My article presentation at the Journal Club on 22 January 2008
Targeting abnormal neural circuits in mood and anxiety disorders: from the laboratory to the clinic
Kerry J Ressler & Helen S Mayberg
VOLUME 10 NUMBER 9
SEPTEMBER 2007
1116-1124
NATURE NEUROSCIENCE
For a free full text of the article:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2444035
To determine anti-anxiety of beta sitosterol , Chandan Chauhan M.S. Research Scholar, Dept. of Pharmacology & toxicology, National Institute of Pharmaceutical Education & Research (NIPER), Hajipur.
To determine anti-anxiety of beta sitosterol , Chandan Chauhan M.S. Research Scholar, Dept. of Pharmacology & toxicology, National Institute of Pharmaceutical Education & Research (NIPER), Hajipur.
Unfrying Your Brain- Tonmoy Sharma, CEO of Sovereign HealthDr. Tonmoy Sharma
Tonmoy Sharma, CEO of Sovereign Health Group, reveals how we must view addiction, and how we can reverse serious cognitive deficits that often go undetected in addiction treatment. Sharma also reviews the need for measurement-based care, and outlines in great detail, how the addiction-treatment industry can evolve to better meet the needs of our patients.
Effect and maintenance of "EEG-biofeedback rTMS" on mood and working memory ...Amin Asadollahpour Kargar
This is a proposal presented in the 1st IBRO/APRC Iranian Associate School of Cognitive Neuroscience “Functional Human Brain Mapping”, Tehran, Iran, May 22-28, 2015
aimed:
1. To evaluate the effect of EEG-biofeedback rTMS on Mood in major depressed patients compare to EEG biofeedback and rTMS
2. To evaluate the maintenance of EEG-biofeedback rTMS on working memory in major depressed patients compare to EEG biofeedback and rTMS
This is a presentation that was given at the Lost in Translation 2013: Exploring the Origins of Addiction conference, that took place on March 25 - 26, 2013 in Vancouver, British Columbia, Canada
Depression as one of the most prevalent and life-threatening
forms of mental illness affects about 1/5 of the world’s population [1], and the number of patients suffering from it is still increasing [2]. The understanding of the pathophysiology and the treatment of this disorder remains greatly challenging to modern medicine. Though many different antidepressants were commercially available during the past years, not all patients were treated satisfactorily accompanied with some potential side effects of these drugs [3,4]. Th is highlights the imperative to the continuous search for new alternatives for the treatment of depression [5,6]. Some recent studies documented that some specific molecules such as chrysin [6], oxytocin [7], P11 [8], and OTX2 [9] are closely related to depression/depression-like behaviors, which suggests potentially important roles of these molecules in the treatment of depression.
Unfrying Your Brain- Tonmoy Sharma, CEO of Sovereign HealthDr. Tonmoy Sharma
Tonmoy Sharma, CEO of Sovereign Health Group, reveals how we must view addiction, and how we can reverse serious cognitive deficits that often go undetected in addiction treatment. Sharma also reviews the need for measurement-based care, and outlines in great detail, how the addiction-treatment industry can evolve to better meet the needs of our patients.
Effect and maintenance of "EEG-biofeedback rTMS" on mood and working memory ...Amin Asadollahpour Kargar
This is a proposal presented in the 1st IBRO/APRC Iranian Associate School of Cognitive Neuroscience “Functional Human Brain Mapping”, Tehran, Iran, May 22-28, 2015
aimed:
1. To evaluate the effect of EEG-biofeedback rTMS on Mood in major depressed patients compare to EEG biofeedback and rTMS
2. To evaluate the maintenance of EEG-biofeedback rTMS on working memory in major depressed patients compare to EEG biofeedback and rTMS
This is a presentation that was given at the Lost in Translation 2013: Exploring the Origins of Addiction conference, that took place on March 25 - 26, 2013 in Vancouver, British Columbia, Canada
Depression as one of the most prevalent and life-threatening
forms of mental illness affects about 1/5 of the world’s population [1], and the number of patients suffering from it is still increasing [2]. The understanding of the pathophysiology and the treatment of this disorder remains greatly challenging to modern medicine. Though many different antidepressants were commercially available during the past years, not all patients were treated satisfactorily accompanied with some potential side effects of these drugs [3,4]. Th is highlights the imperative to the continuous search for new alternatives for the treatment of depression [5,6]. Some recent studies documented that some specific molecules such as chrysin [6], oxytocin [7], P11 [8], and OTX2 [9] are closely related to depression/depression-like behaviors, which suggests potentially important roles of these molecules in the treatment of depression.
