As shown in **Figure 1**, psychotherapy had a significant effect on all applied outcome scales. *Somatization*, as assessed with the somatization sub-scale of the SCL-90-R, was significantly reduced after psychotherapy [*t(*11*)* = 3*.*564; *p*[one−tailed] = 0*.*002∗∗]. *Emotional awareness*, as assessed with the TAS-20, was significantly enhanced after psychotherapy [*t(*14*)* = 2*.*456; *p*[one−tailed] = 0*.*014∗]. In addition, *Mood state* was controlled using the BDI. After psychotherapy, we found a significant reduction of depressive symptoms [*t(*14*)* = 5*.*660; *p*[one−tailed] = 0*.*001∗∗∗]. Finally, *emotion recognition abilities*, which were assessed using the TAB, improved; error rates were significantly lower after psychotherapy [*t(*13*)* = 2*.*747; *p*[one−tailed] = 0*.*008∗].

When checking for correlations between different scales, we found that psychotherapy-induced reductions of SCL-90-somatization scores correlated with reductions of BDIscores (ρ[Spearman] = 0*.*558; *p*[one−tailed] = 0*.*025∗). In addition, psychotherapy induced reductions of TAS-20 scores correlated with reductions of BDI-scores (ρ[Spearman] = 0*.*723; *p*[one−tailed] = 0*.*001∗∗). However, we did not find correlations of psychotherapy induced changes of SCL-90-somatization scores with changes in the TAS-20 (ρ[Spearman] = 0*.*323; *p*[one−tailed] = 0*.*306), of SCL-90-somatization changes with changes of error rates in the TAB (ρ[Spearman] = −0*.*145; *p*[one−tailed] = 0*.*673), of TAS-20 changes with changes of error rates in the TAB (ρ[Spearman] = −0*.*123; *p*[one−tailed] = 0*.*674), or (ρ[Spearman] = 0*.*139; *p*[one−tailed] = 0*.*637).

#### *Intra-scanner empathy ratings*

The 2 × 4 factorial ANOVA with "psychotherapy" ("pretreatment" vs. "post-treatment") as first within-subjects factor and "emotion" ("anger," "disgust," "joy," and "neutral expression") as second within-subjects factor revealed a significant effect of "emotion" [*F(*3*,* 112*)* = 13*.*367; *p <* 0*.*001∗∗∗], whilst we did not find significant effects for the factor "psychotherapy" [*F(*1*,* 112*)* = 1*.*142; *p* = 0*.*288] or the interaction of "psychotherapy" × "emotion" [*F(*3*,* 112*)* = 0*.*586; *p* = 0*.*626]. *Post-hoc t*-tests revealed, that empathy ratings for "anger" trials were significantly higher compared to "disgust" trials [*t(*14*)* = 4*.*715; *p*[two−tailed] *<* 0*.*001∗∗∗] and significantly lower compared to "joy" trials [*t(*14*)* = 5*.*924; *p*[two-tailed] *<* 0*.*001∗]. In addition, empathy ratings for "disgust" trials were significantly lower compared to "joy" trials [*t(*14*)* = 7*.*880; *p*[two-tailed] *<* 0*.*001∗∗∗], and empathy ratings for "neutral expression" trials were significantly lower compared to "joy" trials [*t(*14*)* = 6*.*479; *p*[two-tailed] *<* 0*.*001∗∗∗]. There were, however, no significant differences between empathy ratings for "anger" and "neutral expression" [*t(*14*)* = 0*.*234; *p*[two-tailed] = 0*.*818], and between empathy ratings for "disgust" and "neutral expression" [*t(*14*)* = 1*.*621; *p*[two-tailed] = 0*.*127].

#### **fMRI RESULTS**

#### *ROI based comparison of hemodynamic responses*

In a previous paper, we found 12 brain areas (regions of interest, ROIs) with diminished modulation of hemodynamic responses in pre-treatment somatoform patients compared to healthy control subjects (de Greck et al., 2012). As shown in **Table 2**, we found significant improvement of hemodynamic responses

significant reduction of error rates in the TAB. (Explanations: *h*, *p*1, and *p*2 refer to the scores of healthy subjects (h), pre-treatment somatoform patients (*p*1), and post-treatment somatoform patients (*p*2); error bars indicate the 95%-confidence-interval; ∗*p <* 0*.*05, ∗∗*p <* 0*.*01, ∗∗∗*p <* 0*.*001, with regard to one-tailed *t*-tests.)

after psychotherapy in 6 of the 12 regions—all for the contrast "anger"—"control."

### *Voxel-wise whole brain analysis*

In addition to the above described ROI based approach, we also implemented a voxel-wise whole brain statistical analysis to identify brain regions with altered hemodynamic responses. As presented in **Table 3** and **Figure 2**, four regions showed a significant effect of psychotherapy on hemodynamic modulation: The bilateral parahippocampal gyrus and the left inferior temporal gyrus showed increased modulation of hemodynamic responses after psychotherapy, the left putamen

*(Abbreviations: h, p1, and p2 refer to the mean empathy rating of the according condition, where h indicates data of healthy subjects, p1 indicates data of pre-treatment somatoform patients, and p2 indicates data of post-treatment somatoform patients;* ± *indicates the 95%-confidence-interval).*

had diminished modulation of hemodynamic responses after psychotherapy.

#### *Correlation of psychotherapy induced effects*

We were interested, whether psychotherapy induced alleviations of somatic symptoms (as ascertained with the SCL-90 somatization sub-scale) correlated with psychotherapy induced changes of hemodynamic responses in any of our ROIs. With regard to those ROIs which had previously shown diminished modulation of hemodynamic responses in pre-treatment somatoform patients (i.e., ROIs listed in **Table 1**), we did not find any significant correlations under reasonable statistical thresholds (Spearman correlations, *p*[two-tailed] *<* 0*.*05). With regard to the ROIs found in the voxel-wise analysis (i.e., ROIs listed in **Table 2**), we found only one significant correlation: the reduction in the SCL-90 somatization scores induced by psychotherapy correlated with the reduction of hemodynamic responses in the left putamen (ρ = 0*.*811; *p*[one-tailed] = 0*.*001∗∗).

### *Control for potential effects of the psychotropic medication*

Since 5 of the 15 patients were on psychotropic medication during either on one or both scanning sessions, we implemented two additional fMRI analyses (i.e., an additional ROI-based approach and an additional voxelwise approach) including only data of the 10 patients without medication. These results support the

#### **Table 2 | Effect of psychotherapy on hemodynamic responses—ROI based approach.**

*In a previous study of our group, 12 regions of interest (ROIs) had shown significantly reduced modulation of hemodynamic responses during the same paradigm in pre-treatment somatoform disorder patients. Here, we investigated whether contrast values extracted from these ROIs showed a significant normalization after psychotherapy. In six ROIs, we found a significant enhancement of hemodynamic modulation after psychotherapy. After correction for multiple comparisons using a Bonferroni-correction, two ROIs (i.e., the right parahippocampal gyrus and the left cerebellum) showed a significant effect. (Abbreviations: x, y, and z refer to the Talairach coordinates of the regions; h, p1, and p2 refer to the contrast value of the according contrast, where h indicates data of healthy subjects, p1 indicates data of pre-treatment somatoform patients, and p2 indicates data of post-treatment somatoform patients;* ± *indicates the 95%-interval; ( \*) : p < 0.1; \*: p < 0.05; \*\*: p < 0.01; \*\*\*: p < 0.001; †: p < 0.004, this indicates a significant effect after controlling for multiple comparisons using a Bonferroni-correction.)*

#### **Table 3 | Effect of psychotherapy on hemodynamic responses—voxel-wise whole brain analysis.**

*We implemented a voxel-wise whole brain analysis to identify brain regions with significant changes of hemodynamic modulation for the contrasts all emotions (["anger"*+ *"disgust"* + *"joy"* + *"neutral"]* − *"control"), anger ("anger"* − *"control"), and joy ("joy"* − *"control"). (Abbreviations: x, y, and z refer to the Talairach coordinates of the center of mass of the regions; peak t value refers to the t value of the peak voxel in the cluster; cluster size refers to the number of voxels which survived threshold masking at p*[*uncorrected* ] ≤ *0.001; FWE value describes the probability, that a cluster of the given size would appear as a false positive result in a contrast of the given smoothness; effect refers to an increase (p2 > p1) or a decrease (p2 < p1) of hemodynamic responses after psychotherapy.)*

view that modulation of hemodynamic responses in the left superior temporal gyrus, right parahippocampal gyrus, left posterior insula, and left cerebellum (ROI-based approach), as well as in the in the bilateral parahippocampal gyrus, left putamen, and left inferior frontal gyrus (voxelwise approach) are not caused by the effects of psychotropic medication. Please see the Supplementary Material for a detailed presentation of the according results.

## **DISCUSSION**

#### **SUMMARY OF FINDINGS**

Somatoform disorder patients in a pre-treatment stage show diminished modulation of hemodynamic responses during emotional empathy in several brain areas, including the bilateral parahippocampal gyrus, left amygdala, left postcentral gyrus and others; this was reported in a previous paper by our group (de Greck et al., 2012). Here, we investigated whether brain activity normalized after multimodal psychodynamic psychotherapy. Psychotherapy was successful as demonstrated by a significant reduction of somatization symptoms (based on the SCL-90 somatization sub-scale), alexithymia symptoms (TAS-20), and depressive symptoms (BDI). In addition, psychotherapy led to significant reduction of error rates in an emotion recognition test (TAB).

The analysis of psychotherapy induced changes of brain activity was implemented using two approaches: a region of interest (ROI) based approach and a voxel-wise whole brain analysis. Both analyses came to the matching results that brain activity in the bilateral parahippocampal gyrus during empathy with anger normalized after psychotherapy. With regard to the ROI based analysis, we found that brain activity in almost all of those regions which had shown diminished modulation of hemodynamic responses in the pre-treatment stage for the contrast "empathy with anger" − "control" normalized after psychotherapy. Regions with a normalization after psychotherapy included the left postcentral gyrus, left superior temporal gyrus, left posterior insula, left amygdala (statistical trend), left cerebellum, and the above mentioned bilateral parahippocampal gyrus.

However, none of those regions which had shown diminished modulation of hemodynamic responses of pre-treatment somatoform patients during other contrasts (namely "empathy with all emotions" − "control," and "empathy with joy" − "control"), showed a normalization of hemodynamic responses after psychotherapy.

With regard to the voxel-wise whole brain analysis, we found three regions, which had a significant change in neuronal activity after psychotherapy for the contrast "empathy with anger" - "control" (the bilateral parahippocampal gyrus, and the left putamen), and one region for the contrast "empathy with joy" − "control" (the left inferior temporal gyrus). Interestingly, the left putamen showed *less* modulation of hemodynamic responses after psychotherapy, whereas modulation was increased in all other regions. In addition, the left putamen was the only region in which reduction of hemodynamic responses was correlated with the reduction of somatic symptoms after psychotherapy (over all patients).

#### **PSYCHODYNAMIC MECHANISMS IN SOMATOFORM DISORDER**

From a psychodynamic perspective, the development of somatoform symptoms can be understood as malfunctioning of secondary process mechanisms concerning the handling of emotional conflicts which leads to "resomatization" (i.e., the appearance of somatoform symptoms as "concomitants" or "equivalents" of affective tensions, Schur, 1955). In other words: unreleased affective tensions caused by unconscious emotional conflicts induce the corresponding somatic responses (which appear as somatic symptoms), whereas the corresponding affective component is repressed and can not be experienced (Lipowski, 1988; Hoffmann et al., 2004). In this regard, somatization (i.e., the development of medically unexplained somatic symptoms, Lipowski, 1988) is either seen as a defense mechanism itself (Bond et al., 1983; Lipowski, 1988), or as a correlate of immature defense styles (Nickel and Egle, 2006). In addition to emotional conflicts, the experience of overwhelmingly strong negative emotional reactions, which may occur for instance as a response to childhood adversities, can lead to a breakdown of secondary process thinking and a malfunction of mature defense mechanisms (Nickel and Egle, 2001). As a consequence, these patients are prone to develop reduced emotional awareness as correlate of the repressed emotional component, and somatic symptoms as equivalents of affective tensions (Krystal, 1997). Indeed, there is a strong link between childhood adversities and adult somatization (Spitzer et al., 2008).

#### **HOW DOES PSYCHOTHERAPY HELP PATIENTS WITH SOMATOFORM DISORDERS?**

Psychodynamic psychotherapy, as it was applied in our study, aims to increase the insight and acceptance of unconscious emotions, needs and conflicts (Blagys and Hilsenroth, 2002; Leichsenring, 2005), and to enable patients to gain "mastery over his or her repressed wishes, desires, fears, or anxieties" (Blagys and Hilsenroth, 2002). Regarding this, the development of more mature defense mechanisms and coping strategies is a core aim (Vaillant, 1977). Further treatment goals include the establishment of a psychosomatic disease model, the enhancement of affect differentiation, a better understanding of underlying stresses, and the reduction of medication abuse (Beutel et al., 2008). In the case of somatoform disorder, successful psychotherapy leads to enhanced secondary process thinking, more mature defense mechanisms, improved "desomatization", and decreased somatic symptoms.

