The Trauma Recovery Institute

A Malady of Representations, Dysautonomic Aspects of Borderline Personality Disorder

There is an important category of borderline personality disorder (BPD) phe- nomena that is very often overlooked but that may relate to the core of the disorder. It is overlooked, first, because the patient does not report it and, second, because, if reported, it seems incidental to the main clinical picture and also inexplicable. It appears as an almost literal imprint in the body, particularly the skin, of a fragment of traumatic experience. The symptoms of this phenomenon can be understood in terms of a disconnection theory of BPD. They seem to reflect autonomic nervous activity that is independent of, and unco- ordinated with, higher systems, particularly the prefrontal cortex. Rule et al. (2002) have proposed that the orbitofrontal cortex is central to the top-down regulation of subcortical functioning of structures such as the autonomic system, the hypothalamus, and the amyg- dala, all involved in the induction, activation, encoding, and elicitation of emotion. The phe- nomenon considered in this chapter appears to reflect a loss of this regulation and to mani- fest a “dissociation” of the autonomic nervous system activity from prefrontal regulation, particularly as it controls the dermal vascular bed. Quite intricate patterns of skin sensation and even skin markings arise in some traumatized patients with BPD, like sensory “maps” of parts of the trauma.
Here are some examples:
A young woman who had been in therapy for about a year telephoned her therapist some time after a session, which was an unusual thing for her to do, and reported that as she was preparing for a shower, she noticed a number of bruises behind her knees, which bewildered her. The therapist saw her the next day and found several linear but incomplete lesions behind the patient’s knees. This incident might perhaps have been anticipated since, several years before entering therapy, the patient had been investigated by a physician for large linear bruises that occurred intermittently on her arms and legs. The physician was baf- fled by these bruises and could find no cause for them. They became a focus of therapy. One day the patient recalled being made to face the wall and, while she was caned, to keep her legs perfectly straight. “Phew!” she said. “She used to be cruel. Nowadays you would call it child abuse.” It was following this session that the bruises appeared spontaneously behind the patient’s knees.
A middle-aged woman had an intermittent sensation of a male hand under her chin, grasping it between thumb on one side of her chin and fingers on the other. It turned out that this symptom had its origin in her being forced to commit fellatio regularly with her father as a preadolescent.
A woman in her 30s had the strange sensation, from time to time, of something like a silken cord mov- ing obliquely across her face in a wavering line. This sensation occurred particularly when she was anxious. Eventually a link was discovered that related her facial sensation to a car accident some years before. In the moment before impact, she could see that the accident was about to happen and at that instant felt the ter- ror of knowing she was about to die. She was not, however, seriously injured, but, as she lay on the roadside, blood from a scalp wound trickled obliquely across her face.
A woman in her 40s who had been sexually attacked by two men would feel, intermittently, the skin of her forearms twisting laterally. This was a “body memory” of being held down by the arms by one man while the other raped her.
The skin on the face and hands of a woman in her early 30s would, from time to time during a therapeutic session, become blue and mottled, as if from cold. When her therapist inquired about the skin changes, the patient had no explanation for them. It later emerged, however, that during childhood she was punished by being locked in a closet that was totally dark and in a part of the house that was freezing cold. This experi- ence was frightening.
