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Borderline Personality Disorder Reconsidered

May 28th, 2009 by David Kronemyer · 6 Comments

Overview of Disorder

Borderline Personality Disorder (“BPD”) is an Axis II Cluster B personality disorder. It is defined at DSM-IV-TR 301.83 as a “pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity beginning by early adulthood and present in a variety of contexts.” Five or more of the following nine symptoms must be present:

1. Frantic efforts to avoid real or imagined abandonment.

2. A pattern of unstable and intense interpersonal relationships characterized by alternating between extremes of idealization and devaluation.

3. Identity disturbance: markedly and persistently unstable self-image or sense of self.

4. Impulsivity in at least two areas that are potentially self-damaging (e.g. spending, sex, substance abuse, reckless driving, binge eating).

5. Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior.

6. Affective instability due to a marked reactivity of mood (e.g. intense episodic dysphoria, irritability, or anxiety usually lasting a few hours and only rarely more than a few days).

7. Chronic feelings of emptiness.

8. Inappropriate, intense anger or difficulty controlling anger (e.g. frequent displays of temper, constant anger, recurrent physical fights).

9. Transient, stress-related paranoid ideation or severe dissociative symptoms. DSM-IV-TR in turn defines a “personality disorder” as “an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture.”

The adjective “borderline” is misleading in that BPD has little to do with borders or lines. Originally derived from psychoanalysis (Kernberg, 1967), it was supposed to designate a zone between psychotic and neurotic disorders. With typical hubris psychoanalysis both over-reached and under-stated the phenomena it purported to describe. Psychotic patients suffer from serious Axis I pathology. The term “neurosis” is polythetic and could mean almost anything; it so broad that it has no clinical efficacy. From the standpoint of two-dimensional spatial metaphor it makes more sense to think of BPD as a pathology contained within a circle, not on one side or another of a border or a line. The circle’s diameter is permeable so individual symptoms have the capacity to diffuse in and out in response to social, psychodynamic and neurochemical triggers – much like ligands binding to counterpart receptors.

A second problem with BPD is that the elements of its definition are indeterminate. In this it partakes of the other well-known structural infirmities associated with the DSM. For this reason BPD frequently is confused or comorbid with other mood and personality disorders (Bagge et al, 2004).

Epidemiology

BPD occurs in approximately 1% – 2% of the population (Oldham, 2004; Lenzenweger et al., 2007). DSM-IV-TR states that BPD is diagnosed three times more in (especially young) women than in men, and 75% of these women in turn are middle or upper SES (Ullrich & Coid, 2009). BPD most frequently is reported in North America, Europe and the United Kingdom. There are few reports of it from developing countries where DSM-IV equivalents do not exist (Bjorklund, 2006). These findings suggest that gender or social construction bias, or sampling or diagnostic bias, both may play a role in diagnosing BPD (Sokodol & Bender, 2003). (1)  BPD did not even exist until DSM-III and there is some debate if it (along with all of the other personality disorders) should be carried over into DSM-V (Tyrer, 2009). That being so BPD has moved from being a psychoanalytic colloquialism for untreatable neurotics to becoming a valid clinical diagnosis (Gunderson, 2009).

Symptomatology and Behavioral Presentation

BPD is assessed using the Structured Clinical Interview (“SCI”) for DSM-IV Axis II Personality Disorders (Korfine et al., 2009). The DSM-IV criteria cluster into four categories of symptoms.

Emotional lability. First and foremost BPD is a problem of emotional dysregulation. There is nothing abnormal about having emotions (such as being happy or being sad). BPD patients become pathological when their emotions cross some sort of an internal frontier or “border” (as described above). They ascend an emotional gradient to the point where they become personally distressful or socially maladaptive.

Patients with BPD have a high level of affective instability and cycle rapidly from one emotion to another (Livesly, 2008; Paris, 2007). It would not be correct however to characterize BPD as a cyclothymic mood disorder, which involves swings between depression and mania (DSM-IV-TR 301.13). Rather BPD patients simply experience a wide range of intense emotions, characterized non-pejoratively. They are cross-modal and range idiopathically from anhedonia, dysthymia and dysphoria to euphoria, euthymia, hyperthymia and even hypomania. This is interesting because it implicates decades of philosophical research (and centuries of philosophical speculation) into the nature of lived emotional experience (see Appendix A).

