the problems they have. It can indicate they are experiencing an illness and not a personal failing. Of course, many do not find this diagnosis helpful. We need to retain the benefits and discard the negatives of the term schizophrenia, as we move into a post-schizophrenia era.
What this will look like is unclear. Japan recently renamed schizophrenia as “integration disorder”. We have seen the idea of a new “psychosis spectrum disorder”. However, historically, the classification of diseases in psychiatry has been argued to be the outcome of a struggle in which “the most famous and articulate professor won”. The future must be based on evidence and a conversation which includes the perspectives of people who suffer – and cope well with – these experiences.
Whatever emerges from the ashes of schizophrenia, it must provide better ways to help those struggling with very real experiences.
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