The reduction of somatic symptoms after psychotherapy in our study reflects a decreased use of somatization (i.e., improved "desomatization"). Improved emotion recognition after psychotherapy is probably caused by the uncovering of repressed emotional conflicts and emotional needs, which hampered emotion recognition in the pre-treatment stage.

#### **NEUROPHYSIOLOGICAL MECHANISMS IN SOMATOFORM DISORDER**

The bilateral parahippocampal gyrus seems to play a key role in the affective dysfunctions of somatoform disorder (in particular in the processing of angry facial stimuli), since we found a significantly diminished modulation of hemodynamic responses in this area in the pre-treatment stage (de Greck et al., 2012) and a significant improvement after psychodynamic psychotherapy. Interestingly, the parahippocampal gyrus is involved in the recall of autobiographical memories (Maguire, 2001; Niki and Luo, 2002; Rekkas and Constable, 2005; Gardini et al., 2006), in particular the retrieval of emotional memories (Damasio et al., 2000), or emotional background informations (Smith et al., 2004; Sterpenich et al., 2006). In addition, the recall of conflictual memory content activates the parahippocampal gyrus (Loughead et al., 2010), and it is less activated during free associations to conflict-related themes (Schmeing et al., 2013).

#### **AFFECTIVE PROCESSING IN SOMATOFORM DISORDER AND THE EFFECT OF PSYCHOTHERAPY**

High co-morbidity of somatoform disorder and alexithymia (i.e. diminished awareness of own and other's emotional processes) has been reported by various investigators (Bach and Bach, 1996; Bankier et al., 2001; Duddu et al., 2003; Grabe et al., 2004; Burba et al., 2006; Bailey and Henry, 2007; Mattila et al., 2008; Wood et al., 2009). From a psychodynamic point of view, the link between alexithymia and somatization is explained by a breakdown of secondary process coping with emotional conflicts, followed by the repression of the corresponding affective component and the experience of the somatic component as unexplained body symptoms (Schur, 1955; Lipowski, 1988; Hoffmann et al., 2004). Our data suggests that the parahippocampal gyrus, a region known for its involvement in the processing of autobiographic emotional memories, might be a neural key correlate of this process. In our study, we investigated brain activity during the intentional empathic processing of facial emotions. The process of intentional emotional empathy rests upon emotional sub processes which include emotional and cognitive empathy, emotion recognition, affective and cognitive mentalizing and the processing of autobiographical memory (Shamay-Tsoory, 2011). In order to empathize with somebody else, it is essential to generate a congruent emotional image of the target's emotional state within oneself (Preston and de Waal, 2002). Besides emotional contagion (Preston and de Waal, 2002; Shamay-Tsoory, 2011), this process relies on the recall of autobiographic memory traces (Damasio et al., 2000): If I want to understand from your face, what you feel, and intentionally want to share your emotional state, I may try to recall own memory traces which previously led to a similar emotional response in myself. This process involves the retrieval of emotional autobiographic memory and induces activity in the parahippocampal gyrus. In the case of somatoform disorder, however, it is assumed that overwhelmingly strong emotional conflicts led to a breakdown of emotional processing and a suppression of the corresponding memory traces, resulting in a diminished modulation of the parahippocampal gyrus during emotional empathy. Psychodynamic psychotherapy, however, can restore the retrieval of repressed autobiographic memories, which leads to increased modulation of the parahippocampal gyrus.

#### **PSYCHOANALYTICAL NEUROSCIENCE**

We believe our study is a fine example, which demonstrates how neuroscience can benefit from psychoanalysis. Our main finding (i.e., pre-treatment somatoform disorder patients show diminished modulation of neuronal activity in the parahippocampal gyrus during the empathic processing of angry faces; this pattern normalizes after psychotherapy) fits well to psychoanalytical concepts of somatoform disorder. In fact, it is hard to explain our findings without referencing to psychodynamic concepts, which relate somatoform disorder to repressed emotional memories.

When it comes to the investigation of the neuronal underpinnings of complex emotional processing (and in particular its dysfunctions in psychosomatic diseases such as somatoform disorder) psychoanalytical concepts may provide a profound base to interpret neuroscientific findings.

## **LIMITATIONS**

Our psychotherapeutic intervention was "multimodal", i.e., it included a variety of different therapeutic techniques. Hence, we can not conclude for sure that increased emotional insight in formerly repressed conflicts caused the reduction of symptoms and normalization of brain activity (and not for instance other therapeutic variables such as decreased depression).

Even more important, with the existing design, we can not for sure conclude that changes observed in the pre-post comparison are indeed caused by psychotherapy since they might be related to other factors, such as for instance retest effects, spontaneous remission, or in particular, regression to the mean effects (Barnett et al., 2005). To control for these potential confounds it would have been essential to scan a second control group consisting of somatoform patients, who would have been also scanned for two times without participation in psychotherapy.

However, the fact that we found reduced neuronal activity in the *bilateral* parahippocampal gyrus in the pre-treatment stage, and normalized activity in the *bilateral* parahippocampal gyrus in the post-treatment stage, supports the view that these activations are not related to regression to the mean effects (because it would be rather improbable that regression to the mean effects lead to bilateral effects in the same brain region).

## **CONCLUSION**

Our results are in accordance with the conclusion that the repression of emotional memories, which occurs in

### **REFERENCES**

somatoform disorder in order to defend against overwhelmingly strong emotions, can neurophysiologically be understood in terms of diminished activation of the parahippocampal gyrus. Psychotherapeutic measures aim to increase emotional insight and to accept repressed feelings and emotional memories. After psychotherapy, somatoform patients reported less symptoms and showed stronger neuronal activity in the parahippocampal gyrus. Our results support the assumption that increased access to repressed emotional memories is related to increased neuronal activity of the parahippocampal gyrus.

#### **ACKNOWLEDGMENTS**

The authors thank the staff of the Department of Neurology of the Otto-von-Guericke-University of Magdeburg for their support. We also thank Niall Duncan for his helpful propositions concerning the manuscript. Moritz de Greck had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

## **SUPPLEMENTARY MATERIAL**

The Supplementary Material for this article can be found online at: http://www.frontiersin.org/Human\_Neuroscience/10.3389/ fnhum.2013.00410/abstract

41, 551–559. doi: 10.1016/S0022- 3999(96)00228-0

related activity in somatoform disorder. *World J. Biol. Psychiat.* 12, 296–308. doi: 10.3109/15622975. 2010.539269

841–868. doi: 10.1516/RFEE-LKPN-B7TF-KPDU

**Conflict of Interest Statement:** The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

*Received: 21 March 2013; paper pending published: 23 May 2013; accepted: 11 July 2013; published online: 16 August 2013.*

*Citation: de Greck M, Bölter AF, Lehmann L, Ulrich C, Stockum E, Enzi B, Hoffmann T, Tempelmann C, Beutel M, Frommer J and Northoff G (2013) Changes in brain activity of somatoform disorder patients during emotional empathy after multimodal psychodynamic psychotherapy. Front. Hum. Neurosci. 7:410. doi: 10.3389/ fnhum.2013.00410*

*This article was submitted to the journal Frontiers in Human Neuroscience.*

*Copyright © 2013 de Greck, Bölter, Lehmann, Ulrich, Stockum, Enzi, Hoffmann, Tempelmann, Beutel, Frommer and Northoff. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.*

## What would be the benefits of a collaboration between psychoanalysis and cognitive neuroscience? The opinion of a neuroscientist

## *Perrine Ruby1,2,3\**

*1 Brain Dynamics and Cognition Team, Lyon Neuroscience Research Center (CRNL), INSERM, CNRS, Lyon, France*

*2 University Lyon 1, Lyon, France*

*3 Department of Psychology, University of Swansea, Swansea, UK*

*\*Correspondence<EMAIL_ADDRESS>
#### *Edited by:*

*Nikolai Axmacher, University of Bonn, Germany*

**Keywords: unconscious memory of experienced events, personal meaning, subject's history, affective unconscious, self**

## **CONTEXT OF DEVELOPMENT AND GUIDING PRINCIPLES OF PSYCHOANALYSIS AND COGNITIVE NEUROSCIENCE**

Psychoanalysis was conceived and developed for clinical purposes at the beginning of the 20th century. Freud's main goal was to treat neurotic patients and psychotic patients. As a consequence of this great enterprise he developed a theory to explain the functioning of the human mind. A critical contribution of his work was the theory of the unconscious and the proposal that even if unconscious, a representation can influence a subject's behavior. Freud believed that unconscious thoughts and feelings may cause a patient to experience life difficulties and/or maladjustments. He proposed that the process of freeing unconscious thoughts could help a patient gain insight into and ultimately improve his/her situation. Therefore, Freud developed techniques to decode unconscious images, and to free them through patient insight (e.g., Freud, 1901).

Cognitive neuroscience is a rather young discipline. It was developed in the 1980's and has been strongly linked to the advancement of neuroimaging techniques (mainly positron emission tomography, PET, and functional magnetic resonance imaging, fMRI). The main goal of this discipline is to understand the functioning of the human brain/psyche. A consequence of this great enterprise has been, and hopefully will be, clinical applications. Cognitive neuroscience is fundamentally interested in processes/effects which can be found in several subjects rather than in the specific functioning of single subjects. Of importance, at the moment, this discipline does not provide a consensual and comprehensive theory of the human mind. It has, nevertheless, demonstrated that neuroscientific results can help to shape psychological theories or to disentangle between psychological theories (e.g., Henson, 2005; Poldrack, 2006; Legrand and Ruby, 2009).

## **PITFALLS AND GAPS IN THE TWO DISCIPLINES SHOWING THE NEED FOR A BILATERAL COLLABORATION**

Psychoanalysis is considered by many scientists as an unscientific, an thus untrustworthy discipline. Psychoanalysis needs then to improve its credibility. A collaboration with a scientific discipline such as cognitive neuroscience could certainly help to achieve this aim. In addition, at the theoretical level, one cannot exclude that the investigation of the neurophysiological correlates of psychoanalytical concepts (e.g., Kaplan-Solms and Solms, 2000) could result in a better understanding of the links between some psychoanalytical concepts, as neurophysiological results have already resulted in a better understanding of concepts from experimental psychology (e.g., Henson, 2005; Poldrack, 2006; Legrand and Ruby, 2009).

A current weakness of cognitive neuroscience is to ignore some important brain/mind properties/characteristics, such as (1) what is important to the individual subjects, or in other words the notion of "meaning" in the Freudian sense, (2) the subject's history and preferences, (3) the notion of affective unconscious which is closely related to the Freudian unconscious, (4) the unconscious memory of experienced events (UMEE), which refers to the memory of an episode or a scene that cannot be consciously recollected. All of these issues are at the core of our intimate mind; they are the foundation of our identity. One cannot expect to propose a comprehensive theory of the human mind if neglecting these issues. A collaboration with psychoanalysis, which could be considered as a "science" of singularity, appears then providential to help finding solutions to address private issues in cognitive neuroscience (Ruby, 2011).

## **WHAT WOULD BE THE BENEFITS OF A COLLABORATION? THE CASE OF UMEE UMEE ARE NEGLECTED IN COGNITIVE NEUROSCIENCE**

In cognitive neuroscience, the dominant theory of memory states that long-term memory can be either explicit or implicit. These two types of memory are often referred to as declarative (composed of episodic and semantic memory) and procedural memory or the "knowing what" and the "knowing how." This well-used way of naming explicit and implicit memories show that the notion of "knowing what implicitly/unconsciously" is not emphasized at the theoretical level. It is also true at the experimental level. The issue of UMEE in particular has been barely investigated in cognitive neuroscience. Rather, this concept is often ignored and possibly denied which has important consequences on the interpretation of results and thus theories of the brain/mind.

The consideration of UMEE has been lacking for example in research investigating memory and the self, as illustrated by the article of Klein and Gangi in the Annals of the New York academy of sciences (Klein and Gangi, 2010). In this study, the authors aimed to better understand the link between the different types of self-related memory systems, by investigating the representation of self-personality traits in patients with amnesia. They report results showing that some patients with episodic amnesia (with traumatic or developmental etiologies) can, despite their amnesia, update the representation of their own personality traits. For Klein and Gangi, these cases showed that episodic and semantic memory systems were separate and independent. Interestingly, they also considered at some point the possibility that UMEE may participate in the updating of personality traits since they wrote "K.C. not only had access to semantic knowledge of his own personality traits, but he was also able to acquire new knowledge about his personality. Yet this updating occurred without his being able to episodically recollect any information about the behavioral events on which this updating presumably was based." Unfortunately, the authors did not develop this point and did not discuss the hypothesis of the updating of personality traits based on the UMEE. However, according to their results, one cannot exclude this possibility. How could one otherwise explain their results? The most likely hypothesis is that a semantic representation of one's own personality is elaborated using memories (conscious or unconscious) of past episodes of one's own life, and especially episodes involving human interactions. Klein and Gangi did not provide an alternative explanation but argued against this hypothesis by stating that they "devoted a substantial amount of [their] research (consisting in multiple methods—for example, priming techniques, transfer appropriate processing, the method of reversed association39*,* 55) to show that exemplar-based self-knowledge is not activated (consciously or unconsciously) when participants perform semantic judgments about the self.29*,* 35." However, these results do not exclude the possibility that UMEE participate in the formation of semantic knowledge even if it is not activated during semantic tasks.

