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Innovations

Psychother Psychosom 2007;76:141–153 DOI: 10.1159/000099841

How Does Our Brain Constitute Defense Mechanisms? First-Person Neuroscience and Psychoanalysis

a, c c b d Georg Northoff Felix Bermpohl Frank Schoeneich Heinz Boeker

a Department of Psychiatry, and Psychosomatics, University of Magdeburg, Magdeburg , and b c Department of Psychosomatics, Humboldt University Charité, Department of Psychiatry and Psychotherapy, d Charité-University Medicine Berlin, Berlin , Germany; Department of Psychiatry, University of Zurich, Zurich , Switzerland

Key Words tion in the neural network including the orbitofrontal, the Psychoanalysis Neuroscience Defense mechanisms medial prefrontal and the premotor cortices. In general sen- Neuronal integration Catatonia sorimotor regression and other defense mechanisms are psychoanalytic constructs that are hypothesized to be com- plex emotional-cognitive constellations. In this paper we Abstract suggest that specific functional mechanisms which inte- Current progress in the cognitive and affective neuroscienc- grate neuronal activity across several brain regions (i.e. neu- es is constantly influencing the development of psychoana- ronal integration) are the physiological substrates of defense lytic theory and practice. However, despite the emerging mechanisms. We conclude that first-person neuroscience dialogue between neuroscience and psychoanalysis, the could be an appropriate methodological strategy for open- neuronal processes underlying psychoanalytic constructs ing the door to a better understanding of the neuronal pro- such as defense mechanisms remain unclear. One of the cesses of defense mechanisms and their modulation in psy- main problems in investigating the psychodynamic-neuro- choanalytic psychotherapy. Copyright © 2007 S. Karger AG, Basel nal relationship consists in systematically linking the indi- vidual contents of first-person subjective experience to third-person observation of neuronal states. We therefore introduced an appropriate methodological strategy, ‘first- Introduction person neuroscience’, which aims at developing methods for systematically linking first- and third-person data. The The term ‘defense mechanisms’ was coined over 100 utility of first-person neuroscience can be demonstrated by years ago to describe a construct of psychological mecha- the example of the defense mechanism of sensorimotor re- nisms for coping with intrapsychic conflicts [1] (table 1). gression as paradigmatically observed in catatonia. Com- Defense mechanisms and conflict are two hypothetical bined psychodynamic and imaging studies suggest that constructs that have remained at the core of psychody- sensorimotor regression might be associated with dysfunc- namic approaches to understanding and treating clinical

© 2007 S. Karger AG, Basel Georg Northoff, MD, PhD, Laboratory for and Neurophilosophy 0033–3190/07/0763–0141$23.50/0 Department of Psychiatry, Psychotherapy and Psychosomatics Fax +41 61 306 12 34 Otto von Guericke University Magdeburg, Leipzigerstrasse 44 E-Mail [email protected] Accessible online at: DE–39120 Magdeburg (Germany) www.karger.com www.karger.com/pps Tel. +49 391 671 4234, Fax +49 391 671 5223, E-Mail [email protected] Table 1. Defense mechanisms: hierarchy of mature/cognitively oriented and immature/emotionally driven mechanisms of defense ac- cording to psychoanalytic theory

Mature/cognitively oriented mechanisms of defense Immature/emotionally driven mechanisms of defense Intellectuali- Dealing with emotional stressors by excessive Somatization Dealing with emotional stressors by physical zation use of abstract thinking or complex explanations symptoms involving parts of the body innervat- to control or minimize disturbing feelings. ed by the sympathetic and parasympathetic sys- tems. Rationalization Dealing with emotional stressors by inventing a socially acceptable or logical reason to justify an Derivatives of self/nonself loss of boundaries already taken unconscious emotional action. Dissociation Temporary and drastic modification of one’s self-image to avoid emotional distress. Discon- Repression Moving thoughts unacceptable to the ego into nection from full awareness of self, time and/or the unconscious, where they cannot be easily ac- external circumstances. Often connected with cessed. childhood trauma and posttraumatic stress dis- Displacement Dealing with emotional stressors by redirecting order. emotion from a ‘dangerous’ object to a ‘safe’ ob- Projective Repeated cycle of projection and introjection: ject. identification hateful impulses are projected onto the signifi- Isolation Dealing with emotional stressors by splitting off cant other who becomes the bad object. Some of the emotional components from a difficult the bad impulses are still retained in the self; they thought. The mechanism of isolation is com- are reinforced by taking into one’s self, introject- monly overutilized by people with obsessive- ing, what has originally been projected onto the compulsive personalities. object. Reaction Dealing with emotional stressors by converting Psychotic Psychotic internalization of the object to over- formation an uncomfortable feeling into its opposite. introjection come overwhelming anxieties of loss. Identification Occurs in various stages of development, in par- Psychotic Hallucinatory and paranoid externalization of ticular in its role as an intrinsic part of object projection inaccessible thoughts and their connected af- relationships. Serves the function of structure fects. building and makes it possible to deal with sepa- Splitting Splitting off and rejecting parts of the object im- rations from loved objects. Plays a role in some age and/or of one’s own body. types of conversion. Fragmentation Reflects a primitive stage in psychic develop- Identification By becoming an aggressor towards others, one ment, preceding the formation of part self and (with the avoids becoming a victim of aggression. part object images. Breaking up of the self or the aggressor) object image into components which may oper- Idealization Dealing with emotional stressors by overesti- ate independently. mating the desirable qualities and underestimat- Denial Dealing with emotional stressors by failing to ing the limitations of a desired object. recognize obvious implications or consequences Introjection Dealing with emotional stressors by internaliz- of a thought, act or situation. ing the values or characteristics of another per- Catatonia Psychomotor syndrome showing a specific con- son; usually someone who is significant to the stellation of affective, behavioral and motor individual in some way. symptoms. Sensorimotor regression reflecting Projection The opposite of introjection. Attributing one’s an immature mechanism against the uncontrol- own emotions or desires to an external object or lable overflow of anxieties. person. Autism Extreme withdrawal and avoidance of contact and interpersonal relationships to overcome overwhelming anxieties of losing one’s own self when near the object.

psychopathology. From a psychoanalytical perspective, other. Through specific constellations of affective and defense mechanisms mediate between an individual’s cognitive function, defense mechanisms help resolve wishes, needs and affects on the one hand, and both in- conf licts, whether triggered by internal or external stress- ternalized object relations and external reality on the ors. One could therefore hypothesize that defense mech-

