How Drugs Affect the Brain and Medication‐Assisted Treatment

Total Page:16

File Type:pdf, Size:1020Kb

How Drugs Affect the Brain and Medication‐Assisted Treatment How Drugs Affect the Brain And Medication‐Assisted Treatment Presented by Carl M. Dawson, M.S., MAC, LPC, Q‐SAP Learning Objectives After completing this section, participants will be able to: • Understand the scientific modalities neuroscientists use when studying addictions (Bio‐Psycho‐Social model of addictions, genetics and neuroplasticity) • Explore basic facts regarding the development and function of the human brain • Identify three “Feel Good” chemicals released by the brain (dopamine, serotonin, norepinephrine) • Discuss how addictive behaviors and drugs routinely “hijack” the human brain How Neuroscientists Study Addiction • All addictions (alcohol, drugs, gambling, porn, video games, food) activate the same neurological pleasure (reward) routes (pathways) in the brain • Addictionology uses the “Bio‐Psycho‐Social” model when studying addictions • Research has identified a strong genetic basis for all addiction behaviors (There is no single “addiction” gene, there are approx. 90 genes associated with addictions) How Neuroscientists Study Addiction • Remember: “Our genetics load the gun, but the environment pulls the trigger” • Addictions aren't only hijacking the brain’s activities but they have the ability to modify the neurological structures and activities of the brain (neuroplasticity) Neuroplasticity: is a term used in the field of neuroscience that defines the brain's ability to adapt, adjust and change based upon the strength and reward of the experience ‐ “Neurons that Fire Together, Wire Together” Donald O. Hebb (1904‐1985) Basic Facts and Regions of the Human Brain The average human brain weighs approximately three (3 lbs.) pounds, consisting of 60% protein (fat), possessing approximately 85 to 110 billion neurons and produces 15 watts of electricity, traveling at a speed of one‐half to 250 miles per hour Approximate Ages of the Human Brain 7,000 7,000 480,000 6 to 10 mil. Addiction occurs in the portion of the brain that is 480,000 years old ‐ REMEMBER: “Age Trumps Youth” The “Reward” routes (pathways) Limbic area The “Feel Good” Chemicals in the Brain We possess approximately sixty (60) neurotransmitters in the human brain and nervous system Here are the Big Three (3): Dopamine (DA): Involved in learning, self‐control, seeking‐searching‐wanting behaviours, cravings, euphoria, pleasure and at extreme levels, symptoms of psychosis Serotonin (5ht): Affects feelings of well‐being, anti‐ anxiety, anti‐depression Norepinephrine (NE): Stimulates the brain’s four “Fs” The frontal cortex tells our primitive brain to “STOP” remember our past, predict the future and consider the consequences Important take‐away points • Addiction is a very complex process that is a combination of our biological (genetics), psychological (learning) and social (environmental) influences • Our brains are designed to adapt and change based upon the strength of the experiences we encounter (neuroplasticity) • Our brains consist of sixty (60%) percent protein (fat). Drugs that are attracted to high concentrations of fat will easily hijack the brain and hold it hostage until it is eliminated by the body (opioids, marijuana) • All addictions following the same neurological route (pathway) in the brain and cause a greater than normal release of the pleasure seeking brain chemical, dopamine (DA) Medication‐Assisted Treatment (MAT) in Opioid Use How drug’s “Hijack” and “Turn‐On” the brain Action Potential: The electrical stimulation of a neuron Propagation: To send forth or spread Affinity: The degree of attraction or desirability “Key into a Lock” Model The key either turns “On” or turns “Off” the receptor Receptor Drug FULL NEUROTRANSMITTERS AGONIST ACTION POTENTIAL RECEPTORS “Full” Agonists • Full agonists will occupy all of the receptors • Full agonists create a Receptor stronger potential than partial agonists • Full agonists act like an “On‐Off” light switch • Full agonists, do not have a ceiling threshold which may result in single drug overdose PARTIAL NEUROTRANSMITTERS AGONIST ACTION POTENTIAL RECEPTORS “Partial” Agonist • Partial agonists are designed to only stimulate a portion of the receptor producing a weaker potential Receptor • Partial agonists act like a light “dimmer” rather than an “On‐Off” switch • Partial agonists produce a “ceiling” limit and won’t permit single drug overdosing Antagonists • Antagonists are designed to block all chemicals (full‐partial agonist) from