Running Head: DEPRESSION 1
DEPRESSION 3
Lana Eliot
Depression
Psychology 630
Professor Benton
August 25, 2018
Many people throughout the world experience some type of depression in their lives and it is one of the most common mental disorders. The current statistic show that depression is linked to genetic, environmental, biological and is also psychological. Depression can ben found with any age person. A small child or an adult may have to deal with the depression that is affecting them. Chemical imbalances in the brain is the leading cause for a person dealing with the depressive order. The neurotransmitter is the what we call the communicator between the brain and the limbic system. Researchers study the limbic system in the brain as this is where depression starts; especially for anxiety and stress. The 3 major neurotransmitters; serotonin, norepinephrine, and dopamine all have direct relations with a persons’ depression and anxiety.
Serotonin plays a crucial role in our brain. It is associated with many physical actions that we may portray. The actions associated with serotonin are mood altering, sleeping patterns, eating disorders, and aggression. If a persons’ serotonin levels decrease, they may experience these depressive symptoms. This can also make persons have a feeling of self-worth and suicidal feelings.
Another transmitter in the brain which is associated with the depressive disorder is dopamine. This is the part of the brain that deals with our motivation and how we gain the feeling of self-worth and self-pleasure. Early studies suggested that an existence of neurotransmitter norepinephrine deficiency in some certain areas of the brain resulted in depression. One main cause of depression is the reduction in the concentration of certain neurotransmitters in the brain, such as serotonin and dopamine. The decrease in the concentration of these neurotransmitters leads to disturbed neuronal signal processing which leads to alterations in the structure of the neuronal networks. These basic changes are accepted to be one of the fundamental purposes behind sorrow. The emergence of neuroimaging techniques, magnetic resonance imaging (MRI), positron emission tomography (PET) and functional fMRI, established the importance of the ‘neurocircuit of emotion’ which has been expanded to include other important brain areas and the prefrontal cortex (PFC). These brain sites and their connections, which have been widely studied, are responsible for maintaining emotional stability and their malfunction is considered central to the pathophysiology of depression (Palazidou, E., 2012).
Recent follow up studies also shows that there is a group of individuals with a depression disorder who exhibit low levels of the chemical norepinephrine. In autopsy studies, it has been shown that in comparison,.
Regulation of depression by a new type of brain stimulation in addicted patie...Mrsunny4
Depression is also known as clinical depression and major depressive disorder (MDD). This severe medical illness affects 15 million American adults every year or about 5-8% of the adult population of the US. Women are nearly twice as likely as men to develop major depression.
Psychotherapy the biological dimensionismail sadek
is it real word can affect your brain?
many people say not and don't believe that the psychotherapy change not only our behavior but also it can change the brain structure
Previous research shows deficits in Executive Function (EF) in patients with anxiety and depression. Recent studies have shown that EF measured by neuro-imaging and Neuro-psychological tests predicts treatment outcomes for depression, but it is unclear whether they predict outcomes for anxiety. Neuro-imaging and
Neuro-psychological tests are effective but intensive procedures that may not always be accessible to clinicians. Previous research has explored the viability of questionnaire measures of EF. A previous study suggests that the Revised by executive Questionnaire (DEX-R) predicts concurrent depression and anxiety; however, it is unclear how comorbidity influenced these results. The purpose of the current study was to investigate whether a questionnaire measure of EF could predict concurrent depression and anxiety and well as outcomes following treatment. A total of 206 psychiatric outpatients with major depression or anxiety disorders completed the DEX-R prior to Group Cognitive Behavioral Therapy (GCBT). They also completed anxiety and depression scales at pre-and post-treatment. Executive dysfunction predicted symptom severity for pre-treatment anxiety after controlling for comorbid depression, and for pre-treatment depression after controlling for comorbid anxiety. Symptom severity in anxiety was predicted by specific executive deficits in inhibition; symptom severity in depression was predicted by executive problems with volition and social regulation.