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anisms are complex emotional-cognitive constellations. in emotional-cognitive interaction, which Westen and As such, the recent progress in affective and cognitive Gabbard [13, 14] consider to be crucial in conflict and neuroscience [2–5] raises the question of their underlying compromise. However, despite these studies and the cru- neuronal processes, which, in turn, could also contribute cial role of defense mechanisms in psychoanalytic theory to a more refined and detailed definition of the construct and practice, their underlying neuronal mechanisms re- of defense mechanisms. However, the dialogue between main yet to be explored. psychoanalysis and neuroscience has only recently One of the main methodological challenges in inves- emerged [6–21] . tigating the neuronal processes underlying defense mech- The reception of neuroscience by psychoanalysts rang- anisms is to link first- and third-person data. Being based es from strong skepticism to equally strong enthusiasm. upon subjective experience, psychoanalysis relies on first- Skeptics [22–24] doubt that there can be common con- person data. This contrasts with neuroscience, which re- ceptual grounds for linking the hypothesis about uncon- quires third-person observation of neuronal states. Due scious aspects of the mind (as advanced by psychoanaly- to the neglect of subjective first-person experience, neu- sis) and knowledge about the brain (as framed by neuro- ronal states as third-person data can be quantified and science). They claim that the complexity and richness of objectified. This, in contrast, remains impossible in the subjective human experience can become lost in empiri- case of first-person data (see below for discussion of po- cal neuroscientific investigation. Another argument, as tential criticisms of the concept of first-person data), put forward by Gruenbaum [25] , is that possible psycho- which are rather qualitative and subjective. If, however, dynamic processes cannot be attributed causal relevance the neuronal processes of defense mechanisms are to be in the same way as other scientifically investigable pro- investigated, subjective experience and neuronal states cesses. This makes it rather difficult to empirically test (i.e. first- and third-person data) have to be linked to each and validate psychodynamic processes such as defense other in a systematic way. For this purpose we created an mechanisms. Moreover, skeptics have recently argued appropriate methodological strategy, ‘first-person neu- that it remains impossible to associate the complex sub- roscience’, which aims at systematically linking first- and jective experience with neuronal activity in specific brain third-person data (see below for a discussion of the dis- regions; they thus argue against neuronal localizationism tinctive features of first-person neuroscience when com- of psychodynamic processes [22] . Our answer to these pared to neuroscience and as usually prac- challenges is the following. ticed). After describing first-person neuroscience, the Those endorsing the integration of psychoanalysis and utility of this methodological approach will be paradig- neuroscience usually refer to Freud’s 1895 project, in matically demonstrated by means of the example of sen- which he sought a unitary conception of mind and brain sorimotor regression as observed in patients with catato- [26] . Kandel [10] recently articulated the hope ‘that biol- nia. ogy might reinvigorate the psychoanalytic exploration of Considering sensorimotor regression and other de- the mind’. He emphasized the need for combined re- fense mechanisms, it becomes clear that first-person search approaches in psychopathology (implicit and ex- neuroscience requires a shift from neuronal localization plicit memory, development, etc.) and psychotherapy [17, to neuronal integration: instead of localizing particular 27–29] . This led some authors to investigate the neuronal defense mechanisms in specific brain regions, we hy- mechanisms of psychodynamic processes. For example, pothesize that defense mechanisms might rather corre- emphazising the developmental features of the right or- spond to specific functional mechanisms of integrating bitofrontal cortex, Schore et al. [7, 8] propose neurobio- neuronal activity across several brain regions. We con- logical mechanisms of unconscious processes such as clude that the methodological approach of first-person projective identification. Based on psychoanalytic treat- neuroscience in association with neuronal integration ment in patients with orbitofrontal cortical lesions, Solms might eventually open the door to greater knowledge [6] and Solms et al. [30] make inferences about the local- about the neuronal mechanisms of the various defense ization of early, immature and somatic defense mecha- mechanisms and their modulation in psychoanalytic nisms. Furthermore, Northoff et al. [20] were able to link psychotherapy. sensorimotor regression, as observed in catatonic pa- tients, to a complex neural network including the orbito- frontal, medial prefrontal and premotor cortexes (see be- low for details). The orbitofrontal cortex also plays a role

How Does Our Brain Constitute Defense Psychother Psychosom 2007;76:141–153 143 Mechanisms? Investigation of first-person data, i.e. the person’s subjective experience

Experiencing person

Psychoanalysis

Methods for the systematic linkage First-person neuroscience between first- and third- person data

Commonly practiced neuroscience

Fig. 1. Psychoanalysis and neuroscience: linkage between subjective experience and Investigation of third-person data, i.e. neuronal states in first-person neurosci- the person’s neuronal states ence.

What Is First-Person Neuroscience? person neuroscience, as we understand it here, aims at preserving the individual contents of the psychological Definition of First-Person Neuroscience states, as obtained from the first-person perspective – We define ‘first-person neuroscience’ as a method- this has been called the ‘ideographic approach’. The dif- ological strategy to systematically link subjective first- ference between first-person neuroscience on the one person experience 1 to third-person observation of neuro- hand and third-person neuroscience and psychology on nal states [3, 32–34] . The development of such methods the other thus consists in the difference between the ideo- distinguishes first-person neuroscience from neurosci- graphic and nomothetic approaches, i.e. in whether the ence as it is commonly practiced, which most often relies individual contents are preserved or not. on third-person observation of neuronal states more or The main challenge in establishing first-person neu- less independently of subjective experience ( fig. 1 ). First- roscience, however, does not only consist in pursuing an person neuroscience should also be distinguished from ideographic approach to account for individual contents psychology. Though psychology considers data from the as subjectively experienced in the first-person perspec- first-person perspective as well, for example in the case of tive. An even more demanding challenge is to link the emotional feelings, as in the case of third-person neuro- individual contents of subjective experience to neuronal science, it too relies on third-person observation of psy- states. How can we link subjective experience to neuronal chological states. This means that the individual contents states? The linkage between subjective experience and of psychological states are lost. Such generalization inde- neuronal states requires two steps: (1) subjective experi- pendent of individual contents presupposes what has ence needs to be evaluated systematically, including ob- been called the ‘nomothetic approach’. In contrast, first- jectification and quantification of subjective data – such ‘science of experience’ is a necessary precondition for any

1 linkage between subjective experience and neuronal It should be noted that this also includes introspection of the individ- ual’s own subjective experience. Introspection of subjective experience has states; (2) the systematically objectified and quantified been linked to the second-person perspective, as distinguished from sub- subjective data then enable the linkage to analogous data jective experience itself in the first-person perspective [31–33]. However, about neuronal states. For this, special methodological for pragmatic reasons we refer to introspection and second-person per- spective under the terms ‘subjective experience’ and ‘first-person perspec- strategies need to be developed – this is the core of what tive’, using both in a broader sense. we call ‘first-person neuroscience’: ‘It would be futile to

