How Could Lacanian Theory Contribute to DSM-5?
Discussion of diagnosis of Bipolar disorder and the controversy around grief versus clinical depression


DSM-5, a new updated version of DSM, has been finally published after ten years of a heated debate. DSM-5 raised a lot of controversy. Allen Frances, MD, who chaired the DSM-IV Task Force, expressed his concern that “DSM-5 will result in the mislabeling of potentially millions of people who are basically normal.” With the new version of the manual, grief may quickly turn into Major Depressive Disorder. In this paper, we would like to look at some of the DSM-5 changes mentioned above with the help of Lacanian theory. From a Lacanian point of view depression is not only caused by the accidental loss of a reality object/family member, but also by the lack of loss of a partial object in normal development. By pathologizing grief, psychiatry risks that people may not want to grieve or could feel that they should not grieve, but if they don’t grieve they may thereby be paradoxically predisposed to depression. We also discuss the popular diagnosis of Bipolar disorder, and explore DSM changes in the context of psychoanalytic theories. What could Lacanian theory offer to DSM? Finally, we would like to touch on the never-ending debate between mood swings in the borderline character versus mood fluctuations in the Bipolar II condition.



While the first Diagnostic and Statistical Manual of Mental Disorders (DSM-1) was published in 1952, its origins date back to 1840, at a time when the US government wanted to collect data on mental illness. It is interesting that the census used the terms ‘idiocy/insanity’ without any inhibitions. In a sense someone was either ‘normal’ or ‘insane’ ­the classification was very simple. Over a 40-year period of time ‘insane’ included seven categories: “mania, melancholia, monomania, paresis, dementia, dipsomania and epilepsy.”

From these seven categories, the 1952 DSM-I featured descriptions of 106 disorders, which were referred to as ‘reactions.’ Sixteen years later in 1968, the DSM-II further increased the number of disorders to 182.  Both DSM-I and II were driven mainly by the psychodynamic view up until 1980, when DSM-III came out with a whole new perspective to focus on empirical descriptions. At that point we had an impressive number of 265 diagnostic categories. With DSM-IV in 1994 we reached over 300 categories with not too many changes.  That brings us to DSM-5, with over 1000 pages of checklists of symptoms that psychiatrists around the world use to diagnose their patients.

There seemed to be one big change in the history of DSM that occurred between DSM-II and III. The changes reflect how mental health professionals initially viewed mental illness mostly through psychodynamic lenses, and conceptualized it as the product of conflict between internal drives/wishes and defenses. In DSM-I and II symptoms were largely irrelevant to diagnosis. DSM-III opted to follow Emil Kraepelin rather than Sigmund Freud. The idea of separate syndromes and disorders was created, so that bipolar disorder, schizophrenia and major depressive disorders were supposed to be treated differently and had unique causes.

With DSM-5 we have certainly come a long way from the 1840 ‘one disorder’ of insanity to over 300 nicely described illnesses and disturbances with outlined symptoms and their duration. Unfortunately patients don’t read the textbooks. Psychiatrists and other mental health professionals are often frustrated that their clients rarely fit into neat categories. In addition, symptoms frequently change over time. It often leads to patients becoming sort of “collectors” of different diagnoses, which can be very upsetting to them. It can also lead to polypharmacy, which can be outright dangerous. We try to bring basic research to help with the clarification. We dream about genetic, metabolic and imaging tests that will help us to diagnose better and faster. Unfortunately, the biological tests only support the idea that psychiatric disorders overlap, and that perhaps less is more.


Studies with functional magnetic resonance imaging show that people with anxiety disorders and those with mood disorders share a hyperactive response of the brain’s amygdala region to negative emotion and aversion. Similarly, those with schizophrenia and those with post-traumatic stress disorder both show unusual activity in the prefrontal cortex when asked to carry out tasks that require sustained attention. (Dichter, G. S., Damiano, C. A. & Allen, J. A. J., 2012).