entering the receptor Receptor • When an antagonist enters into the nervous system they will dislodge and remove any chemical on a receptor site resulting in spontaneous (immediate) drug withdrawal Medication‐Assisted Treatment (MAT) In Opioid Treatment Learning Objectives At the end of this session, participants will be able to: • Understand what makes opioid drugs so desirable • Understand Medication‐Assisted Treatment’s (MAT) three (3) main objectives • Know when Medication‐Assisted Treatment (MAT) is indicated • Explore the four (4) most currently prescribed Medication‐Assisted medications (methadone, buprenorphine, naloxone and naltrexone ) What Makes Opioid Drugs Desirable? • Opioid substances are lipophilic (fat‐ loving), meaning that they infiltrate high protein regions of the body quickly (heroin vs. codeine) • Opioid addicts become addicted to the “RUSH” of pleasure produced by the drug What Makes Opioid Drugs Desirable? • Opioid drugs that produce “LESS OF A RUSH“ are less fat‐loving and are more effective in treating opioid dependence (methadone and buprenorphine) • Opioid overdose can be lethal, either when used alone or with other CNS depressant drugs (1 + 1 = 3) effect • The most common cause of opioid related death is due to respiratory arrest Medication‐Assisted Treatment (MAT) Medication‐Assisted Treatment (MAT), combines the use of medications (methadone, buprenorphine) and behavioral therapy (Cognitive‐Behavioral) to treat substance use disorders The most frequently asked question: “Isn’t Medication‐Assisted Treatment just switching one drug for another?” Three (3) Main Objectives of Medication‐Assisted Treatment (MAT) • First (1ST) Objective: STOP the use of illicit drugs! • Second (2ND) Objective: To help abstain from the use of all mood altering substances including alcohol • Third (3RD) Objective: To eliminate the obstacles that lead to relapse The Benefits of Medication‐ Assisted Treatment • MAT has significantly improved opioid treatment admission and retention rates in the criminal justice population • MAT has been found to have significantly reduced rearrests and reincarceration rates, for probationary and paroled individuals The Benefits of Medication‐ Assisted Treatment • Research shows that the use of methadone and buprenorphine has been highly effective at reducing unauthorized and continuous opioid use • Individuals participating in a MAT protocol can be closely monitored by health care professionals for treatment compliance • Currently, buprenorphine can be dispensed through a physician’s office (OBOT) Medication‐Assisted Treatment Tapering: Progressively reducing the dosage or strength of a drug until the body no longer requires that drug in order to maintain normal functioning Maintenance: Providing a medically supervised alternative substance, for chronically drug dependent individuals who are unable or unwilling to stop using Harm Reduction: Providing a medically supervised alternative substance, aimed at reducing the harmful consequences associated with drug use Methadone “Full‐Opioid Agonists” • Methadone, like all full agonists will occupy the entire opioid receptor, producing a greater Opioid action potential and death from a single drug overdose Receptor • Duration of action is 24 to 72 hours • Dosages between 30 to 40 mg will block withdrawal, not cravings • Dosages of 80 to 100 mg are more effective at reducing opioid use Buprenorphine (Subutex) • Partial agonists are designed to only stimulate a portion of the opioid receptor, producing a lesser action potential and less opportunity for a single drug overdose • Subutex is straight Opioid buprenorphine Receptor • Subutex is less lipophilic than morphine • Dosages range from 8‐32 mg • Duration of action is 24 to 36 hours • Buprenorphine has a “Ceiling” limit at 35 mg Buprenorphine (Suboxone) • Suboxone is buprenorphine and naloxone combined • The addition of naloxone to the buprenorphine will insure that any additional Opioid use of an opioid drug or any attempt to divert the Receptor drug will result in an immediate removal of all opioid substances, including buprenorphine, causing spontaneous drug withdrawal • Dosages from 2mg‐0.5mg, 8mg‐2mg Naloxone (Narcan), Naltrexone (Vivitrol) • Naloxone‐Naltrexone are considered opioid and alcohol antagonists • They are designed to block all opioid and ethanol Opioid chemicals (full‐partial Receptor agonist) from entering the opioid receptor • They will remove any opioid or ethanol chemical occupying an opioid receptor • Naloxone lasts for only 30 to 90 minutes • Naltrexone lasts for 1 day