Brain: Orbitofrontal cortex
Approximate location of the OFC shown on a sagittal MRI
Orbital surface of left frontal lobe.
Latin	Cortex orbitofrontalis
Gray's	subject #189 822
NeuroNames	hier-73

The orbitofrontal cortex (OFC) is a prefrontal cortex region in the frontal lobes in the brain which is involved in the cognitive processing of decision-making. In non-human primates it consists of the association cortex areas brodmann area 11, 12 and 13; in humans it consists of brodmann area 10, 11 and 47^[1] Because of its functions in emotion and reward, the OFC is considered by some to be a part of the limbic system.

The OFC anatomically is defined as the part of the prefrontal cortex that receives projections from the magnocellular, medial nucleus of the mediodorsal thalamus.^[2] It gets its name from its position immediately above the orbits in which the eyes are located. Considerable individual variability has been found in the OFC of both humans and non-human primates. A related area is found in rodents.^[3]

Functions of the human orbitofrontal cortex[link]

The human OFC is among the least-understood regions of the human brain; but it has been proposed that the OFC is involved in sensory integration, in representing the affective value of reinforcers, and in decision-making and expectation.^[1] In particular, the human OFC is thought to regulate planning behavior associated with sensitivity to reward and punishment.^[4] This is supported by research in humans, non-human primates, and rodents. Human research has focused on neuroimaging research in healthy participants and neuropsychology research in patients with damage to discrete parts of the OFC. Research at the University of Leipzig shows that the human OFC is activated during intuitive coherence judgements.^[5]

Functional Connectivity of the Orbitofrontal Cortex[link]

Tracer studies in monkeys have shown that the orbitofrontal cortex shares extensive connections with other association cortices, primary sensory and association cortices, limbic systems, and other subcortical areas. Corticocortical connections include extensive local projections to and from other prefrontal regions, as well as with motor, limbic, and sensory cortices. Areas projecting to motor areas are densely interconnected with other prefrontal cortical regions, reflecting integration for executive motor control^[6].

Sensory cortices additionally share highly complex reciprocal connections with the orbitofrontal cortex. All sensory modalities are represented in connections with the orbitofrontal cortex, including extensive innervation from areas associated with olfaction and gustatory somatic responses^[7]. Somatosensory cortices including primary areas 1 and 2, particularly in areas associated with innervation of the hand and trigeminal complex, indicating the importance of the orbitofrontal cortex in face and hand sensation^[6].

Functionally distinct pathways for auditory processing in the orbitofrontal cortex include a rostral stream associated with phonetic processing, and a more caudal stream terminating just posterior to the orbitofrontal cortex in the periarcuate prefrontal cortex associated with auditory-spatial processing, though these connections share extensive overlap. Both ventral and dorsal visual streams share connections with orbitofrontal cortical areas, including rich projections to and from the superior temporal pole, important for integration of spatial and object processing^[6].

Connectivity of the orbitofrontal cortex with limbic areas includes reciprocal projections to granular, dysgranular, and agranular insular cortex, parahippocampal regions, and the hippocampus, particularly CA1 regions in a rostral-to caudal gradient^[6]. The orbitofrontal cortex additionally shares extensive reciprocal connections with the amygdala, and direct and indirect connections to the hypothalamus^[8].

Additional subcortical projections are shared between the striatum, particularly ventral reward-related areas^[9],^[10]. Connectivity with thalamic and periaqueductal grey areas further suggests a role for the orbitofrontal cortex in both inhibitory and excitatory regulation of autonomic function^[6]. Parallel processing loops in connectivity between cortico-striatal networks seem to be involved in the processing of goal-directed and habitual action, whereas cortico-limbic connectivity seems to be of prime importance for action selection, implicating the basolateral amygdala, and the integration of information into behavioral output^[11]

Though invasive tracer studies are largely not possible in humans, diffusion tensor imaging (DTI) tractography studies have also been used to map the connectivity of the orbitofrontal cortex to cortical and subcortical brain structures. Connections in the human orbitofrontal cortex follow a conserved pattern, similar to what is shown in tracer studies in rhesus macaques, but with a distinct pattern of connectivity with regions of the striatum^[12].