UMEE is also barely considered in the field of dream research. Memory (be it conscious or not) is the main source of information available during sleep. Previous studies have looked for episodic recall in the content of dreams (e.g., Fosse et al., 2003), but to my knowledge, no studies have investigated whether UMEE show up in dream content or not. Investigating autobiographical memory in the elderly, Grenier et al. (2005) showed that dreams could bring back very old memories and especially memories from adolescence. Interestingly, these results were not explained by a recent reminiscence of these remote memories because "the participants indicated that to the best of their knowledge, they had not thought of or talked about the different elements experienced in their dreams since the time of the original experience." This type of memory may be closely related to unconscious memory (repressed or not) because according to the participants, the episode recalled in the dream had not reached consciousness since this episode actually happened. It seems thus fairly possible that dreams could bring unconscious memories or representations to consciousness, but this has not yet been tested.

#### **UMEE ARE AT THE CORE OF PSYCHOANALYTIC PRACTICES**

Even if they are difficult to uncover and confirm, UMEE does exist. Here is a tragic example from the French news from the winter of 2012 (e.g., Sud Ouest 29/02/2012; Le Monde 03/03/2012). A women living in Lyon, France (Zahia H.) recalled the memory of being raped and assaulted 37 years prior, in 1973, upon awakening from general anesthesia in 2010. The surgery (one of many previous surgeries) was indicated to treat disabilities caused by this aggression. Thirty seven years ago, Zahia awoke from a coma induced by the episode and had no memory of the rape and the head injury which she had sustained. Zahia's mother decided not to tell her what had occurred. Thirty seven years after, when Zahia recalled the memory of this tragic episode her mother was dead.

This case demonstrates the existence of unconscious memories of important experiences (the facts can be verified). One can easily intuit reading this story, that memories, even if implicit/unconscious, may influence behavior (for example, unexplained fear in particular situations) and play an important role in a subject's life, as hypothesized by Freud. In support of this single case, Mitchell (2006) managed to produce experimental results showing the existence of longlasting unconscious memory of images. He demonstrated that pictures presented 1–3 s could induce a priming effect 17 years after presentation, even in subjects who reported no conscious recollection of their participation in the original laboratory session.

Currently, cognitive neuroscience cannot easily explain the recovery of a memory 30 or 40 years later. By contrast, this phenomenon can be explained from a psychoanalytic perspective (When I previously described Zahia's case in a conference, René Roussillon, psychoanalyst and professor of psychology at the University of Lyon, predicted that the mother of Zahia was dead when she recovered the memory of the rape even though I did not mention this fact). This comes as no surprise since the core of psychoanalytic practice is centered on unconscious memories or representations that induce life difficulties and/or maladjustment and on the means to free them.

#### **WHAT WOULD BE THE BENEFIT OF A COLLABORATION BETWEEN PSYCHOANALYSTS AND NEUROSCIENTISTS ON UMEE**

On the one hand, UMEE is a component that can be easily incorporated into a theoretical model of memory in cognitive neuroscience; on the other hand, this type of memory plays a central role in psychoanalysis since conflicts and trauma may lead (via repression or not) to the creation of UMEE. Therefore, the UMEE (resulting from repression or not) could be a strong convergence point between psychoanalysis and cognitive neuroscience, which may help to built bridges between the two disciplines. Below, possible benefits of a collaboration between psychoanalysis and cognitive neuroscience on UMEE.

## *New hypotheses on the functioning of memory systems in cognitive neuroscience*

Adding a psychoanalytical perspective to reflections on cognitive neuroscience experiments may result in new hypotheses. This can be illustrated by the two examples described above. First, the hypothesis of the possible participation of UMEE in the formation of semantic knowledge about the self derives from a psychoanalytical perspective on the functioning of the mind/brain. Testing this hypothesis would help to better understand the formation of the semantic representation of one's personality traits, which according to Klein and Gangi (2010), is still a mystery: "Of the systems of self we have examined, the semantic self-knowledge system seems the most resilient in the face of the cognitive chaos resulting from developmental and/or environmental damage to the brain. This is both an empirical fact and a mystery for which we have, at present, no explanation." Second, according to Freud (e.g., Freud, 1901), unconscious representation may surface during dreams. Collaboration with psychoanalysts could assist in the design of experiments to test this hypothesis. For example, one could try to use the free association method to test whether free association initiated from the words of a dream would lead to UMEE. The results would help to elucidate whether dreams are indeed the royal road to the unconscious and could also have important implications for theories of sleep, dreams and memory.

#### *New paradigms to test unexplored issues in cognitive neuroscience*

The absence of consideration of the UMEE in cognitive neuroscience is certainly due to the difficulty in investigating such private issue using an experimental approach. Psychoanalysts who work to make unconscious representations conscious may be helpful in developing methods to address this issue in cognitive neuroscience. Previous interdisciplinary work proves that novel paradigms can enable a scientific investigation of concepts that are seemingly impossible to explore. For example, Howard Shevrin, psychoanalyst and Professor of Psychology at The University of Michigan, developed shrewd paradigms to investigate unconscious processes at the experimental level. Using event related potentials and a free association method, his team identified neurophysiologic markers of subliminal perceptions and showed that subliminal images were processed in a complex and associative way (Shevrin and Fritzler, 1968). Using similar means (mild electric shock presented 800 ms after images or words presented subliminally) he also demonstrated that aversive conditioning can occur unconsciously (Shevrin, 2001). These results had a great impact on the neuroscientific community and precipitated an interest in unconscious processes.

#### *Optimize therapeutic means in the psychoanalytic practice*

The investigation of UMEE in cognitive neuroscience should result in a better understanding of the context of formation (repression or not) and the neurophysiological basis of UMEE (possibly dependent on the context of formation). Theoretically, this should help to optimize the therapeutic means to act on or free such memories.

#### **CONCLUSION**

Even if difficult, unconscious processes, private issues (preferences, history, what matters for a subject.) and, more generally, psychoanalytic concepts have to be addressed at the experimental level to achieve a comprehensive theory of the human mind. Another great benefit of such an endeavor would be to provide objective arguments and allow a constructive and scientific debate about whether Freudian or psychoanalytical concepts are plausible and useful. In other words, a collaboration between psychoanalysis and cognitive neuroscience may be the best way to escape from the sterile and counterproductive hostility between the disciplines and to move forward together in order to benefit science and medical practices.

### **REFERENCES**

Fosse, M. J., Fosse, R., Hobson, J. A., and Stickgold, R. J. (2003). Dreaming and episodic memory: a functional dissociation. *J. Cogn. Neurosci.* 15, 1–9. doi: 10.1162/089892903321107774

*Received: 06 June 2013; accepted: 29 July 2013; published online: 23 August 2013.*

*Citation: Ruby P (2013) What would be the benefits of a collaboration between psychoanalysis and cognitive neuroscience? The opinion of a neuroscientist. Front. Hum. Neurosci. 7:475. doi: 10.3389/fnhum.2013.00475*

*This article was submitted to the journal Frontiers in Human Neuroscience.*

*Copyright © 2013 Ruby. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.*

## Subliminal unconscious conflict alpha power inhibits supraliminal conscious symptom experience

#### *Howard Shevrin1 \*, Michael Snodgrass 1, Linda A. W. Brakel 1, Ramesh Kushwaha1, Natalia L. Kalaida1 and Ariane Bazan2*

*1 Program of Research on Unconscious Processes, Ormond and Hazel Hunt Laboratory, Department of Psychiatry, University of Michigan, Ann Arbor, MI, USA 2 Faculté des Sciences Psychologiques et de l'Education, Service de Psychologie Clinique et Différentielle, Université Libre de Bruxelles (ULB), Brussels, Belgium*

#### *Edited by:*

*Nikolai Axmacher, University of Bonn, Germany*

#### *Reviewed by:*

*Gerd T. Waldhauser, University of Konstanz, Germany Henrik Kessler, University of Bonn, Germany*

#### *\*Correspondence:*

*Howard Shevrin, Department of Psychiatry, University of Michigan, B1519 Rachel Upjohn Building, 4250 Plymouth Rd., Ann Arbor, MI 48109, USA e-mail<EMAIL_ADDRESS>
Our approach is based on a tri-partite method of integrating psychodynamic hypotheses, cognitive subliminal processes, and psychophysiological alpha power measures. We present ten social phobic subjects with three individually selected groups of words representing unconscious conflict, conscious symptom experience, and Osgood Semantic negative valence words used as a control word group. The unconscious conflict and conscious symptom words, presented subliminally and supraliminally, act as primes preceding the conscious symptom and control words presented as supraliminal targets. With alpha power as a marker of inhibitory brain activity, we show that unconscious conflict primes, only when presented subliminally, have a unique inhibitory effect on conscious symptom targets. This effect is absent when the unconscious conflict primes are presented supraliminally, or when the target is the control words. Unconscious conflict prime effects were found to correlate with a measure of repressiveness in a similar previous study (Shevrin et al., 1992, 1996). Conscious symptom primes have no inhibitory effect when presented subliminally. Inhibitory effects with conscious symptom primes are present, but only when the primes are supraliminal, and they did not correlate with repressiveness in a previous study (Shevrin et al., 1992, 1996). We conclude that while the inhibition following supraliminal conscious symptom primes is due to conscious threat bias, the inhibition following subliminal unconscious conflict primes provides a neurological blueprint for dynamic repression: it is only activated subliminally by an individual's unconscious conflict and has an inhibitory effect specific only to the conscious symptom. These novel findings constitute neuroscientific evidence for the psychoanalytic concepts of unconscious conflict and repression, while extending neuroscience theory and methods into the realm of personal, psychological meaning.

**Keywords: anxiety, defense mechanisms, repression, alpha, EEG/ERP, avoidance, subliminal, neuropsychoanalysis**

#### **INTRODUCTION**

Oddly as psychoanalysis seems to diminish in the eyes of many, neuroscience appears to be taking a long second look at psychoanalysis. Interest and acceptance of an unconscious has been growing. Leading theoreticians have begun grappling with Freud's theory, even thinking of it as the most comprehensive available to psychiatry (Kandel, 1998, 1999), and offering the best account of recent neuroscience findings (Carhart-Harris and Friston, 2010). A growing number of psychoanalysts are going back to Freud's neuroscience roots, finding in his posthumous Project (1950) insightful anticipation of modern neuroscience concepts (Pribram and Gill, 1976). Some have suggested that neuroscience provides the basic science testing ground to avoid the circularity of many psychoanalytic explanations (Rubinstein, 1977). Yet there remain powerful obstacles on both sides to a true fruitful scientific exchange. The neuroscience investigation of the neural correlates of unconscious processes is often limited to automatic biases, ignoring the importance of unconscious conflict, the role of personal meaning, and unique unconscious processes like repression. In contrast, we present the unconscious that is subject to individual meaning (contained in the unconscious conflict unique to each individual), is comprised of complex unconscious emotional processing including repression, and plays a causative role in the manifestation of symptoms as in social phobias. Moreover, we show that these processes are instantiated in identifiable brain events.

Perhaps the two most controversial psychoanalytic clinical concepts are unconscious conflict and repression. On the basis of these two concepts psychoanalysts seek to explain a variety of psychiatric symptoms and how they can be successfully treated. Unconscious conflict is presumed to arise from opposing desires, working largely unconsciously and subject to unconscious efforts at inhibiting or repressing the conflict that can create great anxiety, shape how a person responds to the challenges of life, and can create a variety of psychiatric symptoms such as the social and specific phobias we have investigated.

Yet unconscious conflict theory is not the only theory of psychopathology psychoanalysts espouse. Psychoanalysts often refer to "conflict theory" as "classical" both in complimentary and pejorative ways. Adherents see it as the original Freudian theory; critics see it as essentially outmoded and replaceable by newer conceptualizations. These different theories all suffer from one fatal flaw-none have achieved the empirical support scientifically required to pass muster as an established scientific theory. Whether you select one theory or another is more a matter of preference than one based on defensible evidence (Rubinstein, 1977). We decided to exercise our preference for conflict theory mainly because it was historically the first and has lasted a considerable time; it was also the one we were best acquainted with by training and clinical experience.

Without doubt one of the most trenchant critics of Freud, Grunbaum (1984) has pointed out that empirical support must come from methods that can be shown to be independent of the clinical method, otherwise circularity is the ever present danger. In response to these challenges, we applied our research method in order to find independent evidence for the validity of the constructs of repression and unconscious conflict. At the same time we believed our research method is theory neutral and could be used by other theories to test their basic hypotheses.