Genetics brings similar findings (Craddock, N. & Owen, M. J., 2010).

Publication of DSM-5 brought a lot of criticism not only from more psychodynamically oriented providers but also from biological psychiatrists and researchers. The National Institute of Mental Health (NIMH) withdrew their funding from DSM two weeks before its publication. Thomas R. Insel, M.D., Director of NIMH, criticized DSM for “its lack of validity” and suggested that “Patients with mental disorders deserve better.” He suggested that a new way for psychiatric nosology is reliance on biology and that “mapping the cognitive, neuronal circuit, and genetic aspects of mental disorders will yield new and better targets for treatment.”

It is a highly promising approach, although we claim here that “anatomy is not destiny”, and that humans are even more complicated than cognitive, neuronal circuits, and genetic aspects of their being.

We would like to look at the process of the creation of DSM 5. It may sound like a cliché but somehow an individual patient is lost in the classification battle. Moreover, no one is asking them how they feel about their ‘disorders’ or why they think they may have them. They become like broken machines spitting out symptoms at the time of diagnosis. The DSM only seems to be interested in what they do rather than why or how or even what they think about it. Sam Kriss’ interesting paper, “Book of Lamentations”, makes such an observation: 


A person who shits on the kitchen floor because it gives them erotic pleasure and a person who shits on the kitchen floor to ward off the demons living in the cupboard are both shunted into the diagnostic category of encopresis. It’s not just that their thought-process don’t matter, it’s as if they don’t exist. The human being is a web of flesh spun over a void.


How could Lacanian theory contribute?


Lacan is one of the most controversial psychoanalysts. One of his most misrepresented statements, “the unconscious is structured like a language,” allowed him to disagree with Freud’s “anatomy is destiny.” He also redefined the concept of drives and did not think that they are purely biologically driven. What interests us most here is that during the 50s, he spent a lot of time trying to combine the topology of surfaces (torus, Moebius band, Klein bottles, crosscaps) with mental life. He claimed that the linguistic signifier, the logic of desire, fantasy, and drives follow the logic of topology. Lacan claimed that it is the best way we can describe the subject in his or her complexity.

When we speak of the human subject, or of the influence of language on the mind/brain, and how culture shapes our otherwise natural inclinations, or how topology may describe psychical structures, we are referring to phenomena beyond the distinction between normality and pathology.

So why is the study of psychopathology necessary and important? The reason is that just as there is health and illness in the body; there is also a mental ‘dis-ease’ of the mind. And nature shows that the dis-ease of the mind tends to break down in discernable patterns and structures. Psychoanalysis is distinguished from psychiatry in that for psychoanalysis there is continuity between normality and pathology. Freud was the first to call his theory of mind a topographical theory. The deep topological structures can manifest via the structures that they are but also through what appears on the surfaces that we could consider symptoms.

Neurosis as representing a divided form of subjectivity is the basic condition of human beings. Human beings are caught between nature, and culture and culture demands that they shape their bodies and minds according to cultural forms. This is where both normality and pathology begin. Such neurosis is built into a person’s characterological structure. The various types of personality traits may or may not turn into dysfunctional and incapacitating symptoms, but the possibilities lie within the traits and the corresponding brain mechanisms.

Consider this clinical vignette. A 22-year-old female with no past psychiatric history arrives for a first consultation to your office. When asked about her goal of the assessment, she says that she “just wants to manage her highs and lows.” She then goes into a detailed description of how both ends of her mood fluctuations wrecked her relationships and her entire semester in college. She says that she experienced her most intense ‘high’ in her senior year of high school. When her boyfriend broke up with her, she started on a self-destructive path; she did not need to sleep and felt very energetic. She described herself as hypersexual, reckless, careless, and very impulsive. She said the episode lasted for about two weeks until her friends stopped talking to her and, completely exhausted, she ‘rolled into’ her ‘low.’ She mentioned that her ‘lows’ are usually marked by extreme sadness, lack of drive, anhedonia, fatigue and ‘complete shutdown.’ Interestingly, she also raised the question as to whether she had an adult ADHD (Attention Deficit Hyperactivity Disorder)–a new feature of DSM-5. She did great in elementary school but since high school has been unable to focus on anything. Upon further questioning, our patient admitted that cutting was the only thing that helped her with mood swings. She said that she tends to get obsessed about people only to drop them when her interest fades. She has a hard time tolerating being dumped by her boyfriends and lists it as the main cause of her ‘highs.’