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stay with first-person descriptions in isolation. We need instrument is the Operationalized Psychodynamic Diag- to harmonize and constrain them by building the appro- nostic (OPD; Arbeitskreis OPD 2004), which, based on priate links with third-person studies. … To make this ICD and DSM, develops five psychodynamically relevant possible we seek methodologies that can provide an open axes (illness experience and expectations, relationship, link to objective, empirically based description’ [35, 36] 2 conflict, structure, and psychic and psychosomatic dis- (fig. 1). turbances). More specific instruments are scales for quantifying defense mechanisms, e.g. the Defense Mech- Science of Psychodynamic Processes anism Rating Scale [45, 46] or the Defensive Style Ques- The systematic examination and evaluation of subjec- tionnaire 40 [47, 48], and psychodynamic psychopathol- tive experience must preserve its richness and complex- ogy in personality disorders (Shedler-Westen Assessment ity on the one hand and objectively quantify its main Procedure 200 [49, 50] ). The functional status of different characteristics on the other 3 . The objectification and psychopathological phenomena as mechanisms of de- quantification of subjective first-person data allows for fense and compensation has been highlighted by several scientific investigation and consequently for establishing former studies (e.g. [51–55] ). what can be called a ‘science of experience’ [40] 4 . Based A potential point of criticism of such science of psy- on a science of experience, a ‘science of psychodynamic chodynamic processes, relying on ideographic approach- processes’ needs to be developed. The science of psycho- es, is that the individual contents from the first-person dynamic processes should place great emphasis on pa- perspective cannot be considered ‘data’ in the way that tients’ mental life or inner experience in order to preserve this term is understood in science. For example, Met- the richness and complexity of subjective experience and zinger [56] argues that the concept of data implies their clinical description [12, 41] . At the same time, these sub- generalizability to groups, their possible validation in an jective features must be objectified to provide reliable and intersubjective process, their extraction by technical quantifiable data. This can be achieved by asking the sub- measuring and their linkage to public procedure. He sub- jects to complete rating scales. For example, visual analog sequently considers first-person data, the individual con- scales [33, 34, 42] with regard to personal identity or id- tents as subjectively experienced from a first-person per- iographic instruments like the Repertory Grid test (see spective, as a fusion of ‘semantic elements with a concept below for further details) might be applied to let the sub- borrowed from the theory of science’ [56]. However, we jects themselves evaluate their experiences. One might do not consider this argument as applicable to the science also apply structured with valid and reliable of psychodynamic processes for the following reasons: instruments for the evaluation of the subjects’ relevant individual contents which are central in psychodynamic psychodynamic features by an experienced investigator. processes can indeed be generalized to groups by com- General instruments include, for example, the Karolins- paring the similarities and differences of individual con- ka scale that assesses different psychodynamically rele- tents between different individual subjects. One of the vant dimensions of a person’s structure [43, 44] . Another main features of psychodynamic theory is that it was able to reveal the same individual contents and structures of psychological processes across different individuals. As 2 the above examples of operationalization demonstrate, it If the ‘science of experience’ is not related to the ‘science of observation’ and thus neuroscience, the former degenerates into ‘first-person mentosci- is quite possible to validate and objectify individual con- ence’, which is occupied with mental states exclusively, without any relation tents in psychological processes. Though not requiring to neuronal states [32, 33, 37] . 3 An interesting development in this respect is the emergence of what has technical measures, it can be considered a public proce- been called ‘clinicometrics’, as distinguished from . Clinico- dure. Thus, in view of these arguments, individual con- metrics arises from clinical observation, clinical methods and clinicians in tents of psychological processes can be understood as its attempt to link clinical phenomena and subjective experience [38, 39] . In contrast psychometrics incorporates methods where all variables have data in the scientific sense. This enables us to refer to the same weight. first-person data characterizing the subjective experience 4 Varela and Shear [35, 36] also refer to ‘first-person methodologies’ in of individual contents. The purpose of our present paper this context. The difference between first-person methodologies and our concept of first-person neuroscience is that only the latter aims at devel- is not to create new methodological approaches but to oping methods to systematically link first- and third-person data, whereas combine existing ones in such a way that it is possible to the former concerns only the quantification and objectification of subjec- link first-person data, characterizing individual contents tive experience, i.e. of first-person data, thus aiming at the development of what we called ‘science of experience’, as distinguished from neuroscience of subjective experience, and third-person data, account- as ‘science of observation’. ing for neuronal states. We believe that this could not

How Does Our Brain Constitute Defense Psychother Psychosom 2007;76:141–153 145 Mechanisms? only provide insight into the underlying neuronal states of neuronal localization we pursue the concept of neuro- but also reveal, diagnose and possibly define psychody- nal integration. Accordingly we have a somewhat critical namic processes in relation to specific individual con- view concerning the nature of defense mechanisms. We tents more clearly and in more detail. This, however, re- therefore prefer to consider them as constructs (see above) mains a scenario of the future. awaiting further psychological and neuronal validation. To avoid misunderstandings, it has to be pointed out that we do not intend to handle defense mechanisms as if they were facts in the same way as, for example, assump- How Can We Investigate the Neuronal Processes of tions about neuronal states. We consider defensive reac- Defense Mechanisms? Sensorimotor Regression in tions as constructs 5 which need to be investigated em- Catatonia pirically, both psychologically, as for example in opera- tionalization scales, and neuronally, as for example by Defense Mechanisms in Disorders: Catatonia and first-person neuroscience. Defense mechanisms – as part Sensorimotor Regression of the psychoanalytic theory – cannot be considered Catatonia is a psychomotor syndrome showing a common psychological functions (as can be, for instance, unique constellation of affective, behavioral and motor working memory, attentional shift, etc.) because, unlike symptoms [58–63] . Acute catatonic patients are totally these functions, they are inherently associated with indi- immobilized, adopting a bizarre posture and becoming vidual contents that are subjectively experienced. Instead, totally mute. Psychodynamically, bizarre motor behavior defense mechanisms are supposed to reflect structures has been interpreted as sensorimotor regression reflect- and processes according to which individual contents of ing an immature and emotionally guided defense mecha- subjective experience are organized across different indi- nism against the uncontrollable overf low of anxieties, i.e. vidual subjects. For example, different individual con- ‘immobilization by anxieties’ [61, 62, 64]. At the same tents of subjective experience might correspond to dif- time more mature and cognitively guided defense mech- ferent defense mechanisms, for instance to more mature anisms like internalization and externalization seem to and cognitively oriented ones or to rather immature and break down in the patients’ handling of their emotional emotionally driven ones (table 1). As such, defense mech- conflicts [65, 66]. According to psychodynamic theory, anisms can only be accounted for by what we called first- unlike schizophrenic patients, catatonic patients are no person data (see above) as distinguished from third- longer able to develop paranoid ideas with respect to their person data. Bearing in mind the methodological short- environment and thus to externalize their emotional comings and problems in operationalizing defense conflicts. Unlike affective patients, catatonic patients re- mechanisms and defining the concept of first-person main unable to attribute emotional conflicts to them- neuroscience, we consider our paper to be a preliminary selves and express them, for example, in ideas of guilt and and speculative attempt to explain defense mechanisms sin and thus to internalize them [66] . These cognitive in psychological and neural terms. mechanisms of internalization or externalization are ap- In this paper we aim to seriously confront the criticism parently no longer available for catatonic patients, whose of empirical validation of psychodynamic processes. One sensorimotor regression aims at compensating for their main point of criticism is that defense mechanisms can- overwhelming anxieties [65–67] . In the following, our not be validated in the same way as other scientific data own findings in catatonia are presented. They will be dis- (see for example Gruenbaum [25] in the ‘Introduction’ cussed in the various sections concerning neuronal inte- section). Our answer to this is the development of first- gration. person methods such as the operationalization of first- person data. Another point of criticism is that defense Methods: Psychodynamic and Biological mechanisms cannot be localized in particular brain re- Measurements of First-Person Psychological Processes gions. In reply to this we would like to state that instead We applied the Role Construct Repertory Grid in cata- tonic and noncatatonic psychiatric patients, as well as in healthy subjects (see [20] for details). The Role Construct 5 Whether defense mechanisms, though being constructs, can be con- Repertory Grid is an idiographic instrument accounting sidered universal of human nature, as is claimed in the case of language, for psychological characteristics from a subjective point for example [57] , is a question to be answered by future investigation. Although psychoanalysis would certainly claim so, it has yet to be con- of view [68–71] . It is based on a semistandardized, opera- firmed. tionalized and validated methodology, combining intra-

