Proceedings of Neuro-psychoanalysis Workshops, Lectures, and Conferences

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Boston Neuropsa Workshop:  CNS Aspects of Pain

Pain is still one of the most fundamental facts of conscious life and the deep interdigitation of pain and conscious state is something that neither traditional cognitive thalamocortical theories of consciousness nor traditional thalamocortical theories of pain can truly accommodate.  Pain is the homeostatic mandate to avoid tissue damage, and its architectures interdigitate with those classically associated with arousal to a conscious state (the reticular activating system) and its extended trajectories interpenetrate with many if not all structures classically thought to be part of the ‘limbic system.”  Indeed, the overlap between structures involved in maintaining a conscious state, those involved in pain, and those involved in emotion is truly enormous.  This is instructive about the intimately related nature of these functions.  The core systems for all of these critical functions probably sit in many upper brainstem regions, particularly the mesodiencephalon, with telencephalic resonances and connectivities that extend up through many subcortical limbic and paralimbic paleocortical systems.  The interdigitation of pain and emotion both functionally and in terms of neural networks, and the interdigitation of pain and homeostasis are major themes for the talk.  Recent work underlining the centrality of the insula for both experienced emotion and for pain is reviewed in detail, including evidence that pain and experienced emotion may recruit somewhat different regions of insula with pain activating more dysgranular areas and emotion more agranular. 

This talk reviews recent work on pain pathways, pain architectures at both spinal cord and CNS levels and looks at several stages of pain processing from peripheral to cord level to CNS structure level.  Critically, c fibers are attuned to a host of homeostatic operators beyond tissue damage, including global and local metabolic state, osmolarity, hypoxia, hypoglycemia, etc.  Review of these architectures suggests that the C fiber system is far more than a nociceptive/temperature system, more the beginning on the afferent side of the brain’s affective systems, critically attuned to all manner of biological operators that affect the body for well or for ill.  In this sense, c fibers are really value-ceptors and not just nociceptors.  The most powerful means to change affective state may all recruit these systems: caresses, massages, playful tickling, physical assault/injury, and sexual intercourse.  There is evidence that maternal care may recruit these C. fiber systems and activate their extended trajectories in early development, and that the absence of this stimulation has serious negative consequences for infant mammals. Thus, the role that these C. fiber systems play in the bootstrapping of attachment in the mammalian brain may be terribly underappreciated.

 The critical role of PAG in both pain and emotion is also reviewed.  Many questions remain about the role of this important midbrain system in both emotion and pain.  There are also many issues re: nature of pain and its relationships to various body maps that are recursively organized at every level of the neuroaxis that remain to be more fully elucidated.  A concerted review of pain has major relevance for understanding emotion, and suggests that emotions may resonate through much the same architectures that map our homeostasis in pain, as emotions anticipate homeostatic challenge before the fact (fear & separation distress being cardinal examples).  Many deep mysteries about the role of multiple RAS and limbic structures in pain remain, along with new frontiers about molecular aspects of pain sensitization/gating with exciting implications for the clinical treatment of various forms of chronic pain.  However the biggest problem in the treatment of pain clinically in this country remains what can only be called "addiction-phobia", and the subsequent reluctance to prescribe opiates even for patients who had no troubles with addictive behavior and for whom other analgesics are simply not adequately effective.  This frequently results in pain being undertreated clinically, and chronic pain syndromes are almost invariably degrading of affective state and functional status.  Given the close relationships between pain and emotion, an interdisciplinary approach to pain control clearly has to look much more closely at every patient's psychosocial and affective status, particularly the presence or absence of viable social support and other psychiatric and psychological co-morbidities.  This simply is not happening in general in our current medical system.

 An understanding of pain, along with the closely allied domains of emotion, attentional function, and organized behavior, all remain linchpins in any viable theory about the neural foundations for conscious states.  Each of these topics is a huge and complex domain within current neuroscience.  However, the current approaches in neuroscience to pain, emotion, attentional function, and the organization of purposeful behavior remain fundamentally fragmented with very little crosstalk between increasingly specialized and even esoteric areas of research.  Bridging these traditionally segmented functions will be required if we are to arrive at any real understanding for how sentience emerges from distributed neural activity in central nervous systems.  In general, the complex and multiple roles played by a host of interconnected upper brainstem systems appear critically integrative and still largely neglected in the dominant corticocentric image of the brain in cognitive neuroscience. 