What does she have? Bipolar disorder type I, II, or could we perhaps explain most of her symptoms with untreated borderline personality disorder? Does she have comorbid adult ADHD? Maybe she has all the above? Why does a seemingly ‘typical’ case presentation present such a challenge? Here we suggest that perhaps because DSM is not a very precise diagnostic tool, symptoms that ‘create’ disorders are not very specific, and they often overlap.

Lacanian topology can help us to be more precise. The main advantage of topology is that shape has no meaning there; we even call it “geometry of the rubber sheet.” We can stretch it, bend it, it does not matter as long as its structure is preserved. If nothing else, it is a wonderful metaphor where for once we don’t judge people by appearances but instead are more interested in their structure. For Lacan it would be a seemingly simple question, mainly because it is a grossly limited choice: is the person sitting in front of me in the consulting room psychotic, neurotic or perverse? There are clearly defined differences between these three diagnostic categories that have serious implications in terms of treatment and prognosis. The differences are not only superficial, but are also present on the level of the unconscious, Oedipal and family structure, the way the subject relates to language, and maybe most importantly the nature of their social link.

We would like to emphasize the fact that what we are suggesting here is not the oversimplification of diagnosis, but in fact a way to make it more sophisticated and closer to what we observe in the clinic and in basic research. We have established that neuroscientific and genetic findings (Dichter et al, 2012; Craddock & Owen, 2010) don’t support the breakdown of many mental disorders into separate categories.

Perhaps the actual state of affairs is that we have a few structural differences/diagnoses that reflect changes on the level of the unconscious, but also the biology (in a broad sense of the term), and additionally, since every subject is unique we observe different symptoms and signs ‘on the surface.’ For example, we may see a patient with a psychotic structure and obsessive, OCD-like behaviors or hoarding on the surface. Another example would be the diagnosis of schizoaffective disorder. Here we would see it as a psychotic structure with mood symptoms on the surface.

Our question remains: how is it that from one disorder of the mind we now have more than 300 illnesses, which seem to just keep multiplying. We think it is because psychiatry has tried to describe all the variations within the main categories as separate disorders. With so many of them, symptoms overlap, and this leads to diagnostic chaos and real difficulties for research.  Some psychiatrists/researchers have made an attempt to modify the approach that DSM has taken. For example, Craddock and Owen (2010) proposed the model of dimensional spectrum–see the image below:

 [click on this image]

 pict 1


From David A. Mental health: On the spectrum 24 April 2013;


Following the model of dimensional spectrum, we propose five diagnostic structural categories: autism-psychosis-borderline-perversion-neurosis. In addition, every structure is further described with specific symptoms and signs that are observed on the surface of a particular subject’s topological structure. There are definite differences between structural categories; for example, a psychotic subject will be very different from a neurotic one. The symptoms and signs are on the spectrum and overlap. Genes and environment interact with each other and with the structure, and produce particular symptoms accordingly.