Clinical Applications of OFC Connectivity Disruptions[link]

When OFC connections are disrupted, varying cognitive, behavioral, and emotional consequences may arise. Research supports that the main disorders associated with dysregulated OFC connectivity/circuitry center around decision-making, emotion regulation, and reward expectation^[13][14][15]

One clear extension of problems with decision-making is drug addiction/substance dependence, which can result from disruption of the striato-thalamo-orbitofrontal circuit^[13][15][16]. Attention Deficit Hyperactivity Disorder (ADHD) has also been implicated in dysfunction of neural reward circuitry controlling motivation, reward, and impulsivity, including OFC systems^[14]. Other disorders of executive functioning and impulse control may be affected by OFC circuitry dysregulation, such as Obsessive-Compulsive Disorder and trichotillomania^[17][18][19]

Some dementias are also associated with OFC connectivity disruptions. The behavioral variant of frontotemporal dementia^[20] is associated with neural atrophy patterns of white and gray matter projection fibers involved with OFC connectivity^[21]. Finally, some research suggests that later stages of Alzheimer’s Disease be impacted by altered connectivity of OFC systems^[19].

Orbitofrontal Cortex and Addiction[link]

Involvement of OFC is often implicated in addictive behavior in addition to the nucleus accumbens and amygdala . The striato-thalamo-orbitofrontal circuit of the OFC has been implicated in the development of addictive behavior via dopaminergic activation of reward circuits as supported by brain imaging studies. The OFC has been associated with compulsive behavior and repetitive behavior^[16], as well as with drive^[22]; in drug dependent individuals, disruption of the striato-thalamo- orbitofrontal circuit leads to compulsive behavior and increased motivation to take the drug.

Addicted individuals show deficits in orbitofrontal, striatal, and thalamic regions^[16]. Conscious and unconscious components are hypothesized to serve as mechanisms responsible for the maintance of drug addiction: conscious mechanisms involve craving associated with loss of control and unconscious elements include anticipated conditioned responses to a drug and impulsivity^[16].

Brain imaging studies show that during cocaine withdrawal, metabolism is increased in the OFC and that this is proportional to drug craving. In contrast, during protracted (up to 3-4 months) withdrawal cocaine abusers show reduced activity in the OFC compared to healthy controls^[23][24].

Similarly, in alcoholics, during withdrawal there is decreased activity in the OFC (compared to the OFCs of healthy controls) ^[16] but, in addition, detoxified alcoholics have significantly lower levels of benzodiazepine receptors in the OFC (compared with healthy controls)^[25]. Hypoactivity in the OFC of alcoholics is also supported by blunted metabolism in the OFC to response to both serotonogenic and GABA- ergic agents^[16].

Anatomy of OFC and Addiction[link]

The OFC projects and is neuronanatomicaly connected (via the mediodorsal nucleus of the thalamus) to the nucleus acumbens - which is associated with the reinforcing effects of drug administration ^[26][27][28]. The nucleus acumbens projects back to the OFC^[29] , as do dopamine cells in the ventral tegmental area (VTA) ^[30] - the latter being associated with the positive, reinforcing effects of drugs. Limbic regions including the amygdala, hippocampus and cingulated gyrus also project to the OFC via direct and indirect pathways^[27][31] and it would appear that the OFC is not only the target for reinforcing drug effects but also serves to integrate information from the limbic system, modulating the response of the limbic areas to drugs of abuse (and their rewarding effects)^[16].