by tablet or 30 days via injection Presentation Review In today’s presentation we covered the following topics: • Reviewed various modalities applied to the science of addiction studies • Explored various regions of the human brain that contribute to addictions • Examined three (3) primary “feel good” chemicals released by the brain Presentation Review In today’s presentation we covered the following topics: • Discussed how all drugs including opioids “hijack” the functions of the brain • Reviewed the three (3) main objectives of Medication‐Assisted Treatment (MAT) • Examined the four (4) MAT drugs currently being used in opioid treatment (methadone, buprenorphine, naloxone, naltrexone) Contact Information: CARL M. DAWSON, M.S., MAC, LPC, Q‐SAP 1320 EAST KINGSLEY SUITE “A” SPRINGFIELD, MISSOURI 65804 E‐mail: ([email protected]).
Recommended publications
  • Targeting Neuroplasticity for Balance Or Gait Deficit
    August 2021 Volume 1 Issue 8 CADTH Horizon Scan The Portable Neuromodulation Stimulator: Targeting Neuroplasticity for Balance or Gait Deficit Health Technology Update Authors: Sara D. Khangura ISSN: 2563-6596 Disclaimer: The information in this document is intended to help Canadian health care decision-makers, health care professionals, health systems leaders, and policy-makers make well-informed decisions and thereby improve the quality of health care services. While patients and others may access this document, the document is made available for informational purposes only and no representations or warranties are made with respect to its fitness for any particular purpose. The information in this document should not be used as a substitute for professional medical advice or as a substitute for the application of clinical judgment in respect of the care of a particular patient or other professional judgment in any decision-making process. The Canadian Agency for Drugs and Technologies in Health (CADTH) does not endorse any information, drugs, therapies, treatments, products, processes, or services. While care has been taken to ensure that the information prepared by CADTH in this document is accurate, complete, and up to date as at the applicable date the material was first published by CADTH, CADTH does not make any guarantees to that effect. CADTH does not guarantee and is not responsible for the quality, currency, propriety, accuracy, or reasonableness of any statements, information, or conclusions contained in any third-party materials used in preparing this document. The views and opinions of third parties published in this document do not necessarily state or reflect those of CADTH.
    [Show full text]
  • The Creation of Neuroscience
    The Creation of Neuroscience The Society for Neuroscience and the Quest for Disciplinary Unity 1969-1995 Introduction rom the molecular biology of a single neuron to the breathtakingly complex circuitry of the entire human nervous system, our understanding of the brain and how it works has undergone radical F changes over the past century. These advances have brought us tantalizingly closer to genu- inely mechanistic and scientifically rigorous explanations of how the brain’s roughly 100 billion neurons, interacting through trillions of synaptic connections, function both as single units and as larger ensem- bles. The professional field of neuroscience, in keeping pace with these important scientific develop- ments, has dramatically reshaped the organization of biological sciences across the globe over the last 50 years. Much like physics during its dominant era in the 1950s and 1960s, neuroscience has become the leading scientific discipline with regard to funding, numbers of scientists, and numbers of trainees. Furthermore, neuroscience as fact, explanation, and myth has just as dramatically redrawn our cultural landscape and redefined how Western popular culture understands who we are as individuals. In the 1950s, especially in the United States, Freud and his successors stood at the center of all cultural expla- nations for psychological suffering. In the new millennium, we perceive such suffering as erupting no longer from a repressed unconscious but, instead, from a pathophysiology rooted in and caused by brain abnormalities and dysfunctions. Indeed, the normal as well as the pathological have become thoroughly neurobiological in the last several decades. In the process, entirely new vistas have opened up in fields ranging from neuroeconomics and neurophilosophy to consumer products, as exemplified by an entire line of soft drinks advertised as offering “neuro” benefits.