Self-image. Second, BPD also implicates a theory of mind. BPD patients have poor self-image and concept of who they are and where their interests lie (Livesly, 2008). “Poor self image” necessarily entails some process of comparison between an existing self-image and an idealized one, both of which are hypothetical mental constructs or self-construals by the BPD patient. This need not be at the forefront of conscious activity; for example it might take the form of an internal soliloquy, dialog, or self-talk. For this reason it might be said that BPD is self-image dystonic in that there is dissonance between these two competing ideations. It does not so much involve deficient mental imaging as it does imaginal ambiguity. People with BPD confront uncertainty and “existential dilemmas” highlighting anxiety-provoking choices, whether real or supposed.

That being so there is no evidence they are cognitively impaired. Phenomenologically they receive the same sense data as everybody else (irradiations on the retina, vibrations in the auditory canal) and process it identically (through the thalamus to the relevant areas of the cerebral cortex). They think in terms of the same idea units. What is different is the emotional valency or “spin” that accompanies them. BPD determines their emotional style.

From the standpoint of differential diagnosis, to some extent BPD shares symptoms of social phobia (social anxiety disorder), DSM 300.23; adjustment disorder, DSM 309; depersonalization disorder, DSM 300.6; or “identity problem,” DSM 313.82, all of which also involve confusion about personal identity (Kihlstrom, 2005). These however also carry with them a measure of reality avoidance, which is not a symptom of BPD. If anything BPD patients suffer from too much reality (reality immersion), not a scarcity of it.

Impulsivity. Third, BPD patients are highly impulsive and frequently engage in socially-inappropriate behavior (Paris, 2007). This leads them into a variety of situational and circumstantial cul-de-sacs. Normal behavior is spontaneous and extemporaneous. There is a sense in which it is impulsive or even “automatic” as one copes with the world and responds to the affordances it presents (Bargh, 1997). BPD patients however carry this natural flexibility to an extreme degree. They are maladaptive in social contexts because they cannot read or process the cultural “cues” that we take for granted. They do not accommodate themselves comfortably to social roles and lack real-world coping skills.

Bodily Harm. Fourth, BPD patients are at risk for more extreme forms of behavior such as suicide and self-mutilation (Oldham, 2006; Paris, 2007).

Etiological Considerations

BPD is caused by two clusters of conditions: neuroanatomical/neurochemical; and sociocultural/psychological. (2)

Neuroanatomical, Neurochemical. There now is a large body of work on the neurophysiology of emotion, which is particularly applicable to BPD given BPD’s status as primarily a condition of emotional dysregulation. Illustrative is Antonio Damasio’s (2003) theory of “somatic markers.” Damasio theorizes that normal decision-making uses two complementary paths. One is cognitive. It prompts options for action, the anticipation of consequences related to particular outcomes, and reasoning strategies. Stimuli are processed through the thalamus to the cerebral cortex and through the hippocampus before reaching the amygdala. The second is emotional. It is far more visceral. Based on previous experience it marks options and outcomes with a positive or negative signal that narrows the decision-making space and increases the probability that the action will conform to past experience. This emotional signal results in “gut feelings” and intuitions that operate entirely beneath the radar of consciousness. Stimuli are processed directly from the thalamus to the amygdala, short-circuiting the cerebral cortex and the hippocampus. Since there is less processing involved, they arrive at the amygdala first and therefore primarily affect emotional response. (3)  These parts of the brain are the oldest phylogenetically.

Damasio supports his work with brain imaging and genotyping techniques. Lack of emotional affect is associated with lesions to the ventral and medial sectors of the orbital prefrontal cortex and in the right parietal lobe. Clearly however not everybody with BPD has brain damage or psychogenic disease. It therefore is necessary also to consider neurochemical explanations if BPD is to be considered as anything more than a psychological phenomenon. BPD’s pathogenesis likely involves reuptake of serotonin transporter proteins (e.g., 5-HT and 5-HTT) and density of dopamine receptors (Figueroa & Silk, 1997). While it is unlikely it ever will be possible to correlate specific emotions with specific neurochemicals (or brain regions), we now are on the verge of being able to identify various neuropeptides with the presence of emotional states or moods. Core limbic brain structures (such as the amygdala and the hippocampus) contain 85% – 95% of the neuropeptide receptors involved in the expression of emotion. Opiate receptors for example are densest in the frontal lobes, which in turn share many connections with the amygdala (Pert, 1997).

Neurophysiologically having an emotion may be similar to experiencing stress (Rohleder et al., 2009). It follows that BPD may release glucocorticoids, which in turn may kill cells in the hippocampus, leading to memory loss. The having of emotions therefore actually changes brain structure by creating new neural pathways, strengthening some, and disabling others (LeDoux, 1996).

Sociocultural, Psychological. There are two basic sociocultural/psychological approaches to emotions. From the standpoint of social psychology emotions are a means of maintaining homeostasis with the environment. They are situational responses to environmental factors such as arousal (Schacter & Singer, 1962). From the standpoint of cognitive psychology they are affective moods or dispositions implicating appraisal and attribution, both components of personality (Oatley et al., 2006).