[click on this image]

Moncayo 3a 


Now, following Freud, we can differentiate the topological structures according to a specific defense formation and a point of developmental fixation. See the table below.







against being born and to live in diachronic or chronological time

absolute primary narcissism


identification with imaginary phallus and foreclosure of Name-of-the-Father

relative primary narcissism


Intersubjective splitting

on the specular image

ideal ego


disavowal of the law

on the lack 


identification with- avowal of the law: repression

on ego ideal



The autistic pre-subject lives in a solipsistic timeless bubble that includes the individual and his mother/Other, and this One contains the entire world. Freud described absolute primary narcissism as the condition of intrauterine life, where the body of the mother and the baby are not differentiated. No distinction between self and other exists, yet the mother and the child are related to each other within the One bubble. The autistic pre-subject refuses to be born outside the One body/bubble and may not speak or use language. The father as a function is irrelevant for the autistic pre-subject.

In psychoses, the pre-subject is identified with the breast-child as a phallic object of the jouissance of the Other (what object am I for the Other?). The psychotic is primarily a relative narcissistic object of the mother. There is no ‘subject proper’ or integrated specular body image. The psychotic speaks, but the order of language, not being tied together by the paternal metaphor or NoF (Name of the Father), results in loose associations. It is a primary form of narcissism because the subject has not been differentiated from the object and the libido rests entirely on the pre-subject as an object (of the mother’s fantasy). The father is either brutal and cannot be symbolized as a function, or fails to mediate/castrate the mother/child fusion.

The borderline subject has attained secondary narcissism, a symbolic name and an integrated imaginary ideal ego (body image), but remains fixated to the whole image and to being the object of the mother’s desire. The borderline cannot recognize the flaws in the image or the aspect of the mother’s desire that is turned towards the Other/father. Any flaw in the other turns the other bad and, by the same token, the borderline subject good and perfect. Conversely, if the other is seen as embodying the good and perfect specular image, then the subject becomes bad and unlovable, and a failure in being the object ‘cause of the other’s desire’. Here the borderline risks psychotic disintegration and regression to a malevolent form of depersonalization. To the right of the structure, or upward in development, the borderline subject can also manifest overt asocial or non-normative traits. The borderline can typically have problems with drug addiction, wear atypical clothing, have problems with impulse control, engage in sexual acting out, and have many body piercings and tattoos.

The pervert/sociopath has encountered the lack/flaw in the specular image and recognized the presence of the father, but the law and Name-of-the-Father is disavowed, and the subject remains fixated on the lack as a pure negativity without a constructive function. Otherwise, the pervert can appear to be perfectly normal, charming, and conventional.

The latter takes us to the neurotic structure where conventionality is structural and not only on the surface as in the pervert. The neurotic avows the Law, identifies with it, and modifies/inhibits/adapts itself accordingly. The neurotic uses repression as a defense and is fixated on the narcissism of the ego ideal. The neurotic aspires to be complete and consistent by being a good boy/girl and lovable to the ego ideal and the normative values of society.


Medical History of Bipolar Disorder


A good question that we may pose here is where should we locate bipolar disorder in the maze outlined above? We suggest that perhaps we could take another travel in time and look at the medical history of bipolar disorder. It seems that the earliest written description of the illness can be traced back to 30-150 A.D. Around that time Aretaeus, a Greek medical phylosopher from Cappadocia, wrote texts referring to a unified concept of manic-depressive illness originating in disorders of ‘black bile.’

Then, the illness was seemingly lost in the custom to describe all mental diseases as insanity, until the mid-19th century publications of PhilippePinel’s Treatise on Insanity (1806) and John Haslam’s Observations on Madness and Melancholy (1809) reintroduced the concept of bipolar disease back into Western medicine. On January 31, 1854, Jules Baillarger described to the French Imperial Academy of Medicine a biphasic mental illness causing recurrent shifts between mania and depression, which was defined two weeks later by Jean-Pierre Falret as folie circulaire (‘circular insanity’). Emil Kraepelin also provided a detailed clinical description for bipolar disorder: “Manic-depressive insanity [as it will be described in this section] …includes on the one hand the whole domain of so-called periodic and circular insanity, on the other hand simple mania, [and] the greater part of the morbid states termed melancholia.”