In each of these examples, the symptom represents an element of traumatic memory that was initially unconscious. Janet called hysteria an “ensemble of maladies of representation” (1901, p. 488). Breuer and Freud concurred, noting that “the hysteric suffers mostly from reminiscences” (1895, p. 4). Until recent years, there have been few reports of phenomena such as these. Presumably they were ignored as medically meaningless or discounted as mere fabrica- tions. In the years before World War I, how- ever, they formed part of the descriptive background of the complex condition then called hysteria. The possibility that at least some of these phenomena reflect changes in the blood supply to the skin is suggested by the observations of Janet. He found, for example, that anesthesia of the arm is as- sociated with markedly reduced blood flow (Janet, 1901, p.11). He also described the re- markable case of a young woman, observed over a period of 10 years, who had a persis- tent pulse of 100 and a temperature about 2 degrees Fahrenheit above the normal, sug- gesting a disturbance of autonomic regula- tion of body temperature (Janet, 1925, pp. 1050–1051). Her symptoms could not be explained in terms of illnesses such as thy- rotoxicosis. Her abnormal temperature did not inconvenience her. She complained, however, of fever when she had a slight attack of influenza. Janet noted that the “disorders of the peripheral circulation tak- ing the form of passive dilation of the blood vessels or of vasomotor spasm” (1925, p. 1051) were not uncommon. “A great many of these patients are continually becoming affected with redness or pallor of the skin of various regions” (p. 1051). In several of his patients, “patches on the skin, at first red and hot, and then pale and very cold, [fusion_builder_container hundred_percent=”yes” overflow=”visible”][fusion_builder_row][fusion_builder_column type=”1_1″ background_position=”left top” background_color=”” border_size=”” border_color=”” border_style=”solid” spacing=”yes” background_image=”” background_repeat=”no-repeat” padding=”” margin_top=”0px” margin_bottom=”0px” class=”” id=”” animation_type=”” animation_speed=”0.3″ animation_direction=”left” hide_on_mobile=”no” center_content=”no” min_height=”none”][are] apt to become blue on the following day, and that for a long time in these areas a bruise is left” (p. 1052). In one case the bruising was associated with “actual ecchy- moses” (p. 1051).
The sensations and/or marks on the skin representing traumatic memory in some patients with BPD are like analogues of the PTSD flashback and nightmare. The dermal imprint might be conceived as another form of what Lenore Terr (1988) called a “burning in” of the trauma (p. 105). The visual repre- sentation, which “is often the repetition of the actual experience without transforma- tion of any kind,” as W. H. R. Rivers remarked (1922, as cited by McDougall, 1926, p. 138), is larger and more coherent than the dermal one. The latter is also qualitatively different from PTSD in that the individual is typically unaware of the origin of the skin phenom- ena. Are they, then, dissociative?
In terms of the hypothesis being put for- ward at the beginning of the chapter about the origins of this category of BPD phenom- ena, the imprints on the skin representing trauma are dissociative. They can be under- stood in terms of Rivers’s use of the great neurologist Sir Henry Head’s (1918) definition of dissociation. Head considered it a process “whereby one set of nervous functions are separated from others with which they are normally associated so that they become ca- pable of independent study” (Rivers, 1922, p. 71). Rivers considered “the word ‘dissocia- tion’ [to be] peculiarly appropriate to the psy- chological process” (p. 72).
Janet’s description of cases involving der- mal representation and trauma suggest a dissociative basis. The famous case of Marie provides an example (Janet, 1901, pp. 282– 285). Marie was a young girl from the coun- try who had been hospitalized because she was judged insane and incurable. Janet dis- covered a number of traumatic incidents in her past. A principal one involved the onset of menstruation at the age of 13. For some reason, “she took it into her head that there was some shame connected with the affair, and sought some means whereby to stop the flow as soon as possible. In the course of some twenty hours she went out and secretly plunged into a big tub of cold water. She suc- ceeded completely, the courses stopped sud- denly, and notwithstanding the severe chill that followed, she was able to reach home” (pp. 283–284). This episode was followed by an illness in which she was delirious for several days.
Her periods stopped for 5 years but when they returned, she suffered a crisis at each menstruation. Twenty hours after the onset, the flow stopped suddenly and a severe chill shook her whole body. Then followed a dis- sociative delirium with florid symptomatol- ogy, including hallucinatory representations from other traumata. The episode, which lasted about 48 hours, “ended with several blood vomitings.” She remembered noth- ing of the experience. Janet remarked that the scene of the cold bath “takes place be- low the surface of consciousness” (1901, p. 284).