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Notes prepared by Brian Johnson

Summary Notes of Presentations at the International Neuro-Psychoanalysis Meeting,  Rome September 2004.  By Brian Johnson

Howard Shevrin

• Administered the Hysterical-Obsessional Scale
• Obsessionals saw spiders, not snakes
• Hysterics didn’t see
• Results very statistically significant

 Panksepp 

             Panksepp-Shevrin bet on unconscious affect, tested with the tachistoscope.  10 positive or 10 negative words.  Subject marks intensity of feeling: happy/sad, power.  Power shifted significantly (larger) after positive words.  (Panksepp feels sad reflects endorphin lack.)

            Affect not read out of the cortex, is one component (with cognition) of emotion.

            Intense feeling suppresses cortical functioning.

            Conscious affects of distress with unconscious cognitive correlates drive people to treatment.

 Guido Gainotti

                    Denial as it relates to right hemisphere lesions:

Amytal in left carotid causes depression

Amytal in right carotid causes euphoria

Left lesions cause anxiety and bursts of tears (appropriate)

Right lesions cause joking and lack of attention to results of injury

Emotional system – rapid and mostly ucs responses

Cognitive system – slow and mostly cs

            Leventhal’s categories of emotions

Sensorimotor – innate

Schematic – stored in memories

Conceptual – thinking about experiences

Patients with right hemisphere injuries decode emotional experiences poorly

Largest galvanic skin response when stimuli presented to right hemisphere

Upsetting films – Normal and left brain damaged patients turned away, right damaged patients tolerated/watched. Gainotti (2002) –

• Right brain processes schematic emotions
•  Left – conceptual, left brain damaged patients
• Masked (ucs) stimuli decoded in right amygdala
• Conscious stimuli decoded in left amygdala
• Thalmus input transmitted to right amygdala, procedural ucs
• Thalmus input transmitted to visual cortex, then left amygdala, dynamic unconscious.

 For Gainotti and Panksepp, take home message was that only cortical material can be repressed.

 Maggie Zellner, “Neonatal isolation reduces food-rewarded operant responding in rats”

 DEPRESSION                                   causes                                     EARLY STRESS

 Depression/dec dopamine     REDUCED MOTIVATION             dec dopamine

 Animals with maternal deprivation administer more drugs

No decrease in consummatory behavior, but decreased locomotion and anticipatory behavior

Blunted response to change in sucrose concentration

No difference in sucrose-maintained lever pressing

No difference in total acquisition of learning how to press lever

BUT

Difference in rate of acquisition of learning

Non-isolated rats had a higher break point – how hard they will work to get the next pellet

  Gokce Ozkarar

             Left frontal hypoactivation in schizophrenia: words presented to left and right ear.  Loose associations (lack of relatedness to original word) occurred only when word registered in the wild right hemisphere, (Freud: id not monitored by ego).  Left frontal lesions also lead to schizophrenia-like symptoms.

 Bottom line: find ways to empirically test psychoanalytic ideas.

Neuropsychoanalysis Seminar Minutes.         

             Brian Johnson began the discussion by noting that Freud was born 19 years after the publication of Darwin’s Origin of Species.  Darwin’s work was both dominant in 19^th century science as a style of approaching the explanation of a complex phenomenon, and entirely retrodictive.  Darwin’s theory gives no way to predict the future evolution of a species which can be tested by observation.  Freud’s neurologically-based metapsychology is hampered by the same retrodictive style; look at how we can suggest the childhood origins and internal workings of this or that form of psychopathology!  Psychoanalytic therapy has been informed by this intellectual stance, with no particular motivation to form testable hypotheses; the basis of pragmatic science.  (N.B.  William James’ definition of pragmatism in psychology is that the experimental method is how to settle an argument where neither side can convince the other of the veracity of their claims.)

             Brian then went on to praise the Robert Scaer paper, “The neurophysiology of dissociation and chronic disease,” Applied Psychophysiology and Biofeedback, 2001, 26:73-91, as presenting a persuasive model of the pathophysiology of mysterious diseases such as reflex sympathetic dystrophy, irritable bowel syndrome, fibromyalgia, chronic fatigue, interstitial cystitis, chronic and phantom pain.  Scaer reviewed animal and human experiments and observations of the freeze/immobility response.  He suggested that recurrent dissociation was the behavioral manifestation of CNS arousal due to environmental cues of previous trauma which resulted in pathologic oscillating autonomic activity originating in the dorsal vagal nucleus.  Parasympathetic/vagal predominance, which could be specifically directed to body parts which were affected by the original trauma, resulting in insidiously noxious manifestations such as hypoperfusion, inhibition of sensory feedback, or pain.  Unresolved and unconsciously perceived procedural memories of threat would trigger symptoms with concomitant dissociation.  Scaer seemed especially informed by previous work of psychoanalyst Henry Krystal.