When we think about diagnosis in terms of the DSM, it was in the DSM-III that the term ‘bipolar disorder’ replaced the term ‘manic depressive disorder.’ It was also DSM-III that for the first time mentioned pediatric bipolar disorder. DSM-III-R brought further classification of the disorder into subtypes such as Bipolar Disorder-Mixed, Bipolar Disorder-Manic, Bipolar Disorder-Depressed, Bipolar Disorder-Not Otherwise Specified, and Cyclothymia. In the DSM-IV and DSM-IV-TR, it was decided to divide the illness into two separate types distinguished by the type of mania: Bipolar I and Bipolar II. In Bipolar I Disorder, patients suffer from at least one manic episode and one depressive episode, while in Bipolar II Disorder, individuals experience at least one hypomanic episode and at least one major depressive episode. DSM-5’s main change was adding the criteria of increase in energy in addition to mood changes, which can be seen at as an attempt to tighten the criteria. Also, bipolar not otherwise specified (BP NOS) has been replaced by bipolar not elsewhere classified (BP NEC), with a better defined subthreshold for bipolar variations. At the same time, the committee created an interesting hybrid of ‘mixed state’ with a very broad spectrum of manic and depressive symptoms.

To quickly summarize the above, we went from simple ‘manic-depressive’ single illness to many different ones with various subgroups and additional qualifiers. The question remains: does ‘more’ mean a better, more accurate diagnosis or just more confusion? The question is important because diagnosis has tremendous implications in treatment, research studies, etc.

Psychoanalytic Understanding of Manic-Depression


Early on in the psychoanalytic movement, Karl Abraham noted that in mania, complexes overcome inhibitions and the patient reverts to the carefree state of childhood.

               Freud (1917) saw mania as a reversal of depression and as the psychopathological counterpart to the socially sanctioned group celebration of festivals. In many cultures funerals are also viewed as a time for celebration. So what an individual does as a function of individual pathology may constitute a split-off derivative of normative ritual behavior wherein opposite feelings (grief and joy, for example) are included.

               So what an individual does as a function of individual pathology may be equivalent to normative and normal group psychology and behavior in other cultures.

               Freud distinguishes depression and mania by the relations between the ego and super-ego. In depression the super ego is the exacting and cruel (sadistic) master of the ego. In mania the ego has triumphed over the super-ego and dances a victory dance over the body of the dead super-ego. It is the victory over the super-ego that frees the narcissistic ego from the inhibitions of the super-ego and allows the ego to reinstate an infantile form of omnipotence.

               For Freud, mania involved the denial of the primal ‘manic’ and cannibalistic crime of killing and eating the primal father. However, Abraham believed that the murderous fantasies of the manic patient were primarily directed towards the mother.

               ‘Manic defense’ was a term first used by Melanie Klein (1935) to describe a set of mental mechanisms aimed at protecting the ego from depressive and paranoid anxieties. Omnipotence, denial and idealization are the three constituents of manic defense. Omnipotence is used to control objects but without any recognition of the object as a subject (or what object relations call a genuine concern for the other). The other is an imaginary object of fantasy similar to the omnipotence of the mother-child fusion, where the child functions as the imaginary phallus of the mother that completes her and closes her lack of being. In this state of affairs, the function of the Name of the Father that symbolically castrates and humanizes the subject is not operative, at least on the surface. This would seem to, psychoanalytically speaking, place acute mania at least as a psychotic symptom, but not necessarily a structure, since the symptom is episodic and does go into spontaneous remission even if untreated with mood stabilizing medication.

