Our metapsychological discussion of identity formation has enabled us to distinguish a position of the subject in relation to (a) and the Other where the secondary defense and psychological processing have not taken place. The initial problem—which is simultaneously the motive for identity formation—remains focused on the body, that is to say, on the demand arising out of the real body and the impotence of the Other to answer it.
Should such a subject position be empirically verifiable, the consequences would be the following. First, in the psychodiagnostic field, the differential diagnostic becomes relatively simple. For such a subject position, there will be no symptoms a fortiori, that is, no signifying constructions in the Symbolico-Imaginary. The accent will remain on the starting point of the development, namely, on certain somatic phenomena and their accompanying (un-)pleasure and anxiety. Still within the context of diagnosis, this implies that such patients today will initially find themselves in the medical field and only later in a clinical psychological setting. Secondly, at the level of treatment we are confronted with a problem that is structurally different from our customary psychopathology, the latter having already undergone secondary processing. The usual psychotherapeutic treatment will be of little use here, and the potential psychotherapeutic approach to such problems must also be completely reconsidered in the light of the structural diagnostic.
There are two arguments in favor of the existence of such an actualpathological position. One is classical and conceptual: we must look again at what has long since been a forgotten part of Freudian theory and clinical practice, at what in 1898 he called the “actual neuroses.” The other draws on more recent empirical work: we must call upon the flood of contemporary research into somatization, alexithymia, and the panic disorders.
At its outset, clinical practice was utterly unlike that of today. One of the chief differences was its lack of specialization, with the result that doctors could be confronted with more or less any type of patient. Into this often vaguely differentiated group, Freud quickly introduced divisions. On one side is what he called the neuro-psychoses of defense (Freud 1978 [1894a], [1896b] and manuscript B and E).1 The origin of these disorders must be sought in infantile sexual development; its associated symptoms are signification-rich and their typical characteristic is defense against an inner conflict at the level of sexuality and desire. On the other side are the actual neuroses. Their origin is also sexual, by which we must understand that it is located in the present life of the patient, not in the past. The symptoms are limited to somatic phenomena and have no further meaning, the emphasis lying largely on anxiety and the somatic anxiety equivalents (Freud 1978 [1895b], [1896a]).
Throughout the subsequent course of his career, Freud will place his emphasis on elaborating the first group, which will come to form the basis of many of today’s psychodiagnostic categories. The second group remains underdeveloped, despite Freud’s continuing to confirm its existence right to the end. The reason for this relative lack of interest is a pragmatic one. This group failed to respond to the psychoanalytic treatment of his time. Indeed, the symptomatic superstructure and accompanying fantasmatic developments are completely absent; there is quite simply nothing to analyze.
Nevertheless, this didn’t stop him from providing a thorough description of this group, for whose etiology he offers a number of hypotheses. Within the actual neuroses, he distinguishes between anxiety neurosis and neurasthenia, later adding hypochondria to these (Freud, 1978 [1914c], pp. 82–85).
Freud’s emphasis is clearly on anxiety neurosis, whose name and discovery are both Freud’s (Freud 1978 [1895b], [1898a]). It is worth recalling his clinical description. He identifies seven characteristics:
General irritability. This indicates an increase of excitation and an inability to tolerate it. Sleeplessness is fairly common.
Anxious anticipation. There is a quantum of free-floating anxiety that can be secondarily associated with any content whatsoever. For Freud, this is the symptomatic kernel.
Anxiety attacks. Such attacks occur suddenly, without any connection with a preceding train of thought. This anxiety can be secondarily associated with fears of dying or of becoming mad. The combination of anxiety with disturbances in certain bodily functions is fairly common, such as “spasms of the heart,” respiratory difficulties, sweating, ravenous hunger.
A continuum from rudimentary anxiety attacks to somatic anxiety equivalents. The proportional combination of the two varies widely in the clinic, but the central phenomenon remains anxiety. Among the somatic anxiety equivalents, Freud distinguishes heart palpitations, disturbances of respiration, sweating, tremor and shivering, ravenous hunger, diarrhea, locomotoric vertigo, congestion, and paresthesias. Freud calls such somatic anxiety-equivalents “larval anxiety-states” and adds that the anxiety is not always experienced as such by the patient.2
Nocturnal fears (pavor nocturnis). An anxiety attack at night, usually in combination with sweating and respiratory difficulties, although not associated with a nightmare.
Vertigo. Also usually in combination with anxiety, although not always. The patient’s legs feel like they are giving way and it seems impossible to remain standing but without actually falling.
Two kinds of phobias. The first group boils down to the reinforcement of previously existing and, according to Freud, probably instinctive aversions in the patients (anxiety about thunderstorms, vermin, darkness), thereby turning them into a phobia. The second group concerns agoraphobia, often beginning with an attack of vertigo and later taking hold of the patient’s motor abilities. Freud highlights the difference between both types of phobias and psychopathology: there is no associative link to an underlying repressed train of thought—thus making it impossible to moderate this phobia through analysis or psychotherapy—and the underlying affect is anxiety as such (Freud 1978 [1895b], pp. 92–97).
For Freud, the etiological ground of anxiety neurosis or, more broadly, of the actual neuroses, must lie in the somatic-sexual factor, operating as an endogenic arousal. More specifically, he locates its etiology in the failure to psychically process this excitation and thus abreact it—and hence gives general irritation as its first characteristic. The accumulated tension is immediately transformed into anxiety. Freud will further specify this etiology by referring to the role of sexual abstinence. Its kernel nevertheless remains the absence of psychological elaboration of something that pertains to the body.