Although accounts as exotic as that of Marie are rare, it is becoming evident that much lesser forms of the phenomenon are not uncommon. This evidence suggests that they may be an aspect of dissociation. For example, Madhulika and Adilya Gup- ta (Gupta & Gupta, 2006) asked 360 peo- ple—44 psychiatric outpatients and 314 non- clinical participants—to complete both the Dissociative Experiences Scale (DES) and an extensive checklist of cutaneous symp- toms. They found that the symptom score correlated with the DES total score. They then considered those 17 people whose DES scores were considered pathological and found that their mean score on the cutaneous symptoms scale, 360, was much higher than the mean score of the remaining par- ticipants, which was 70. Pain, itching, and numbness were the best predictors of the DES score.
Although numbness, and to some extent pain, have long been associated with the phenomenon of dissociation, itching has not. Pruritic states, however, may repre- sent “body memories” of traumatic mem- ory. One of our own cases supported this possibility. The patient, a woman of late middle-age, presented to a physician with a 15-month history of recurrent episodes of formication and pruritus, particularly in the pubic area. This formication, described as a creepy feeling that bugs were crawling un- der her skin, was accompanied by feelings of being “unclean” and unfit to be around others. A provisional diagnosis was made of connective tissue disorder. She was inten- sively reviewed by an immunologist, who found no abnormalities. Since she was also depressed, she was referred to our clinic. It emerged that her symptoms had begun soon after an incident in which she felt as if she had been physically assaulted in the stairwell of the apartment house in which she lived. During this “assault,” an obese male neighbor thrust his large abdomen into her abdomen in an intimidating way, as if he were trying to bump her out of the way. She was extremely distressed by this incident. Her symptoms remitted during therapy (Meares & Jones, 2009). A traumat- ic precursor to the bumping incident was not revealed, nor was it sought.
Two remarkable case histories from R. L. Moody, reported in The Lancet in 1946 and 1948, suggest an association between the state of dissociation and the representation of trauma by vascular changes in the skin. In the first of these cases a man of 35 was admitted to a hospital in 1944 “because of somnambulism accompanied by aggressive behaviour” (Moody, 1946, p. 934 ). He was an Army man, but no account was given of his military service. In a previous hospital ad- mission in 1935 for a minor septic condition, he had been “retained five months because of somnambulism” (p. 935). During this admission various restraints were imposed upon him to prevent his nocturnal wander- ings. “On one such occasion his hands had been tied behind his back during sleep, as a precautionary measure. Waking in a disso- ciated state he had struggled unsuccessfully to free himself. He had then managed to evade his bodyguard and had escaped into the surrounding countryside from which he had returned a few hours later” (p. 935).
One night, during a later admission in 1944, “the patient was observed to be toss- ing and turning violently in his bed. He was holding his hands behind his back and ap- peared to be trying to free them from some imaginary constriction. After carrying on in this way for about an hour, he got up, and with his hands still in the same position, crept stealthily into the hospital grounds” (Moody, 1946, p. 935). He came back after 20 minutes in an apparently normal state of mind.
Two nights later Dr. Moody abreacted the patient by means of intravenous narcosis: He slept for a few minutes and then began reciting poetry (this was a com- mon prelude to his somnambulism). Then minutes later he began to toss and turn on the couch, with his hands behind his back. As he appeared to be in a completely dissociated state, I turned the light full on him. I watched him writhing violently for at least three quarters of an hour. After a few min- utes weals appeared on both forearms; gradually these became indented; and finally some fresh petechial haemor- rhages appeared along their course. (Moody, 1946, p. 935). A photograph of these indentations was included in Moody’s Lancet paper.
In this article, Moody briefly mentioned three other cases of abreaction of traumata being followed by bodily “representations” of an aspect of the trauma. Swelling at points on a man’s body recurred where he had been injured by a flying bomb; a seaman who had been immersed in very cold water for a long time showed localized ischemia of the extremities; a woman injured in a riding accident at the age of 10 showed petechial hemorrhages along the tenth rib, which had been fractured in the accident.