    [Show full text]
  • Brain Stimulation and Neuroplasticity
    brain sciences Editorial Brain Stimulation and Neuroplasticity Ulrich Palm 1,2,* , Moussa A. Chalah 3,4 and Samar S. Ayache 3,4 1 Department of Psychiatry and Psychotherapy, Klinikum der Universität München, 80336 Munich, Germany 2 Medical Park Chiemseeblick, Rasthausstr. 25, 83233 Bernau-Felden, Germany 3 EA4391 Excitabilité Nerveuse & Thérapeutique, Université Paris Est Créteil, 94010 Créteil, France; [email protected] (M.A.C.); [email protected] (S.S.A.) 4 Service de Physiologie—Explorations Fonctionnelles, Hôpital Henri Mondor, Assistance Publique—Hôpitaux de Paris, 94010 Créteil, France * Correspondence: [email protected] Electrical or magnetic stimulation methods for brain or nerve modulation have been widely known for centuries, beginning with the Atlantic torpedo fish for the treatment of headaches in ancient Greece, followed by Luigi Galvani’s experiments with frog legs in baroque Italy, and leading to the interventional use of brain stimulation methods across Europe in the 19th century. However, actual research focusing on the development of tran- scranial magnetic stimulation (TMS) is beginning in the 1980s and transcranial electrical brain stimulation methods, such as transcranial direct current stimulation (tDCS), tran- scranial alternating current stimulation (tACS), and transcranial random noise stimulation (tRNS), are investigated from around the year 2000. Today, electrical, or magnetic stimulation methods are used for either the diagnosis or exploration of neurophysiology and neuroplasticity functions, or as a therapeutic interven- tion in neurologic or psychiatric disorders (i.e., structural damage or functional impairment of central or peripheral nerve function). This Special Issue ‘Brain Stimulation and Neuroplasticity’ gathers ten research articles Citation: Palm, U.; Chalah, M.A.; and two review articles on various magnetic and electrical brain stimulation methods in Ayache, S.S.
    [Show full text]
  • The Brain That Changes Itself
    The Brain That Changes Itself Stories of Personal Triumph from the Frontiers of Brain Science NORMAN DOIDGE, M.D. For Eugene L. Goldberg, M.D., because you said you might like to read it Contents 1 A Woman Perpetually Falling . Rescued by the Man Who Discovered the Plasticity of Our Senses 2 Building Herself a Better Brain A Woman Labeled "Retarded" Discovers How to Heal Herself 3 Redesigning the Brain A Scientist Changes Brains to Sharpen Perception and Memory, Increase Speed of Thought, and Heal Learning Problems 4 Acquiring Tastes and Loves What Neuroplasticity Teaches Us About Sexual Attraction and Love 5 Midnight Resurrections Stroke Victims Learn to Move and Speak Again 6 Brain Lock Unlocked Using Plasticity to Stop Worries, OPsessions, Compulsions, and Bad Habits 7 Pain The Dark Side of Plasticity 8 Imagination How Thinking Makes It So 9 Turning Our Ghosts into Ancestors Psychoanalysis as a Neuroplastic Therapy 10 Rejuvenation The Discovery of the Neuronal Stem Cell and Lessons for Preserving Our Brains 11 More than the Sum of Her Parts A Woman Shows Us How Radically Plastic the Brain Can Be Appendix 1 The Culturally Modified Brain Appendix 2 Plasticity and the Idea of Progress Note to the Reader All the names of people who have undergone neuroplastic transformations are real, except in the few places indicated, and in the cases of children and their families. The Notes and References section at the end of the book includes comments on both the chapters and the appendices. Preface This book is about the revolutionary discovery that the human brain can change itself, as told through the stories of the scientists, doctors, and patients who have together brought about these astonishing transformations.