The second form of actual neurosis is what was called neurasthenia. Originally described by Beard, this category enjoyed immense success and was extensively developed by Janet, for one. Freud remained critical of this broadening of the term, limiting his description of its core characteristics to three elements.3 Firstly, the characteristic physical exhaustion that has no physical explanation. Secondly, the accompanying somatic phenomena, normally headaches, dyspepsia, constipation, and spinal paresthesia. Thirdly, the decline of sexual activity. An important difference between this and the previous group is that here anxiety is almost entirely absent. Its etiology is the same as that of anxiety neurosis, that is, the impossibility of psychically processing an internal sexual somatic arousal. In neurasthenia, the cause is not so much anxiety as exhaustion resulting from a conflict between the subject and its drive. As a special etiological factor, Freud mentioned masturbation, something that accorded perfectly with the medical-moral discourse of that time.
This more or less sums up the Freudian theory of actual neurosis (with the exception of hypochondria; see Chapter 15). As I said, it gets little attention in the rest of his oeuvre and, after Freud, this piece of his theory and clinical praxis becomes more or less forgotten. One reason for this has to do with the supposed etiology of the condition: these days, sexual abstinence and masturbation no longer mean the same thing as in the 1900s—although I am still convinced that their psychological impact should not be underestimated even today. However, along with this one tends to forget how these are merely the specific etiological manifestations of an underlying general cause, that is, the fact that the endogenic arousal has not been psychically processed. As far as this arousal is concerned, Freud even accounts for the classic psychiatric “surmenage,” or in contemporary terms stress by overwork (Freud 1978 [1898a], [1905d]). The second reason why it has been forgotten doubtless has to do with the fact that, because of the growing medical specialization, such patients tend to arrive in an increasingly exclusive medical setting. We will have to wait for the reconciliation of the medical and clinical psychological discourses before this problem is addressed. However, this brings us to two contemporary topics that have been widely researched: panic disorders and somatization phenomena.
Panic disorder is a modern success story. Psycinfo cites only 22 studies for the 1970s; this increases to 2.588 in the 1980s, and that number more than doubles over the next decade. As has often happened, the discovery of this condition was purely coincidental, occurring moreover outside the context of any historical awareness. In the 1960s, an American psychiatrist, Donald Klein, conducted research into the pharmacological treatment of schizophrenia. One particular group of schizophrenic patients, characterized by an absence of delusions and hallucinations, and displaying acute anxiety attacks, failed to react to the usual medication of those days. This was in contrast to the other group that did indeed display hallucinations and delusions, along with a chronic anxiety.4 He then discovered that another drug (imipramine) diminished the acute anxiety and concluded that the anxiety in both groups must be essentially different (D. Klein 1964).
After that, things begin to move fast. This particular form of anxiety is described as the so-called panic attack. This, in turn, will give rise to a number of diagnostic entries in the DSM. We will first discuss the description of the panic attack itself, and then the diagnostic entries in the light of the associated empirical research.
In the DSM-IV (American Psychiatric Association 2000, p. 432), panic attack is described as an isolated, acute-anxiety experience in which the patients display at least four of the following symptoms, arriving at a peak in a very short time:
Panic Attack
A discrete period of intense fear or discomfort, in which four (or more) of the following symptoms developed abruptly and reached a peak within 10 minutes:
1) palpitations, pounding heart, or accelerated heart rate
2) sweating
3) trembling or shaking
4) sensations of shortness of breath or smothering
5) feeling of choking
6) chest pain or discomfort
7) nausea or abdominal distress
8) feeling dizzy, unsteady, lightheaded, or faint
9) derealization (feelings of unreality) or depersonalization (being detached from oneself)
10) fear of losing control or going crazy
11) fear of dying
12) paresthesias (numbness or tingling sensations)
13) chills or hot flushes
Comparing this description with the characteristics of anxiety neurosis described above, we are forced to conclude that they both concern the same thing. Not only does the DSM contain all of the phenomena described by Freud, Freud moreover contains more. The shortcoming of the DSM lies for the most part in its lack of a certain insight not absent in Freud, namely, that the somatic anxiety equivalents can appear in place of anxiety, with the result that the patient is barely aware of his own anxiety. Recent discussion since then has revolved around the paradoxical NFPD, the “non-fearful panic disorder,” as yet unmentioned in the DSM. Research has shown that such panic attacks without anxiety may occur in both clinical and nonclinical populations (Kushner and Beitman 1990). The difference between both groups is relatively small, although with the understanding that the nonclinical population suffers less from agoraphobia and expectance anxiety. As such, NFPD remains an unintelligible clinical phenomenon for which even the cognitive approach must rely on the probably unconscious “cognitions” of this group as an explanation (Clark 1986). The explanation today resides in linking NFPD with alexithymia (see below).