DEX-R significantly predicted post-treatment symptoms of anxiety but not depression following treatment in GCBT. It was concluded that EF deficits are associated with both anxiety and depressive disorders and predict responsiveness to treatment for anxiety patients. Screening of psychiatric patients for EF and, where indicated, incorporation of neurocognitive training strategies into therapy, may improve treatment outcomes.
Previous research shows deficits in Executive Function (EF) in patients with anxiety and depression. Recent studies have shown that EF measured by neuro-imaging and neuropsychological tests predicts treatment outcomes for depression, but it is unclear whether they predict outcomes for anxiety. Neuro-imaging and neuropsychological tests are effective but intensive procedures that may not always be accessible to clinicians. Previous research has explored the viability of questionnaire measures of EF. A previous study suggests that the Revised Dysexecutive Questionnaire (DEX-R) predicts concurrent depression and anxiety; however, it is unclear how comorbidity influenced these results.
Previous research shows deficits in Executive Function (EF) in patients with anxiety and depression. Recent studies have shown that EF measured by neuro-imaging and neuropsychological tests predicts treatment outcomes for depression, but it is unclear whether they predict outcomes for anxiety. Neuro-imaging and neuropsychological tests are effective but intensive procedures that may not always be accessible to clinicians.
Application of The Cognitive Psychology in Mental Illness or Traum.docxspoonerneddy
Application of The Cognitive Psychology in Mental Illness or Trauma
Melvin Coe
Capella University
Professor Theresa Crawford
Research Foundation of History Systems in Psych
June 7, 2020
Running Head: APPLICATION OF THE COGNITIVE PSYCHOLOGY 1
APPLICATION OF COGNITIVE PSYCHOLOGY 2
Application of The Cognitive Psychology in Mental Illness or Trauma
Introduction
In the present times, the number of people suffering from mental challenges has been on the rise. It is a time that demands psychologists to have better and effective scientific methods that would help them handle the different psychological issues being brought to their attention. Cognitive psychology is one of the scientific methods that can be used by psychologists to study the mind as an information processor. Using the method, psychologists are able to develop cognitive theories and models that would align and seems applicable in individual cases they are handling for instance, how one perceives, understands, remembers, attentiveness, makes use of language and is conscious of things.
The principal goals of clinical psychology are to generate knowledge based on scientifically valid evidence and to apply this knowledge to the optimal improvement of mental and behavioral health (Baker, McFall, Shoham, 2008). The values, principles, and methods of cognitive psychology and psychodynamic psychotherapy are anticipated to be utilized in an investigation which replaces maladaptive behaviors. The interest in the study is centered around increasing social response while decreasing maladaptive behaviors by utilizing differential reinforcement of alternative behaviors. Differential reinforcement of alternative behaviors is a procedure that reduces a problematic behavior by reinforcing an appropriate alternative behavior that serves the same function.
Research topic (Cognitive Psychology in the influences of patient with trauma or mental illness)
The research paper revolves around understanding how cognitive psychology influences patients with trauma and mental illness. It is evident that cognitive psychology revolves around the study of the process within the brain and they vary from learning, perception, attention, memory, thinking, language, attention and problem-solving (Maslow, 1943). The mental illness and trauma are a result of some of the brain processes thus with embracing the school of cognitive psychology it is easier to understand and comprehend the potential solutions. The problem of mental illness has become complaisant in the current era and with the limited resources and technology in the past made it a challenge to contain it but the advancement in field of psychology has made it easier to find solutions to the problem. There is no specific treatment for trauma or mental illness in this era of medical advancement and technology but cognitive psychology is making it easier to help under.
Application of The Cognitive Psychology in Mental Illness or Traum.docxssusera34210
Application of The Cognitive Psychology in Mental Illness or Trauma
Melvin Coe
Capella University
Professor Theresa Crawford
Research Foundation of History Systems in Psych
June 7, 2020
Running Head: APPLICATION OF THE COGNITIVE PSYCHOLOGY 1
APPLICATION OF COGNITIVE PSYCHOLOGY 2
Application of The Cognitive Psychology in Mental Illness or Trauma
Introduction
In the present times, the number of people suffering from mental challenges has been on the rise. It is a time that demands psychologists to have better and effective scientific methods that would help them handle the different psychological issues being brought to their attention. Cognitive psychology is one of the scientific methods that can be used by psychologists to study the mind as an information processor. Using the method, psychologists are able to develop cognitive theories and models that would align and seems applicable in individual cases they are handling for instance, how one perceives, understands, remembers, attentiveness, makes use of language and is conscious of things.