    [Show full text]
  • Michael M. Merzenich
    Michael M. Merzenich BORN: Lebanon, Oregon May 15, 1942 EDUCATION: Public Schools, Lebanon, Oregon (1924–1935) University of Portland (Oregon), B.S. (1965) Johns Hopkins University, Ph.D. (1968) University of Wisconsin Postdoctoral Fellow (1968–1971) APPOINTMENTS: Assistant and Associate Professor, University of California at San Francisco (1971–1980) Francis A. Sooy Professor, University of California at San Francisco (1981–2008) President and CEO, Scientifi c Learning Corporation (1995–1996) Chief Scientifi c Offi cer, Scientifi c Learning Corporation (1996–2003) Chief Scientifi c Offi cer, Posit Science Corporation (2004–present) President and CEO, Brain Plasticity Institute (2008–present) HONORS AND AWARDS (SELECTED): Cortical Discoverer Prize, Cajal Club (1994) IPSEN Prize (Paris, 1997) Zotterman Prize (Stockholm, 1998) Craik Prize (Cambridge, 1998) National Academy of Sciences, U.S.A. (1999) Lashley Award, American Philosophical Society (1999) Thomas Edison Prize (Menlo Park, NJ, 2000) American Psychological Society Distinguished Scientifi c Contribution Award (2001) Zülch Prize, Max-Planck Society (2002) Genius Award, Cure Autism Now (2002) Purkinje Medal, Czech Academy (2003) Neurotechnologist of the Year (2006) Institute of Medicine (2008) Michael M. Merzenich has conducted studies defi ning the functional organization of the auditory and somatosensory nervous systems. Initial models of a commercially successful cochlear implant (now distributed by Boston Scientifi c) were developed in his laboratory. Seminal research on cortical plasticity conducted in his laboratory contributed to our current understanding of the phenomenology of brain plasticity across the human lifetime. Merzenich extended this research into the commercial world by co-founding three brain plasticity-based therapeutic software companies (Scientifi c Learning, Posit Science, and Brain Plasticity Institute).
    [Show full text]
  • Protocol Title: Cracking Addiction
    Protocol Title: Cracking addiction: does BRAIN Stimulation-induced neuroplasticity reverse prefrontal cortex hypoactivity in cocaine and neW stImulanTs addiCtion in Humans (BRAIN SWITCH)? Abbreviated title: Transcranial Magnetic Stimulation for Cocaine Addiction Protocol Number: 1496 Date of Approval: June 29, 2017 Principal Investigator Name, Degree Branch/Institute Phone E-mail Massimo di Dept. of +39 0871358928 [email protected] Giannantonio, Neuroscience, MD Imaging and Clinical Sciences (ITAB) – University of Chieti Co- Principal Investigator Name, Degree Branch/Institute Phone E-mail Giovanni Dept. of +39 08713556914 [email protected] Martinotti, M.D., Neuroscience, Ph.D. Imaging and Clinical Sciences (ITAB) – University of Chieti Villa Maria Pia Clinic - Rome Associate Investigators Name, Degree Branch/Institute Phone E-mail Chiara MNB/NINDS +39 3281264713 [email protected] Montemitro, M.D. Mauro MNB/NINDS +39 3391979487 [email protected] Pettorruso, M.D. Lamberto Office of +39 3474727282 [email protected] Manzoli, Ph.D. Biostatistics/ University of Ferrara Referral Contact Name, Degree Branch/Institute Phone E-mail Mauro Pettorruso, MNB/NINDS +39 3391979487 [email protected] M.D. 1 Accountable Investigator Name, Degree Branch/Institute Phone E-mail Giovanni Dept. of +39 08713556914 [email protected] Martinotti, M.D., Neuroscience, Ph.D. Imaging and Clinical Sciences (ITAB) – University of Chieti Villa Maria Pia Clinic - Rome 2 A. Précis Background: Cocaine use disorder (CUD) are a major public health concern, associated with high relapse rates, significant disability and substantial mortality. In Italy, it has been recently estimated that up to 4.8% of subjects between the ages of 15-64 have assumed cocaine at least once, whereas 1.3% subjects currently have a diagnosis of CUD.