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subjective self-appreciation with intersubjective catego- Results: Grid and fMRI rial evaluation [68–71] and thus enabling the nomotheti- The Grid test, which was applied after significant re- cal use of idiographic data by means of different covery from the acute symptoms, revealed that catatonic mathematical-statistical procedures. This methodology patients characterized themselves by the terms ‘low emo- was developed in the context of the psychology of per- tional arousal’, ‘low self-esteem’ and ‘lack of social con- sonal constructs [72, 73]. The psychology of personal tact’ in both the acute and postacute states. The imaging constructs [69] follows the assumption that subjective ex- results showed an altered pattern of signal changes in the periences of the self and other persons are actively cre- medial orbitofrontal cortex [MOFC; Brodman areas (BA) ated or constructed and that therefore certain related psy- 11 and 12 ] and lateral orbitofrontal cortex (LOFC; BA 11, chological characteristics are manifest, which, in turn, 47) in catatonic patients compared to noncatatonic psy- determine personal constructs. These psychological chiatric and healthy controls. Specifically, we observed characteristics include various emotional and cognitive reduced signal changes in the MOFC (BA 11, 12) and en- functions whose particular ways of interacting might hanced signal changes in the LOFC (BA 11,47) during correspond to different defense mechanisms. Personal negative stimulus presentation (see [32, 33] for details). constructs might subsequently be well suited to give in- Analysis of functional connectivity revealed abnormal sight into the first-person experience of psychological connections from the orbitofrontal to the medial prefron- mechanisms associated with defense mechanisms. tal cortex (BA 8, 10) and to the premotor (BA 6) and mo- In addition to the Repertory Grid, we used functional tor cortex (BA 4) in catatonic patients when compared to magnetic resonance imaging (fMRI) to investigate cata- noncatatonic psychiatric and healthy controls. tonic patients, noncatatonic psychiatric control patients Correlation analysis between Grid and fMRI results (bipolar depressive, unipolar depressive, unipolar manic revealed the following specific findings in catatonic pa- and schizoaffective) and healthy subjects during emo- tients: emotional arousal and self-esteem correlated sig- tional stimulation with a motor response (see [32, 33] for nificantly with signal changes in the MOFC (BA 11, 12). details). In this paradigm the subjects viewed emotional In contrast the dimension of social contact correlated sig- pictures and had to give an immediate response to the nificantly with motor symptoms as well as with signal picture by the arbitrary pressing of buttons. The focus of changes in the orbitofrontal and medial prefrontal cortex our analysis was on those regions presumed to be in- (BA 8, 10) and their connectivity to the premotor cortex volved in emotional (orbitofrontal and medial prefrontal (BA 6). cortex) and motor (premotor and motor cortex) process- ing. Moreover we performed an analysis of functional connectivity between these regions [32, 33] . Finally we What Is Neuronal Integration? correlated signal changes in the relevant regions with catatonic symptoms and results from the Repertory Grid Neuronal Integration: Organization of Neuronal test to determine the relationship between psychological Activity across Different Regions characteristics and regional neuronal activity in cataton- Neuronal integration describes the coordination, or- ic patients. One should be aware that other paradigms ganization and adjustment of neuronal activity across might be used to elicit implicit nonconscious emotional different regions. Neuronal organization and modulation processing, as for example in masking, and to distinguish is mirrored in specific functional mechanisms of inte- it clearly from explicit and conscious processing. The grating neuronal activity [32, 33]. Even though the exact paradigm in our investigation might be considered a functional mechanisms of neuronal organization under- mixture of both, since the duration of emotional picture lying emotional-cognitive interaction are largely un- presentation was about 4 s, without any request to give an known, we would like to discuss two possible examples emotional judgment which would have induced the ex- derived from recent imaging studies on emotional-cog- plicit and conscious component. Finally neurochemical nitive interaction in relation to specific defense mecha- challenge studies during emotional stimulation, for ex- nisms. We should, however, emphasize the hypothetical ample with lorazepam that relieves the acute catatonic nature of our reflections, since neither the exact mecha- state [61, 62], might also be of interest. This is especially nisms of neuronal integration nor the defense mecha- so given the fact that lorazepam in healthy subjects mod- nisms have been completely and satisfactorily validated ulates neural activity in those regions (the orbitofontal at this point. cortex) [74] that are altered in catatonia.

How Does Our Brain Constitute Defense Psychother Psychosom 2007;76:141–153 147 Mechanisms? Reciprocal Modulation: Cognitively and Emotionally Based on these observations, we assume that the orbi- Guided Defense Mechanisms tofrontal cortex plays a crucial role in constituting more Recent studies [32, 33, 75, 76] demonstrated a pattern mature and cognitively guided defense (like intellectual- of opposite signal changes in the medial and lateral pre- ization, rationalization, isolation or reaction formation). frontal cortex during emotional-cognitive interaction. Dysfunction in this region and consecutive dysbalance in These results are compatible with the assumption of reciprocal modulation with lateral regions might make functional mechanisms of reciprocal modulation and re- the constitution of cognitively guided defense mecha- ciprocal attenuation during emotional-cognitive interac- nisms impossible. This, in turn, might induce regressive tion. Reciprocal modulation can be defined by signal processes with the consecutive predominance of rather changes in opposite directions (i.e. signal increases and immature and emotionally guided defense mechanisms decreases) in different regions. While emotional process- like splitting, projective identification, denial and psy- ing is known to lead to signal increases in the medial pre- chotic introjection/projection. For example, one would frontal cortical regions (BA 8, 10, 11) and concurrent sig- suspect dysfunction in the orbitofrontal cortex in pa- nal decreases in the lateral prefrontal cortex (BA 9, 46, tients with a borderline personality, where projective 47), cognitive tasks might induce the reverse pattern with identification predominates. Imaging studies indeed signal increases in the lateral prefrontal cortex (BA 9, 46, show severe alterations in the orbitofrontal cortex and 47) and signal decreases in the medial prefrontal cortex connected subcortical regions (amygdala, hippocampus) (BA 8, 10, 11). Emotional-cognitive interaction is then as- during emotional stimulation in these patients (see [7, 8, sociated with the functional mechanism of reciprocal at- 77–79] for a detailed neurobiological account of projec- tenuation: the inclusion of an emotional component in a tive identification). However, altered reciprocal modula- cognitive task leads to smaller signal decreases in the me- tion between the medial and lateral prefrontal regions dial prefrontal cortical regions and, at the same time, remains to be demonstrated in these patients. smaller signal increases in the lateral prefrontal cortical regions, which shall be called attenuation. Since attenua- Functional Unit: Sensorimotor Regression and tion concerned both the medial and lateral prefrontal Hysterical Conversion cortical regions in opposite directions (i.e. smaller signal Another example of a possible functional mechanism decreases/increases, respectively), one can call it recipro- of emotional-cognitive interaction might be the constitu- cal attenuation. tion of functional units among several brain regions over Catatonic patients showed an altered pattern of recip- a certain time period. Such transient functional units rocal signal increases and decreases in MOFC and LOFC might be identified based upon the psychophysiological (see above and [32–34] for further details). There were characteristics or the functional connectivity of the re- diminished signal increases in MOFC (BA 11, 12) and spective regions [80–86] . For example, in contrast to oth- more signal decreases in LOFC (BA 11, 47) during emo- er regions (like the lateral prefrontal cortex), so-called tional stimulation. This indicates that the reciprocal cortical midline structures (CMS, [32] ) show a continu- modulation (and possibly reciprocal attenuation) of emo- ously high level of neural activity during resting condi- tional-cognitive interaction might be altered in these pa- tions, such as passively focusing on a certain point (cross) tients. We assume that altered reciprocal modulation [87–91] . Moreover regions in the CMS seem to be charac- could possibly be related to their inability to use cognitive terized by close anatomical connections. Finally Greicius defense mechanisms and thus to cognitively defend the et al. [92] investigated the functional connectivity among emotional overflow. The exact relationship between al- CMS regions in both resting and activation states. They tered reciprocal modulation and the inability to use cog- observed increased functional connectivity between an- nitive defense mechanisms, however, remains unclear. terior and posterior CMS regions in the resting state, Either the altered reciprocal modulation causes changes whereas it was decreased during active cognitive tasks. in defense mechanisms, or a different use of defense These data provide compelling evidence for the exis- mechanisms leads to changes in neural patterns with al- tence of CMS as a functional unit, which seems to be par- tered reciprocal modulation. Alternatively, changes in ticularly active and cohesive in the resting state [92–95] . both reciprocal modulation and cognitive defense mech- Interestingly analogous observations of the CMS as a anisms could possibly be traced back to a third factor un- functional unit have been made during the processing of derlying and thus causing both, possibly resulting in a self-referential stimuli as distinguished from non-self- bidirectional relationship. referential stimuli [32, 88, 96]. Since the resting state can