             Giovanni Liotti took on some of the same territory in a developmental way with his “Trauma, dissociation and disorganized attachment: three strands of a single braid,” Psychotherapy: Theory, Research, Practice, Training, 2004, 41:472-86.  After reviewing the research on attachment in infants and adults, Liotti had a complex discussion of the relationship of child neglect, dissociation, AAI “unresolved” patients, trauma, intergenerational transmission of trauma, internal working models, PTSD, borderline personality disorder, and various forms of psychotherapy.  Two especially impressive aspects of Liotti’s discussion was his use of the experimental observation literature to underpin his explanations of clinical phenomena, and his pragmatic/experimental stance.  The latter is summarized in his ending, “All these innovative guidelines for the psychotherapy of complex trauma-related disorders may…yield outcomes studies supporting, or falsifying, the hypothesis implied by the research finding reviewed in this article: when the contribution of disorganized attachment to the disorder is successful dealt with, traumatic memories become more easily integrated and dissociative defenses are less difficult to relinquish.”

             Hence, Liotti has a scientific-predictive method in mind.  Since we can’t agree which psychotherapy is best, let’s test each with patients, and have quantitative outcome measures. This is not a huge leap from Freud’s idea that childhood trauma is manifest in adult psychopathology.  But it adds a pragmatic/predictive approach to the retrodictive model-building which is evident in Freud, Scaer and Liotti.

             A jail-break of discussion then ensued.  Without being able to recapitulate most comments, Michelle Shuder gave several examples from her clinical practice which elaborated on these papers.  Like Liotti, she moved from research findings to clinical material and back.  David Mann suggested that Alexander’s “corrective emotional experience” was suggested by the clinical material.  Brian Johnson agreed, but suggested that the method of “correction” might be addressed with empirical research.  In particular the Boston Process of Change study group believes that amelioration of psychopathology does not have to occur via conscious interpretations, but can occur via procedural exchanges between analyst and patient.  Toni Greatrex strongly objected, insisting that things must be put into words. (It occurred to me subsequently that another application of neuropsychoanalytic principles which I observe daily is that patients often start an hour with autobiographical information, “news of the day,” which I listen to without response.  Invariably, often punctuated with something like, “that’s about all,” they plunge into procedural free associations which then bring forth my interpretations.  The procedural associations are organized unconsciously, and listening without comment then does the patient no good.  They require my verbal interpretations, which tend to move procedural relatedness into the conscious/autobiographical sphere, “Oh, I’m apologizing about being ‘off topic’ as if you are my father, and are about to abandon me if I don’t conform to your expectations of me.”)  Brian responded to Toni that he was not insisting that words were not necessary for change, but that with Liotti’s approach, we are now thinking of designing prospective experiments to test our dearly-held hypotheses.

Notes on the Sixth International Neuro-Psychoanalysis Congress  

Do dreams and psychosis share a common brain mechanism?  If so, what is it?                                 

 Mark Solms

 Mark showed a picture of the mesocortical dopamine system (SEEKING, reward, curiosity, wanting – all synonyms).  Mark noted that in both dreams and psychosis:

• It is hyperactive
• The dorsolateral prefrontal cortex (DLPFC) is hypoactive
• Posterior sensory and memory areas are relatively active

Mark noted that the following evidence supports a common pathway:

• that  both dreams and psychosis are eliminated by lesions which cut the ventral tegmental area (VTA) pathway to the frontal cortex

• Neuroimaging  shows hyperactivation in both conditions
• Neurochemical studies show that dopaminergic agents enhance both and block both; for example Ernst Hartmann’s studies that L-dopa enhances dreaming and psychosis is a side effect of this medication.  Hartmann let subjects sleep, then gave half of his subjects L-dopa.  Their dreams were longer, more bizarre, more emotionally intense, and they had more nightmares
• Prefrontal leucotomy causes both loss of dreaming and ameliorates psychosis.  Dreaming is stopped by leucotomy despite the preservation of REM sleep
• Prefrontal leucotomy with preservation of dreaming was regarded as a sign of poor prognosis of its efficacy for psychosis.  The therapeutic goal of the psychosurgeons of the 50s was elimination of dreaming.
• PET scans show activation of the prefrontal, limbic and zone of convergence (confluence of temporal, parietal and occipital lobes) and suppression of the DLPFC
• PET scans of hallucinating subjects show hyperactivity of the nucleus accumbens (part of the VTA pathway)
• Dopamine release in the nucleus accumbens is maximal during REM