In each of these cases, the history given was insufficient to infer a BPD diagnosis. However, the background of the case pre- sented in Moody’s 1948 article was very like that told by a person who would now be given the borderline diagnosis. The patient was a married woman in her late 30s, who had had “an extremely unhappy childhood in which a sadistic father had played a promi- nent part” (p. 964). During Dr. Moody’s ab- reactions of her traumata, “swelling, bruising and bleeding were observed on at least thirty occasions” (p. 964). They included the fol- lowing: (1) “The morning after abreacting an incident in which she had been thrashed with a cutting whip at 8 years, three large bruises of appropriate shape appeared on her left buttock” (p. 964). (2) A few minutes after abreacting an incident in which she had cut herself rushing through a window, long red streaks appeared down each leg. The patient reported that these bled during the night. (3) Bruising after an abreaction had a “curi- ous sharply defined pattern” resembling an elaborately carved stick her father had used to beat her.
None of the symptoms observed by Dr. Moody or by my colleagues and myself could have been explained by trickery or as factitious. Certain of the phenomena resembled the famous story of Padre Pio, whose body at times bore the signs of the stigmata, the wounds that Christ suffered on his hands, feet, and side at the crucifixion. In the 1920s the Vatican suspected that the oozing blood observed at the sites of the stigmata was factitious, and he was banned from cel- ebrating Mass in public for over a decade. However, no evidence was ever found to suggest that the bleeding was self-inflicted and that he was a fraud. Padre Pio was ex- tremely popular. Hundred of thousands of people converged on the Vatican for the occasion of his canonization by Pope John Paul II in 2002.
The mechanisms underpinning the rep- resentations on the skin have not been in- vestigated. They are likely to be complex. Nevertheless, the data suggest the hypoth- esis that shock to the central nervous sys- tem causes a disruption and destabilization of the autonomic system that is manifest particularly in the regulation of blood flow to the skin. In a mild way, the phenomena might resemble the syndrome of dysauto- nomia that may complicate severe head injury. The name of this specific syndrome may soon be changed, since it is often con- fused with a more general disturbance. Ian Baguley and his colleagues (2009) report that although dysautonomia can result from any form of acquired brain injury, it oc- curs most frequently after a moderate to se- vere traumatic brain injury. In most of these cases, there are episodes of accelerated heart rate, blood pressure, respiration rate, and body temperature, which, when they occur together, suggest a paroxysmal and widespread increase in sympathetic activa- tion. Usually, these episodes pass; in about 10% of cases, however, they persist and are indicative of a poor prognosis.
Baguley and his colleagues regard dysau- tonomia as a spectrum disorder, ranging from mild to severe. It seems possible that just as a blow to the head might be followed by a period of dissociative-like amnesia, re- sembling psychogenic shock, such a shock may precipitate a minor form of dysauto- nomia, manifest particularly in the vascular. The data suggest the hypothesis that shock to the central nervous system causes a disruption and destabilization of the autonomic system that is manifest particularly in the regulation of blood flow to the skin system. Minor disturbances of blood supply to the skin, such as displayed in Raynaud’s phenomenon, are now sometimes diag- nosed as dysautonomia, although there is little research evidence to back up such a diagnosis.
It is of interest that Baguley and his colleagues (2009) suggest that, in dysautono- mia, it is not the presence of overreactivity, per se, but rather a loss of the inhibitory processes for control over reactivity that contributes to dysautonomic “storming,” in line with observations of emotion and pain dysregulation in BPD. Porges and his coworkers found that a disturbance of heart rate in neonatal distress could be explained as the outcome of a disconnection between the activities of two vagal systems, one of which evolved later than the other.
In an earlier paper Baguley (2008) put forward the hypothesis that symptoms of dysautonomia, in common with a number of similar syndromes of autonomic dysreg- ulation, display an increase in the ratio be- tween excitatory and inhibitory influences. There is also a tendency of the individual to develop an overreaction to non-noxious stimuli (Baguley, 2008). These phenomena are not dissimilar to aspects of the patho- physiology of BPD.