               The feeling of concern for the intersubjective other is predicated on the other existing as a subject rather than as an object. The other as a subject is differentiated from the other as an object of fantasy. The other as a subject cannot exist without the symbolic function of the father or the paternal metaphor (Name of the Father/Desire of the Mother). The Kleinian depressive position (even if it is considered as an anaclitic or attachment based form of depression), or the early maternal super-ego, that Klein theorized in relationship to the good and bad breast, cannot be thought independently from the symbolic phallic function. With Lacan’s formula for the relationship between the objet a and the phallus (a/-phi=objet a closes a gap or lack of imaginary phallus), the symbolic dimensions of the breast and the phallus can be properly understood in their structuring psychical/subjective function. The fantasized fear that the child may have hurt the mother or the good breast cannot exist without some awareness of being a subject. The latter does not happen before the specular image and the name of the subject as unary traces have been established. For the mother to give of herself and of her breast to the child, and for the child to have a specular image, requires that the mother relinquish the objet a as predicated by the function of symbolic castration.

As stated above, from a Lacanian point of view depression is not only caused by the accidental loss of a reality object/family member or the loss of the love of an important childhood figure, but also by the lack of loss of a partial object in normal development.  In both cases, the losses are not grieved: however, in the second case, the partial object is not grieved not because a loss took place and was denied, but because the necessary structural loss never happened in the first place (Hassoun, 1997; Moncayo, 2008).

According to psychoanalytic theory, in ‘normal’ development a child has to lose: the breast during weaning and the oral phase; feces during the anal phase and the acquisition of sphincter control; and the phallus during the genital phase. These are not accidental losses of a partial object, but losses that are necessary for the development of human subjectivity. By pathologizing grief, psychiatry risks that people either may not want to grieve or could feel that they should not grieve, but if they don’t grieve they may thereby be paradoxically predisposed to depression. This would occur not because they didn’t grieve the accidental loss of a reality object but because they didn’t grieve the necessary losses that take place during the course of normal development. Pathologizing grief is consistent with the consumer society of late capitalism, where everyone is expected to be happy and where there is no place for the positive and constructive function of lack and grief. 

               Regarding the psychoanalytic treatment of manic depression, the resistances to treatment have to be understood from the structure rather than from the surface of the symptoms. The manic symptom may temporarily hinder the patient’s capacity for insight or the desire to know something about their symptom, or to take responsibility for it or desire to change or alter their relationship to the symptom. But once the symptom goes into remission, the question of future relapses and accessibility to treatment will be decided by the structure in which the symptom takes place. 

With regards to the Lacanian understanding of manic depression proper, the following observations can be made. First of all, in our opinion, the fact that Lacan did not speak much about manic depression as Freud had previously done follows from a very important consideration: forLacan, the most important question was whether this patient’s Bipolar Disorder stemmed from a neurotic, pervert or psychotic structure—to which we suggest adding Borderline. The mania is only a symptom that can be present in all structures. 

If Bipolar Disorder stems from a neurotic structure, then the person with Bipolar Disorder can be stable between episodes, with or without medication–something impossible for the psychotic, who is always psychotic. Moreover, in Bipolar Disorder with a neurotic structure, psychotic features are driven by the intensity of the affect during episodes, while mood fluctuations in bipolar patients seem to have continuity with mood fluctuations in normal neurotics (most people are neurotic) and even with the mood swings observed in the borderline character that often cannot be distinguished from the mood fluctuations in the Bipolar II condition.

The question of success and failure and of competition is a crucial question and value, especially for modern capitalist societies. It is in fact difficult to separate the goals and objectives leading to success (or failure) from feelings of positive or negative self-esteem. Thinking that one is good or bad, successful or a failure, lovable or unlovable, and feeling good or bad, up or down, euphoric or dysphoric, are closely tied together.  

In addition, psychoanalytic theory prior to Lacan had a consistent theme related to what Klein called a manic defense against depression. However, in the clinic the same mechanism or presentation is not always observed. Every bipolar patient is different and they engage in their manic symptoms for different reasons. Some patients may be purely biological; others are seriously narcissistic subjects who present their grandiosity in such a way that it looks like mania, while others are psychotics, who can present their psychosis through grandiosity and elation (“I am god”).