 Mark noted the following correlations with sleep/dreaming in Freud’s “Interpretation of Dreams” chapter 7

• Increased drive state/increased VTA functioning
• Weakened ego/hypoactivation of DLPFC
• Regression to perceptual and memory functioning/activation of posterior sensory and memory cortical areas

 Mark then drew the following implications

• One can translate Freudian metapsychology into neuroscience terminology
• “Libido” = mesolimbic/mesocortical dopamine system.  More specific information can be researched using this concept
• A partial answer as to the reason for the confluence of psychosis and dreaming is that this system drives the animal to enter the world looking for gratification of survival needs.  Dreaming allows for rehearsal of solutions to obtaining gratification.
• Kapour’s hypothesis regarding psychosis is that it involves aberrant salience attachment due to hyperactivation of this system, which “…converts neutral entities into attractive, appealing entities.”  Delusions are therefore an attempt to make sense of aberrant salience.
• Similarly dreams involve attaching unusual value to neutral information; seeking by sifting through one’s mental representations
• Freud’s view of primary process (lessened ego function/hypoactivation of DLPFC) involved representation of desires as fulfilled; instant gratification – which allowed continued sleep rather than having to awaken to seek real gratification

 Discussion

• Dopamine causes cathexis
• The quantity of cathexis must be correlated with the amount of dopamine in response to a stimulus
• Irene Mathis, “Dopamine has nothing to do with meaning.  Psychoanalysis has to uncover the meaning of the dream.”
• Mark Solms, “Understanding this helps the patient translate psychotic ideas into current relationships.  The patient lacks the ability to reflect.

Private reflections

• Nora Volkow, in her Pfeffer Prize Lecture (New York Psychoanalytic Institute, May 2005), showed how much more (11X) dopamine is released by seeking cocaine than by seeking natural reinforcers such as food (2X).  This must be a corollary of the suggestion that the amount of cathexis is related to the amount of dopamine release, or why patients pursue cocaine in preference to food or love.
• In impending delirium tremens, patients have an intense need to sleep, but are terrified and beginning to hallucinate.  I treat this with haloperidol, which puts results in sleep with the patient awakening feeling well.  I must be blocking the dopamine seeking of psychotic goals so that the patient can respond to their need for sleep.  My one failure of this treatment was a delirious patient who did not sleep in response to haloperidol, was sent to the emergency room, and diagnosed with gonococcal sepsis (i.e. seeking aberrantly salient goals was not the reason for psychosis and delirium).
• This idea would explain nightmares; seeking is accompanied by a warning of danger as the dreamer proceeds towards the goal.

 Neuroimaging of psychosis                David Silbersweig 

• There is decreased activation of frontal areas which monitor volitional speech during auditory hallucinations
• In an experiment where the voice was distorted and fed back to subjects, subjects with schizophrenia were unable to identify the speech as their own thoughts
• In paranoia there is increased activation of the limbic danger system

 Psychosis model

• Decreased prefrontal function: VMPFC, DMPFC
• Increased mesotemporal/limbic and subcortical threat/emotional valence/salience activation
• This system is triggered inappropriately by neutral stimuli

 Discussion

            Mark Solms noted that there were no studies of the effects of antipsychotic medications on dreaming

 Private reflections

            This system is more obsessional, less coherent, but in basic agreement with the model of Solms.

The neurochemistry of dreams and psychosis

Claude Gottesmann

 Dr. Gottesmann showed a slide of the balance of acetylcholine (Ach), norepinephrine (NE), serotonin (5HT) and dopamine (DA) in various states which I will crudely reproduce 

                                                                                                                                    X

                                                                                                                                    X

 X        X         X                                 X                                    X           X                X

 X        X         X                                 X                                    X           X              X                                                X            X         X         X         X         X                                    X           X                X

 X        X         X         X         X         X              X         _        X           X       _       X

________________________________________________________________

         5HT                              5HT                                  5HT                         5HT

ACh   NE    DA          ACh   NE   DA              ACh    NE   DA          ACh   NE   DA

   WAKING                    SWS                        INTERMEDIATE                   REM

             There is bursting of dopamine in REM and in schizophrenia

             In schizophrenia there is disconnection between system: temporal/frontal and between system hippocampal/frontal

 Activated in REM

• parahippocampal cortex
• pontine tegmentum
• amygdala
• anterior cingulated

 Deactivated in REM

• primary visual cortex
• posterior cingulated
• DLPFC

 The lack of activation of the primary visual cortex is a marker of disconnection from the outside world

             Slides were shown indicating that in normal functioning the nucleus accumbens receives input from the hippocampus, amygdala and prefrontal cortex.  In schizophrenia input from the hippocampus and prefrontal cortex is attenuated but input from the amygdala is highly activated.