Within psychoanalysis sharply critical voices along the same lines as Dr. Grunbaum have been heard as well. Outstanding theoreticians such as Rapaport (1959) have written extensively on these same issues. It is important to note that Rapaport's influence as a thinker and theoretician went beyond psychoanalysis. He was an early influence on Daniel Kahneman, as Kahneman (2003) noted in his Autobiography. Kahneman's monograph "Attention and Effort" contained a theory of attention as a limited resource to which Rapaport had originally led him (Kahneman, 1973, 2003). Kahneman also incorporated the concept of psychic energy, another important Rapaport theoretical preoccupation and central to Freud's concept of repression that Kahneman found useful and renamed effort (Kahneman, 1973, 2003). Kahneman was intending to spend more time studying with Rapaport; unfortunately Rapaport died prematurely at 50 before Kahneman could pay his return visit. Interactive contacts between psychoanalysts and cognitive and neuroscientists, as between Rapaport and Kahneman, have likely occurred a number of times, but were not sustained or further exploited.

Our research group set about some years ago to venture onto this difficult terrain. The tripartite approach was a natural next step from the senior author's previous research in which he was the first to report event related potential markers of subliminal unconscious processes (Shevrin and Fritzler, 1968), to demonstrate unconscious inhibition (Snodgrass et al., 1993a,b), and to devise methods for investigating two different modes of thought related to Freud's concepts of primary and secondary process: [Shevrin and Luborsky (1961), Brakel et al. (2000), see also Brakel and Shevrin (2003) for a comparison of Freud's theory of primary and secondary processes with more recent cognitive dual process theories].

Our early studies were designed as straightforward cognitive investigations incorporating subliminal and electrophysiological methods. What they all lacked was any clinical data from which the existence of unconscious processes and repression were inferred. The new method sought to correct this lack by including in depth interviews of patients who were also the research participants on whom the inferences derived from the interviews were tested. The initial study we conducted utilizing this tripartite method involved social phobic subjects (described in section The Initial Social Phobia Study: Establishing Clinical and Brain Evidence for Unconscious Conflict). A detailed account of the tripartite method and the encouraging findings emerging from this initial study were published in Consciousness and Cognition (Shevrin et al., 1992) and subsequently in a book length treatment including additional findings and three detailed case studies (Shevrin et al., 1996). The main objective of the initial study was to determine that our method would provide objective evidence for the existence of unconscious conflict; secondarily it was hoped that the data would also show a repressive cause and effect relationship between unconscious conflict and conscious symptom experience. This first study (summarized below in section The Initial Social Phobia Study: Establishing Clinical and Brain Evidence for Unconscious Conflict) succeeded with its primary objective, but results for the second were ambiguous at best. We realized that we lacked a neural correlate for the nature of the causal relationship between unconscious conflict and conscious symptom experience. A series of subsequent studies (summarized below Previous Studies With Spider Phobia: Alpha Power Serves as an Inhibiting Brain Mechanism in Phobic Experience) were aimed at investigating the role of alpha power as an inhibitory agent that might provide the neural causal link. Following the presentation of these two sets of earlier findings, we describe our new previously unpublished study (section The New Investigation: Establishing a Repressive Causal link Between Unconscious Conflict and Conscious Symptom Experience) replicating and extending these earlier findings, and we believe identifying the neural correlate we were seeking.

## **THE INITIAL SOCIAL PHOBIA STUDY: ESTABLISHING CLINICAL AND BRAIN EVIDENCE FOR UNCONSCIOUS CONFLICT**

The subjects were eleven social phobics who met DSM IV-R criteria. Four clinician judges selected individual words to be presented as stimuli for each subject. In a within subject design three groups of words were selected. The words were chosen individually for each subject to represent the unconscious conflict, conscious symptom experience, and a group of general negative valence words [see Shevrin et al.(1996, p. 139 Appendix B) for a detailed description of the word selection procedure]. The three word groups were equated for frequency, length, and part of speech (nouns and verbs). All words were presented subliminally and supraliminally. The brain responses were measured by timefrequency features derived from event-related potentials (ERPs). The essential idea behind time-frequency analytic approaches is simple: While standard ERP methods depict brain responses in two dimensions (time and amplitude), time-frequency methods add a third dimension—frequency. Time-frequency methods thus represent event-related brain responses as the frequency and amplitude (more accurately, power) present at each time bin on each trial, rather than only the amplitude at each time bin, as in usual ERP methods. "Time-frequency features," then, refer to points in this three-dimensional space. The application of time-frequency features was a relatively new approach to ERPs at the time pioneered by co-author Williams (Moser and Avnon, 1986; Williams et al., 1987, 1994; Cohen, 1989; Williams and Jeong, 1989, 1992; Zaveri et al., 1992). See Supplement 1 and Shevrin et al. (1992) for further description.

In this earlier study, we used discriminant analysis to select the t-f features which best differentiated the critical unconscious conflict and conscious symptom word stimulus categories (vs. general negative words). These disciminant analysis/classification findings were then internally cross-validated by performing a standard development vs. test set (i.e., odd vs. even-numbered trials) analysis. The t-f feature analysis and its use are explained in the book length presentation (Shevrin et al. 1996, p. 139 Appendix B).

The main finding was a significant two way interaction between word category (unconscious conflict vs. conscious symptom) and duration (subliminal vs. supraliminal). The brain responses to the unconscious conflict words were more correctly classified subliminally as compared to the general negative valence control; the reverse was found for the brain responses of the conscious symptom words (Shevrin et al., 1992, 1996). A second finding concerned repressiveness as measured by a Hysteroid-Obsessoid Questionnaire (HOQ) that the subjects completed. The HOQ is a self-report personality trait instrument originally developed to measure obsessive vs. hysterical personality styles (Caine and Hawkins, 1963; Caine and Hope, 1967). Psychoanalytic theory suggests repressive defenses should be prominent in those with the latter style. Further, earlier work (Ludolph, 1981; Shevrin et al., 2002a) found significant positive relationships between hysterical/repressive HOQ scores and various other indicators of repressive defenses (e.g., related indexes on the Rorschach). These two tests arrive at measures through largely different methods. Here, in the initial social phobic study, the HOQ predicted better classification of UC stimuli subliminally, but poorer classification of UC stimuli supraliminally. This finding suggested that an inhibitory repressive process was at work when the unconscious conflict words were presented supraliminally, inhibiting conscious recognition of their unconscious significance. The comparable correlations for the conscious symptom words and the control words were both non-significant (Shevrin et al., 1992, 1996). These two findings, inferred from clinical material by subjective clinical judgments, and hypothesized to be a cause of the symptom, were paralleled by objective time-frequency measures of unconscious processes.

The conflict stimuli selected were unique for each subject, a practice rare in cognitive research. Nevertheless, the positive results demonstrated that these different stimuli across subjects produced similar results (Shevrin et al., 1992, 1996). We further tested whether the unconscious conflict and conscious symptom words formed unique categories by scrambling the words across categories to form new pseudo-categories. We used an information flow measure (Kushwaha et al., 1992), an adaptation of Shannon-type information measures, to assess stimulusrelated information flow between pairs of electrodes. Although this measure cannot tell us what aspects of the ERP response (e.g., amplitude, frequency, etc.) are carrying this information, it does—critically—measure specifically stimulus category-related information (vs., e.g., other information flow analytic techniques which do not distinguish category-related vs. background activity). See Supplement 1 of the current manuscript for further explanation the information flow technique, and Kushwaha et al. (1992) for full details. Substantively, Kushwaha et al. found that significantly more stimulus related information flowed between electrodes for the true categories than for the pseudo-categories, convergently indicating that the former were indeed true categories. Additionally, we found greater information flow when the unconscious conflict words were presented subliminally as compared to supraliminally (Kushwaha et al., 1992).

The evidence from the first study with social phobics established the existence of unconscious conflict on the basis of clinical and independent non-clinical methods. It seemed clear that the unconscious conflict stimuli formed unique, individually meaningful categories. However, what was not clear is how these stimuli acted as causes of conscious symptom experience.

## **PREVIOUS STUDIES WITH SPIDER PHOBIA: ALPHA POWER SERVES AS AN INHIBITING BRAIN MECHANISM IN PHOBIC EXPERIENCE**

We then set about to investigate the link between unconscious conflict and conscious symptom experience. In our subsequent studies, we shifted our primary measure of physiological brain activity from time-frequency features to alpha power measures. We did so because much recent evidence had suggested that alpha power may be an important brain mechanism for inhibiting task irrelevant stimuli. For example, if the same frequency light was presented to each eye and the subject was instructed to pay attention only to the left eye, alpha power contralateral to the right eye increased significantly. Alpha power played a role in inhibiting attention to the right eye (Kelly et al., 2006). If this inhibitory function were generalizable it might provide the inhibitory function involved in repression. Charles Brenner, a leading psychoanalytic theoretician, had earlier hypothesized that psychodynamic defenses like repression were made up of normal cognitive functions that were put to specific unconscious motivational uses (Arlow and Brenner, 1964; Brenner, 1976, 1982). It would follow from this hypothesis that alpha power might provide the inhibitory function needed for repression, while the motivation for the inhibition would derive from the person's unconscious conflict. If so then alpha power might be the means by which to quantitatively measure the causal inhibitory link between unconscious conflict and conscious symptom experience.

We set about conducting a series of experiments with spider phobics. We presented phobic spider images and controls, subliminally and supraliminally. An FFT measured alpha power in the 8–13 frequency range. Subjects also completed a standard detection procedure with subliminal images, and rated their fear of spiders before and after the subliminal presentations (Shevrin et al., 2010; see Supplement 2 for the published poster abstract). Snake phobics served as a control for phobic state and rectangles served as a neutral stimulus control. In this study with spider phobics we did not assess unconscious conflict; our limited aim was to see if for spider phobics alpha power inhibited responses to spider stimuli and other spider related responses. If this turned out to be the case, then the inhibiting function of alpha power could be generalized beyond the purely cognitive inhibition of distracting or irrelevant stimuli to inhibiting relevant but emotionally disturbing stimuli. It might then approximate, from a psychoanalytic standpoint, a defense resembling repression once it could be linked to a related unconscious conflict.

The results were encouraging. Increased alpha power correlated with: (1) diminished attention to the phobic spider stimulus as reflected in smaller N100 amplitude and delayed N100 latency, (2) below chance (inhibited) detection of spider stimuli in a standard detection procedure, (3) greater self-reported levels of spider fear, (4) worsening spider fear after repeated subliminal exposure. Control results for snake phobics and rectangles for these comparisons were all non-significant (Shevrin et al., 2010; see Supplement 2 for the published poster abstract).

The results from this study with spider phobics demonstrated that alpha power went far beyond inhibiting attention to purely cognitively irrelevant stimuli. Rather, alpha power played an inhibitory role: (1) when the perceptual stimulus was emotionally significant (a feared spider), (2) when the task was to attend to an emotionally significant stimulus, (3) when the phobic stimulus elicited greater anxiety and fear, and (4) when multiple subliminal exposures did not decrease phobic spider fear. The finding that avoidance worked against improvement following multiple subliminal presentations of spiders suggested that the research might have treatment implications (Shevrin et al., 2010). It was as if the inhibitory process was flexible and not bound to a particular task. Rather, it served a specific unconscious motivation that could be imagined in these words, "I am afraid of spiders and I don't want to have anything to do with them. I will inhibit any process that increases the likelihood of exposure to spiders." When put in these terms it begins to sound like repression. Indeed, as cited previously, Brenner defined defenses from a psychoanalytic standpoint as a particular cognitive function linked to a particular motive. In this instance the particular cognitive function was inhibition associated with alpha power, and the motive was to avoid or minimize fear or anxiety with respect to spiders. These strong indications that alpha power may serve as the inhibitory brain mechanism of repression lead us to focus on the role of alpha power in the new, original study to be reported below.

## **THE NEW INVESTIGATION: ESTABLISHING A REPRESSIVE CAUSAL LINK BETWEEN UNCONSCIOUS CONFLICT AND CONSCIOUS SYMPTOM EXPERIENCE**

Much cognitive research had long called attention to the central role of avoidance in anxiety disorders. In our research we sought to demonstrate that avoidance was related to unconscious conflict and repression, and generalizable across many different tasks. Moreover, these processes could all go on unconsciously. It is notable that recently, Klimesch et al. (2011) have provided extensive cognitive neuroscience evidence that alpha power serves a general inhibitory function not limited, as heretofore believed, to distracting and irrelevant stimuli. Its inhibitory function can be applied to different tasks and stimuli determined by a variety of top down influences such as expectations. These considerations parallel our own conclusions reported in Shevrin et al. (2010).

In our first social phobia study (section The Initial Social Phobia Study: Establishing Clinical and Brain Evidence for Unconscious Conflict) we showed that unconscious conflict based on in-depth clinical data exists, but we could not claim that the evidence established a causal link between unconscious conflict and conscious symptom experience. In the spider phobia study (section Previous Studies With Spider Phobia: Alpha Power Serves as an Inhibiting Brain Mechanism in Phobic Experience; Shevrin et al., 2010) we showed how alpha power functioned to inhibit responses to a subliminal phobic stimulus on different tasks (e.g., attention, detection, etc.). From a psychoanalytic standpoint, the important missing piece in the spider phobic study was the underlying unconscious conflict creating the necessary motivation for inhibition or repression of spider stimuli. It seemed clear that now we needed to show that alpha power served as the causal neural link between unconscious conflict and clinically based conscious symptom experience.