The principal goals of clinical psychology are to generate knowledge based on scientifically valid evidence and to apply this knowledge to the optimal improvement of mental and behavioral health (Baker, McFall, Shoham, 2008). The values, principles, and methods of cognitive psychology and psychodynamic psychotherapy are anticipated to be utilized in an investigation which replaces maladaptive behaviors. The interest in the study is centered around increasing social response while decreasing maladaptive behaviors by utilizing differential reinforcement of alternative behaviors. Differential reinforcement of alternative behaviors is a procedure that reduces a problematic behavior by reinforcing an appropriate alternative behavior that serves the same function.
Research topic (Cognitive Psychology in the influences of patient with trauma or mental illness)
The research paper revolves around understanding how cognitive psychology influences patients with trauma and mental illness. It is evident that cognitive psychology revolves around the study of the process within the brain and they vary from learning, perception, attention, memory, thinking, language, attention and problem-solving (Maslow, 1943). The mental illness and trauma are a result of some of the brain processes thus with embracing the school of cognitive psychology it is easier to understand and comprehend the potential solutions. The problem of mental illness has become complaisant in the current era and with the limited resources and technology in the past made it a challenge to contain it but the advancement in field of psychology has made it easier to find solutions to the problem. There is no specific treatment for trauma or mental illness in this era of medical advancement and technology but cognitive psychology is making it easier to help under.
Similar to Targeting abnormal neural circuits in mood and anxiety disorders:from the laboratory to the clinic (20)
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...
Targeting abnormal neural circuits in mood and anxiety disorders:from the laboratory to the clinic
1. Targeting abnormal neural circuits in mood and anxiety disorders: from the laboratory to the clinic Kerry J Ressler & Helen S Mayberg VOLUME 10 NUMBER 9 SEPTEMBER 2007 1116-1124 NATURE NEUROSCIENCE 14.805, for 2006; 4th of 341 neuroscience journals http://www.nature.com.libaccess.lib.mcmaster.ca/neuro/index.html
2. Kerry J. Ressler MD, Ph.D Assistant Professor of Psychiatry and Behavioral Sciences 1- Department of Psychiatry and Behavioral Sciences, Emory University, School of Medicine, Atlanta, Georgia 2- Yerkes National Primate Research Center http://userwww.service.emory.edu/~kressle/ http://userwww.service.emory.edu/~kressle/kerry.htm
3. B.S. in molecular biology @ M.I.T. PhD (1995) Department of Neurobiology, Harvard University M.D. (1997) Harvard School of Medicine Residency in Psychiatry at Emory University School of Medicine Research fellow with Dr. Michael Davis at Emory studying behavioral neuroscience
4. Dr. Ressler's lab at Yerkes Research Center is focused on the molecular and cellular mechanisms of fear learning and the process of extinction of fear in mouse models. He hopes that by understanding how fear works in the brain, it will improve our understanding of and advance treatments for fear-based disorders, such as PTSD and Panic Disorder.
5. The goal of my laboratory is to create a program which utilizes the enormous power of molecular biology to approach difficult and important questions in systems neuroscience. I use genes known to be involved in synaptic plasticity to examine plasticity in the amygdala and regions which connect with it during the consolidation phase of fear memory formation. http://www.emory.edu/NEUROSCIENCE/facultyprofiles_Z.html
6. I am also initiating a program to create transgenic animal models for visualizing the amygdala neurons, some of its sensory inputs and the neuromodulatory projections which together mediate some of the important behavioral responses of fear and stress.
7. During his clinical time, Dr. Ressler is co-director with Dr. Ann Schwartz of the newly created Post-traumatic Stress Disorders Clinic at the Adult Outpatient Psychiatry Clinic at Grady Memorial Hospital. Dr. Ressler was recently nominated as an Investigator with the Howard Hughes Medical Institute .