    [Show full text]
  • Gut Microbiota and Neuroplasticity
    cells Review Gut Microbiota and Neuroplasticity Julia Murciano-Brea 1,2, Martin Garcia-Montes 1,2, Stefano Geuna 3 and Celia Herrera-Rincon 1,2,* 1 Department of Biodiversity, Ecology & Evolution, Biomathematics Unit, Complutense University of Madrid, 28040 Madrid, Spain; [email protected] (J.M.-B.); [email protected] (M.G.-M.) 2 Modeling, Data Analysis and Computational Tools for Biology Research Group, Complutense University of Madrid, 28040 Madrid, Spain 3 Department of Clinical and Biological Sciences, School of Medicine, University of Torino, 10124 Torino, Italy; [email protected] * Correspondence: [email protected]; Tel.: +34-91394-4888 Abstract: The accumulating evidence linking bacteria in the gut and neurons in the brain (the microbiota–gut–brain axis) has led to a paradigm shift in the neurosciences. Understanding the neurobiological mechanisms supporting the relevance of actions mediated by the gut microbiota for brain physiology and neuronal functioning is a key research area. In this review, we discuss the literature showing how the microbiota is emerging as a key regulator of the brain’s function and behavior, as increasing amounts of evidence on the importance of the bidirectional communication between the intestinal bacteria and the brain have accumulated. Based on recent discoveries, we suggest that the interaction between diet and the gut microbiota, which might ultimately affect the brain, represents an unprecedented stimulus for conducting new research that links food and mood. We also review the limited work in the clinical arena to date, and we propose novel approaches for deciphering the gut microbiota–brain axis and, eventually, for manipulating this relationship to boost mental wellness.
    [Show full text]
  • Neural Plasticity in the Brain During Neuropathic Pain
    biomedicines Review Neural Plasticity in the Brain during Neuropathic Pain Myeong Seong Bak 1, Haney Park 1 and Sun Kwang Kim 1,2,* 1 Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Korea; [email protected] (M.S.B.); [email protected] (H.P.) 2 Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea * Correspondence: [email protected]; Tel.: +82-2-961-0491 Abstract: Neuropathic pain is an intractable chronic pain, caused by damage to the somatosensory nervous system. To date, treatment for neuropathic pain has limited effects. For the development of efficient therapeutic methods, it is essential to fully understand the pathological mechanisms of neuropathic pain. Besides abnormal sensitization in the periphery and spinal cord, accumulating evidence suggests that neural plasticity in the brain is also critical for the development and mainte- nance of this pain. Recent technological advances in the measurement and manipulation of neuronal activity allow us to understand maladaptive plastic changes in the brain during neuropathic pain more precisely and modulate brain activity to reverse pain states at the preclinical and clinical levels. In this review paper, we discuss the current understanding of pathological neural plasticity in the four pain-related brain areas: the primary somatosensory cortex, the anterior cingulate cortex, the periaqueductal gray, and the basal ganglia. We also discuss potential treatments for neuropathic pain based on the modulation of neural plasticity in these brain areas. Keywords: neuropathic pain; neural plasticity; primary somatosensory cortex; anterior cingulate cortex; periaqueductal grey; basal ganglia Citation: Bak, M.S.; Park, H.; Kim, S.K.