The thirteen characteristics can be ordered in line with our theory. The group 1 through 8, 12, and 13 are the somatic anxiety equivalents, where the “chills or hot flushes” signals the connection that Freud already pointed out with menopause. We have previously encountered characteristic Number 9, derealization or depersonalization; both can be understood as a reaction to a failed confrontation with the Real of the body. The failure lies in the absence of the psychic processing, causing these phenomena—derealization and depersonalization—to acquire a dissociative character. Hence, it is not by chance that we will come across the same phenomena later on in our study of the traumatic neuroses. Numbers 10 and 11 are the sole psychological characteristics and can be interpreted as an expression of anxiety over the disappearance of the subject itself, in the wordlessness of the Real.
On the basis of this description, the DSM-IV-TR distinguishes between panic disorders with or without agoraphobia. At this point we reencounter the original Freudian description, albeit outside of any conceptual framework. The kernel of the agoraphobia is described as:
Anxiety about being in places or situations from which escape might be difficult (or embarrassing) or in which help may not be available in the event of having an unexpected or situationaly predisposed Panic Attack or panic-like symptoms. Agoraphobic fears typically involve characteristic clusters of situations that include being outside the home alone; being in a crowd or standing in a line; being on a bridge; and traveling in a bus, train, or automobile. [American Psychiatric Association 2000, p. 433]
This disorder is then described as follows:
Panic disorder with agoraphobia (300.21)
A. Both 1) and 2):
1) recurrent unexpected Panic Attacks
2) at least one of the attacks has been followed by 1 month (or more) of one (or more) of the following:
a. persistent concern about having additional attacks
b. worry about the implications of the attack or its consequences (e.g., losing control, having a heart attack, ‘going crazy’)
c. a significant change in behavior related to the attacks
B. The presence of Agoraphobia
C. The Panic Attacks are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hyperthyroidism)
D. The Panic Attacks are not better accounted for by another mental disorder, such as Social Phobia (e.g., occurring on exposure to feared social situations), Specific Phobia (e.g., on exposure to a specific phobic situation), Obsessive-Compulsive Disorder (e.g., on exposure to dirt in someone with an obsession about contamination), Posttraumatic Stress Disorder (e.g., in response to stimuli associated with a severe stressor), or Separation Anxiety Disorder (e.g., in response to being away from home or close relatives). [American Psychiatric Association 2000, p. 441]
The need to couple panic attack and agoraphobia with panic disorders comes from the experience that in practice they are frequently found in combination. The majority of studies devoted to this link come to more or less the same conclusion: agoraphobia is a consequence of a preceding panic attack (Clum and Knowles 1991). Such an approach pays most attention to the cognitive factors (catastrophic interpretations and social concerns). For me, however, the most interesting angle is that found in Klein and Gorman (1987), who offer the following typical sequence: the “spontaneous” occurrence of the first panic attack is followed by help-seeking behavior, after which chronic expectance anxiety is installed, succeeded by the final development of avoidance behavior.
The reason I find this the most interesting approach is because it no longer focuses on the phobic “object” that must be avoided—the agora—but rather on the patient’s motivation that lies at its base. One can also see this motivation in the DSM’s description of the panic attack: “Anxiety about being in places or situations from which escape might be difficult (or embarrassing) or in which help may not be available.” To my mind, when understood from our metapsychological perspective, such a panic attack is always a reaction to an internal, unprocessed excitation (a), in response to which the subject makes an almost instant appeal to the Other. Typically, for actualpathology in general, and for anxiety neurosis in particular, the other’s intervention will never suffice but the appeal will nevertheless persist. “Agoraphobia” is the expression of this need for the other, and the avoidance of all situations where this other could be absent. In this sense, panic disorder may well be accompanied by claustrophobia, understood as the feeling of being locked up on one’s own in a small space. In both cases, agoraphobia and claustrophobia, the anxiety will be tempered by the presence of a significant other, although this presence will never be enough.
Empirical research has meanwhile shown that panic disorders demonstrate a high comorbidity with other anxiety disorders, such as affective disorders and addiction (Rosenbaum 1997).5 Addiction corresponds with the phenomenon of auto-medication, and can be minimally understood as the drinking or injecting away of anxiety.6 Freud already indicated the high correlation between anxiety neurosis (panic disorder) and depression (Freud 1978 [1892–1899], Manuscript B to Fliess). This correlation is indeed pretty high (44 percent in the research by Clum and Pendrey 1987), and again can be understood in light of our conception of subject-formation. Here, depression is the actualpathological position of the subject who was unable to satisfy the Other’s desire from the start (see Chapter 10). Typical of this comorbidity is that, in these other disorders, symptoms (in our sense of the word) are also entirely absent: there’s no secondary elaboration, making classic psychotherapy all the more problematic.
Comparing recent studies with Freud’s classical notions of actual neurosis and of anxiety neurosis in particular reveals certain similarities. This is probably true for classical neurasthenia and contemporary chronic fatigue syndrome as well, although I will not go into that here. The questions now concern etiology: What is the source of the actualpathology? Can contemporary studies provide an answer for this? and What relevance will it have for the treatment?
The etiological question is all the more of a challenge because the anxiety is always described as spontaneous. Given the pharmacological discoveries, it is no surprise that its etiology was initially purely sought in the biological discourse. The fact that imipramine has a favorable effect on panic attacks but not on chronic anxiety led Klein and his colleagues (1987) to hypothesize that there were two different neurobiological systems at work that could be considered the cause of two different anxieties. This theory contains an error of logic; although certain pharmacological items operate selectively on anxiety, that doesn’t mean that the cause of anxiety must be sought in the absence of those molecules. Other research concentrated on “challenge tests” that artificially provoked or inhibited anxiety attacks through the administration of certain products (caffeine, among others). This produced a surprising result: the substances worked on a number of different systems in the human body. The hypothesis that panic attacks were caused by one specific bodily system or function consequently had to be rejected (McNally 1994).