8. Helen S Mayberg M.D., FRCPC Professor of Psychiatry & Neurology http://en.wikipedia.org/wiki/Helen_S._Mayberg http://neurology.emory.edu/Faculty/Mayberg.htm 1- Department of Psychiatry and Behavioral Sciences, Emory University, School of Medicine, Atlanta, Georgia 2- Department of Neurology, Emory University, School of Medicine, Atlanta, Georgia She is also affiliated with Rotman Research Institute at Baycrest Centre and the Departments of Psychiatry and Neurology, University of Toronto
9. Born in 1956 in California B.A. (1976) Psychobiology @ UCLA M.D. (1981) University of Southern California University of California, Irvine Graduate studies: Department of Radiological Sciences Residency (1985) @ Columbia University’s Neurological Institute in New York City Research fellowship (1987) at Johns Hopkins University’s PET facility from
10. Research Focus My research concerns the characterization of neural systems mediating mood and emotions in health and disease using functional neuroimaging. Defining brain mechanisms underlying major depression is the primary goal, with an emphasis on development of algorithms that will discriminate patient subgroups, optimize treatment selection, and provide markers of disease vulnerability.
11. INTRODUCTION Major depressive disorder (MDD) is the most common of all psychiatric disorders. MDD ranks among the top causes of worldwide disease burden and disability, with lifetime risk of 7–12% in men and 20–25% in women. 20% completely fail to SSRIs, 60% may not achieve adequate response.
12. The different anxiety disorders, including panic disorder, post-traumatic stress disorder (PTSD) and phobias, are also extremely common, with a combined lifetime prevalence of over 28%, and with a similar societal cost-burden with similar rates of failure to respond to treatment with that in MDD.
13. In this review, MDD and anxiety disorders will be considered together: 1- comorbidity 2- a significant problem of diagnostic classification with highly overlapping symptom criteria 3- similar involved brain circuits 4- similar treatments (e.g., SSRIs, CBT) Current clinical descriptions are probably not identifying the phenotypic clusters of disorders that may be most useful from a neurobiological and treatment perspective. Problem in current clinical descriptions!
14.
15. New neurostimulatory therapies based on progress in understanding emotion circuitry and new pharmacological therapies based on understanding emotional learning are likely to provide more rapid and robust methodologies for treating MDD and anxiety disorders .
16. 1- Abnormal circuit modulation in mood and anxiety disorders PET and fMRI studies have examined differences in brain regional activation in depressed and anxious subjects relative to controls and in patients before and after treatment.
17. Many brain areas may underlie some of the different symptom clusters of depression. nucleus accumbens along with other areas involved in reward processing, are also likely to be involved in the anhedonic components of depression. http://en.wikipedia.org/wiki/Nucleus_accumbens http://www.biopsychiatry.com/nucleus-accumbens.htm
18. The areas most reproducibly found to be dysregulated in common emotional disorders are the prefrontal cortex (PFC) and subgenual cingulate cortex (Cg25) , which seem to be involved in emotion experience and processing , as well as the hippocampus and amygdala , which are involved in emotional memory formation and memory retrieval .
19. Review focuses on: role of Cg25 in emotion regulation and processing, the role of the amygdala in emotional memory formation and expression. 1 = BA25 (subcallosal gyrus), 2 = BA24sg (SGPFC) 3 = BA32 (paracingulate gyrus)
20. Cg25 is involved in the production of sad emotions and in antidepressant treatment response. activated during transient sadness Decreased activity in Cg25 after treatment, even after placebo. Also in social phobia. Activity in Cg25 before treatment predicts treatment response with CBT.
21. A- Transient sadness in healthy volunteers increases activity in Cg25 measured by PET B- Decreased Cg25 activity with chronic fluoxetine treatment for MDD. C- Cg25 decrease in recovery with chronic fluoxetine from Parkinson’s disease related depression. D- Natural recovery with decreased Cg25 activity in patients treated with placebo. E- Predictors of response in subjects responding to CBT for depression included low pretreatment Cg25 activity. F- Subgenual cortical decreased activity was common in responders compared with nonresponders for those responding both to citalopram and CBT for social phobia.
22. Overactivation of the amygdala is also implicated in depression and anxiety. Amygdala activation decreases with recovery from mood symptoms. Studies that implicate Cg25 also find significant amygdala decreases with response to CBT treatment for social phobia. http:// www.psycheducation.org/emotion/amygdala.htm
23. A genetic polymorphism has repeatedly been implicated in gene by environment interactions for disorders of emotional dysregulation: the serotonin promoter polymorphism 5-HTTLPR .