OFC and Addiction in Animal Studies[link]

(for a review see Porrino & Lyons, 2000) Stimulating OFC in laboratory animals results in drug self administration^[16]. In animal studies OFC is hypothesized not only to associated with response to reward but also respond and adjust animal behavior when the rewarding properties of the reinforcement change^[32] as well as learning the association between stimulus and reward. The damage to OFC results in deficits in reversal of stimulus reinforcement in which an animal perseverates on a behavior and fails to extinct a behavior^[33]. This perseveration and inability to extinct a behavior can be related to drug administration in substance abuse and substance dependence where individuals compulsively self-administer a drug even with drastic decrease of reinforcing effects of that drug and tolerance to the pleasurable effects and in the presence of adverse consequences of drug use. Rats who are reintroduced to an environment in which they used cocaine experience activation of the OFC^[34]. In addition, in rats, repeated alcohol use causes degeneration of the OFC^[35].

Neuroimaging research in healthy participants[link]

Using functional magnetic resonance imaging (fMRI) to image the human OFC is a challenge, because this brain region is in proximity to the air-filled sinuses. This means that signal dropout, geometric distortion and susceptibility artifacts are common when using EPI at higher magnetic field strengths. Extra care is therefore recommended for obtaining a good signal from the orbitofrontal cortex, and a number of strategies have been devised, such as automatic shimming at high static magnetic field strengths^[36].

The published neuroimaging studies have found that the reward value, the expected reward value, and even the subjective pleasantness of foods and other reinforcers are represented in the OFC. A large meta-analysis of the existing neuroimaging evidence demonstrated that activity in medial parts of the OFC is related to the monitoring, learning, and memory of the reward value of reinforcers, whereas activity in lateral OFC is related to the evaluation of punishers, which may lead to a change in ongoing behaviour^[37]. Similarly, a posterior-anterior distinction was found with more complex or abstract reinforcers (such as monetary gain and loss) being represented more anteriorly in the orbitofrontal cortex than less-complex reinforcers such as taste. It has even been proposed that the human OFC has a role in mediating subjective hedonic experience^[1].

The orbitofrontal cortex (OFC) represents the main neocortical target of primary olfactory cortex. In non-human primates, the olfactory neocortex is situated along the basal surface of the caudal frontal lobes, encompassing agranular and dysgranular OFC medially and agranular insula laterally, where this latter structure wraps onto the posterior orbital surface. Direct afferent inputs arrive from most primary olfactory areas, including piriform cortex, amygdala, and entorhinal cortex, in the absence of an obligatory thalamic relay.^[38].

Neuropsychology research in patients[link]

Visual discrimination test[link]

This has two components. In the first component, "reversal learning", participants are presented with one of two pictures, A and B. They learn that they will be rewarded if they press a button when picture A is displayed, but punished if they press the button when picture B is displayed. Once this rule has been established, the rule swaps. In other words, now it is correct to press the button for picture B, not picture A. Most healthy participants pick up on this rule reversal almost immediately, but patients with OFC damage continue to respond to the original pattern of reinforcement, although they are now being punished for persevering with it. Rolls et al.^[39] noted that this pattern of behaviour is particularly unusual given that the patients reported that they understood the rule.

The second component of the test is "extinction". Again, participants learn to press the button for picture A but not picture B. However this time, instead of the rules reversing, the rule changes altogether. Now the participant will be punished for pressing the button in response to either picture. The correct response is not to press the button at all, but people with OFC dysfunction find it difficult to resist the temptation to press the button despite being punished for it.

Iowa gambling task[link]

A simulation of real life decision-making, the Iowa gambling task is widely used in cognition and emotion research.^[4] Participants are presented with four virtual decks of cards on a computer screen. They are told that each time they choose a card they will win some game money. Every so often, however, when they choose a card they will win lose some money.^{[further explanation needed]} They are told that the aim of the game is to win as much money as possible. The task is meant to be opaque, that is, participants are not meant to consciously work out the rule, and they are supposed to choose cards based on their "gut reaction." Two of the decks are "bad decks," which means that, over a long enough time, they will make a net loss; the other two decks are "good decks" and will make a net gain over time.