According to psychoanalytic conflict theory (Freud, 1955, 1957, 1959; Brenner, 1982), neurotic disturbances are the consequence of a conflict of motives operating largely unconsciously. Any effort to investigate this proposition must: (1) infer from appropriate clinical material that a particular conflict causes a specific neurotic disturbance, (2) demonstrate that only when the conflict is activated via subliminal presentation (so that it is active outside of the person's awareness) does it produce an inhibitory response in the conscious neurotic disturbance, (3) show that when the unconscious conflict stimuli are supraliminal (so that they are processed consciously) they will not produce these inhibitory effects specific to the conscious neurotic disturbance, (4) ascertain that when control conscious experiences other than the specific neurotic disturbance are involved there will be no evidence of an unconscious conflict inhibitory effect either subliminally or supraliminally. To summarize: The relevant unconscious conflict specific to the neurotic disturbance has its inhibitory effect on the neurotic disturbance only when the unconscious conflict is activated subliminally, and only with respect to that neurotic disturbance (i.e., the conscious symptom stimuli). In short, the inhibition is unconscious and specific to the particular neurotic disturbance.

But why should the inhibitory repressive process triggered by the activation of unconscious conflict also lead to inhibition related to the conscious symptom experience? In the current experiment, the critical condition involves initially subliminally presenting words related to participants' unconscious conflict, rapidly followed by words related to their conscious symptom experience. These conscious symptom words describe the aspects of the social situation that are most anxiety provoking and fearful to the participant, as well as the physiological signs of anxiety the participant experiences in the uncomfortable social situation. In effect, the presentation of these words places the participant consciously into the dreaded socially feared situation. But—and this is critical—these social situations are dreaded precisely because they themselves also resemble the participant's unconscious conflict. If they did not, participants would not exhibit symptoms in response to such situations. This fact highlights a fundamental point—that conscious symptoms (taken together with the situations that trigger them) are related to and interconnected with the underlying unconscious conflict. The participant experiences social situations as if they contain an aspect of the unconscious conflict, although the participant does not realize that their unconscious conflict is influencing their conscious experience. For example, if the participant's unconscious conflict revolved around his relationship with his father (as suggested by example in Supplement 3), then the participant will experience certain social interactions in the same framework as he experienced his conflictual interactions with the father. Consciously, it becomes a struggle between enjoying the social occasion and tolerating increasing anxiety generated by its unconscious significance. Thus, from a psychodynamic perspective, repression must be directed from the activated unconscious conflict toward the social situation, or the most (unconsciously) conflictual aspects of it. Accordingly, attempts to inhibit and repress activation of the unconscious conflict should predict attempts to inhibit and repress responses to the conscious symptom stimuli. Therefore, we would expect to find a positive correlation between inhibition of unconscious conflict, and inhibition of the following conscious symptom reminders. By contrast, purely cognitive accounts, which lack any concept of unconscious conflict, would predict no relationship at all between the two kinds of stimuli.

The novel methodological innovation in this new study was to show that inferences drawn from entirely qualitative psychoanalytic clinical material can be tested by objectively measurable brain processes so that what is ultimately demonstrated is an underlying commonality of function between psychodynamic and brain processes.

The major change from the original experimental design of the first social phobia study was to shift to a priming model in which the unconscious conflict stimuli preceded the conscious symptom stimuli. A priming model allowed us to empirically assess the effects of the unconscious conflict stimuli on the following conscious symptom stimuli, and to scrupulously control for any potential confounding influences. In all other respects the design of this new study, presented in detail below, was exactly the same as of our first study, described in Shevrin et al. (1992).

## **METHODS AND MATERIALS**

#### **PARTICIPANTS**

Ten subjects (7 women, 3 men) who met DSM IV-R criteria for social phobia were selected. The subjects provided written informed consent prior to participation in the study. The study was approved by the University of Michigan Medical School Institutional Review Board (IRBMED) Ethics Committee.

#### **PROCEDURE**

After the participants had been selected, 3–4 hour taped diagnostic interviews were obtained from each participant and transcribed for examination and word selection [see Shevrin et al. (1996, 59–90) for details; Chapters 9, 10, 11 for detailed case studies]. This procedure yielded the Unconscious Conflict (UC) and Conscious Symptom (CS) primes, selected individually for each participant. Conscious Symptom (CS) word targets were also drawn from these interviews, and when such words appeared both as primes and targets they were always non-identical. A set of Osgood Negative Valence (ON) words, selected uniquely for each participant, served as the control (Osgood et al., 1975). For each of the word groups (UC, CS, and ON) judges selected seven words for each participant. The three word groups were equated for frequency, length, and part of speech (nouns and verbs). In Supplement 3, we present a sample set of words for each of the three categories of stimuli for one subject.

The selected words were presented tachistoscopically to the participants. The key experimental condition was subliminal unconscious conflict primes followed by supraliminal conscious symptom targets. This critical condition was embedded in a Prime Type (unconscious conflict vs. conscious symptom) × Target Type (conscious symptom vs. Osgood negative valence) × Prime Duration (subliminal vs. supraliminal) 2 × 2× 2 withinparticipants factorial design. Every presentation consisted of two words, the prime and the target, presented 1000 ms apart. All primes were presented subliminally as well as supraliminally, whereas the targets were always supraliminal. Each prime word was paired with every target word for a total of 196 subliminal and 196 supraliminal trials (e.g., unconscious word prime 1 was paired with all 14 CS and ON targets). All subliminal prime trials were presented first, followed by all supraliminal trials. Otherwise, prime–target pairs were randomized. Participants were simply instructed that at a prearranged signal they should fixate on a dot in the center of a blank field and not blink or move their eyes until signaled that the trial was complete.

The subliminal stimuli were presented for 1 ms duration, 10 ft/lamb.; supraliminal duration was set at 30 ms, 10 ft/lamb. These durations are much briefer than in typical subliminal studies. We used a Gerbrand Model 3-field Dodge-type tachistoscope, which is capable of much faster durations than a computer that requires backward masking to achieve subliminal presentations. Ambient light was set at 10 ft./lamb., matching the luminance of the stimuli [see Shevrin et al. (1996) for successful application of these settings].

#### **MEASURES**

EEGs were recorded from 10 electrodes (SCR, OB muscle, Corrugator muscle, F3, F4, CzPz, P3, P4, Oz, EOG) with reference to linked ears (A1 + A2). A 10–20 electrode placement system was used for application of electrodes. Silver-silver chloride electrodes were used with impedance kept below 5 K Ohms. Originally data was collected at 500 samples per second and then down sampled to half at 250 samples per second for 2 s and 400 ms. A total of 600 bins or 2400 ms of data were collected. Grass model 8 EEG machine was used to amplify EEGs and a hardware filter of 0.3–125 Hz was used. LabView on a Macintosh computer was used to digitize EEGs. Digitized data were then transferred to a LINUX PC for further analysis. MATLAB was used for doing FFT and Alpha band power calculations. Alpha power (8–13 Hz), calculated via the Fourier transform, was determined for the subliminal and supraliminal prime (1000 ms) and target (1000 ms) epochs post-stimulus for each trial, and then averaged within-condition (e.g., subliminal UC primes when followed by CS targets, etc.). For each participant there were a total of 49 trials averaged for each prime and target category. The experimenter visually inspected EEG recordings online for artifacts resulting from eye movement, muscle movement and 60 Hz. Trials containing such artifacts were rejected online. The stimuli were then repeated in the next trial and EEG data was re-recorded. Because we did not initiate trials until participants indicated their readiness and the ongoing EEG was artifact-free, very few trials (1–3%) needed to be repeated, and the proportions of such trials did not differ between conditions. Because the alpha power distribution was notably skewed across participants, alpha power was log-transformed before further analysis.

The measure of alpha power we used was absolute alpha power. We did not divide prime or target alpha by a baseline so the units in the figures simply reflect alpha power for both the *x*and *y*-axes. While some researchers divide post-stimulus alpha by a preceding baseline, others often simply analyze unmodified post-stimulus alpha power. Both methods are equally valid. For example, Cooper et al. (2003) and Kelly et al. (2006), cited as prior research for our own, found increases in absolute alpha power to play inhibitory roles.

#### **DATA ANALYSIS**

Our main interest was in examining the influence of prime alpha power on target alpha power. To this end, we analyzed prime influences using a regression approach in which alpha power for the two primes (UC and CS) were predictors, and target alpha power was the dependent (criterion) variable. The regression approach allows estimation and comparison of the unique (i.e., uncorrelated) abilities of the two prime types to predict target alpha. In contrast, in the more commonly used difference score approach (e.g., UC—CS primes) to examining prime-target relationships, it is not possible to examine the contributions of the UC vs. CS primes independently, thus leaving it ambiguous as to which of the two factors caused a positive result. Although not presented here, the main difference results from these data largely converged with the regression results presented below.

One might also maintain that the main analysis, rather than regression, should have been a comparison of mean effects in an ANOVA. In many situations analyzing the means is helpful. Here, however, such analyses are of secondary interest, because we are critically interested in the *relationship* between prime and target alpha (i.e., the predictive/causal relationships between the two). Further, correlations as in regressions are independent of means and mean differences. For example, mean 1 could be larger than mean 2, but this says nothing about whether scores in condition 1 are correlated with scores in condition 2. We have previously documented in our review (Snodgrass et al., 2004a), extremely subliminal conditions (i.e., wherein detection *d*- = 0) frequently yield exclusively *bidirectional* effects—that is, effects driven by individual differences but with no main (i.e., mean) effects. This is exactly the case with our data: An ANOVA on our data produced no mean effects, while the regression analysis was strikingly productive. For a comprehensive report of the data, we present means for all prime and target categories, as well as an ANOVA analysis in Supplement 4.

Because the subliminal vs. supraliminal prime duration manipulation is of great interest, we wished to analyze these conditions separately, so that any differences between subliminal vs. supraliminal effects would emerge. Regarding reporting R-square, often cited in regression analyses, in our case this would be uninformative or even confusing, for several reasons. First, we are only interested in possible differences in effects associated with UC vs. CS prime types (i.e., in regression language, their unique contributions to predicting target alpha). Such differences are captured precisely by the (unique) partial correlations currently reported in the text. In contrast, overall R-square reflects not only the predictors' unique contributions, but also any predictive contribution made by the predictors' shared (common) variance—and this variance is not of interest here. The current focus on unique prime type contributions to predicting target alpha removes these uninformative effects.

Our core hypothesis was that the degree of alpha power-related (i.e., inhibitory/repressive) brain activity in the UC primes should predict increased alpha power in the CS targets (i.e., signaling increased inhibition/avoidance), but not for unrelated ON targets. In keeping with our prior results from the first social phobic study (section The Initial Social Phobia Study: Establishing Clinical and Brain Evidence for Unconscious Conflict; Shevrin et al., 1992, 1996), this effect should manifest with UC subliminal but not UC supraliminal primes. In parallel fashion, any CS prime influences on CS or ON targets should manifest more strongly supraliminally than subliminally, an expectation based on the first social phobic study in which CS effects were only supraliminal (section The Initial Social Phobia Study: Establishing Clinical and Brain Evidence for Unconscious Conflict; Shevrin et al., 1992, 1996).

## **RESULTS**

Four separate regressions were performed: (1) Subliminal primes (UC, CS) with CS target; (2) Supraliminal primes (UC, CS) with CS target; (3) Subliminal primes (UC, CS) with ON target; and (4) Supraliminal primes (UC, CS) with ON target. We began by averaging across all six electrodes (F3, F4, CzPz, P3, P4, Oz).

## **UNCONSCIOUS CONFLICT PRIMES (UC): SUBLIMINAL AND SUPRALIMINAL RESULTS**

Subliminal UC prime alpha as hypothesized positively predicted CS target alpha, [*t(*7*)* = 2*.*47, *p* = 0*.*043, β = 1*.*08, partial *r* = 0*.*68]. (The scatter plot showing this central hypothesized relationship is presented in **Figure 1**.) By contrast, subliminal UC prime alpha had no effect on ON control target alpha [*t(*7*)* = 0*.*79, *p* = 0*.*45, β = 0*.*36, partial *r* = 0*.*29]. (The scatter showing an absence of an effect for this control condition is presented in **Figure 3**). When UC primes were supraliminal they no longer predicted CS target alpha: [*t(*7*)* = 0*.*74, *p* = 0*.*49, β = 0*.*28, partial *r* = 0*.*27], and had no effect on control ON targets [*t(*7*)* = −0*.*81, *p* = 0*.*45, β = −0*.*44, partial*r* = −0*.*29]. Thus, only when the UC primes were subliminal, and only when they preceded the CS targets did they produce an enhanced alpha effect.

## **CONSCIOUS SYMPTOM PRIMES (CS): SUBLIMINAL AND SUPRALIMINAL RESULTS**

Subliminal CS primes, unlike subliminal UC primes, did not predict CS symptom alpha [*t(*7*)* = −0*.*21, *p* = 0*.*84, β = −0*.*09, partial *r* = −0*.*08]. (The lack of a relationship in this control condition is shown in the scatter plot in **Figure 2**.) The subliminal CS primes also did not predict control ON target alpha

**the following conscious symptom target alpha.** Alpha power units are in squared microvolts, log-transformed. This graph includes measures averaged across all electrodes.

log-transformed. This graph includes measures averaged across all electrodes.