Both of these perspectives are true, though trivially, and they do not shed much light on BPD. If one regards BPD solely as a malaise of 20th – 21st century Western culture, then arguably the social and psychological construction of emotions is pertinent. For example BPD may be triggered or exacerbated by stressful emotional interactions with people in certain social contexts, which would place it in the range of being a sociocultural/psychological phenomenon.

This type of analysis is unsatisfactory though. For one thing it is impossible to clearly distinguish the individual psychological from the systematic social components (Butler & Gross, 2009). Second, it ignores all of the neuroanatomical and neurochemical issues previously discussed. It seems unlikely that social interaction alone would be capable of producing an emotional response absent some neurophysiological or somatic correlate. A zombie (for example) might be capable of engaging with people on a group level without affective experience, but people are not zombies. (4)  The reciprocal also is true. Someone (say) in the throes of cortisol flooding is going to experience something, which we now call (say) an emotion. This occurring does not depend on the presence or absence of social interaction. It could take place when the person is by herself/himself, confronting danger in the natural/ecological environment, or experiencing feelings or intuitions unprompted by a social event. Changing the label to something else is not going to change its fundamental attributes. Third, socio-cognitive theories of emotion lead to a paradox, which is as follows. Social interaction engages the neocortex, which evolutionarily is the most modern part of the brain (Damasio, 1994). If emotions are outcomes of social interaction, and social interaction by and large is cognitive, then what becomes of the neuroanatomical pathway directly from the thalamus to the amygdala? It becomes effectively (and affectively) displaced, which seems unlikely.

Treatment Considerations

Relevant psychotherapeutic orientations. BPD has attracted a variety of psychoanalytic theorists. Illustrative is Fonagy (1991) who characterizes BPD as a form of psychic organization characterized by active primary-process id-dominated thinking and weak or unstable secondary-process ego management. BPD patients have short-lived, chaotic yet intense interpersonal relations; a fragmented concept of self; overwhelming affective response; and mental disorganization. The function of psychoanalysis is to restore the patient’s ability to understand her/his beliefs and desires, thereby enabling her/him to function as a whole person.

The main problem with psychoanalysis is that it presents a taxonomy for viewing the world that lacks empirical validation and predictive power. It has a well-developed vocabulary of concepts and principles, which have some degree of inter-subjective meaning among its adherents and practitioners, but which lack real-world reference. Constructs such as the “ego” and the “id” for example are opaque and seemingly arbitrary. They readily are substitutable (and have been replaced) with others such as “striving for individual success” (Adler) or “personal individuation” (Jung). The question the clinician must ask is: “What recourse is available to the BPD patient when introspection fails?” This is particularly salient in light of BPD’s main pathology, which is lack of affective regulation and cognitive homeostasis.

For these same reasons it seems unlikely that CBT would be a useful treatment for BPD. Conceptually the whole premise of CBT is that thought precedes feelings and emotions, see Appendix A. In other words emotions are something one can think one’s way out of by deploying conscious, rational thought processes. This is not likely to assuage somebody who is adrift in an emotional backwater. Any effective therapy for BPD necessarily must address emotions first, not as an artifact or precipitate of mental activity.

In Damasio-like terms (supra), BPD involves the direct signal path of emotions from the thalamus to the amygdala. CBT on the other hand requires activity in the cerebral cortex and the hippocampus. This seems so obvious that it is difficulty to see how the myriad articles in the style of Wenzel, 2006 (advocating CBT for BPD) ever got traction. Recently there has been a new crop of psychologists such as Linehan (1993) who view BPD as more of an existential malaise that can be treated with new age-ish psycho-babble which she calls “dialectical behavior therapy” (though what is “dialectical” about it is not susceptible to discernment).

Given this lack of operational definition and clinical precision it is likely that BPD by and large is refractory to psychotherapy and CBT, though it may have modest efficacy in connection with psychopharmacological treatment.

Psychopharmacological treatment. There is no specific pharmacologic treatment for BPD. Given BPD’s comorbidity with Axis I disorders with emotion-related components (depression, Bipolar II) it stands to reason that low-dose atypical neuroleptics (e.g. seroquel), specific serotonin reuptake inhibitors (e.g. lamictal) and mood stabilizers (e.g. alprazolam) will alleviate many of its symptoms (Paris, 2005).