24. Takahashi T, Suzuki M, Kawasaki Y, Hagino H, Yamashita I, Nohara S, Nakamura K, Seto H, Kurachi M.Biol Psychiatry. Perigenual cingulate gyrus volume in patients with schizophrenia: a magnetic resonance imaging study. 2003;53:593-600. Carriers of the risk-conferring 5-HTTLPR polymorphism have reduced gray matter volume in the perigenulate region surrounding Cg25 as well as in the amygdala .
25. prefrontal-limbic circuits, the Cg25 and amygdala areas in particular, may be critically involved in emotional processing and regulation in mood and anxiety disorders.
26. 2- Neurostimulation therapies modulate dysregulated circuits Several somatic therapies , available or under investigation, may modulate the disrupted circuit activity. Vagus nerve stimulation therapy (VNS) Transcranial magnetic stimulation (TMS) Magnetic seizure therapy (MST) Deep brain stimulation (DBS) Deep Brain Stimulation for Treatment-Resistant Depression: An Expert Interview With Helen S. Mayberg, MD @ http://www.medscape.com/viewarticle/520659 Posted 01/05/2006
27. VNS approved by the FDA for treatment of medication-resistant depression and was approved earlier for the treatment of epilepsy. Promising but long-term efficacy in refractory patients still remains to be demonstrated. Mechanism: may help correct dysfunctional neurotransmitter modulatory circuits in patients with depression. the nucleus of the tractus solitarius
28. Functional imaging suggests that VNS leads to acute changes in hypothalamus , orbitofrontal cortex , amygdala, hippocampus , insula , medial prefrontal cortex and cingulate cortex . Chronic VNS treatment leads to significant ventromedial prefrontal cortex deactivation, similarly to other approaches to depression treatment. Low rates of relapse, well-tolerated VNS may be an important adjunct for refractory depression.
29. TMS Repetitive transcranial magnetic stimulation (rTMS) and electroconvulsive therapy (ECT) are both somatic treatments relying upon altering local and distant neural circuits within the brain. rTMS is also potentially useful as a probe for understanding brain activity changes with response to treatment with rTMS and ECT.
30. When PET and TMS combined it was seen that, Baseline hypometabolism responds better to high-frequency stimulation that seems to enhance excitability, Baseline hypermetabolism responds better to low-frequency stimulation that seems to dampen excitability.
31. In preclinical studies, rTMS modulates neural circuits and neurotransmitter systems thought to be involved with mood regulation. rTMS modulates cortical β -adrenergic receptors, serotonergic receptors in frontal cortex, and increases NMDA receptors in hypothalamus and basolateral amygdala. Furthermore, rTMS at 10 Hz in a rat model of depression leads to enhanced hippocampal plasticity after stress. rTMS acutely modulates dopamine and serotonin levels .
32. MST involves the induction of relatively focal seizure activity using focused magnetic stimulation. MST seems to offer greater control of intracerebral current intensity than is possible with ECT and thus may result in fewer cognitive side effects. . Relatively new May 2000. in Switzerland. But yet promising as it has the ability to focally stimulate cortical areas. It will provide a new tool to dissect the critical circuitry involved in recovery from depression.
33. DBS Parkinson’s disease DBS may also modulate disorders of emotion, in addition to its known role in treating disorders of motion . DBS targeting the left caudate may lead to recovery from depressive symptoms.
34. BA25 has been investigated in treatment-resistant depressive patients more extensively. DBS can reduce elevated BA25 activity. Distal effects on remote cortical and brainstem areas might arise from indirectly from BA25 or directly from the WM tracts passing through the field of stimulation. Early data on DBS suggest that it might be a powerful tool to specifically target dysregulated neural circuits.
35. 3- Pharmacological therapies to modulate emotional learning 3a- Enhancing extinction of fear 3b- Preventing consolidation of traumatic memories 3c- Preventing reconsolidation of traumatic memories
36. 3a- Enhancing extinction of fear From an operational perspective, Extinction may thus be defined as “ a reduction in the strength or probability of a conditioned fear response as a consequence of repeated presentation of the conditioned stimulus in the absence of the UCS”.