 Discussion

            Mark Solms speculated that schizophrenia (1%) could be selected into the population because of the need for dreaming; which enhances adaptive behaviors by using sleep to model various solutions to gratifications of drive needs.  He also speculated that dreaming might prevent schizophrenia.

            On a similar theme Jaak Panksepp suggested that there is no compensatory REM sleep in subjects with schizophrenia; could this be because they are having “REM sleep” while awake?  He noted that the prefrontal cortex regulates the VTA/nucleus accumbens (NA).  When the PFC is lesioned, there is more dopamine activity in the NA.

            Mark Solms asserted that REM is neither necessary nor sufficient to generate dreams; it is simply a correlate of dreaming.

  July 26, 2004

 Psychosis in relation to the seeking system

Jaak Panksepp

Jaak started by explaining that we can generate enthusiasm via data, not argumentation.  Subjectivity evolved; how can we measure it?

The data about hypofrontality in dreams and schizophrenia comes from neuroscience.  The Freudians have abundant ideas with little agreement about fundamental issues, which means that we will not be listened to.  First person accounts provide no privileged view of brain mechanisms.

The function of the brain is to generate psychological processes that regulate behavior.

ES=(Mc-Ms)/SDp

ES – effect size, Mc – control group mean, Ms – schizophrenia group, SDp – standard deviation of pooled data

             Schizophrenia is a disconnection syndrome.  There is diminished cortico-glutamatergic control and diminished GABA inhibition; top-down disconnections.  The cortex continually thins.  Reelin, a protein which organizes cortical layering, is low.  Norepinephrine and serotonin are underactive, just like in dreams.  Acetylcholine and dopamine are overactive, just like in dreams.  Choppy smooth pursuit eye movements may represent a disconnection between self and eye movements.

             Psychoendophenotypes are internal goal-directing programs which include seeking, lust, fear, etc.  All basic emotions are initially objectless, a tool, a goad without a goal.  Using these tools requires learning.  Emotional operating systems have intrinsic inputs and coordinated physiologic and behavioral outputs.  Cognitions instigate emotions.

             The seeking system is a foraging system.  Knutson, a former doctoral student of mine, showed that anticipation of money lights up the nucleus accumbens on fMRI.  Nojar and Panksepp (2002) showed that amphetamine seeking increases seeking of food and sex.  Olds, pairing a tone and food, showed that “the subcortex is the first to learn and the neocortex is the first to know.”  This means that seeking occurs unconsciously at first, and it is only later that one realizes one’s goal, reinforcing the seeking, now in a conscious state.  The seeking system was first described by me in 1971, before S. Snyder first described the dopamine receptor in 1974.  W. Freeman (2001) showed that each level of brain reinterprets inputs from other levels.  The seeking system sets the stage for internal learning systems to be engaged.  The dopamine system creates realities out of correlative connections.

             REM deprivation leads to increased self-stimulation and increased seeking; shown by hyperactive exploration.  This self-stimulation eliminates REM rebound, and psychosis eliminates REM rebound.  (As I write these notes, I assume that Jaak meant that therefore, psychosis is an alternative to REM sleep.)

Dreams and psychosis in psychoanalysis                   Howard Shevrin

            Freud described the first phase of psychosis as withdrawal of cathexis from the world.  (It was evident by now that cathexis and seeking were much the same.)  The second phase was the creation of delusions and hallucinations in an attempt to reconnect.  Drives were described in “Instincts and their vicissitudes.” A drive is a state of energized expectancy.  The drive is connected to the object and the aim; consummation, a motor act.  Drives are a demand for work.

             The method of convergence is a top-down attempt to combine many findings, and prove an assertion by showing that all available information is explained by a parsimonious hypothesis.  The method of validation is a bottom-up use of data to show a specific hypothesis to be validated by the experiment.  (My note – I use the terms idiographic and nomothetic in a similar manner.)  Therefore the top-down assertions of psychoanalysis must be validated by bottom-up neurophysiologic experiments.  These experiments are obviously not done via observation of psychoanalysis, but rather via observation of phenomena related to psychoanalysis.  This leads to the “method of convergence,” which is a way to substantiate psychoanalytic hypotheses.

             Primary and secondary processes were used to understand a narrative of a psychosis.  The subject had the psychotic realization the “number 3 is an important number for Americans.”  Primary process is feature-based and secondary process is relation-based.  The subject realized how often Americans use “3” – The Holy Trinity, Mil-wau-kee (3 syllables), U.S.A. (3 letters).  The subject’s thinking broke down into primary process thinking.