Appendix A

Brief History of Emotions

The history of emotions is that for a long time they were thought to be a philosophical problem. The Greek philosopher Aristotle (384 – 322 B.C.E.) concluded that emotions are a kind of lens or filter that mediate conscious thought and intentional action. For example one becomes aware one has been slighted or ignored; becomes vengeful; and retaliates. They are undesirable because fundamentally they are irrational impulses and the goal of philosophical reflection is to eradicate them. Fast-forward two millennia to René Descartes (1649) who famously differentiated between res cogitans (the mind) and res extensa (the world; everything other than the mind, including the physical body). One’s perceptions of the latter always are subject to doubt. The only thing one knows indubitably is that one has cognitions (ego cogito ergo sum, “I think therefore I am”). Because they are elements of cognition, emotions (what Descartes called “passions”) are distinct from the body, considered as a biological organism. Rather they are markers or vehicles for insight into this specialized cognitive state – what we now might call personal identity or the “self.”

Contemporary theory of emotions begins with Darwin, James and Freud. Darwin (1872) concluded that emotions are vestiges or residues of behaviors that arose in the EEA where they were functionally useful. They are triggered or activated by situations that are perceptually analogous to their primitive origins. For example “sneering” (like Elvis Presley, who famously would lift one side of his lip) substitutes for snarling, a fight response involving the baring of teeth. James (1890) attempted to integrate emotions with a theory of action. Naively, emotions are situated between an “exciting fact” and activity. One sees a snake; is frightened; then reacts by jumping away. James rearranged this equation so that reaction precedes emotion. Emotion is the perception of the somatic change caused by one’s reaction to the exciting fact. James was correct in concluding that there is a close relationship between bodily states and emotions. However it follows from his theory that one cannot be having an emotion unless one is conscious of doing so and perceives it as such, which is unlikely. Freud (1895) theorized that emotions arose in the unconscious as one component of the drives comprising the id. Because they are repressed (together with other id-originating instincts) they cause personality disorders such as neurosis.

Psychoanalysis by and large was replaced by CBT in the 1960s. The central principle of CBT is that cognitive thought precedes emotions and then subsequent behavior. How one thinks largely determines how one feels and behaves. Different CBT theorists contrived different names for the “thinking” part of this equation. What they shared is the concept that once one has become aware of or achieved some degree of insight into one’s thoughts and thinking patterns then they can be cognitively restructured. Albert Ellis for example characterized the belief as “irrational” and developed “rational emotive behavior therapy,” the objective of which was to demonstrate to a patient how his or her belief system was dysfunctional and lead to inappropriate behavior. Aaron Beck identified the dysfunctional belief as part of a “schema,” which is a cognitive structure comprising a person’s fundamental assumptions and concepts about self, others and reality. David Burns called it a “cognitive distortion” and developed a taxonomy of them with a view towards assisting clients to identify them by category. Martin Seligman conceived it was part of one’s “explanatory style,” which is how one sees the world and how one explains adversity.

It is a fair assessment to state that the fundamental tenet of CBT (thoughts precede feelings and behavior) now has been discredited by the work of Damasio and related predecessors and successors such as Eric Kandel (2006) and Joseph LeDoux (1996) (see main text).

References

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Bagge, C., Nickell, A., Stepp, S., Durrett, C., Jackson, K. & Trull, T. (2004). “Borderline personality disorder features predict negative outcomes 2 years later.” J. Abnormal Psych., 113(2), 279 – 288.

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Footnotes

(1) By analogy, the now-discredited diagnosis of “hysteria” was frequently and exclusively applied to women in fin de siècle Vienna (Makari, 2008, p. 44).

(2) Other etiological factors include genetic predisposition (Livesley, 2008) and early childhood trauma (Paris, 2007). The varied presentation of BPD and the difficulty in isolating any one set of symptom clusters as necessary or sufficient virtually compel the adoption of an integrative approach to symptom classification, or a multidimensional diathesis-stress theory.

(3) Though confusingly Damasio also believes that one does not “have” an emotion unless one can cognitively construct a mental representation of the somatic state. The brain constructs a (transient) representation of a local body-state change. It then “perceives” this and the percept is what counts as an emotion. Thus for example “pain” is the perception of a certain class of sensory signals, as opposed to “suffering” which is the feeling that comes from perceiving the emotional reaction to that perception. The reason why this is dubious is because pain is pain; it is not culturally variable or cognitively mediated. Damasio would say, “you just think you’re in pain” without conceding that you actually are. However a second level of conscious processing (“knowing” one is in pain) is superfluous. Emotions originate in the body and are integral to rational thought. This doesn’t mean one has to think them, or think about them, in order for them to exist.

(4) From the standpoint of cognitive science zombies are just like us physically (neuroanatomically) but have no conscious experience or emotions.