In the field of psychological science, Ste- phen Porges has been prominent in the in- vestigation of autonomic regulation in men- tal illness. He has put forward a theory that is resonant with Jacksonian principles (Porg- es, 2009). The basis of his theory is derived from his experiences as a neonatal physi- cian. Porges and his coworkers found that a disturbance of heart rate in neonatal dis- tress could be explained as the outcome of a disconnection between the activities of two vagal systems, one of which evolved later than the other. During the distress period the more primitive system remained opera- tive, whereas the later evolved form was no longer functioning (Reed et al., 1999).
Porges’s (2009) polyvagal theory focuses on regulation of the heartbeat and an or- ganization of parasympathic activity that is determined by evolutionary history. The early, or reptilian, element of vagal regu- lation of the heart depends on an unmy- elinated efferent pathway originating in the dorsal motor nucleus and terminating primarily below the diaphragm. The later evolved mammalian component is myeli- nated in the process of evolution. This new system is involved not only in the regulation of the heart but also of the muscles in the face and head subserving emotional expres- sion via cranial nerves V, VII, IX, X, XI. These nerves together create an integrated social engagement system and provide the neural regulation of the muscles controlling eye gaze, facial expression, listening, and pros- ody (Porges, 2007). This mammalian myeli- nated system also links the rhythms of the heart to breathing, producing respiratory sinus arrhythmia (RSA).
In a study of patients with BPD, Porg- es and his colleagues (Austin et al., 2007) reported that at baseline there was little difference to be found between the BPD cohort and controls. However, when the two groups were stressed by means of film clips selected to elicit a strong emotional response, the patients with BPD showed diminishing RSA whereas the controls showed increasing RSA. In 1992, Porges had proposed that vagal tone, derived from an RSA measure, be used as an index of rel- ative stress vulnerability.
In addition to the differences in RSA, the two groups showed another contrast dur- ing the stress condition. A correlation was found between the changes in RSA and heart beat period in the control group but not in the patients with BPD, suggesting that vagal mechanisms mediated the heart period responses only in the control group. These findings can be understood as a fail- ure of connection between the vagal signals originating in the brainstem and the heart’s response in those with BPD.
Porges and his colleagues saw the change in the patients with BPD as evidence of a stress-induced “dissolution,” the term Hughlings Jackson (1958) gave to the rever- sal of the evolutionary trajectory of devel- opment of the human brain–mind. Dissolu- tion implies a disconnection between neural systems that usually function together. Porges describes a phylogenetically or- dered and hierarchical sequence of auto- nomic response strategies to environmental challenges. The highest-order system oper- ates in an atmosphere of safety. It depends upon an increase in the influence of the later evolved
The notion of “bi-directional coupling” is particularly important and intriguing. It implies that a particular state of vagal ac- tivity is likely to foster social engagement and that, conversely, certain kinds of social engagement have the capacity to promote activation of the later evolved vagal com- ponent. The latter possibility is supported by an interesting study from Schwerdtfeger and Friedrich-Mai (2009). Heart rate was re- corded over 22 hours by means of ambula- torymonitoringofsubjectswithdepressive symptoms. The group was divided into those deemed high and low in depression. When those with high depression were alone, they had less heart rate variability (i.e., RSA) and a higher negative affect. However, when they were engaged with partners, family, or close friends, the heart rate variability in- creased, approaching that of subjects with low depression, and their mood improved. This effect was not achieved when the in- teractions occurred with strangers or colleagues.
When the sense of safety is lost, and when threat appears in the environment, an earlier evolved network of neural circuitry is triggered that leads to the fight–flight mode of experiencing and behaving. This system, which is necessary to immediate survival, overrides the calming, social engagement system. Porges proposes, in addition, a third and more primitive circuitry involving inhibition and manifest in freezing and im- mobilization. It is a response to extreme terror.