Case presentation


Let’s use another vignette to clarify the concepts described above, that of a 31-year-old Caucasian male with a clearly defined history of bipolar disorder. During the intake interview he reported that his first manic episode lasted one week, occurred during his teenage years, and ended in hospitalization for several months. His last major manic episode was a few years prior to starting psychotherapy and apparently lasted a few months. During that time he experienced euphoria, a decreased need for sleep, racing thoughts, and some delusional thinking. He also got into some fights and spent a lot of his money. He stopped taking his medications, and was using alcohol to help with his racing thoughts.

The patient started psychotherapy treatment every two weeks. He continued to refuse to take any medications and instead decided to manage his mania with three hours of exercise a day. He also said that he received a lot of support from his girlfriend whom he’s been seeing twice a week. He went to Psychiatric Emergency soon after beginning his treatment, after he woke up from a beating.  It was discovered that he had skull fractures, and a plate had to be inserted in his forehead, which left him temporarily bald and with ear-to-ear stitches in his skull. The only thing that he could remember was that he had gotten drunk at a bar and had had an argument with a bouncer outside.

The patient, a very smart undergraduate philosophy student who had finished all his coursework but had never obtained his degree, had been working at the gym and as a cook on weekends. His personal history was filled with significant mood swings, unstable relationships, and poor performance at school and work.

In significant distress, he also had odd perceptual experiences such as feeling that the walls and floor were moving and buildings were bending over. In a closed space, he thought there was a hole in the wall and thirteen floors beneath him. He also had some out-of-body experiences, where the seat of perception was removed from his body and he felt likeapieceoffurnitureintheroom. While manic, the patient described an euphoric mood, grandiosity (thinking he is god), pressured speech and lack of sleep.

At the beginning of treatment, the patient not only did not want to take medications, but also questioned the entire therapeutic endeavor by saying that he enjoyed the suffering produced by his symptoms.  He explained that the values that claim that health is better than illness were signs of a corrupt social system in which he did not want to participate   So the question thus arose as to why he was coming to treatment at all, what did he want, what was he looking for?  Although the patient could not answer any of these questions, the psychotherapist went along with his rejection of the health and well-being ideal and stated to him, “You also don’t mind when the floor moves under you or the walls undulate like water.”  At that point, the patient began having the symptom and became very distressed.  The psychotherapist responded by normalizing his experience in support of what the patient had said earlier, stating “Well, sometimes objects can stand still, and sometimes they can move just like people”after which the patient’s symptom disappeared as quickly as it had appeared a minute prior.  With this intervention the therapeutic relationship was strengthened, given that it had had an obvious immediate benefit to the mental state of the patient. The patient never returned to the position of either defending the suffering produced by the symptom, or questioning the value of the treatment.

The patient’s father had killed himself when he was young.  His mother has been about to leave the father when he shot himself.  The patient saw his father, who was illiterate, as a failure in life, and had never been close to him.. For his mother, the father’s suicide had been a relief.  She remarried, but he had never become very close to his stepfather in twenty years.  He blamed his mother for ‘over-sharing’ the details of her romantic life, and for his father’s death. The patient described her as a good caretaker but a“gatekeeper,”angry more than anything else, and not very affectionate.


Original Diagnosis: (DSM-IV)


Axis I             Bipolar I Disorder with psychotic symptoms, currently depressed

Alcohol Abuse

Panic disorder with no agoraphobia

Axis II           Borderline Personality Disorder 

Axis III           Multiple head injuries

Axis IV          Problems related to social environment and economic problems

Axis V            GAF: 50


The DSM-5 diagnosis does not have axial representation.  There is no GAF.  And agoraphobia and panic disorder are now separate diagnoses.  However, the part that most interests us here is the diagnosis of bipolar disorder, which would stay the same.  Perhaps this is a case where we would add Anxious Distress Specifier.  Apparently, as per DSM-5 guidelines, this specifier is intended to identify patients with anxiety symptoms that are not part of the bipolar diagnostic criteria.  Regardless of how we try to narrow down the diagnosis, there are still many of them to consider.