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Motor symptoms

Somatic defense Catatonic symptoms: sensorimotor regression

Behavioral symptoms Social contact

Cognitive defense

Premotor/motor cortex Emotional arousal and self-esteem

Orbitofrontal cortex

Fig. 2. Sensorimotor regression and orbi- tofrontal-premotor/motor cortical func- tion in catatonia.

be characterized by strong self-directed and thus internal ther supported by studies in patients with conversion activity, it might also show a high degree of self-referen- symptoms. Conversion with hysterical paralysis might be tial stimulus processing. This might explain analogous regarded as a form of somatic defense in relation to an CMS results during both rest and self-referential process- emotional-cognitive conflict which can no longer be ing. solved by cognitive defense exclusively. Imaging studies Catatonic patients showed alterations in anterior CMS in acute paralytic patients revealed deficits in various re- with decreased functional connectivity among the gions of the anterior CMS, including the orbitofrontal MOFC, the LOFC and the premotor/motor cortex (see and the premotor/motor cortex [97–100]. Why, however, above). These changes significantly correlated with the is there a symptomatic difference in somatic defense be- patients’ alterations in their self-esteem, which reflects tween hysterical and catatonic patients, the former show- changes in self-referential processing (see above). This in- ing conversion and the latter sensorimotor regression? It dicates that decreased functional connectivity in the should first be noted that hysterical patients can show a CMS as a functional unit is somehow related to changes catatonic-like picture and that, conversely, catatonic pa- in self-referential processing, as manifest in low self-es- tients can appear strongly hysterical [61, 62, 101–103]. teem and abnormal social contact. Decreased functional Such a symptomatic overlap suggests that both catatonia connectivity from the orbitofrontal to the medial pre- and hysteria overlap in the neuronal mechanisms under- frontal and to the premotor cortex might not only disrupt lying somatic defense. They might share the abnormal self-referential processing but also concurrent behavior. functional unit of anterior CMS resulting in abnormal We speculate that such concurrent disruption of self-ref- motor behavior. However, reciprocal modulation (and re- erential processing and behavior might ultimately result ciprocal attenuation) of neuronal activity across the in the manifestation of predominantly somatic defense MOFC and the LOFC might be altered to different de- mechanisms with catatonic motor symptoms as a form of grees in both disorders, being stronger in catatonia and sensorimotor regression ( fig. 2). less pronounced in hysteria, possibly corresponding to The relationship between an abnormal functional unit emotional and behavioral differences and thus to differ- of anterior CMS and somatic defense mechanisms is fur- ent forms of somatic defense. Finally, additional regions

How Does Our Brain Constitute Defense Psychother Psychosom 2007;76:141–153 149 Mechanisms? might be implicated in hysterical conversion. This is in- tegration across multiple brain regions. We hypothesize dicated by a recent study by Lanius et al. [104] . They in- that the various defense mechanisms – constructs as hy- vestigated patients with posttraumatic stress disorder in pothesized in psychoanalytic theory – may correspond to whom f lashbacks or dissociative responses to script-driv- specific functional mechanisms by means of which neu- en imagery were observed in fMRI. Patients with disso- ronal activity is coordinated and thus integrated across ciative responses could be characterized by an increased different brain regions. As our knowledge of the func- connectivity between the anterior cingulate cortex and tional mechanisms of neuronal integration grows, the fu- the ventrolateral prefrontal cortex. This suggests that (i) ture holds the promise of a deeper understanding of the different additional regions like the ventrolateral pre- different neuronal processes associated with the various frontal cortex might be involved in hysterical conversion defense mechanisms. A better understanding of these and (ii) functional connectivity might also increase, neuronal processes will open the door to an appreciation which might possibly compensate for the decreased con- of the neurophysiology underlying the transition from nectivity among other regions. However, at present we immature defense mechanisms to more mature ones in remain unable to fully explore the similarities and differ- psychotherapy. ences between hysterical and catatonic conversion. Final- Since the emotional interaction between patient and ly one might use different forms of stimulation, for ex- therapist is crucial for inducing changes in the pattern of ample emotional pictures [33, 34] or trauma-oriented defense mechanisms, investigating the underlying neu- script-driven imagery [104] , in both hysterical and cata- ronal changes in the brains of both might be of future tonic conversions. We speculate that both types of pa- interest. First-person neuroscience – in contrast to third- tients might eventually show differential response pat- person neuroscience – subsequently considers that our terns to both types of stimulation6 . brain is embedded in social interaction. One could con- sequently use the terms embedded first-person neurosci- ence and embedded neuropsychoanalysis [32, 33, 37, 106] . Conclusion First-person neuroscience in this sense will provide in- sight into the neuronal processes of defense mechanisms We introduced an appropriate methodological strate- and emotional interaction. This, in turn, might help lay gy, first-person neuroscience, to overcome the method- the foundation for the development of a neurophysiolog- ological problem of linking first- and third-person data. ically informed psychoanalytic psychotherapy. Psychodynamic processes such as defense mechanisms must be considered first-person data, since they reflect the individual contents as they are subjectively experi- A c k n o w l e d g m e n t s enced in the first-person perspective, whereas neuronal states as observed in the third-person perspective are typ- We are grateful to Moritz de Greck for his critical suggestions, which considerably improved the manuscript. Moreover we thank ically regarded as third-person data. As such, first-person Christian Lücke for the formal preparation of the manuscript. neuroscience allows for psychodynamic processes associ- The work on this paper was financially supported by a grant from ated with defense mechanisms to be related to neuronal the German Research Foundation to G.N. (DFG, 304/4-1), a grant activity in our brain. Concerning neuronal activity, first- from the Swiss National Foundation to G.N. and H.B. and a grant person neuroscience requires a shift from neuronal local- within the BMBF-funded study group ‘Functions of Conscious- ness’ of the Berlin-Brandenburg Academy of Sciences to F.B. ization within one or more brain regions to neuronal in-

6 Another issue is the question of lateralization. A large body of literature (Lanius et al. [104] and especially for a very good overview Schore 2003 [7, 8] ) suggests the right hemisphere to be involved in primitive defenses. Though in this paper we have focused on cortical midline structures, this is still compatible with catatonia. In other studies right hemispheric dys- function in the lateral parietal cortex was observed to correlate with spatial deficits [105] . The exact relationship between the midline and the right lat- eral parietal cortical changes, however, remains unclear [74] . What is ulti- mately needed are studies that link the different subjective experiences and their different individual contents in catatonic and hysterical conversion to different though probably overlapping neural networks with specific pat- terns of increased and decreased functional connectivity.