A second explanatory model was found in psychology, with the accent on learning and cognitive psychology. Here, the cause of a panic attack was thought to lie in the so-called catastrophic misinterpretation of bodily sensations (Beck 1988; Clark 1986). These bodily sensations can be quite diverse (anger, excitation), and the emphasis is on the patient’s mistaken and thereby anxiety-provoking interpretation (heart attack, suffocating, becoming mad), resulting in an increasingly vicious circle. This view received extensive research (Barlow and Craske 1988; Craske and Barlow 1988; Rachman et al. 1988; Wolpe and Rowan 1988), and produced the following result. Catastrophic misinterpretations are developed only after the first panic attack and therefore cannot explain this attack. What this model does explain, however, is the spiral that sets in after the first attack and that gives rise to agoraphobia, for example, and other avoidant behaviors.
The conclusion is that neither a simple neurobiological line of reasoning, nor a cognitive learning psychological approach can provide a conclusive answer to the question of etiology. This means that we can return to Freud’s hypothesis, albeit with a number of important additions. The starting point of the first anxiety attack lies in the body, and more specifically in an increase in arousal or excitation. It is not at all clear whether this arousal is of a phallic-sexual nature: neurobiological research indicates that this excitation can be associated with a number of different bodily systems. To my mind, this argues for the certainly vague, but nevertheless causal character of (a) as the drive excitation that only after the secondary processing through the oedipal structure acquires a phallic character. The rise in tension itself is not the cause of anxiety per se, but rather the fact that such excitation cannot be adequately psychically elaborated. It is precisely this lack of secondary processing that lies at the basis of the development of anxiety and/or somatic anxiety equivalents.
With this we return to Freud’s general hypothesis: the absence of psychological processing of the endogenous excitement is the cause of the actual neurosis. Nevertheless, such a hypothesis remains relatively biological-medical. The crucial supplement we can and must add to it is founded on recent research.
The first aspect concerns the experience of analysts in the course of treating patients with panic disorders (Milrod 1995, 1998; Milrod et al. 1997; Shear et al. 1993; Shear and Weiner 1997). Time and again, it became clear that for such patients the stress factors preceding the panic disorder invariably had to do with physical or emotional separation from significant persons or with fantasies concerning this. Faravelli’s research (Faravelli and Pallanti (1989); Faravelli et al. 1985) confirms that, compared with a normal control group, such patients were significantly more frequently confronted with the death or a life-threatening disease of a partner or relative or good friend. The crux of the problem lies in these patients’ inability to express situations of conflict, or even simply the impossibility of experiencing such situations in a psychological way; we will discuss the pertinent connection with alexithymia shortly.
These studies were confirmed from a different angle by research into biological psychiatry. Recently it has been shown that there is a correlation between separation anxiety and panic disorder (de Ruiter and van IJzendoorn 1992; Free et al. 1993; Miliora and Ulman 1996; Silove et al. 1995). Separation anxiety is defined as an intense anxiety about losing contact with a caretaker or a protective person. Here, it is not so much the actual departure of this person that is anxiety provoking but the loss of the subjective feeling of union with him or her. Hence, even a purely fantasized experience of loss can be as effective as a real loss.
We can therefore conclude that the causal factor of actualpathology, and of anxiety neurosis/panic disorder in particular, lies in the fact that the subject’s internal drive excitation is not—or is insufficiently—answered by the Other. The transition from (a) to A through which the Other supplies an answer and sets the secondary processing into motion does not occur, with the result that the initial arousal turns into anxiety and even into separation anxiety (see the element of separation in so-called agora-phobia). Anxiety neurosis is situated between (a) and A, and has no further reach. The ensuing phenomenon we are now in a position to examine—somatization disorder—also lies in between, if somewhat closer to (a) and therefore probably closer to neurasthenia.
Following the explosion of medical science and the power of its application, it is becoming increasingly clear that a number of apparently organic disorders escape medical discourse. These are indicated as “MUS”—as in medically unexplained symptoms, or somatization phenomena.7 Epidemiological studies are constantly demonstrating their high frequency in both the normal population (Drossman et al. 1993; Kroenke and Price 1993) and in every medical setting (Escobar et al. 1998; Fink 1992). The numerous studies attempting to understand this phenomenon often make the following distinction. On the one hand is a group of patients possessing a relatively clear link between somatization and an underlying psychological complaint; for them, the question then concerns the nature of this link. On the other hand, we have a group of patients where this relation is not at all clear, and where somatization occurs in itself, apparently without any connection to psychological history (De Gucht 2001; De Gucht and Fischler 2002).
The confusion here (see below) has to do with the disappearance of the category of hysteria in the DSM, thus making it necessary to place one of its core symptoms, conversion, into another category. Ever since Briquet (1859) and Freud (1978 [1894a]), conversion has been understood as the somatic and meaningful expression of a psychological conflict and its accompanying defense (repression) within a certain psychopathology, namely, hysteria; conversion is, thus, a symptom. The DSM’s atheoretical approach has thrown out this category, resulting in the need for a new distinction as far as the problem of somatization is concerned.