    [Show full text]
  • The Portable Neuromodulation Stimulator (Pons)
    The Portable Neuromodulation Stimulator (PoNS™) FACT SHEET What is the PoNS? The Portable Neuromodulation Stimulator (PoNS) device is an investigational medical device being studied for the treatment of neurological symptoms caused by disease or trauma. The PoNS is currently being studied in the United States for the treatment of balance disorder related to mild to moderate Traumatic Brain Injury (mTBI), and in Canada for the treatment of gait and balance disorder for patients with Multiple Sclerosis (MS). It represents the first in a series of non-invasive devices -- based on the patented PoNS platform -- designed to amplify the brain’s powerful ability to heal itself. This is part of a new approach being studied for “symptom treatment” for the rising number of patients who have experienced loss of function as a result of neurological disease or trauma. What is the potential impact of the PoNS? As a result of their disease or injury, many patients are left with disrupted neural networks in the brain that are unable to carry neural impulses completely or efficiently. Neural impulses are the signals responsible for directing the functions of the body, such as movement control or sensory perception. Researchers believe that significantly increasing the activation of these neurons through electrical stimulation, combined with targeted functional therapy, may help reorganize and reactivate the networks responsible for those functions. While physicians and patients turn to available options to manage a host of neurological symptoms today, for millions living with these chronic disorders, there exists limited treatment options that actually help patients rehabilitate lost functions. The PoNS device is being studied as new potential option for the treatment of these chronic neurological symptoms of disease or trauma.
    [Show full text]
  • Neuroscience Discoveries and Clinical Practice Resource List
    TENTH ANNUAL INTERPROFESSIONAL Spring Symposium Neuroscience Discoveries and Clinical Practice Resource List A list of resources prepared by UNE Library Services Books Addiction Neuroethics: The Ethics of Cognitive Neuroscience Addiction Neuroscience Research and Marie T. Banich and Rebecca J. Compton Treatment Wadsworth, Cengage Learning, 2010 Adrian Carter Academic Press, 2011 Addiction Neuroethics: The Promises and Cognitive Neuroscience of Aging: Linking Perils of Neuroscience Research on Addiction Cognitive and Cerebral Aging Adrian Carter Roberto Cabeza, Lars Nyberg, & Denise Park Cambridge University Press, 2012 Oxford University Press, 2009 Advances in the Neuroscience of Addiction The Compass of Pleasure: How Our Brains Cynthia M. Kuhn, George F. Koob Make Fatty Foods, Orgasm, Exercise, CRC Press, 2010 Marijuana, Generosity, Vodka, Learning, and Gambling Feel So Good David J. Linden Viking, c2011 Art Therapy and Clinical Neuroscience Creating Modern Neuroscience : The Revolu- Noah Hass-Cohen and Richard Carr tionary 1950s Jessica Kingsley Publishers, 2008 Gordon M. Shepherd Oxford University Press, 2010 The Behavioral Neuroscience of Empathy: From Bench to Bedside Adolescence Jean Decety Linda Patia Spear MIT, 2011 W. W. Norton, c2010 Brain Culture: Neuroscience and Essential Neuroscience Popular Media Allan Siegel and Hreday N. Sapru Davi Johnson Thornton Wolters Kluwer/Lippincott Williams & Wilkins Rutgers University Press, 2011 Health, c2011 Braintrust: What Neuroscience Tells Us Foundations of Behavioral Neuroscience about Morality Neil R. Carlson Patricia S. Churchland Prentice Hall, 2010 Princeton University Press, 2011 Cajal’s Butterflies of the Soul: Science From Brain to Mind: Using Neuroscience to and Art Guide Change in Education Javier DeFelipe James E. Zull Oxford University Press, 2010 Stylus, 2011 Clinical Neuroscience: Psychopathology Fundamentals of Computational and the Brain Neuroscience Kelly G.