150 Psychother Psychosom 2007;76:141–153 Northoff /Bermpohl /Schoeneich /Boeker

References

1 Freud S: The neuro-psychoses of defense; in 19 Westen D: Implications of developments in 34 Northoff G, Kotter R, Baumgart F, Danos P, Strachey J (ed): The Standard Edition of the for psychoanalytic Boeker H, Kaulisch T, Schlagenhauf F, Wal-

Complete Psychological Works of Sigmund psychotherapy. Harv Rev Psychiatry 2002; ter H, Heinzel A, Witzel T, Bogerts B: Orbi-

Freud. London, Hogarth, (original work 10: 369–373. tofrontal cortical dysfunction in akinetic published 1894), 1962, pp 43–68. 20 Northoff G, Böker H, Richter A, Tempel- catatonia: a functional magnetic resonance 2 Gazzaniga MS: Mark D’Esposito with Mi- mann C, Bogerts B, Heinze HJ: Emotional- imaging study during negative emotional

chael S. Gazzaniga. J Cogn Neurosci 2004; behavioral disturbances in catatonia: a com- stimulation. Schizophr Bull 2004; 30: 405–

16: 1–3. bined study of psychological self-evaluation 427.

3 Panksepp J: : The and fMRI. Neuropsychoanalysis 2003; 3: 35 Varela FJ, Shear J: First-person methodolo-

Foundations of Human and Animal Emo- 151–167. gies: what, why, how? J Consc Studies

tions. New York, Oxford University Press, 21 Northoff G: Phänomenale, tiefenpsycholo- 1999a;6: 1–14. 1998. gische und neurowissenschaftliche Perspe- 36 Varela FJ, Shear J (eds): The views from with- 4 Panksepp J: At the interface of the affective, ktiven der Katatonie: Eine epistemische Be- in: first-person methodologies in the study behavioral and cognitive neurosciences: de- trachtung; in Böker H (ed): Depression, of consciousness (special issue). J Consc coding the emotional feelings of the brain. Manie und schizoaffektive Psychosen. Gies- Studies 1999b, vol 6.

Brain Cogn 2003; 52: 4–14. sen, Psychosozial-Verlag, 2000. 37 Northoff G: Philosophy of the Brain. The 5 Damasio AR: How the brain creates the 22 Schneider P: Psychoanalyse und Neurowis- Brain Problem. Amsterdam, John Ben-

mind. Sci Am 1999; 281: 112–117. senschaft: Inkompatibilität!; in Böker H jamins, 2004. 6 Solms M: What is consciousness? J Am Psy- (ed): Psychoanalyse und Psychiatrie – Ge- 38 Fava GA, Ruini C, Rafanelli C: Psychometric

choanal Assoc 1997; 45: 681–703, discussion schichte, Krankheitsmodelle und Therapie- theory is an obstacle to the progress of clini-

704–778. praxis. Heidelberg, Springer Medizin Verlag, cal research. Psychother Psychosom 2004;

7 Schore SE, Sumner CJ, Bledsoe SC, Lu J: Ef- 2006. 73: 145–148. fects of contralateral sound stimulation on 23 Jones H: Preserve psychoanalysis from too 39 Nierenberg AA, Sonino N: From clinical ob-

unit activity of ventral cochlear nucleus neu- much neuroscience. Br J Psychiatry 2003; servations to clinimetrics: a tribute to Alvan

rons. Exp Brain Res 2003; 153: 427–435. 182: 552–553. R. Feinstein, MD. Psychother Psychosom

8 Schore SE, El Kashlan H, Lu J: Effects of tri- 24 Edelson SM: Implications of sensory stimu- 2004; 73: 131–133. geminal ganglion stimulation on unit activ- lation in self-destructive behavior. Am J 40 Varela FJ: Neurophenomenologie: a meth-

ity of ventral cochlear nucleus neurons. Neu- Ment Defic 1984; 89: 140–145. odological remedy for the hard problem. J

roscience 2003; 119: 1085–1101. 25 Gruenbaum A: Precis of The Foundations of Consc Studies 1996; 3: 330–349. 9 Kandel ER: A new intellectual framework for Psychoanalysis: A Philosophical Critique. Be- 41 Gabbard GO: The psychodynamic perspec-

psychiatry. Am J Psychiatry 1998; 155: 457– hav Brain Sci 1986; 9: 217–284. tive: a conversation with Glen O. Gabbard, 469. 26 McCrone J: Freud’s neurology. Lancet Neu- MD. by Norine J Kerr. Perspect

10 Kandel ER: Biology and the future of psycho- rol 2004; 3: 320. Psychiatr Care 1992; 28: 6–12. analysis: a new intellectual framework for 27 Pugh G: Freud’s ‘problem’: cognitive neuro- 42 Northoff G: ‘Brain-paradox’ and ‘embedd-

psychiatry revisited. Am J Psychiatry 1999; science and psychoanalysis working togeth- ment’ – Do we need a ‘philosophy of the

156: 505–524. er on memory. Int J Psychoanal 2002; 83: brain’? Brain and Mind 2001; 2: 195–211.

11 Gabbard GO: Psychodynamic psychiatry in 1375–1394. 43 Weinryb RM, Rossel RJ, Asberg M: The Ka- the ‘decade of the brain’. Am J Psychiatry 28 Anderson DL: You don’t need a licence (or rolinska Psychodynamic Profile. II. Inter-

1992; 149: 991–998. PhD) to use your brain. Nature 2004; 430: disciplinary and cross-cultural reliability.