Most healthy participants sample cards from each deck, and after about 40 or 50 selections are fairly good at sticking to the good decks. Patients with OFC dysfunction, however, continue to perseverate with the bad decks, sometimes even though they know that they are losing money overall. Concurrent measurement of galvanic skin response shows that healthy participants show a "stress" reaction to hovering over the bad decks after only 10 trials, long before conscious sensation that the decks are bad. By contrast, patients with OFC dysfunction never develop this physiological reaction to impending punishment. Bechara and his colleagues explain this in terms of the somatic markers hypothesis. The Iowa gambling task is currently being used by a number of research groups using fMRI to investigate which brain regions are activated by the task in healthy volunteers as well as clinical groups with conditions such as schizophrenia and obsessive compulsive disorder.

Faux pas test[link]

This is a series of vignettes recounting a social occasion during which someone said something that should not have been said, or an awkward occurrence. The participant's task is to identify what was said that was awkward, why it was awkward, how people would have felt in reaction to the faux pas and to a factual control question. Although first designed for use in people on the autism spectrum,^[40] the test is also sensitive to patients with OFC dysfunction, who cannot judge when something socially awkward has happened despite appearing to understand the story perfectly well.

Consequences of damage to the OFC[link]

Destruction of the OFC through acquired brain injury typically leads to a pattern of disinhibited behaviour. Examples include swearing excessively, hypersexuality, poor social interaction, compulsive gambling, drug use (including alcohol and tobacco), and poor empathising ability. Disinhibited behaviour by patients with some forms of frontotemporal dementia is thought to be caused by degeneration of the OFC^[41].

See also[link]

• BELBIC
• Emotional Learning
• Phineas Gage
• Witzelsucht
• Obsessive-compulsive disorder

Additional images[link]

• 

  Orbital gyrus shown in red.

• 

  Medial surface of cerebral cortex - gyri

• 

  Basal surface of cerebrum. Oribital gyrus shown in red.

References[link]

External links[link]

• Cerebral Cortex special issue on orbitofrontal cortex
• Camille et al. (2004) The Involvement of the Orbitofrontal Cortex in the Experience of Regret

This article has multiple issues. Please help improve it or discuss these issues on the talk page. This biography of a living person needs additional citations for verification. Tagged since January 2011. It relies on references to primary sources or sources affiliated with the subject, rather than references from independent authors and third-party publications. Tagged since January 2011. It is written like a résumé. Tagged since January 2011.

Antonio Damasio

Antonio Damasio (born February 25, 1944 in Lisbon, Portugal) is David Dornsife Professor of Neuroscience at the University of Southern California, where he heads USC's Brain and Creativity Institute and Adjunct Professor at the Salk Institute. Prior to taking up his posts at USC, in 2005, Damasio was M.W. Van Allen Professor and Head of Neurology at the University of Iowa Hospitals and Clinics. His career at Iowa lasted from 1976 to 2005.

Besides being a well-known researcher in several areas of neurology and neuroscience, Damasio is the author of several best-selling books which describe his scientific thinking. "As a leading neuroscientist, Damasio has dared to speculate on neurobiological data, and has offered a theory about the relationship between human emotions, human rationality, and the underlying biology."^[1]

Life and work[link]

Damasio was born in Lisbon and studied medicine at the University of Lisbon Medical School in Portugal, where he also did his neurological residency and completed his doctorate. He worked as a research fellow at the Aphasia Research Center in Boston in 1967, prior to receiving his MD in Lisbon. His work there on behavioral neurology was done under the supervision of the late Norman Geschwind, the Harvard neurologist who created the field.