The solution was the creation (from the DSM-III onward) of the categories of Somatization on the one hand, and Conversion Disorder on the other, whose connection with psychological factors was presupposed. Thus we end up with two different categories, as is confirmed over and over again by research: somatization as such and somatization as the bodily expression of psychological distress. The two categories are sometimes called “functional” somatization and “presenting” somatization (Kirmayer and Robbins 1991), and have been amply confirmed by other research (Escobar 1997; Fava et al. 1995; P. Fink 1996; Portegijs et al. 1996).
The difference between these two groups is then defined as follows: the presenting somatization group is typified by the presence of an affective disorder (anxiety, depression) and the manner in which these patients present their symptoms to the doctor (MUS instead of, or in combination with, psychological symptoms). Here, the dimension of the Other is quite clear. In contrast, patients with functional somatization fail to mention any relation with psychological problems or even explicitly deny a relation between their complaints and a supposedly psychosocial origin. The latter—the real, functional or idiopathic somatization patients—are in the minority (Craig et al. 1993; Kirmayer and Robbins 1991; Kirmayer et al. 1993). The comorbidity between somatization on the one hand, and anxiety and the depressive disorders on the other is fairly high: up to 53 percent for affective disorder (depression), up to 40 percent for anxiety disorder (P. Fink 1995; Rief et al. 1992). Nevertheless, in the DSM-IV, the emphasis is on functional somatization and the other group is confusingly spread out over a number of categories.8
With respect to the “presenting somatization” group, the question remains whether one can consider somatic symptoms as a substitute for psychological problems or as mere manifestations of those problems. The first thesis follows the classical conception of conversion hysteria, where somatic phenomena are regarded as meaningful symptoms (see Chapter 13). The second thesis, in all its vagueness, is right but of little value, and testifies largely to the absence of any theoretical support.9 The contemporary notion is that somatization can be understood as a somatic equivalent of anxiety disorder or depression (Bridges and Goldberg 1985; De Gucht 2001). The connection with the classical Freudian position regarding actual neurosis (phenomena rather than symptoms) is easily made but is ignored by contemporary research.
As I said earlier, the high frequency of the somatization phenomenon has given rise to extensive research. One of the aims was to find an explanation: What is the difference between this group and a normal population, and what is the underlying mechanism? Today’s research results come to the same conclusion: at the root of MUS is a personality factor, called alexithymia (De Gucht 2001; De Gucht and Heiser 2003b). Translated literally, this means “to have no words for feelings.” The concept comes from psychoanalytic discourse (Sifneos 1973) and was later taken up in the cognitive model as a defect in the “cognitive processing and regulation of emotions” (Bagby and Taylor 1997). The concept itself was initially understood as having four dimensions; after empirical verification, a threefold structure was maintained: (1) a difficulty identifying feelings; (2) a difficulty describing feelings to others; and (3) externally oriented thinking.
Further investigation of the results (De Gucht 2001; De Gucht and Heiser 2003b) delivered the following.10 All English empirical studies (1985–2000) demonstrate a significant correlation between alexithymia and the number of reported MUS-phenomena, particularly with regard to the first factor. The correlation with the second factor is lower, but still significant; the correlation with the third is unclear. All studies comparing patients from the functional somatization group to a healthy control group demonstrate a significantly higher presence of alexithymia in the patient group. Conversely, all except one find a significantly higher presence of somatization phenomena in the alexithymia group as compared to a normal control group (that is to say, without alexithymia). The temporal stability of alexithymia in both clinical and in nonclinical populations has moreover been confirmed; this is in contrast to anxiety, depression, and negative affect, which can change considerably during the follow-up period (Haviland et al. 1988; Marinez-Sanchez et al., 1998; Salmien et al. 1994; Schmidt et al. 1993; Wise et al. [all as quoted in De Gucht 2001]). With regard to this latter affect, it is worth looking at the item analysis of De Gucht’s research (2001). Analysis of the applied instrument (the TAS-R) clearly shows how the highest correlation between the MUS and alexithymia is to be found in the first subscale “Difficulty identifying feelings,” and then particularly with regard to the following items: “I have physical sensations which even the doctors do not understand” and “I am often puzzled by sensations in my body.” This corresponds moreover with earlier research cited in the same paper.
What can we conclude from this? First, we find a confirmation of our thesis—namely, that a subject position characterized by an absence of psychological processing with regard to bodily excitations and/or phenomena does exist, and that such a structure is quite stable. Second, there are evidently two groups that can be distinguished from one another, one in which such somatizations are apparently unrelated to a psychological problem, and another that shows a clear correlation, particularly with regard to anxiety and depression but also with other psychopathological disorders, and which is brought up as such by the patients.