12 Gabbard GO: Psychodynamics of panic dis- 965. Acta Psychiatr Scand 1991; 83: 73–76. order and social phobia. Bull Menninger 29 Anderson CS, Hackett ML, House AO: In- 44 Weinryb RM, Rossel RJ, Asberg M: The Ka-

Clin 1992; 56(suppl 2A):A3–A13. terventions for preventing depression after rolinska Psychodynamic Profile. I. Validity

13 Westen D, Gabbard GO: Developments in stroke. Cochrane Database Syst Rev 2004; 2: and dimensionality. Acta Psychiatr Scand

cognitive neuroscience. I. Conflict, compro- CD003689. 1991; 83: 64–72. mise and connectionism. J Am Psychoanal 30 Solms M, Turnbull OH, Kaplan-Solms K, 45 Perry JC, Cooper SH: An empirical study of

Assoc 2002; 50: 53–98. Miller P: Rotated drawing: the range of per- defense mechanisms. I. Clinical interview 14 Westen D, Gabbard GO: Developments in formance and anatomical correlates in a se- and life vignette ratings. Arch Gen Psychia-

cognitive neuroscience. II. Implications for ries of 16 patients. Brain Cogn 1998; 38: 358– try 1989; 46: 444–452. theories of transference. J Am Psychoanal 368. 46 Vaillant GE, Bond M, Vaillant CO: An em-

Assoc 2002; 50: 99–134. 31 Bollas L: Der Schatten des Objekts: Das pirically validated hierarchy of defense

15 Westen D: The scientific status of uncon- ungedachte Bekannte. Zur Psychoanalyse mechanisms. Arch Gen Psychiatry 1986; 43:

scious processes: is Freud really dead? J Am der frühen Entwicklung. Stuttgart, Klett- 786–794.

Psychoanal Assoc 1999; 47: 1061–1106. Cotta, 1997. 47 Kipper L, Blaya C, Teruchkin B, Heldt E, Iso- 16 Brockman R: Toward a neurobiology of the 32 Northoff G, Bermpohl F: Cortical midline lan L, Mezzomo K, Bond M, Manfro GG:

unconscious. J Am Acad Psychoanal 2001; structures and the self. Trends Cogn Sci Brazilian patients with panic disorder: the

29: 601–615. 2004; 8: 102–107. use of defense mechanisms and their asso-

17 Beutel ME, Stern E, Silbersweig DA: The 33 Northoff G, Heinzel A, Bermpohl F, Niese R, ciation with severity. J Nerv Ment Dis 2004;

emerging dialogue between psychoanalysis Pfennig A, Pascual-Leone A, Schlaug G: Re- 192: 58–64. and neuroscience: neuroimaging perspec- ciprocal modulation and attenuation in the 48 Andrews G, Singh M, Bond M: The Defense

tives. J Am Psychoanal Assoc 2003; 51: 773– prefrontal cortex: an fMRI study on emo- Style Questionnaire. J Nerv Ment Dis 1993;

801. tional-cognitive interaction. Hum Brain 181: 246–256.

18 Solms M, Lechevalier B: Neurosciences and Mapp 2004; 21: 202–212.

psychoanalysis. Int J Psychoanal 2002; 83:

233–237.

How Does Our Brain Constitute Defense Psychother Psychosom 2007;76:141–153 151 Mechanisms? 49 Shedler J, Westen D: Dimensions of person- 67 Arieti S: Volition and value: a study based on 79 Vollm B, Richardson P, Stirling J, Elliott R, ality pathology: an alternative to the five- catatonic schizophrenia; in Post SC (ed): Dolan M, Chaudhry I, Del Ben C, McKie S,

factor model. Am J Psychiatry 2004; 161: Moral Values and the Superego Concept in Anderson I, Deakin B: Neurobiological sub-

1743–1754. Psychoanalysis. New York, International strates of antisocial and borderline personal- 50 Shedler J, Westen D: Refining personality Universities Press, 1972. ity disorder: preliminary results of a func- disorder diagnosis: integrating science and 68 Boeker H: Selbstbild und Objektbeziehungen tional fMRI study. Crim Behav Ment Health

practice. Am J Psychiatry 2004; 161: 1350– bei Depressionen. Untersuchungen mit der 2004; 14: 39–54. 1365. Repertory Grid Technique und dem Giessen 80 Friston KJ, Josephs O, Rees G, Turner R: 51 Smith N, Freeman D, Kuipers E: Delusions: Test an 139 Patienten mit depressi ven Er- Nonlinear event-related responses in fMRI.

an experimental investigation of the delu- krankungen. Darmstadt, Steinkopf, 1999. Magn Reson Med 1998; 39: 41–52.

sion as defence. J Nerv Ment Dis 2005; 193: 69 Kelly GA: The Psychology of Personal Con- 81 Friston KJ, Fletcher P, Josephs O, Holmes A,

480–487. structs. New York, Norton, 1955, vol I and Rugg MD, Turner R: Event-related fMRI: 52 Wilkinson-Ryan T, Westen D: Identity dis- II. characterizing differential responses. Neu-

turbance in borderline personality disorder: 70 Winter DA: Repertory grid technique in the roimage 1998; 7: 30–40. an empirical investigation. Am J Psychiatry evaluation pf therapeutic outcome; in Beail 82 Friston KJ: Imaging neuroscience: principles

2000; 157: 528–541. N (ed): Repertory Grid Technique and Per- or maps? Proc Natl Acad Sci USA 1998; 95:

53 Schauenburg H, Schussler G, Leibing E: Em- sonal Constructs. London, Croom Helm, 796–802. pirical assessment of defense mechanisms 1985, pp 154–172. 83 Friston K: Learning and inference in the

with a self evaluation questionnaire (accord- 71 Winter DA: Personal Construct Theory in brain. Neural Netw 2003; 16: 1325–1352. ing to Bond et al.). Psychother Psychosom Clinical Practice. London, Routledge, 1992. 84 Friston KJ, Harrison L, Penny W: Dynamic

Med Psychol 1991; 41: 392–400. 72 Böker H, Budischewski K, Eppel A, Härt- causal modelling. Neuroimage 2003; 19:

54 Schibuk M, Bond M, Bouffard R: The devel- ling F, Rinnert H, von Schmeling F, Will H, 1273–1302. opment of defenses in childhood. Can J Psy- Schöneich F, Northoff G: Personality and 85 Friston KJ, Penny W: Posterior probability

chiatry 1989; 34: 581–588. object relations in patients with affective dis- maps and SPMs. Neuroimage 2003; 19: 1240– 55 Barglow P, Jaffe CM, Vaughn B: Psychoana- orders: ideographic research by means of the 1249. lytic reconstructions and empirical data: re- repertory grid technique. J Affect Disord 86 Friston KJ, Price CJ: Degeneracy and redun-

ciprocal contributions. J Am Psychoanal As- 2000; 60: 53–59. dancy in cognitive anatomy. Trends Cogn

soc 1989; 37: 401–435. 73 Böker H: Persons with depression, mania Sci 2003; 7: 151–152. 56 Metzinger T: Being No One. The Self Model and schizoaffective psychosis: Investiga- 87 Gusnard DA, Raichle ME: Searching for a Theory of Subjectivity. Cambridge, MIT tions of cognitive complexity, self-esteem, baseline: functional imaging and the resting

Press, 2003. social and object relations by human brain. Nat Rev Neurosci 2001; 2: 685– 57 Chomsky N: Universals of human nature. means of the repertory grid-technique; in 694.