As a researcher, Damasio's main interest is the neurobiology of the mind, especially neural systems which subserve memory, language, emotion, decision-making and consciousness. Damasio's most influential contribution to date is the demonstration that emotions play a critical role in high level cognition, an idea that ran counter to dominant 20th c. views in psychology^{[citation needed]}, neuroscience^{[citation needed]} and philosophy^{[citation needed]}. He showed that emotions and their biological underpinnings are involved in decision-making (both positively and negatively, and often non-consciously); provide the scaffolding for the construction of social cognition; and are required for the self processes which undergird consciousness. "Damasio provides a contemporary scientific validation of the linkage between feelings and the body by highlighting the connection between mind and nerve cells...this personalized embodiment of mind."^[2]

This idea has inspired many systems-neuroscience experiments carried out in laboratories in the U.S. and Europe, and has had a major impact in contemporary science^{[citation needed]} and philosophy^{[citation needed]}. It is often discussed in peer-review experimental and theoretical work (an index of its relevance can be gleaned from the fact that Damasio has been named by the Institute of Scientific Information as one of the most highly cited researchers in the past decade). Damasio has formulated the somatic markers hypothesis, which captures the essence of these ideas. Current work on the biology of moral decisions, neuro-economics, social communication, and drug-addiction, has been strongly influenced by Damasio's hypothesis.

Damasio also proposed that emotions are part of homeostatic regulation and are rooted in reward/punishment mechanisms. He recovered James' perspective on feelings as a read-out of body states, but expanded it with an "as-if-body-loop" device which allows for the substrate of feelings to be simulated rather than actual (foreshadowing the simulation process later uncovered by mirror neurons). He demonstrated experimentally that the insular cortex is a critical platform for feelings, a finding that has been widely replicated, and he uncovered cortical and subcortical induction sites for human emotions, e.g. in ventromedial prefrontal cortex and amygdala.

In another development, Damasio proposed that the cortical architecture on which learning and recall depend involves multiple, hierarchically organized loops of axonal projections that converge on certain nodes out of which projections diverge to the points of origin of convergence (the convergence-divergence framework). This architecture is applicable to the understanding of memory processes and of aspects of consciousness related to the access of mental contents.

In “The Feeling of What Happens”, Damasio lays the foundations of the “enchainment of precedences”: “the nonconscious neural signaling of an individual organism begets the protoself which permits core self and core consciousness, which allow for an autobiographical self, which permits extended consciousness. At the end of the chain, extended consciousness permits conscience. ^[3]

Damasio's research depended significantly on establishing the modern human lesion method, an enterprise made possible by Hanna Damasio's structural neuroimaging/neuroanatomy work complemented by experimental neuroanatomy (with Gary Van Hoesen and Josef Parvizi), experimental neuropsychology (with Antoine Bechara, Ralph Adolphs, and Dan Tranel) and functional neuroimaging (with Kaspar Meyer, Jonas Kaplan, and Mary Helen Immordino-Yang).

As a clinician, he and his collaborators have studied and treated disorders of behavior and cognition, and movement disorders.

Damasio's books deal with the relationship between emotions and feelings, and what their bases may be within the brain. His 1994 book, Descartes' Error: Emotion, Reason and the Human Brain, won the Science et Vie prize, was a finalist for the Los Angeles Times Book Award, and is translated in over 30 languages. It is regarded as one of the most influential books of the past two decades. His second book, The Feeling of What Happens: Body and Emotion in the Making of Consciousness, was named as one of the ten best books of 2001 by the New York Times Book Review, a Publishers Weekly Best Book of the Year, a Library Journal Best Book of the Year, and has over 30 foreign editions. Damasio's Looking for Spinoza: Joy, Sorrow, and the Feeling Brain, was published in 2003. In it, Damasio suggested that Spinoza's thinking foreshadowed discoveries in biology and neuroscience views on the mind-body problem. Spinoza was a protobiologist. His latest book is Self Comes to Mind: Constructing the Conscious Brain. In it Damasio suggests that the self is the key to conscious minds and that feelings, from the kind he designates as primordial to the well-known feelings of emotion, are the basic elements in the construction of the protoself and core self.

Damasio is a member of the American Academy of Arts and Sciences, the National Academy of Sciences' Institute of Medicine, and the European Academy of Sciences and Arts. Damasio has received many awards including the Prince of Asturias Award in Science and Technology, the Kappers Neuroscience Medal, the Beaumont Medal from the American Medical Association, the Nonino Prize, the Reenpaa Prize in Neuroscience, and, most recently, the Honda Prize. He has received honorary doctoral degrees (Doctor honoris causa) from the University of Aachen (2002), University of Aveiro (2003), University of Copenhagen (Copenhagen Business School; 2009), University of Leiden (2010), University Ramon Llull, Barcelona (2010), University of Coimbra (2011) and from the Swiss Federal Institute of Technology, Lausanne (2011).