[*t(*7*)* = 1*.*38, *p* = 0*.*21, β = 0*.*63, partial *r* = 0*.*46]. Supraliminal CS primes came close to positively predicting CS target alpha: [*t(*7*)* = 1*.*81, *p* = 0*.*11, β = 0*.*70, partial *r* = 0*.*56], and did positively predict ON target alpha [*t(*7*)* = 2*.*62, *p* = 0*.*034, β = 1*.*42, partial *r* = 0*.*70]. Finally, given the similar results for supraliminal CS primes with both CS and ON targets, we also pooled both targets, yielding an overall near-significant result; [*t(*7*)* = 2*.*15, *p* = 0*.*069, β = 1*.*11, partial *r* = 0*.*63].

**FIGURE 3 | This figure shows that the relationship presented in Figure 1 is absent in another control condition.** Here, the conscious symptoms targets (as presented in **Figure 1**) are replaced with the control Osgood negative valence target. The graph shows the partial *r* between subliminal unconscious conflict prime alpha and Osgood negative valence target alpha. Alpha power units are in squared microvolts, log-transformed. This graph includes measures averaged across all electrodes.

#### *POST-HOC* **FINDINGS**

Upon examining parallel analyses for individual electrodes, we noticed an apparent frontal (F3, F4, CzPz) vs. parietal (P3, P4, Oz) pattern. We then averaged across these electrode subgroups. For economy of exposition we focus on the main results; other findings never approached significance and showed no frontal vs. parietal differences. These analyses suggested that the critical subliminal UC/CS finding was strongly present parietally: UC prime alpha [*t(*7*)* = 3*.*95, *p* = 0*.*006, β = 1*.*37, partial *r* = 0*.*81], but non-significant frontally: UC prime alpha [*t(*7*)* = 1*.*16, *p* = 0*.*28, β = 0*.*57, partial *r* = 0*.*40]. Conversely, the supraliminal CS prime findings were stronger frontally [CS target: *t(*7*)* = 2*.*33, *p* = 0*.*05, β = 0*.*65, partial *r* = 0*.*66; ON target: *t(*7*)* = 3*.*67, *p* = 0*.*008, β = 1*.*27, partial *r* = 0*.*81], but non-significant parietally [CS target: *t(*7*)* = 1*.*43, *p* = 0*.*20, β = 0*.*69, partial *r* = 0*.*48; ON target: *t(*7*)* = 1*.*27, *p* = 0*.*24, β = 1*.*01, partial *r* = 0*.*43]. Again we note the inverse reciprocal relationships between unconscious conflict and conscious symptom results as a function of category and duration, paralleling findings from the first social phobic study (Shevrin et al., 1992, 1996).

#### **BOOTSTRAP APPROACH REGRESSIONS**

While the above findings confirmed our key hypotheses, one might worry that regression methods with small samples such as ours could yield unreliable results. Bootstrap methods, which repeatedly reanalyze the sample data using random resamples, are a useful tool to check this concern because they nonparametrically estimate the sampling distribution using the actual sample data rather than relying on standard assumptions (Fox, 2008). Here, we reran our primary regression analyses, now incorporating related bootstrapping techniques. For all electrodes combined, the critical subliminal UC prime/CS target effect actually improved slightly (*p* = 0*.*018), while the subliminal CS prime/CS target effect remained non-significant (*p* = 0*.*79), as did both UC prime controls (subliminal UC prime/ON target, supraliminal UC prime/CS target), *p*s *>* 0.35. Further, the relevant univariate distributions and regression diagnostics indicated no outliers with these key effects, suggesting these findings were not distorted by this potential problem. Finally, the nonpredicted supra CS prime/CS target and supra CS prime/ON target effects also improved slightly (*p*s = 0.084 and 0.009, respectively). Overall, then, applying bootstrapping to the critical effects suggested they were reasonably stable.

## **DISCUSSION**

The pattern of results supported our main hypothesis for unconscious conflict. Only when the unconscious conflict primes were subliminal did they significantly predict conscious symptom target alpha power. The alpha effect was not present: (1) when the unconscious conflict primes were supraliminal, (2) when the conscious symptom stimuli were the subliminal primes (3) when the control Osgood Negative words were the supraliminal target stimuli. In short, there was only one condition in which the unconscious conflict primes were associated with enhanced alpha power: when the subliminal unconscious conflict primes were followed by supraliminal conscious symptom targets.

These findings strengthen the interpretation of a cause and effect relationship between unconscious conflict and conscious symptom experience. Of particular importance to supporting our hypotheses, we did not simply obtain some single, isolated finding consistent with this hypothesis. Rather, based on coherent, interrelated psychoanalytic theory relevant to our hypothesis, we predicted—and obtained—an interrelated *pattern* of findings, including not only specifying where we *should* obtain the predicted result (i.e., with subliminal UC primes and CS targets), but also where we *should not* obtain the result (i.e., with ON targets or with supraliminal UC primes). Notably, we obtained this entire pattern, strengthening the likelihood that the key results are genuine—and meeting specific recommendations by Grunbaum regarding testing this fundamental psychoanalytic causal hypothesis.

The one seemingly anomalous finding, not in itself central to our hypotheses, was the alpha power effect found for the supraliminal CS primes and the ON target alpha power. Since these results were not predicted, they may possibly represent a false positive finding. Nevertheless, one might wonder that if any inhibitory effects can occur with CS primes whether that challenges the specificity of the relationship between UC primes and repression. We deal in some detail with this troublesome issue below, calling attention in particular to the findings that CS prime inhibition never occurs subliminally, it is not correlated with repression in the initial social phobia study, and it does not cleanly discriminate between conscious symptom experience and the ON control targets [the near significant conscious symptom result (*p* = 0*.*11)], suggesting that the inhibition is directed at negative valence words rather than specifically directed at the CS primes.

From this pattern of converging experimental and control results we are in a position to infer that only the unconscious conflict stimuli selected *a priori* by psychoanalysts from clinical data *causally link clinical inferences based on psychological meaning* *(unconscious conflict over emotionally incompatible desires) with brain processes (patterns of electrophysiological inhibition).* If so, then to our knowledge this is the first *psychophysiological* evidence for Freud's unconscious conflict theory of psychopathology. Repression emerges as a function of these inhibitory patterns, as it does in the patterns of psychological avoidance and choice. From this standpoint, repression is not a neural or psychological "force," but a series of unconscious decisions creating a pattern of interactions with oneself and the world. That was what we found with the pattern of interactions for the unconscious conflict primes in the current study in which inhibition occurs subliminally, but not supraliminally.

Could alternative cognitive explanations account for some of the effects described in our results? The simple answer is that semantic priming would not predict any relationship at all between the unconscious conflict primes and the conscious symptom targets because the unconscious conflict primes do not constitute a semantic category at all, let alone one with any relation to the conscious symptom category. Indeed, as mentioned in the text, the participants in our earlier social phobia study themselves did not regard the unconscious conflict primes as a category when asked to consciously categorize the stimuli post-experimentally. On the other hand semantic priming accounts could explain the results involving the conscious symptom primes and conscious symptom targets, as these do constitute standard "related" categories. This is perfectly fine with us; we never thought such accounts would not apply to purely conscious symptom-related effects. Similar reasoning applies to emotionattention accounts; like semantic priming, they would predict no relationship between UC primes and CS targets (because the UC primes do not comprise a standard emotional category), but could account for relationships between CS primes and CS targets (which do). Furthermore, attentional blink phenomena require much shorter prime-target SOAs (c. 200–300 ms) than ours (c. 1000 ms), so this mechanism could not account for our results.

What is it that needs to be explained and further understood about the phobic experience and how would our findings based on psychoanalytic concepts advance that understanding? It is clear that the phobic experience is one of fear, anxiety, avoidance, at times revulsion and disgust. Most important is the general observation that the phobic person is aware that these reactions are not substantiated by the nature of the actual phobic object or situation. Moreover, there is no agreed upon explanation on how a phobia develops or is sustained. For the psychoanalyst there might be an answer to be found to these questions when the role of unconscious conflict is taken into account. Perhaps surprisingly, we learn that it is not the phobic object or situation taken in its literal significance that is the source of the phobic experience amply reflected in the conscious symptom accounts. Instead, it is the way these accounts are related in significance to unconscious conflict, so that the conscious symptom experience falls prey to the same repressive influences as are present in the unconscious conflict and are reflected in our key findings. The conscious phobic experience is transformed into a stage on which invisible actors reenact the unconscious conflict scenario, out of keeping with what is happening visibly. Thus, the repression triggered by the activation of the unconscious conflict, should in a similar manner be directed toward the conscious symptom experience. Our results support this understanding with new evidence drawing on brain based inhibitory processes, as well as clinically based accounts of unconscious conflict. However, the influence of unconscious conflict on conscious symptom formation, and the role of repression and inhibition in this process presents a complex system which may unfold differently in different situations, such as different psychopathology or different experimental measures. The exact mechanism of this complex relationship is for future research to determine. But our findings tell us that, beyond the immediate largely conscious avoidant reactions, there are important new parameters to be take into account, namely unconscious conflict and repression.

Two findings require further examination: (1) for the unconscious conflict primes to have an alpha power effect on the conscious symptom experience they must first be subliminal, (2) whereas the conscious symptom primes exercise alpha power effects only supraliminally.

#### **THE SUBLIMINAL CONDITION AND ALPHA POWER EFFECTS AT THE OBJECTIVE DETECTION THRESHOLD (ODT)**

At the beginning of the senior author's program of research on unconscious processes, he decided to present stimuli at the fastest duration possible with equipment available at the time. The tachistoscope was the equipment of choice because it could deliver reliably (checked by oscilloscope) a 1ms duration at moderate luminance (10 ft/candles). Under these conditions stimulus detection was at chance (50%). In a series of studies (Shevrin, 1973) replicable subliminal effects were obtained under these conditions.

Snodgrass in a series of subsequent studies (Snodgrass et al., 1993a,b, 2004a,b) combined a signal detection theory approach with Shevrin's earlier psychophysical method, making it possible to go beyond the limitations of classical psychophysics and assess accuracy separately from bias. This made it possible to obtain an accurate measure of the objective detection threshold (ODT) free of criterion bias at which detection (*d*- ) was not different from zero. Subsequent research revealed that at the ODT different things happen than at the supraliminal threshold. For example, in a series of replicated studies (Snodgrass et al., 1993a,b, 2004a,b), Snodgrass discovered inhibitory processes at the ODT that were a function of individual differences, findings quite germane to our current study. These effects were based on standard cognitive tasks (e.g., word choices). At the ODT different kinds of thought processes might be occurring. This was borne out in another study on language processing in which palindrome, or reverse word priming, was found at the ODT, but not in the supraliminal condition where only standard forward priming occurred (Villa et al., 2006a,b). The ODT may not only be the purest unconscious state our current methods can produce, but may also constitute a qualitatively different psychophysiological state susceptible to unconscious conflict activation. (It is also possible that similar findings might occur at other subliminal thresholds such as the subjective threshold at which *d*- *>* 0, but participants aver that they do not see the stimulus, hence subjective (Snodgrass et al., 2004a,b). This remains for future research to determine). These ODT findings raise the possibility that when the unconscious conflict primes are processed at the ODT they become sensitive to individual differences, among them, the inhibitory and repressive processes we have found that do not happen when the same words are processed supraliminally.

## **THE SUPRALIMINAL CONDITION AND THE CONSCIOUS SYMPTOM EXPERIENCE**

If the reasoning offered above for the unconscious conflict primes at the ODT is correct, why doesn't it also work for the conscious symptom primes when they are subliminal, but appear to work only when they are supraliminal? Here two findings from the initial social phobic study (section The Initial Social Phobia Study: Establishing Clinical and Brain Evidence for Unconscious Conflict) are pertinent. First, the repressiveness personality measure predicted t-f subliminal vs. supraliminal classification for the unconscious conflict primes only. This relationship was not found for the conscious symptom stimuli. Moreover, supraliminally the unconscious conflict primes were not significantly grouped together either by the t-f feature analysis or by participants' own category groupings. They simply did not form a category supraliminally (Shevrin et al., 1992, 1996). This was further confirmed by Kushwaha et al.'s (1992) information flow analyses, which showed that the unconscious conflict category showed more information flow subliminally than supraliminally, and more than control pseudo-category analyses. Thus, the unconscious conflict primes were a meaningful category only subliminally in the first study (section The Initial Social Phobia Study: Establishing Clinical and Brain Evidence for Unconscious Conflict), and it was only this category that had a significant subliminal alpha power inhibitory effect on the supraliminal conscious symptom targets, in the new, or second social phobic study (section The New Investigation: Establishing a Repressive Causal Link Between Unconscious Conflict and Conscious Symptom Experience). By contrast, participants in the initial study (section The Initial Social Phobia Study: Establishing Clinical and Brain Evidence for Unconscious Conflict) had no difficulty in treating the supraliminal conscious symptom primes as a category expressing what the participant had previously described as disturbing about the phobic experience. None of this could be said about the supraliminal unconscious conflict primes (Shevrin et al., 1992, 1996).