Psychother Psychosom 2005; 74: 263–268. Klapp BP, Jordan J, Walter OB (eds): Role 88 Gusnard DA, Akbudak E, Shulman GL, 58 Bush G, Fink M, Petrides G, Dowling F, Repertory Grid and Body Grid – Construct Raichle ME: Medial prefrontal cortex and Francis A: Catatonia. II. Treatment with Psychological Approaches in Psychosomatic self-referential mental activity: relation to a lorazepam and electroconvulsive therapy. Research. Frankfurt/M., VAS – Verlag für default mode of brain function. Proc Natl

Acta Psychiatr Scand 1996; 93: 137–143. Akademische Schriften, Reihe Klinische Acad Sci USA 2001; 98: 4259–4264. 59 Bush G, Fink M, Petrides G, Dowling F, Psycholinguistik, 2004, pp 119–146. 89 Raichle ME: Cognitive neuroscience: bold

Francis A: Catatonia. I. Rating scale and 74 Northoff G, Witzel T, Richter A, Gessner M, insights. Nature 2001; 412: 128–130. standardized examination. Acta Psychiatr Schlagenhauf F, Fell J, Baumgart F, Kaulisch 90 Raichle ME, MacLeod AM, Snyder AZ, Pow-

Scand 1996; 93: 129–136. T, Tempelmann C, Heinzel A, Kotter R, Hag- ers WJ, Gusnard DA, Shulman GL: A default 60 Fink M: Catatonia and psychotic (delusion- ner T, Bargel B, Hinrichs H, Bogerts B, mode of brain function. Proc Natl Acad Sci

al) depression, distinct syndromes in DSM- Scheich H, Heinze HJ: GABA-ergic modula- USA 2001; 98: 676–682.

IV. Am J Psychiatry 1993; 150: 1130–1131. tion of prefrontal spatio-temporal activation 91 Mazoyer B, Zago L, Mellet E, Bricogne S, 61 Northoff G: What catatonia can tell us about pattern during emotional processing: a com- Etard O, Houde O, Crivello F, Joliot M, Petit ‘top-down modulation’: a neuropsychiatric bined fMRI/MEG study with placebo and lo- L, Tzourio-Mazoyer N: Cortical networks

hypothesis. Behav Brain Sci 2002; 25: 555– razepam. J Cogn Neurosci 2002; 14: 348–370. for working memory and executive func- 577, discussion 578–604. 75 Goel V, Dolan RJ: Explaining modulation of tions sustain the conscious resting state in

62 Northoff G: Catatonia and neuroleptic ma- reasoning by belief. Cognition 2003; 87:B11– man. Brain Res Bull 2001; 54: 287–298. lignant syndrome: psychopathology and B22. 92 Greicius MD, Krasnow B, Reiss AL, Menon

pathophysiology. J Neural Transm 2002; 109: 76 Goel V, Dolan RJ: Reciprocal neural response V: Functional connectivity in the resting

1453–1467. within lateral and ventral medial prefrontal brain: a network analysis of the default mode

63 Taylor MA: Catatonia: a review of the behav- cortex during hot and cold reasoning. Neu- hypothesis. Proc Natl Acad Sci USA 2003;

ioral neurologic syndrome. Neuropsychiatry roimage 2003; 20: 2314–2321. 100: 253–258.

Neuropsychol Behav Neurol 1990; 3: 48–72. 77 Johnson PA, Hurley RA, Benkelfat C, Her- 93 Wicker B, Ruby P, Royet JP, Fonlupt P: A rela- 64 Perkins K: Catatonia as an immobilization pertz SC, Taber KH: Understanding emotion tion between rest and the self in the brain?

reflex. Aust NZ J Psychiatry 1982; 23: 282– regulation in borderline personality disor- Brain Res Brain Res Rev 2003; 43: 224–230. 288. der: contributions of neuroimaging. J Neu- 94 Wicker B, Keysers C, Plailly J, Royet JP, Gal-

65 Böker H, Lempa G: Psychosen; in Senf W, ropsychiatry Clin Neurosci 2003; 15: 397– lese V, Rizzolatti G: Both of us disgusted in Broda M (eds): Praxis der Psychotherapie. 402. my insula: the common neural basis of see-

Ein integratives Lehrbuch. Stuttgart, 78 Tebartz van Elst L, Hesslinger B, Thiel T, ing and feeling disgust. Neuron 2003; 40:

Thieme, 1996. Geiger E, Haegele K, Lemieux L, Lieb K, Bo- 655–664. 66 Johnson DR: Representation of the internal hus M, Hennig J, Ebert D: Frontolimbic 95 Wicker B, Perrett DI, Baron-Cohen S, De- world in catatonic schizophrenia. Psychiatry brain abnormalities in patients with border- cety J: Being the target of another’s emotion:

1984; 47: 299–314. line personality disorder: a volumetric mag- a PET study. Neuropsychologia 2003; 41:

netic resonance imaging study. Biol Psychia- 139–146.

try 2003; 54: 163–171.

152 Psychother Psychosom 2007;76:141–153 Northoff /Bermpohl /Schoeneich /Boeker

96 Kelley WM, Macrae CN, Wyland CL, Ca- 101 Modestin J, Bachmann KM: A third kind 104 Lanius RA, Williamson PC, Bluhm RL, glar S, Inati S, Heatherton TF: Finding the of psychosis. Analysis of the literature. Densmore M, Boksman K, Neufeld RW,

self? An event-related fMRI study. J Cogn Schweiz Arch Neurol Psychiatr 1992; 143: Gati JS, Menon RS: Functional connectivi-

Neurosci 2002; 14: 785–794. 307–323. ty of dissociative responses in posttraumat- 97 Marshall JC, Halligan PW, Fink GR, Wade 102 Modestin J, Bachmann KM: Is the diagno- ic stress disorder: a functional magnetic DT, Frackowiak RS: The functional anato- sis of hysterical psychosis justified? Clini- resonance imaging investigation. Biol Psy-

my of a hysterical paralysis. Cognition cal study of hysterical psychosis, reactive/ chiatry 2005; 57: 873–884.

1997; 64:B1–B8. psychogenic psychosis and schizophrenia. 105 Northoff G, Richter A, Gessner M, Schla-

98 Vuilleumier P, Chicherio C, Assal F, Compr Psychiatry 1992; 33: 17–24. genhauf F, Fell J, Baumgart F, Kaulisch T, Schwartz S, Slosman D, Landis T: Func- 103 Northoff G, Eckert J, Fritze J: Glutamater- Kotter R, Stephan KE, Leschinger A, Hag- tional neuroanatomical correlates of hys- gic dysfunction in catatonia? Successful ner T, Bargel B, Witzel T, Hinrichs H, Bo-

terical sensorimotor loss. Brain 2001; 124: treatment of three acute akinetic catatonic gerts B, Scheich H, Heinze HJ: Functional

1077–1090. patients with the NMDA antagonist aman- dissociation between medial and lateral 99 Halligan PW, Athwal BS, Oakley DA, Fra- tadine. J Neurol Neurosurg Psychiatry prefrontal cortical spatiotemporal activa-

ckowiak RS: Imaging hypnotic paralysis: 1997; 62: 404–406. tion in negative and positive emotions: a implications for conversion hysteria. Lan- combined fMRI/MEG study. Cereb Cortex

cet 2000; 355: 986–987. 2000; 10: 93–107. 100 Spence SA, Crimlisk HL, Cope H, Ron MA, 106 Tononi G, Edelman GM: Schizophrenia Grasby PM: Discrete neurophysiological and the mechanisms of conscious integra-

correlates in prefrontal cortex during hys- tion. Brain Res Brain Res Rev 2000; 31: 391– terical and feigned disorder of movement. 400.

Lancet 2000; 355: 1243–1244.

How Does Our Brain Constitute Defense Psychother Psychosom 2007;76:141–153 153 Mechanisms?