His current work involves the social emotions, consciousness and the creative interface between neuroscience and the arts, especially music and film.

Damasio is married to Dr. Hanna Damasio, his colleague and frequent co-author.

Scientific philosophy[link]

'Damasio himself notes, in fallibilist fashion, "I have a difficult time seeing scientific results, especially in neurobiology, as anything but provisional approximations"'.^[4] Whether despite or because of that fallibilism, Damasio writes in the belief that 'scientific knowledge can be a pillar to help humans endure and prevail'.^[5]

Bibliography[link]

Selected books and articles[link]

• Descartes' Error: Emotion, Reason, and the Human Brain, Putnam, 1994; revised Penguin edition, 2005

• The Feeling of What Happens: Body and Emotion in the Making of Consciousness, Harcourt, 1999

• Looking for Spinoza: Joy, Sorrow, and the Feeling Brain, Harcourt, 2003

• Self Comes to Mind: Constructing the Conscious Brain, Pantheon, 2010

• Meyer K, Kaplan JT, Essex R, Damasio H, Damasio A. Seeing touch is correlated with content-specific activity in primary somatosensory cortex. Cerebral Cortex, vol 21, 2113-2121, 2011.

• Meyer K, Kaplan JT, Essex R, Webber C, Damasio H, Damasio A. Predicting visual stimuli based on activity in auditory cortices. Nature Neuroscience, vol 13, 6, 667–668, 2010.

• Meyer K, Damasio A.Convergence and divergence in a neural architecture for recognition and memory. Trends in Neurosciences, vol. 32, no. 7, 376–382, 2009.

• Immordino-Yang MH, McColl A, Damasio H, Damasio A. Neural correlates of admiration and compassion. Proceedings of National Academy of Sciences, vol. 106 no. 19, 8021–8026, 2009.

• Damasio A, Meyer K. Behind the looking glass. Nature, vol. 454: 167–168, 2008.

• Parvizi J, Van Hoesen G, Buckwalter J, Damasio A. Neural connections of the posteromedial cortex in the macaque: Implications for the understanding of the neural basis of consciousness. Proceedings of National Academy of Sciences, 103: 5, 1563–1568, 2006.

• Shiv B, Lowenstein G, Bechara A, Damasio H, Damasio A. Investment behavior and the negative side of emotion. Psychological Sciences, 16: 435–439, 2005.

• Parvizi J, Damasio AR. Neuroanatomical correlates of brainstem coma, Brain, 126: 1524–1536, 2003.

• Parvizi J, Damasio AR. Consciousness and the brainstem, Cognition, 79: 135–160, 2001.

• Damasio AR, Grabowski TJ, Bechara A, Damasio H, Ponto LLB, Parvizi J, Hichwa RD. Subcortical and cortical brain activity during the feeling of self-generated emotions. Nature Neuroscience, 3: 1049–1056, 2000.

• Damasio AR. How the brain creates the mind. Scientific American, 281: 74–79, 1999.

• Damasio AR. Investigating the biology of consciousness. Transactions of the Royal Society (London), 353: 1879–1882, 1998.

• Bechara A, Damasio H, Tranel D, Damasio AR. Deciding advantageously before knowing the advantageous strategy. Science, 275: 1293–1294, 1997.

• Damasio AR. The somatic marker hypothesis and the possible functions of the prefrontal cortex. Transactions of the Royal Society (London), 351: 1413–1420, 1996.

• Adolphs R, Tranel D, Damasio AR. Impaired recognition of emotion in facial expressions following bilateral damage to the human amygdala. Nature, 372: 669–672, 1994.