The DSM categorization is therefore insufficient. Despite its isolation of somatization from depression and anxiety disorder, the entry contains a confusing mix. The core description is as follows:
300.81 Somatization Disorder
B. Each of the following criteria must have been met, with individual symptoms occurring at any time during the course of disturbance:
four pain symptoms: a history of pain related to at least four different sites or functions (e.g., head, abdomen, back, joints, extremities, chest, rectum, during menstruation, during sexual intercourse, or during urination)
two gastrointestinal symptoms: a history of at least two gastrointestinal symptoms other than pain (e.g., nausea, bloating, vomiting other than during pregnancy, diarrhea, or intolerance of several different foods)
one sexual symptom: a history of at least one sexual or reproductive symptom other than pain (e.g., sexual indifference, erectile or ejaculatory dysfunction, irregular menses, excessive menstrual bleeding, vomiting throughout pregnancy)
one pseudoneurological symptom: a history of at least one symptom or deficit suggesting a neurological condition not limited to pain (conversion symptoms such as impaired coordination or balance, paralysis or localized weakness, difficulty swallowing or lump in throat, aphonia, urinary retention, hallucinations, loss of touch or pain sensation, double vision, blindness, deafness, seizures; dissociative symptoms such as amnesia; or loss of consciousness other than fainting. [American Psychiatric Association 2000, p. 490]
Characteristic Number 4 is called “conversion,” and the description itself is in fact quite classical (pseudoneurological syndromes). In this way, one opens the door to psychopathology, while in their isolated character characteristic Numbers 1 to 3 pertain to actualpathology. In addition, there is a separate category in the DSM for conversion—thus making the confusion complete. It is striking that the above-mentioned research is far more nuanced in this respect than the DSM.
The explanation found in contemporary research—alexithymia as a stable personality trait—is simply a redefinition of what used to be called actual neurosis. The Freudian definition corresponds perfectly with the previously mentioned item analysis of the TAS-R, and makes the core problem clear: “something” bodily presents itself but is neither nameable nor communicable. In a further development, this “something” clearly correlates with a psychological problem, resulting in a different population from the purely actualpathological or alexithymic. Yet this correlation is not a necessary one. What is unmistakable is how the presence of what is called “negative affect”—beside alexithymia—is the best predictor for MUS (De Gucht 2001; De Gucht and Fischler 2002; P. Fink 1995; Simon et al. 1996). This, too, fits in perfectly with what we have already described in identity formation.
Here we find ourselves back in our metapsychology. Something bodily presents itself in a negative way (unpleasure) and calls for processing. It is by way of the Other that this processing is expected to occur. Should it fail, the only possibility for the subject is to maintain this problematic at the same somatic level; the secondary elaboration is absent. That this frequently gives rise to anxiety and depression is confirmed by empirical research, and was predicted by our metapsychology. Opposed to this are the conversion symptoms, where the somatic problem is also present—albeit in a completely different way: conversion belongs to the psychopathological relation toward the Other (see Chapter 13).
What is initially a little unclear is the failure of the Other. For us, it is indeed not so much the somatic arousal itself that is the cause of the actualpathology or alexithymia, but the Other’s failing intervention. The Other must be understood, moreover, as the concrete first and second others (the parents), as well as the cultural discourse. Indeed, a study by Shorter (1994) shows that the Other, in the sense of the sociocultural discourse, has a clear influence on the specific forms of appearance of somatic symptoms. It seems as if patients obtain their somatic phenomena from a culturally determined symptom pool that varies throughout different times and places. The failure of the first and/or second other is not directly indicated in the cited research results, nor in Freud’s description of actual neurosis. As with the panic disorders, therefore, we must take a look at some studies that are more expressly focused on the treatment.
Despite the fact that such studies derive from quite different therapeutic approaches, all of the data point in the same direction. The resultant hypothesis can be summed up thus: the Other has failed in its meaning-providing function and, hence, in its protective interventions with respect to the bodily excitation. A number of studies posit somatic and sexual abuse during childhood as the etiology (Drossman et al. 1995; McCauley et al. 1997; Reilly et al. 1999). In the next chapter we will discuss the post-traumatic stress disorders that center around the Other’s impact and the dissociative somatization phenomena. Other studies discuss “social learning” as a causal factor, where once again the Other appears as a decisive factor (Barsky 1992; Pennebaker and Watson 1991; Whitehead et al. 1994). In a metastudy (Medline search, 1990–99), Van Houdenhove (2001) concludes that early attachment problems and emotional, physical, and sexual abuse play a clear role in the etiology of somatization, and that these moreover form the foundation of dysfunctional help-seeking behavior.
Within each of the different theoretical frameworks, then, the same element appears: the Other failed in its answer to the subject’s question concerning something at the level of the body.
The empirical studies cited above persuasively confirm the existence of an actualpathological structure in the subject, understood as the impossibility of translating somatic arousal into psychological representations. The correlation with the Other’s failure is also confirmed by the frequently mentioned problem of separation. The connection with our metapsychology, particularly with regard to primary identity acquisition, is clear. Clear, too, is the analogy with Fonagy’s core argument regarding the development of the subject’s first identity through the other’s mirroring of the child’s somatic arousal, although these authors fail to make the link to actualpathology (Fonagy et al. 2002).
Differential diagnostics in actualpathology must be approached from two aspects. On the one hand, the clinician must distinguish between the neurotic, psychotic, or the perverse structure of the subject. On the other, adequate attention must be paid to the nature of the affect and the accompanying phenomena.
With regard to the subjective structure, it is striking to find that the majority of research has focused almost exclusively on neurotic patients, while the post-Freudian starting point (D. Klein) took off from psychotic patients. The clinician must be aware that the actualpathological position of the subject can occur in every subjective structure, and that the typical actualpathological characteristics will be fully colored by that structure. In psychosis, this will often be hypochondria, understood as the subject’s anxious preoccupation with “something” in the body that cannot be named. Again, in psychosis, we also encounter paroxysmic anxiety attacks. In perversion, the application is considerably less clear, largely because of the lack of clinical material.