            My research shows that children use primary process and adults mostly use secondary process.  Under stress, more primary process thinking is evident.  My recent research showed that victims of sexual, but not physical, abuse before the age of 10 persist in primary process thinking as young adults.

             A second example of neurophysiologic research proving psychoanalytic ideas was my study of social phobia published in 1992.  Clinical interviews were listened to by teams of researchers.  Words were selected which would have relevance only to the fears of that particular person.  The words caused electrophysiologic responses different from neutral words – only when presented subliminally, and not when presented supraliminally. 

 Hence, we can do individual research which is more relevant to the general theory than other studies which use the same words across different individuals; and showed heterogeneous and nonspecific results.  Without the underlying psychoanalytic theory regarding the generation of conflict/anxiety in the subjects, the general case could not have been proven.  Both the method of convergence and the method of validation are scientific.  But a pillar of the method of validation is that the unconscious influences behavior in a way that requires inference.

 Discussion

            Jaak Panksepp said that incentive salience not only works on the external world, but also on our own thoughts.  In paranoia there is increased salience of thought.

            Howard Shevrin replied that the salience is then externalized from internal thoughts to external objects.  (My note - In hypochondriasis, the salience is displaced from internal thoughts to the body.)

            Jaak Panksepp clarified an earlier statement; Darwin and Freud are heroes, but of an earlier time.  They do not have to do with current science.

 Annual General Meeting

            The next international conference, July 2006, will be in Los Angeles, “Love, desire and attachment.”

            Neuropsychoanalysis is vibrant; a 12 page article in Der Spiegle, a long TV program about it, Howard Shevrin had the most cited neuroscience paper in 2004.

 Dreams and psychosis in psychoanalysis               Victor M. Andrade

             Freud asserted that in both dreams and psychosis there was a regression to primitive thinking.  There is a kind of wish fulfillment in both which satisfies both id and superego.  Antiwish dreams satisfy the superego.  In a letter to Fleiss in 1998 Freud equated metapsychology and biology.  In dreams of trauma, neither id nor superego is satisfied.  Freud thought these were a manifestation of the repetition compulsion, which he linked with the death instinct.  Repetition dreams prepare the ego for danger, which is why they occur despite their painful content.

             Freud’s theory is that dreams bind id energy.  Might they bind it via decreasing norepinephrine and serotonin, which energize cortical glutamate?  Cortical glutamate inhibits dopamine.  There is a transient loss of regulation in dreams, and a permanent loss of regulation in psychosis.

             Alan Schore’s work shows that interactions with a caregiver enhance both dopaminergic functioning, and cortical development – which regulates the dopamine.  Might psychoanalysis correct brain pathology by regression in the transference to early maternal/baby interactions, allowing rebalancing of this dopamine/cortex interaction?

             What in psychoanalytic technique helps?  Hobson’s critique of psychoanalysis was invoked, but his “critique” seems a validation of our method.  We are in fact trying to use the couch and free association to expel the DLPFC from our office, allowing uncensored ideas to float out of the patient in a dreamlike way.  E. Hartmann has suggested that there is little difference between dreaming and free association.

 Research Day, July 27

 Sleep and dreaming                                                           Fred Levin

          Dreams identify and deal with conflicts or threats by means of deferred action plans.  Memory is consolidated during REM sleep.  The dream pathway runs through the lateral hypothalamus, which regulates appetites.  In fact, there is an appetite for dreaming.  When the organism knows that its appetites will be taken care of by evolving action plans, it relaxes, and continues to sleep.

             Learning is intimately connected with the motor system.

1. Spontaneous initiative activates working memory for what we are learning
2. Action primes memory in general
3. Our actions follow our interests, which activates primary association cortices for various sensory systems.  The subjective experience is, “Aha!”
4. Every action is an experiment

 Why we dream

1. Dreams facilitate learning by creating specific emotion-based action plans as probes for the discovery of the exact nature of potential dangers
2. Dreams are exercises in emotional/instinctual potentials
3. Dreams simulate threatening events, rehearse threat perception and threat avoidance, and therefore improve self-performance in dealing with danger.  This improves the probability of survival and sexual reproduction by well-dreaming individuals.

Dreaming is the only time we are not required to take action.  Therefore we are free to analyze, including at levels we would not consciously acknowledge.