• Damasio AR, Tranel D. Nouns and verbs are retrieved with differently distributed neural systems. Proceedings of the National Academy of Sciences, 90: 4957–4960, 1993.

• Damasio A, Tranel D, Damasio H. Face agnosia and the neural substrates of memory. Annual Review of Neuroscience, 13: 89–109, 1990.

• Damásio AR. Time-locked multiregional retroactivation: A systems level proposal for the neural substrates of recall and recognition. Cognition, 33: 25–62, 1989.

• Tranel D and Damasio A. Knowledge without awareness: An autonomic index of facial recognition by prosopagnosics. Science, 228(21): 1453–1454, 1985.

• Hyman B, Van Hoesen GW, Damasio A, Barnes C. Alzheimer's disease: Cell-specific pathology isolates the hippocampal formation. Science, 225: 1168–1170, 1984.

• Damasio A and Geschwind N: The neural basis of language. Annual Review of Neuroscience, 7:127–147, 1984.

See also[link]

References[link]

External links[link]

Wikimedia Commons has media related to: Antonio Damasio

Wikiquote has a collection of quotations related to: António Damásio

• USC Faculty page
• Brain and Creativity Institute
• Audio of Antonio Damasio's 2003 lecture, "Emotion, Feeling, and Social Behavior: The Brain Perspective" at Walter Chapin Simpson Center for the Humanities
• Ideas of Antonio Damasio – JRSM book review

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Nora Volkow in 2009.

Nora Volkow (b. 27 March 1956) is director of the National Institute on Drug Abuse (NIDA). She is the great-granddaughter of Russian revolutionary leader and Head of the Fourth International, Leon Trotsky. Her father was the son of Leon Trotsky’s elder daughter.^[1]

Born in Mexico City, Volkow and her three sisters grew up in the house where Trotsky was killed.^[1] She attended the Modern American School, then earned a medical degree from National University of Mexico before going to New York University for psychiatric residency. She chose a career in brain research after reading an article on the use of positron emission tomography in studying brain function. She did research at Brookhaven National Laboratory before becoming director of NIDA in 2003.^[1]

Research[link]

She has stated that her imaging studies of the brains of people addicted to drugs have helped to clarify the mechanisms of drug addiction. She also maintains that they have also helped to change the public's view of drug addiction, from that of a moral violation or character flaw to an understanding that pathological changes to brain structure make it very difficult for addicts to give up their addictions.^[1] Volkow says that she has shown that abnormalities in the prefrontal cortex of addicts create a feeling of need or craving that addicts know is irrational but cannot prevent. Prefrontal abnormalities also make it difficult to override compulsions to take drugs by exercising cognitive control. The main areas affected are the orbitofrontal cortex, which maintains attention to goals, and the anterior cingulate cortex, that mediates the capacity to monitor and select action plans. Both areas receive stimulation from dopamine centers lower in the brain. A steady influx of dopamine makes it difficult for addicts to shift their attention away from the goal of attaining drugs. It also fastens their attention to the motivational value of drugs, even though these drugs have long stopped providing pleasure. It is now understood that dopamine activation does not signal pleasure. Rather, it signals the importance or relevance of sought-after goals. Addicts have a hard time turning their attention —and their actions— away from the goal of acquiring and consuming drugs. They are caught, she states, in a vicious circle of physical brain changes and the psychological consequences of those changes, leading to further changes.

References[link]

External links[link]

• Nora D. Volkow, M.D., Director's Page, National Institute of Drug Abuse
• Appearances on C-SPAN
• Nora Volkow on Charlie Rose
• Hooked: Why Bad Habits are Hard to Break on 60 Minutes
• Nora Volkow: Two Paths to the Future (Vanderbilt University Medical Center Article - February 2006)
• Works by or about Nora Volkow in libraries (WorldCat catalog)
• Nora Volkow - the Time 100, 2007
• NIDA's New Leader JAMA
• Why Is It So Damn Hard to Change? by Rebecca Skloot, O, the Oprah Magazine

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