As far as the nature of the affect is concerned, three aspects can be distinguished. The first concerns a special form of anxiety—traumatic, automatic anxiety, or panic. Where this anxiety is predominant, we are facing panic disorder or anxiety neurosis (or, anxiety psychosis—see D. Klein [1964, 1980]—and schizophrenia in particular). The second concerns somatization, whether in combination with the previous form or not. Once more I must underscore how these are not constructed and therefore signifying symptoms, but anxiety equivalents of the accompanying phenomena of anxiety. Their distinction from meaningful conversion symptoms must be taken fully into account. The applicable categories here are functional somatization, neurasthenia, and, in all probability, chronic fatigue syndrome. The third point concerns the possible presence of an affective disorder, chiefly depression. This has to be clearly distinguished from its psychopathological counterpart (see Chapter 10 and Chapters 13 and 15).
These three aspects of the differential diagnostic cannot be easily isolated. The most important argument for a diagnosis of actualpathology has to do with the presence of a specific characteristic relation between the subject and the Other, understood as both language and as concrete others. This relation boils down to the fact that the Other failed in its initial verbalization of (a), with the result that the secondary elaboration was not set in motion, or only barely. The above-cited clinical studies describe a problem of separation. Our metapsychology enables us to be more precise: it is in fact a problem of alienation, in the sense that the Other failed to present sufficient signifiers with which the subject could have identified so as to have been able to cope with the bodily arousal. As a result, such patients were unable to have access to separation, being the logical-temporal process that comes after the alienation. In such cases, separation lies on the side of the Other: it is the Other that separates from the subject.
Consequently, the clinical diagnostic examination must contain a thorough exploration of the case history. This is all the more imperative because patients themselves seldom make a connection between their actualpathological phenomena on the one hand, and anxiety and depression on the other. This clinical exploration of the primary relation between the subject and the Other is particularly vital because it is precisely this relation that will repeat itself in the transference and become the aim of the treatment. To help such patients, it is this relation that must be changed.
If we understand actualpathology as an effect of a primary disturbance in the relation between the subject and the Other that results in the impossibility of a secondary elaboration and symptom construction by the patient, it will become clear that the treatment will not just be different from that for psychopathology, but will in fact be the exact opposite. To follow Freud, it is impossible to classically analyze actualpathology precisely because there is no symptom formation. Psychopathologies with accompanying secondary elaborations allow symptoms to be analyzed—to be stripped of their meaning—albeit always with the accent on the relation through which these meanings came into being. In actualpathologies, the primary aim of the treatment is the restoration or even installation of the primary relation between the subject and the Other through the therapeutic relation. It is this that will enable the subject to build up a secondary elaboration and, through the transferential relation, embed the original bodily arousal into signifiers, enabling symptoms to be constructed. To put it concretely, one must begin with an exploration of the original relation between the subject and the Other (with the emphasis on separation anxiety) and on the remaining signifiers, that is, the minimal original inscriptions of the somatic in the Symbolico-Imaginary order.11 Rather than subject analysis, the therapeutic goal here is subject amplification.12
Along with subject amplification, the need to make the therapeutic relation the goal of the treatment is shown by empirical outcome studies. Short-term outcome studies demonstrate that cognitive behavioral therapy produces the best results (Barlow 1997; Gould et al. 1995). Outcome studies in long-term treatments that focus solely on the actualpathological phenomena present a considerably less rosy picture: residual symptoms, relapse, alcoholism, and comorbidity with anxiety and affective disorders are the rule (Milrod and Bush 1996; Shear and Weiner 1997; Shear et al. 1993) for 40 to 80 percent of the patients (Rosenbaum 1997). These studies have a larger scope than the former, where improvements are almost exclusively measured in terms of the reduction of the number of somatic phenomena and panic attacks, and not on the basis of the improvement in the overall state of the patient (McNally 1994; Pollack and Otto 1997).13 It must be admitted that from a scientific perspective this latter is far harder to measure. A recent review of empirical outcome studies of mainly cognitive treatments for panic disorder (Bakker 2001) demonstrates that with longer follow-up periods the risk of relapse is fairly considerable, and that patients run a significantly higher risk of developing depression.
Clearly, to focus on somatic phenomena and/or anxiety is not enough for the treatment. Even more, the failure of such an approach—recently becoming increasingly clear—leads to a repetition of the original problem, hence the higher risk of depression in these patients. Such patients were recently designated “therapy resistant” (Lydiard and Brawman-Mintzer 1997; Rosenbaum 1997). In terms of the dialectics of the therapeutic relation, this amounts to blaming the patient—it is the patient who is the reason for the failure, she or he is “resistant”—leaving the therapist in the position of the Other. This is nothing but a repetition of the original failed relation between the subject and the Other, where the Other was unable to fulfill its task and left the subject in the lurch. The same process is recognizable in the medical approach as well: realizing that medical science is inapplicable14—that is, having inadequate signifiers at his or her disposal, the medical doctor refers the patient to a psychiatrist or clinical psychologist with whom the same process will once again be repeated. This is a painful illustration of what was already described in our metapsychology, where the original, pathogenic relation between the subject and the Other will repeat itself in the subsequent therapeutic relation! As clinicians, we need to be well aware of this so as to make this relation the precise focus of the diagnosis and the therapeutic medium.