On these grounds it seems reasonable to suppose that the supraliminal conscious symptom words were overtly disturbing to the participants because they brought back the conscious social phobic experience itself. And when at the same time participants in the second study (section The New Investigation: Establishing a Repressive Causal Link Between Unconscious Conflict and Conscious Symptom Experience) were exposed supraliminally to other quite negative stimuli (other conscious symptom words or Osgood Negative words), participants would be disposed to respond with efforts at inhibition or avoidance, now completely conscious.

When we compare the *supraliminal conscious symptom prime condition* with the *subliminal unconscious conflict prime condition*, in both of which evidence for inhibition appears, differences are found that inform us of the difference between conscious and unconscious inhibition. For example, there is no evidence that the inhibition following the supraliminal conscious symptom prime condition has any of the characteristics of repression. In contrast, multiple sources of evidence point to an association between the subliminal unconscious conflict prime condition and repression. The unconscious conflict prime condition showed a relationship to the repression personality measure in the first study (section The Initial Social Phobia Study: Establishing Clinical and Brain Evidence for Unconscious Conflict; cf. Shevrin et al., 1992, 1996), as well as to an independent projective behavioral measure of repression, with both of these indexes of repression being highly correlated (Caine and Hawkins, 1963; Caine and Hope, 1967; Ludolph, 1981; Shevrin et al., 2002a,b). But at the heart of the matter is the second study's central finding that only the subliminal unconscious conflict primes activate the unconscious conflict; while the supraliminal conscious symptom prime condition activates the conscious phobic experience. This difference between what the participant is aware of fearing consciously and seeks to avoid consciously and what constitutes repressed unconscious knowledge related to these conscious fears lies at the heart of the psychoanalytic conception of psychopathology.

## **LIMITATIONS**

Although a substantial amount of prior work (cited above) supports the inhibition interpretation that we provide for alpha power, some (e.g., Palva and Palva, 2007) have suggested other functions of alpha. However, we note their position is based on phase-locked alpha, not non-phase-locked alpha as in our research and in the alpha/inhibition literature generally (e.g., Kelly et al., 2006). Also, Palva and Palva's alternative interpretation is specifically linked to supraliminal stimuli (see their p. 157, box), and is hence likely not applicable here in any case.

It also might have been useful to have here included a behavioral measure as an independent indicator of inhibition. We note, however, that our previous spider phobia study (Shevrin et al., 2010) suggested that greater alpha power was indeed associated with inhibited performance on a behavioral signal detection task. Nonetheless, our and others' future work would benefit from routinely including behavioral measures of inhibition. We also note that our stimulus materials (especially UC words), while balanced on many factors (frequency, length etc.), could not be balanced for all possibly relevant dimensions (e.g., arousal). This is a necessary limitation due to their completely individualized nature, a unique feature of this study perhaps essential to investigating the impact of intrinsically idiographic UC (and to a lesser extent, CS) stimuli—a fundamental goal of the current line of research.

Finally, our sample size is small, which raises potential statistical bias/instability issues with regression approaches such as ours. The bootstrap analyses, however, suggested our regression results were reasonably stable, and there was no indication of potentially distorting outliers. Nonetheless, because this is a small-sample single study, further replication with larger samples is needed to more firmly establish our conclusions. We plan such a larger-scale replication, which would additionally include other valuable data-analytic approaches such as single-trial analyses and robust regression methods, as well as a behavioral measure of inhibition.

## **FUTURE DIRECTIONS**

One future direction would take us to applied clinical research. We would expect that following successful psychodynamic, conflict oriented treatment, the same unconscious conflict prime words presented after treatment would no longer have an enhanced inhibitory effect on conscious symptom targets. It would no longer be needed. Another direction might take us into the curious inverse reciprocal relationship between conscious and unconscious processing as a function of threshold. We have suggested that this inverse reciprocal relationship can be understood as determining what is limited to conscious processing as contrasted with unconscious processing. From this standpoint the Snodgrass discovery of the ODT may open the door to investigations of the complex relationships between conscious and unconscious processing in normal and abnormal states.

Lastly, our findings may offer an opening for studying the neurophysiology of repression. The *ad hoc* results of the second study suggest that the repressive effect of the subliminal unconscious conflict primes is more closely associated with parietal alpha, while the alpha power effect of the supraliminal conscious symptom primes is more closely associated with frontal alpha. Also it seems that repression emerges as the outcome of complex interacting decisions and choices rather than as a punctiform cause acting at one particular time.

## **CONCLUSION**

We set out to seek evidence for a cause and effect relationship between unconscious conflict alpha power and conscious symptom experience. Our findings supported our hypothesis. Only when the unconscious conflict primes were subliminal did they have an inhibitory effect on the processing of conscious symptom targets, and this relationship was physiologically instantiated through inhibitory alpha power activity. The study also yielded unexpected findings concerning the effects of supraliminal conscious symptom primes. In both the initial and the new social phobic studies, the effects of conscious symptom primes and unconscious conflict primes appeared inversely related to each other. Specifically, in the new social phobic study, the unconscious conflict primes only produced inhibition when presented subliminally and only selectively for conscious symptom targets, while conscious symptom primes only produced inhibition when presented supraliminally, and did not discriminate between targets. We concluded that the supraliminal conscious symptom effects were due to conscious re-experiencing of the phobia with attendant efforts at conscious inhibition and avoidance, as occur in many cognitive phobia experiments. Only when subliminal unconscious conflict primes enter the picture is another level of meaning involved that engages repression. We can thus distinguish between conscious inhibition and unconscious repression, only the latter involving unconscious conflict.

#### **ACKNOWLEDGMENTS**

We would like to acknowledge the interest in our research by Professor Adolf Grunbaum, a foremost critic of psychoanalysis and a leading figure in the philosophy of science. Professor Grunbaum challenged our claim that our evidence in the first study demonstrated a cause and effect relationship between unconscious conflict and conscious symptom experience. In a subsequent exchange of letters the senior author accepted Professor Grunbaum's position. It was this agreement that led to the new study reported in the paper. There have been many contributors to the research and its execution whom we wish to acknowledge: James Bond, Richard Hertel, John Hartman (clinical judges); James Abelson, Ariane Bazan (co-authors of 2010 phobia study); ML Brown, (biosignal analysts); Beverly Knickerbocker, Adrienne Young (administrative assistant) who smoothed the way through many roadblocks, Brian Silverstein

## **REFERENCES**

*Int. J. Psychophysiol.* 47, 65–74. doi: 10.1016/S0167-8760(02)00107-1

(research assistant) for his able development of graphs and figures; An earlier version of this paper was presented at the *Conference on the Freudian Unconscious: Between Neuroscience and Psychoanalysis*, Lausanne Federal Polytechnical School, sponsored by the Agalma Foundation, Lausanne, Switzerland, on October 29, 2011.

## **SUPPLEMENTARY MATERIAL**

The Supplementary Material for this article can be found online at: http://www.frontiersin.org/Human\_Neuroscience/10.3389/ fnhum.2013.00544/abstract

sustained visuospatial attention. *J. Neurophysiol*. 95, 3844–3851. doi: 10.1152/jn.01234.2005

*B. Rubinstein, M.D., also Psychol. Issues Monograph 63, Originally published in Psychoanalysis and Contemporary Science, 4, 1975*, ed R. R. Holt (Madison, WI: International Universities Press), 273–324.

*Conscious. Cogn.* 1, 340–366. doi: 10.1016/1053-8100(92)90068-L

A. W. (2006a). Testing Freud's hypothesis that word forms and word meanings are functionally distinct: subliminal primary-process cognition and its links to personality. *Neuropsychoanalysis* 8, 117–138.

theory and applications," in *IEEE International Symposium on Circuits and Systems*, Vol. 2 (Portland, OR), 1243–1247.

**Conflict of Interest Statement:** The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

*Received: 02 April 2013; paper pending published: 23 April 2013; accepted: 19 August 2013; published online: 05 September 2013.*

*Citation: Shevrin H, Snodgrass M, Brakel LAW, Kushwaha R, Kalaida NL and Bazan A (2013) Subliminal unconscious conflict alpha power inhibits supraliminal conscious symptom experience. Front. Hum. Neurosci. 7:544. doi: 10.3389/fnhum.2013.00544*

*This article was submitted to the journal Frontiers in Human Neuroscience.*

*Copyright © 2013 Shevrin, Snodgrass, Brakel, Kushwaha, Kalaida and Bazan. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.*

## Addiction and will

## *Brian Johnson\**

*Department of Psychiatry, State University of New York Upstate Medical University, Syracuse, NY, USA*

#### *Edited by:*

*Henrik Kessler, University of Bonn, Germany*

#### *Reviewed by:*

*Claudio Colace, AUSL Viterbo, Italy Andrea Clarici, University of Trieste, Italy*

#### *\*Correspondence:*

*Brian Johnson, Department of Psychiatry, State University of New York Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA e-mail<EMAIL_ADDRESS>
A hypothesis about the neurobiological bases of drive, drive reduction and will in addictive illness is presented. Drive reduction seems to require both SEEKING and gratification. Will is the everyday term for our experience of drives functioning within us. Addictive drugs take over the will by altering neurotransmission in the SEEKING system. As a result of this biological change, psychological defenses are arrayed that allow partial gratification and reduce anxiety about the consequences of drug use. Repeated partial gratification of the addictive drive creates a cathexis to the drug and the drug seller. It also keeps the addicted person in a permanent state of SEEKING. The cathexis to the drug and drug seller creates a difficult situation for psychoanalytic therapists. The actively addicted patient will have one set of feelings for the analyst, and a split off set of feelings for the drug dealer. Addictive neuroses, which feature a split transference, are contrasted with Freud's concept of transference and narcissistic neuroses. For treatment of an actively addicted patient, the treater must negotiate the split transference. By analyzing the denial system the relationship with the drug dealer ends and the hostility involved in addictive behavior enters the transference where it can be interpreted. Selling drugs that take over the will is a lucrative enterprise. The addictive drug industry, about the size of the oil and gas industry worldwide, produces many patients in need of treatment. The marketers of addictive drugs understand the psychology of inducing initial ingestion of the drugs, and of managing their addicted populations.The neuropsychoanalytic understanding of addiction might be used to create more effective public health interventions to combat this morbid and mortal illness.

 *Toxoplasma* in the environment gain entry into the rat by skin contact. They multiply in brain and muscle tissue. The immune response of the rat results in cyst formation.

The pathways for the defensive and reproductive pathways run in parallel from the olfactory bulb to the medial amygdala and hypothalamus in close anatomical proximity (House et al., 2011). *Toxoplasma* cysts elaborate tyrosine beta hydroxylase, the ratelimiting enzyme in the pathway from the tyrosine in food to dopamine. Prandovszky et al. (2011) found that infected brain cell cultures had a threefold increase in dopamine compared to uninfected cells. Alteration in brain dopamine results in a subtle shift in behavior. Rats infected with *T. gondii* shift their behavior from fearing/avoiding cats to approaching them as if they were desirable mates. The rats get eaten by the cats.

The organism makes its way into its preferred host, the cat, by taking over the brain of the rat (House et al., 2011). The rat behaves normally in all ways except that instead of avoiding cats, it seeks them out. This behavioral change is not for the survival of the rat, but for the survival of the *T. gondii* parasite.

The goal of this communication is to ask the question about whether a homologous process in the human has to do with the sale of addictive drugs. Like the process involving *T. gondii*, the mechanism would involve the dopaminergic system. The conclusion would be that, like the rat serving the *Toxoplasma* organism, the behavior of a human taking addictive drugs into their brain has to do with the benefit of the drug seller; even at the cost of the life of the addicted human.

There is almost no clinical material in this paper. Psychoanalytic and neuropsychoanalytic treatment of addiction has been extensively presented by the author in numerous clinical papers covering alcohol (Johnson, 1992, 1993, 2003a, 2011), marijuana (Jones et al., 2005), cocaine (Johnson, 2009a), heroin (Johnson, 1999, 2001, 2010), nicotine (Johnson, 2003a), and drug dreams (Johnson, 2001, 2003b, 2006, 2012) including papers describing whole psychoanalyses with 9-year follow ups after treatment for alcohol addiction (Johnson, 2011) and heroin addiction (Johnson, 2010). After 10 mostly clinical papers, this discussion focuses on the general implications of concepts derived from the confluence of neuroscience and clinical psychoanalytic work.

## **DRIVE AND CATHEXIS: KEY CONCEPTS FOR ADDICTION NEUROPSYCHOANALYSIS**

Drive and cathexis are concepts that originated during Freud's pre-psychoanalytic period of neuroscience research (Compton, 1983a). Since then, the field has struggled with the problem of how to combine clinical observational data with theoretical constructs that involve a completely unconscious aspect of motivation. Freud originally identified drive as the engine of relatedness, the primary conceptual device in psychoanalysis for explaining mind, body, and environment relationships (Compton,1983b). For some

"fnhum-07-00545" — 2013/9/10 — 15:20 — page 1 — #1

psychoanalysts, the concept of drive has taken on the extreme opposite quality. For example, Aron (1999, p. 259) stated, "...The classical drive/structure metapsychology ... narrows our view of people, deprives them of subjectivity, and reduces them to objects. This limitation is true of any asocial, 'one-person' psychology."