Recent work in the neurophysiology of development correlates with Fonagy’s developmental model of emotion and cognition. He and his colleagues suggest that mentalized affectivity, by which they mean the mature capacity for regulation of one’s own feelings and the capacity to discover the subjective meaning of states of one’s own feelings, lies at the heart of treatment.  This complex capacity, which includes the ability for appreciating similarity and difference between self and other, as well as agency and self-awareness, is embodied in mature love.  The hypothesis is that these changes represent not just maturing psychological capacities but have neurophysiological correlates.

Reported by Brian Johnson

Chapter 6 – "A psychoanalytic model for the development of subjectivity"

Psychic equivalence mode – internal reality is external reality

Pretend mode – internal reality is marked and different from external reality

Integration of these modes leads to the capacity to mentalize, a reflexive mode of thought.

 An example of psychic equivalence: An obsessional person “knows” the door is locked, but checks because the internal image of an unsecured house has more meaning and power than external images provided by the senses. 

 Theory of Mind – ability of children to attribute intentional mental states – goals, desires and beliefs – to oneself and others.

 E.g., In play, children can be developmentally advanced.  A 3-year-old child shown a candy box, and believes it is full of candy until shown that it is filled with pencils.  He then believes that he always thought it was full of pencils, and believes that another child shown the candy box will believe it to be full of pencils.  But a 3-year-old child told to pretend that an adult drinks an imaginary glass of chocolate milk, and then to pretend that the glass is now full of lemonade, will remember that at first it was “filled” with chocolate milk.

 This capacity to mentalize has the following advantages:

 a.  The child can have a sense of continuity of the self as the world changes.  The world changes do not change the child.

b.  The child sees others’ actions as meaningful through attribution of thoughts and feelings.  It makes people predictable.

c.  The child acquires a distinction between inner and outer truth, distinguishing between bad people and bad behavior (valuable in the case of abusive parents).

d.  It enables communication between people with two points of view.  Conversation becomes a collaboration.

e.  It allows higher intersubjectivity, deeper experience with others.

             Play with parents and other children reflects the child and reality, while breaking away from psychic equivalence.

             Fonagy describes the psychoanalysis of Rebecca, 4 and without a father.  Rebecca could not play through not having a father with her 22 year old mother because the mother reacted too severely.  Rebecca had pretended that her grandfather was her father, and his death and her mother’s grief precipitated the depression which brought her to treatment.  Her fantasies were forced into a mode of psychic equivalence.  Her feelings of hurt and shame about being fatherless could not be discussed with anyone.  Mother’s reflection of Rebecca included the feeling that Rebecca had “pirated” her independence.

            Fonagy tolerates her feelings and plays this all through in typical analytic style.

             The adult adopts the child’s mental stance and represents it to him as a “third object,” the scaffolding of the child’s sense of self.  If the adult cannot think about a piece of reality, neither child nor adult can “metabolize” the thoughts.  The development of the child’s perceptions of mental states depends on the psychic reality of the caregiver.

            This shifts our language/thinking from “internalization of the object” to “internalization of the thinking self from the object’s thinking.”

 

Reported by Brian Johnson

by Brian Johnson, M.D.  .   Notes on:   Schore, A.  (2003).   Affect dysregulation and disorders of the self.  NY: W.W. Norton.  

Temperamental attunement with a good caregiver is the result of ventral tegmental development via positive interactions.  The opiate system is originally sculpted by infant/mother interactions.  The eventual result is the ability to gain pleasure (endorphins) from being related.  Insecure avoidance may be the result of selective pruning of this system, coupled with expansion of the lateral tegmental inhibitory system.

 The right brain relational regulation system is formed or deformed by early experiences.

• The orbitofrontal cortex forms internal working models of interactions
• CRF is excessive, and results in excessive catecholamine states, in D infants
• In D infants, parasympathetic “unseen” states are upregulated, results in “dazed” dissociation
• The brain areas which mediate stress and fear are: orbitofrontal cortex (receives input from body and combines it with perception), prefrontal cortex (sorts out complex interaction, does planning), anterior cingulate cortex (alerts brain to incoming data, orders data), amygdala (reads fearful interpersonal situations/faces), hippocampus (memory of past interactions), brain stem (supplies “energy” to brain via cholinergic, serotoninergic, noradrenergic and dopaminergic tonic stimulation), periaqueductal grey (switching zone for mode of interaction: consummatory, drive, panic, play, etc), hypothalmus (“headganglion of ANS”, source of regulatory hormones and neurotransmitters: thyroid, cortisol, hunger, thirst, etc), pituitary and adrenals (endorgans regulated by hypothalmus), vagus (parasympathetic regulation of heart).
• Hyperactivation of dopaminergic and noradrenergic systems in infants results in excessive parcellation via NMDA/glutamate excitotoxicity.  Thus amygdala inputs are relatively strengthened, orbitofrontal weakened, “emotional perseveration” and lack of flexibility and complex cognition.
• Lack of orbitofrontal input to hypothalamic aggression sites leads to unmodulated aggression.
• Orbitofrontal (head of this system) deficits may predispose to: autism, mania, depression, schizophrenia, obsessive-compulsive, alcoholism, drug addiction.
• Dissociation/PTSD may be result of non-functioning of memory-integrating parts of this system, in part because of hypercortisolism/smaller hippocampal volume
• The mammalian “smart” vagal system uses the nucleus ambiguous, the reptilian “vegetative” parasympathetic system the dorsal motor nucleus.  The first can incorporate facial expression, vocalization and gestures vial contingent social interactions, the latter only immobilization, death feigning or hiding behaviors