Accordingly, merely to focus on the symptoms during the treatment—or more accurately, on the phenomena—will never be enough. There has recently been renewed interest in a broader psychoanalytic treatment of these disorders that combines classical Freudian data with contemporary research results (Bush et al. 1999; Comptom 1998; Hebbrecht 1998; Miliora and Ulman 1996; Milrod et al. 1997). The hardest part in such a therapeutic approach is the analyst’s ever-present tendency to interpret somatic phenomena and/or anxiety as meaningful symptoms, while the patient is not yet able to do so. The patient’s complaints are thereby turned into metaphors, which is precisely what they are not. Inevitably, such a misunderstanding induces guilt in the patient.15 Rather, the emphasis must be on the creation of a therapeutic context through which the patient—with the help of the Other’s interventions—can develop his or her own meanings.
Once more, this testifies to the importance of making a correct diagnosis, one focusing on the original relation between the subject and the Other. The diagnostic distinction between an actualpathology and psychopathology must re-emerge in a clearly differentiated therapeutic approach. This will also be true for the differential diagnostic group to be discussed in Chapter 12: The post-traumatic stress disorders and the borderline spectrum.
1. Let us not forget that the term “neurosis” originally covered almost the entire field of psychopathology, including what are known today as psychosis and perversion. These latter categories are more recent and appear at least partly thanks to Freud. In order to take account of today’s differentiation, we will talk about actualpathology versus psychopathology.
2. Equivalents, that is to say, not substitutes. With substitutes we would be dealing with signifying symptoms and therefore with psychopathology.
3. Freud isolated anxiety neurosis from what was then a very broad description of neurasthenia that encompassed practically everything. This is shown in the title of his paper: “On the grounds for detaching a particular syndrome from neurasthenia under the description anxiety neurosis” (Freud 1978 [1895b]).
4. Note that this supports the distinction between the actualpathological and a psychopathological position in the psychotic structure. A psychotic structure without symptoms does indeed exist, that is to say, without delusions and hallucinations. Freud’s original study of the anxiety neurosis was mainly concerned with the neurotic spectrum. Only later did he add schizophrenia because of the presence of hypochondria (Freud 1978 [1914c]).
5. During a certain period, the relation between hyperventilation attacks and panic disorders was also the topic of intensive research. On the basis of this research, hyperventilation is now considered a side phenomenon that can occur during an anxiety attack, that is, as part of what Freud regarded as respiratory difficulties.
6. Through research into primates, it was shown that there is a clear relation between addiction (alcoholism) and separation (Higly et al. 1996). As we will see later on, the failure of the primary relation between the subject and the Other is also central to actualpathology.
7. Lipowski (1988, p. 1359) classically defines it as “the tendency to experience and communicate somatic distress and symptoms unaccounted for by pathological findings, to attribute them to physical illness, and to seek medical help for them.”
8. The major confusion lies in the way Conversion belongs to the description of the Somatization Disorder (300.81, ad B4), while also receiving its own separate category (300.11 Conversion Disorder). Moreover, in yet a third category, “Pain Disorder,” a relation with psychological factors is also presupposed (American Psychiatric Association 2000, p. 503), so that part of the “old” conversion hysteria also assumes its place here (more specifically: paresthesias).
9. What has been confirmed up till now is a parallel increase in the number of MUS-symptoms on the one hand, and the extent of psychological distress reported by the patients on the other (Simon et al. 1996; Simon and Gureje 1999). To imagine that there is a relation between them would call for a theory but clearly that would be going too far today.
10. The most validated and internally consistent instrument is the TAS-R (the Toronto Alexithymia Scale) (Bagby et al. 1994).
11. This means that the clinician must look for things like childhood diseases and the parental reaction to them—there are almost always residual signifiers to be found concerning both the original relationship to the Other and its inscription on the body. Beginning with these signifiers, the clinician needs to create the context through which this originally omitted process can nevertheless be carried out inside an expressly guaranteeing therapeutic relation. Where the therapist him or herself produces signifiers and significations from within a University or Master discourse, the risk of inducing guilt on the patient’s part is immense (see Note 3 in Chapter 10).
12. It is striking how Fonagy et al. (2002) come to the same conclusion: classical interpretations do not work with these patients. Instead, they propose a therapeutic approach in which the original mirroring process is reperformed, founded on the actual reality of the therapeutic interaction.
13. These new studies resulted in a surprising discovery: the majority of patients (up to 80 percent) underwent additional treatment during the follow-up period after the first treatment that the outcome studies were attempting to measure. Because most of the studies following the first treatment failed to inquire into the possibility of additional treatment during the follow-up period, their results are dubious (de Beurs et al. 1999).
14. It is no coincidence that medical doctors experience such patients as “difficult and frustrating.” Consequently, their referral is actually a rejection (Hahn et al. 1996; Walker et al. 1997). Nor is it a coincidence that these patients frequently decide to organize self-help groups—that is to say, with the exclusion of the professional Other; sometimes these organizations even take juridical steps to get their members’ status as patients officially recognized.
15. In Chapter 10 we referred to Sontag (1979) with regard to the guilt-inducing impact of a certain so-called “psychosomatic” approach. In the words of Sontag herself: “Nothing is more punitive than to give a disease a meaning—that meaning being invariably a moralistic one” (p. 57).