We would like to emphasize that the patient was initially refusing medications, said they made him feel worse, that he couldn’t think when he was on them, and that they took away all his motivation, etc.  The psychotherapist helped him to understand that the continuum between self and no-self is normal, but in his case what was missing was the ability to also differentiate between them.  The therapist also linked this developmental achievement with the body image and the ideal ego as a product of the relationship with the mother.  It is interesting that the patient responded to intervention.  Treating his character seemed to help with his bipolar symptoms.  He was also able to discuss the question of his desire.  Despite his reporting occasional psychotic-like symptoms, in sessions he did not show any language disturbances or loose associations.  He was able to use metaphors well, associate to his dreams, and have some insight into his delusions.  With all the above, the patient was diagnosed as having a neurotic structure with psychotic symptoms, mood swings, and alcohol abuse.

With the help of his therapist, the patient was able to accept that mania was a defense against depression.  Here cognized the difference between grief and depression, and the fact that he did not have feelings when his father died when he was a teen.  He then recalled becoming depressed a few years later, which was followed by his first manic episode.  During the course of therapy, the patient used disavowal of the law as a defense.  He struggled with the idea of starting a job versus being homeless and spending his days just studying in the library.  His desire to be stable is above all his girlfriend’s desire, and he alternates between following it and defying it.


Discussion of the Case


In Frieda Fromm-Reichmann’s (1954) interpersonal studies and treatment of manic-depressive patients, she observed many significant parent-child interactions that seemed to characterize the families of patients suffering from manic depression.  Consistent with the findings of the histories of patients with Major Depression, they had sustained significant environmental losses during their childhood.  It remains unclear why some patients sustain losses and do not develop Major Depression, or why some people sustain losses, develop Major Depression, but do not develop manic episodes/defenses.

If we follow Freud’s theory of the complemental series, then the environmental traumatic factors by themselves are not sufficient to produce a symptom or a structure for that matter.  Oedipal structure is as important if not more important than the family history/narrative in question.  In addition, the two series may have various ways of interacting.

For example, the patient may have failed to grieve the Oedipal loss of his mother due to the family failures of the father, who was too weak to have a significant impact on the mother-son dyad.  Not only did the father perform poorly as a provider and in the family, but his failure as a provider may have also affected the status and isolation of the family within the community, a finding that is consistent with the families of the patients that Fromm-Reichman studied.

Then the question is: why the additional tendency towards mania? This patient may well have been emboldened as the mother’s ‘prince’ to take a ‘greater’ role in the family, even to the extent of replacing his father, especially upon his death.  The mother may have enlisted the son to remedy the problematic situation with the father.  The patient may have also experienced the suicide of his father as a personal triumph and victory in battle, similar to how Freud described the dance of the victor over the body of the dead enemy/father. The disturbance in the patient’s work ethic may also be seen as an identification with the same disturbance in the father, and as an extension of the poor example and authority figure that the father represented and that the son challenged.  The patient said that the father’s suicide made him question reality and mistrust people.




Lacanian topology may have a lot to offer in the process of improving our diagnostic process.  Lacan’s division of people’s structure into psychotic, perverted and neurotic brings an interesting point of view in terms of nosology.  There are clearly defined differences between these three diagnostic categories not only on a superficial level but also in the unconscious, in the Oedipal and family structure, in the way the subject relates to language, and maybe most importantly, in the nature of their social link.

Such a classification seems to be closer to what we observe in the clinic and in basic research.  In this paper, we suggest diagnosing patients based on their psychical structure, describing their symptoms present on the surface, and mentioning genetic and environmental factors that may play a role.  It seems that such an approach holds the promise of being more individualized and truer to particular subjects.  It could also help in tailoring therapeutic interventions better and more effectively.  Most important, it will allow for a better prognosis and plan for future treatments.




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