On the other hand, drive or motivation has become a focus of the neuroscience approaches to addiction. For example, Kalivas and Volkow (2005, p. 1403) stated, "As the pursuit for the neural basis of addiction advances, it is clear that the search intimately involves understanding the neurobiological basis of motivation and choice for biological reward, such as food and sex, as well as more cognitively and experientially based reward, such as friendship, family and social status." Neuroscientists working in the field of motivation and volition have varying opinions as to the origin of motivation. Some reviews (Zhu, 2003; Haggard, 2008) look to cortical pathways as the initiators of actions. Others (Berridge, 2004; Kalivas and Volkow, 2005) focus on the dopaminergic pathway that leads from the ventral tegmental area (VTA) of the midbrain through the lateral hypothalamus to the nucleus accumbens as the central structural pathway involved in motivation. This is the SEEKING system (Panksepp, 1998).

In neuropsychoanalyst Jaak Panksepp's model, derived from his extensive experimentation with animals, the SEEKING system has the capacity to shift activity from one to another motivational system, depending on internal and environmental inputs. This supraordinate flexibility is exactly what Berridge (2004, p.201) cited against the drive model. "The most dramatic evidence against dedicated drive neurons came from studies of motivation by electrical brain stimulation... For example, if one stimulated the lateral hypothalamus of different rats, many rats might show eating behavior. But a few rats might show drinking behavior, a few show sexual behavior, or others show predatory aggressive behavior, depending on the availability of stimuli and on the disposition of the individual rat being stimulated." This phenomenon, that various motivated behaviors are prompted by one system, is exactly the concept of drive; a constant pressure from inside the organism to do work (Freud, 1915; Shevrin, 1997; 2003).

In an earlier contribution (Johnson, 2008) I considered addiction researchers Robinson and Berridge (1993), Berridge and Robinson (2003) distinction between "wanting" and "liking." In that paper I posited that Panksepp's SEEKING system is the same system that Freud (1915) hypothesized to exist deep in the brain, libidinal drive. My assumption was not based on a historical study. I was and am using Freud's thinking only because, in many cases, it is still the most perspicacious description integrating nomothetic neuroscience with ideographic psychoanalytic observation. I suggested that Freud's concept of the pleasure principle was connected to Panksepp's many observations of endorphin/opioid function in the brain (Panksepp, 1981, 1990, 1998, 1999; Panksepp and Watt, 2011, etc.). Importantly, the pleasure system is tied to the drive system via opioid receptors in the VTA and nucleus accumbens shell (NAS), where they potentiate glutamatergic and dopaminergic processes that intensify drive.

Using the SEEKING system to stand in for Freud's drive system obviates the objection that it excludes a focus on relatedness, since SEEKING and other instinctual systems, CARE, PLAY, LUST, and PANIC (Panksepp, 1998), offer a biologically based and much

more articulated set of instinctual drivers toward forming relationships. It gives us a model for clinical work that preserves Freud's concept of libidinal drive while responding to Aron's concern that drive produces an "asocial, one person psychology." We SEEK relationships. Panksepp's neuropsychoanalytic formulation of instinct, which is based in animal research, solves problems which could not be understood by an approach that is purely based on clinical experiences with patients.

Freud described "cathexis" as an initially mobile instinctual energy that could be bound to persons, body parts, ideas, or dream elements (Freud, 1920, p.34). In the 21st century we have information that allows us to describe the neuroscience of libidinal investment (Johnson, 2008). Dopamine is released in the nucleus accumbens of mother rats following pup exposure. VTA or nucleus accumbens (drive/SEEKING system) lesions disrupt maternal behavior (Insel, 2003). Dopamine (D1) receptors are necessary for rats to develop place conditioning for opioids. Opioid receptor antagonists block the development of partner preference in rats after mating. Both drive and pleasure need to be functioning to produce attachment. Without the drive of the dopaminergic system, there can be no libidinal investment. In order to form a sexual bond, rats have to remember that mating was a pleasant, not just a driven, experience.

Other neural systems are involved when animals come to prefer specific mates. Medial orbital frontal, amygdalar, and hippocampal memory inputs are involved. Hormonal systems interact with drive and pleasure systems. Oxytocin potentiates endorphin release during mating. Oxytocin is essential for partner preference, as has been demonstrated repeatedly in experiments comparing the prairie vole, which has an oxytocin system, with the montane vole, which does not (Insel, 2003; Johnson, 2008). Prairie voles form sexual partnerships, montane voles do not. In summary, cathexis has to do with an ensemble of drive, pleasure, memory, hormones – but there is no cathexis without drive.

One conclusion of the 2008 paper was that versions of the 1993 Robinson and Berridge distinction between wanting and liking had already been discovered by previous investigators. Freud had described it in 1920 in his essay, "Beyond the Pleasure Principle." Panksepp had shown the distinction between wanting and liking in his papers on the SEEKING and endorphin systems (Panksepp, 1981, 1990, 1998; Panksepp and Watt, 2011, etc.). But the main conclusion of the paper was that in biological or "physical" (Johnson, 1999, 2003b) addiction, addictive drugs had changed the drive system so that they were urgently wanted; whether intoxication was pleasant or not. This conclusion is an elaboration of the concept that is generally accepted in the neuroscience community that addiction begins with an alteration in the mesolimbic dopamine system (Hyman et al., 2006; Koob and Volkow, 2010). Addiction represents the usurpation of neural processes that underlie pursuit of food, water, sex, and relationships. Implicit was an idea about cathexis that will be developed below; cathexis for drugs or drug sellers can complete with cathexis for people who are loved.

#### **DRIVE REDUCTION AND DRIVE**

Why is the concept of drive reduction dead? I believe it is because Freud's thinking about this topic has been ignored by current neuroscientists. For example, when Berridge (2004) discussed why

"fnhum-07-00545" — 2013/9/10 — 15:20 — page 2 — #2

drive reduction had been disproved by animal experiments, he explained that animals who only SEEK will do it forever, and animals who are only gratified, for example by having caloric requirements satisfied by gastric feeding, were still motivated to pursue food. An important source of his confusion is the behaviorist term "reward," which conflates the concepts of SEEKING/drive and gratification. It is only by separating these two components of drive reduction that we can understand how they operate.

Freud gave the fullest description of drive reduction in his 1923 paper, "The Ego and the Id" (Freud, 1923, pp. 21–23).

"Internal perceptions yield sensations of processes arising in the most diverse and certainly also the deepest strata of the mental apparatus...they are more primordial, more elementary than sensations arising externally...

Sensations of a pleasurable nature do not have anything inherently impelling about them, whereas unpleasurable ones have it in the highest degree. The latter impel toward change, toward discharge, and that is why we interpret unpleasure as implying a heightening and pleasure a lowering of energetic cathexis...

This something behaves like a repressed impulse. It can exert driving force without the ego noticing the compulsion... Not until there is a resistance to the compulsion, a hold-up in the discharge reaction, does the 'something' at once become conscious as unpleasure...

The part played by word-presentations now becomes perfectly clear. By their interposition internal thought-processes are made into perceptions... We are all 'lived' by unknown and uncontrollable forces."

The ego's relationship with the id, "Is like a man on horseback, who has to hold in check the superior strength of the horse... Often a rider, if he is not to be parted from the horse, is obliged to guide it where it wants to go."

Drive reduction involves a combination of the rapacious, insistent drive building to a state where it demands satisfaction, and the pleasure of complete gratification. Both must operate sequentially for the drive to be reduced. Drive alone, in the case of addiction the constant drive for addictive drugs, is only increased by exposure to drugs. Once addicted, exposure to alcohol, cocaine, nicotine, or opioids causes a brief diminution of desire, followed by an increase of the urgent wish for the drug.

In the case of self-stimulation of the drive center (lateral hypothalamus), animals wired to be able to activate this area will push the "on" button constantly until they die. The unpleasure of briefly relieved drive apparently causes endless fruitless attempts to achieve drive reduction. In contrast, pure gratification without activation of SEEKING is in the end unsatisfying. Pornography addiction may be an example of gratification that is endlessly unsatisfying. Masturbation may be unsatisfying because it gratifies sexually without engaging the SEEKING system. Apparently, animals or humans who can't reduce drive by combining SEEK-ING and satisfaction sometimes endlessly engage in activities that activate only one or the other half of drive reduction.

We have taken as a hypothesis that drive involves activation of the ventral tegmental dopaminergic SEEKING system running from the midbrain through the lateral hypothalamus to the nucleus accumbens. A second hypothesis is that drive reduction requires both activation of the SEEKING system and gratification; food, sex, a relationship, something that requires work (Freud, 1915; Shevrin, 1997), and involves the complete relaxation of gratification. Addictive behaviors cause a brief and incomplete reduction of drive that result in endless drug seeking. The Freudian concept of will is necessary to understand how drive and drive reduction operate in the individual to change behavior.

## **THE CONCEPT OF WILL**

In the Project for a Scientific Psychology (aka "Psychology for Neurologists") Freud explained, "...in the interior...there arises the impulsion which sustains all psychical activity. We know this power as the *will* – the derivative of the drives" (quoted/translated by Schmidt-Hellerau, 2001, p. 61). The experience of drives operating inside us can impel us to do things that we do not consciously "want" to do. This often leads to an interpretation by the analyst that certain behaviors are, "intentional but not conscious." The reasons that we do things are often not apparent to us.

In fact, the lay term "will power" sometimes seems to exist as a denial of true intention. People will say things like, "I wanted to eat the whole pint of ice cream, but I exercised will power and only had half." Or even less consciously, "I really wanted to stay on my diet and I struggled not to eat all that ice cream, but I did it anyway; I ate that ice cream against my will." Much of the work of psychoanalysis has to do with patients becoming conscious of their real motives, what the true goals of their will is (Wheelis, 1956; The philosophical and psychoanalytic intersection of will and drive was reviewed in Young and Brook, 1994).

As Freud said so presciently, it is the repeated stimulation of neuronal pathways that leads to cathexis (Schmidt-Hellerau, 2001, pp. 54–58). The process of facilitation of neuronal pathways, leading to structural changes in the brain, would nowadays be referred to as long-term potentiation (Kandel, 2006). The combination of experience and brain changes under the influence of neurotransmitters, neuropeptides, and hormones leads to the development of interests that are different for every person (Johnson, 2008). In other words, inborn givens take shape and definition through the interaction with the social environment and establish patterns of maintaining contact and relatedness with others. This phenomenon of modulation of cathexis by a combination of innate biology, development, and experience means that every person is a little different in their tastes. The urgent needs generated by the drive system, once specific tastes in object and patterns of relatedness become fixed, are matched up against external reality. The degree of pleasure and fulfillment resulting from actualization of one's drives and cathexes lead to either gratification or neurotic frustration (Johnson, 2008). In the case where expression of will leads to frustration, individuals feel that their life is not going well and yet are often not be able to articulate where the problem lies.

Interpretation of conflicts between conscious and unconscious goals, often described as "neurotic conflict," is the constant occupation of any psychoanalyst. Meissner (2005, p. 28) discussed "intrasystemic id conflicts" involving motivational systems. One might love one's mother consciously, and yet also wish to destroy her unconsciously. Both urges could be described as id-driven. This conflict generates anxiety – a signal that there is trouble in a relationship (Freud, 1926; Watt and Panksepp, 2009). There is

"fnhum-07-00545" — 2013/9/10 — 15:20 — page 3 — #3

a conflict between the wish for additive drugs and the wish for relationships. Both could be characterized as id-driven.

In a typically parallel neuropsychoanalytic way, the intrasystemic id conflict of addiction can be seen psychologically and also neurobiologically. Psychologically, one might love one's mother consciously, and also unconsciously want to destroy her by destroying oneself with heroin. The use of addictive drugs can be understood as an unconscious expression of rage (Dodes, 1990). Neurobiologically, the conflict has to do with a conflict between urgently wanting a drug, and still wanting other goals of the drive system including a relationship with one's mother. The experience that the mothers of heroin users are wildly upset while the heroin user sees themselves is single-mindedly pursuing drug use, is an everyday experience on an addiction treatment service.

## **HOW THE WILL IS TAKEN OVER BY ADDICTIVE CHEMICALS**

There are only about 20 chemicals known to humans that alter the drive system so as to create a new drive (Johnson, 2008). These substances: alcohol, nicotine, benzodiazepines, opioids, stimulants, marijuana, phencyclidine, etc., all work by diverse mechanisms (Nestler, 2005), but with the same uniform end result. They cause sensitization of the ventral tegmental dopaminergic SEEKING system to the chemical (Robinson and Berridge, 1993). After sufficient exposure to the chemical, the person begins to want the drug; irrationally and insistently.

There is a triangle on the lower right half of **Figure 1** which shows the hypothesized mechanism of physical addiction for stimulant drugs. The corners of the triangle are the VTA, the NAS, and the prefrontal cortex. Cocaine and methamphetamine increase

"fnhum-07-00545" — 2013/9/10 — 15:20 — page 4 — #4

dopaminergic neural activation from the VTA directly to the NAS (Niehaus et al., 2009) by blocking the dopamine reuptake transporter protein. Nicotine has receptors on the VTA, and stimulates activating signaling from the amygdala (Nestler, 2005).