Amygdala inhibition of hippocampal function at high levels of arousal mediates diminution of conscious explicit memory in traumatic events, yet implicit memory is retained

Reported by Jenai Wu

talked about the details of brain sensing through the hair cells of the inner ear which convert a sound wave (mechanical) to an electrical signal picked up by neurons.  He showed images and models of details of the tip of the inner ear hair cell called stereocilia which respond to tension caused by a sound vibration.  He graphically demonstrated how these cilia are not only bundled but linked by tiny filaments called tip links which respond in organized direction (collectively and directionally), and through the action of the mechanical stimulus, gate and regulate the ion channels in the tips of the stereocilia, using K ions to convey an electrical impulse. 

John Assad, Ph.D. Asst Prof Neurobiology, Harvard Medical School,

brought in a metapsychological perspective to visual perception at the level of neuronal activity and raised the question of how the brain plays a role in interpreting the raw data of perception.  By this he raised the brain’s active versus passive role in constructing meaning to what is seen, a “dynamic interplay between bottom-up and top-down” processes.  Using electrophysiological recording of awake monkeys, Assad’s lab studies how neurons in the parietal cortex respond to the same visual stimuli in different perceptual contexts – specifically neurons that become activated when spots don’t actually move but from the context might be construed as moving.  Hence there are neurons in the visual perceptual systems that are responding to more than the visual cues.  He thus raises a tantalizing question of how the brain’s semiotic activity can be traced to a neuronal level and opens the field for more questions this raises.

Cori Bargmann, Ph.D., Prof of Anatomy, University of California at San Francisco,

reviewed her research of how neurons find their synaptic partners throughout development.  She demonstrated how there is a hierarchy of synaptic formations of neurons given dozens to hundreds of neuronal sybtypes, and the rules that neurons use to connect to each other.  She demonstrated that presynaptic cells (specifically a neuron that regulates egg-laying in the nematode) don’t need post-synaptic cells or targets to form synapses where they should.  Instead, she introduced the concept of synaptic guidepost cells  based in the epithelial lining of the egg-laying region being essential for the correct synapses to form, or avoid scattering in a disorganized fashion. 

Carla Shatz, Ph.D., Prof of Neurobiology, Harvard Medical School,

presented her sweeping research elucidating the precision of cellular and molecular mechanisms and wiring in neural development,  given the sheer magnitude of potential connections.  She demonstrated the difference between adult brain (visual) connections and its equivalent in the fetal brain.  While connections between each eye’s retina and their targets in the thalamic nucleus and lateral geniculate nucleus (LGN) are well differentiated and layered in adults, it is not the case with the fetal brain.  Before the retina is developed in the fetus and vision is occurring, the brain generates its own activity to fire at and create synaptic structures, both short-term and long-term.   While studying these phenomena she discovered that class I major histocompatibility complex antigens (class I MHC), normally viewed as molecules present in immune cellular functions, are not only expressed during synaptic plasticity in the CNS, but bear similarity to hippocampal synaptic activity, and therefore may provide insights into learning and memory as well as mechanisms of developmental synaptic differentiation and structure building. 

Eric Kandel, M.D., Ph.D., University Professor,  Columbia University, and 2000 Nobel Laureate in Medicine, 

 discussed his research in the molecular and synaptic underpinnings of two areas of memory: sensitization or learned fear, and explicit or declarative memory storage, working with the sea slug Aplysia.  Specifically, he demonstrated a link between subcellular processes and chemical signaling including defining the genes and proteins that express synaptic connections, leading to coordinated behavior change.  This work is significant in its implications of linking molecular cell biology and neurochemistry, genetics to behavior, psychiatry and psychopharmacology.  During Q&A he discussed “Memory Pharmaceuticals” which is working on drugs to enhance memory based on his research, as well as implications of his work on PTSD.