37. Extinction is a form of learning and not ‘unlearning’ or the forgetting of a conditioned association so why not enhance the neurotranmission of NMDA receptors the D-Cycloserine (DCS) partial NMDA agonist, used in the treatment of tuberculosis, potential use in facilitating extinction-based therapies for human anxiety disorders. Subjects receiving DCS (one dose) showed greater decreases in physiological measure of anxiety. Placebo-compared trials also showed promising results in favor of DCS in patients with anxiety. Seromycin ® http://www.coccyx.org/treatmen/cycloser.htm
38. 3b- Preventing consolidation of traumatic memories With certain disorders, notably PTSD, the time of the insult that created the disorder is known—it is when the initiating trauma occurred. Memories do not immediately become permanent at the time of the initial experience. Instead they exist in a labile state for at least hours and possibly days, during which they become consolidated into a more permanent memory.
39. There is a host of in vitro and in vivo data in animals outlining the molecular, synaptic, neurotransmitter and systems-level changes that may occur during this consolidation process. Trauma Labile memories Consolidation of memories (after hours/days) Labile again when recalled = Reconsolidation (following retrieval)
40. Differential memory systems are encoding different aspects of a memory in parallel. Declarative memory systems [hippocampal-cortical pathways] are likely to be encoding the ‘what, when and where’ of an event, in parallel amygdala-cortical pathways are encoding the emotional salience and aversiveness of the memory.
41. Therefore, agents that block the ‘emotional overconsolidation’ of a traumatic memory perhaps could preserve the declarative aspects of the same memory. This idealized approach would not render the patient fully amnestic, but would potentially prevent PTSD.
42. Fear consolidation is blocked after training by an antagonist of noradrenergic activation. Propranolol , a common β -blocker used for hypertensioncan block central β 1 and β 2 adrenergic receptors.
43. Patients after a trauma (motorcyle accident) took propranolol and placebo for 10 days. After 1 month; patients who were on propranolol PTSD measures trended lower, as well as physiological symptoms of PTSD.
44. Another consolidation-blockade approach is based on the findings that lower cortisol levels after trauma predict subsequent PTSD. Glucocorticoids are involved in emotional memory encoding and retrieval and high doses of glucocorticoids decrease the catecholamine. Early data with small # of subjects support that when cortisol given after the trauma it decreases the number of subjects with PTSD.
45. Every memory recall event is accompanied by competition between molecular events that strengthen the original memory (reconsolidation) and those that inhibit that memory (extinction). By differentially enhancing or inhibiting these processes, opposing effects on the state of the existing fear memories may be obtained.
46. Other neuromodulators including dopamine and glutamate-NMDA receptor activation are implicated in the consolidation of fear memories. This work remains in its early stages, but there is room for optimism. In emergency rooms, in the future, on the battlefield or after a disaster the early routine medical interventions in later PTSD prevention may be as important as the ones we do after stroke and MI today.
47. 3c- Preventing reconsolidation of traumatic memories Memories remain labile and associative when they are recalled. Reactivated memories are also sensitive to pharmacological disruption. Local infusion of protein synthesis inhibitors into discrete brain regions prevents the reconsolidation of the memory, but do not cross the blood-brain barrier easily, so unlikely to be used in humans.
48. More benign drugs, given in animals acutely with recall of fear memories, may also act to reduce later memory expression, possibly through inhibiting reconsolidation mechanisms. NMDA receptor agonists β -adrenergic antagonists timolol or propranolol block reconsolidation, and thus may serve as useful agents in future human studies of reconsolidation.
49. Reconsolidation occurs for recently learned memories but not distant memories. Propranolol has not been reported to block reconsolidation in humans, as the initial report about animals was a decade ago but it is safe to try in humans as well.
50. Disrupting the remote memories from chronic PTSD may not be possible using reconsolidation-impairing approaches. Extinction of fear may eventually be optimal in more chronic cases.
51. Conclusions This is a very exciting time in the fields of learning and memory and psychiatry, because the growing literature on the differential processes involved in memory formation are now increasingly amenable to translational human studies. This review has focused on recent developments in understanding the neural circuit processes underlying mood and anxiety disorders.
52. It is hoped that recent progress in understanding the neurobiology of emotional regulation and dysregulation will lead to powerful and exciting new treatments for mood and anxiety disorders. New experimental treatments may alleviate symptoms through the correction of dysregulated circuit activity as well as prevent overlearning or enhance extinction learning in circuits mediating negative emotional memories.