    [Show full text]
  • Brain-Machine Interface: from Neurophysiology to Clinical
    Neurophysiology of Brain-Machine Interface Rehabilitation Matija Milosevic, Osaka University - Graduate School of Engineering Science - Japan. Abstract— Long-lasting cortical re-organization or II. METHODS neuroplasticity depends on the ability to synchronize the descending (voluntary) commands and the successful execution Stimulation of muscles with FES was delivered using a of the task using a neuroprosthetic. This talk will discuss the constant current biphasic waveform with a 300μs pulse width neurophysiological mechanisms of brain-machine interface at 50 Hz frequency via surface electrodes. First, repetitive (BMI) controlled neuroprosthetics with the aim to provide transcranial magnetic stimulation (rTMS) intermittent theta implications for development of technologies for rehabilitation. burst protocol (iTBS) was used to induce cortical facilitation. iTBS protocol consists of pulses delivered intermittently at a I. INTRODUCTION frequency of 50 Hz and 5 Hz for a total of 200 seconds. Functional electrical stimulation (FES) neuroprosthetics Moreover, motor imagery protocol was used to display a can be used to applying short electric impulses over the virtual reality hand opening and closing sequence of muscles or the nerves to generate hand muscle contractions movements (hand flexion/extension) while subject’s hands and functional movements such as reaching and grasping. remained at rest and out of the visual field. Our work has shown that recruitment of muscles using FES goes beyond simple contractions, with evidence suggesting III. RESULTS re-organization of the spinal reflex networks and cortical- Our first results showed that motor imagery can affect level changes after the stimulating period [1,2]. However, a major challenge remains in achieving precise temporal corticospinal facilitation in a phase-dependent manner, i.e., synchronization of voluntary commands and activation of the hand flexor muscles during hand closing and extensor muscles [3].
    [Show full text]
  • Neuroplasticity & Implications for Stroke Recovery
    4/6/2016 Neuroplasticity Mechanisms: Selected Neural Plasticity References How Therapy Changes the Brain • Bryck & Fisher (2012) Training the Brain: Practical Applications of Neural Plasticity From the Intersection of Cognitive Neuroscience, Developmental Psychology and Prevention Science. Am Psychol. 67(2): 87–100 Review as applied to perdiatrics After Injury Part 2 • Kerr, AL, Cheng, SY, Jones, TA (2011) - Experience-dependent neural plasticity in the adult damaged brain. Commun Disord. 44(5): 538–548 • Kleim, Jeffrey (2011) Neural plasticity and neurorehabilitation: Teaching the new MSHA brain old tricks. Journal of communication disorders, 44(5) • Kleim, J. and Jones, T.A. (2008) Principles of experience-dependent neural plasticity. JSHR 51(1), S225-S239. • Murphy & Corbett (2009) Plasticity during stroke recovery: from synapse to Martha S. Burns, Ph.D. behaviour. Nature Reviews Neuroscience • Pekna,M., Pekny, M., Nilsson,M.(2012) Modulation of Neural Plasticity as a Basis Joint Appointment for Stroke Rehabilitation. Stroke 43: 2819-2828 Thorough review for all disciplines Professor • Takeuchi, N & Izumi, S (2013) Rehabilitation with Poststroke Motor Recovery: A Review with a Focus on Neural Plasticity. Stroke Research and Treatment. Volume Northwestern University 2013, Article ID 128641 Excellent review for PT and OT • Warraich Z, Kleim JA. (2010) Neural plasticity: the biological substrate for neurorehabilitation. PM R. 2:S208 –S219. , References – EB task specific References on Recovery procedures • Corbetta M, Kincade MJ, Lewis C, Snyder AZ, Sapir A. (2005) Neural basis and • Harris, J., Eng, J., Miller, W., Dawson, A.(2009) A Self- recovery of spatial attention deficits in spatial neglect. Nature Neuroscience 8:1603-10. Administered Graded Repetitive Arm Supplementary • Castellanos, N et al.
    [Show full text]