Data presented by Porges and his group (Austin et al., 2007) lead to two main infer- ences: (1) Patients with BPD are more eas- ily tipped into physiological states of fight– flight than controls; and (2) this physiology shows a failure of coordination between neural systems that were previously con- nected.When the sense of safety is lost, and when threat appears in the environment, an earlier evolved network of neural circuitry is triggered that leads to the fight–flight mode of experiencing and behaving. This system, which is necessary to immediate survival, overrides the calming, social engagement system.
. . . myelinated vagal motor pathways on the cardiac pacemaker that slows the heart, inhibits the fight–flight mechanism of the sympathetic nerv- ous system, dampens the stress re- sponse system of the HPA axis (e.g., cortisol), and reduces inflammation by modulating immune reaction (e.g., cytokines). Second, through the pro- cess of evolution, the brainstem nuclei that regulate the myelinated vagus became integrated with the nuclei that regulate the muscles of the face and head. This link results in bi-direc- tional coupling between spontane- ous social engagement behaviors and bodily states. (Porges, 2009, p. 588)
The Porges data and related observa- tions suggest a disturbance in autonomic function in BPD that can be conceived figu- ratively as “vertical” in the sense that later evolved higher-order systems become inac- tive and are thus disconnected from lower- order, more primitive systems. A second kind of disconnection may also occur in the autonomic function of those with BPD, which is metaphorically “horizontal”: A fail- ure of coordination between sympathetic and parasympathetic activity is suggested by findings from the research by my colleagues and myself, the data being collect- ed prior to formal recognition of the border- line concept.
Four decades ago our patients were given the diagnosis of “chronic hysteria” (Meares & Horvath, 1972). Most of them would have fulfilled DSM criteria for BPD. The essential diagnostic criteria were evidence of a poly- symptomatic personality disorder and a his- tory of conversion, defined as loss of neural function. These patients showed a habitu- ation failure of the electrodermal response to an intermittently sounded neutral tone. Such a deficit in selective inattention was shown in no other nonpsychotic group, but was characteristic of a nonparanoid form of schizophrenia (Horvath & Meares, 1979).
In a nonpsychotic population, a failure of habituation occurs only in the presence of extremely high levels of the arousal (e.g., Lader, 1967). Using spontaneous fluctua- tions of skin conductance, which Lader (1969) had shown to be a better measure of arousal than the level of skin conductance, we found that our group of patients had levels of arousal considerably lower than people with anxiety disorders. The anxiety group, however, did not show impairment of habituation to the extent of our group of patients who would now be diagnosed with BPD.
In this study, the two measures of habit- uation and spontaneous fluctuation of skin resistance reflect inhibitory activity, in the former case, and excitation, in the latter. Since the level of arousal could not explain habituation failure in “chronic hysteria,” we put forward the hypothesis that a deficiency in higher-order processes of inhibition was a primary disturbance in this condition (Hor- vath et al., 1980). Seen in the light of data such as that of Porges, our findings give rise to a second hypothesis: They suggest a relative failure of coordination between in- hibitory and excitatory neural systems. The normal reciprocal or inverse linear relation- ship between these systems was upset.
Against our inferences are the earlier findings of Lader and Sartorius (1968). They had shown, in a group of patients similar to our own, not only very deficient habituation but also very high arousal, higher than those with anxiety states. These patients, howev- er, were different from ours in one crucial re- spect: They were still suffering from conver- sion symptoms, whereas the symptoms had remitted in our patients. Their remission status may have explained their low arousal, relative to the Lader and Sartorius cohort.
It is only in the last decade or so that some interest has been taken in the auto- nomic peculiarities of BPD. Herpertz et al. (1999) and Schmahl, Elzinga, et al. (2004) measured skin conductance in patients with BPD and found no evidence of sympa- thetic overarousal relative to controls. On the other hand, Ebner-Priemer et al. (2007) found that those suffering from BPD do show evidence of increased heart responses to emotional stimuli, relative to controls, when ambulatory monitoring is used. Cru- cial observations of parasympathetic activ- ity were lacking in the studies of Herpertz et al. (1999) and Schmahl, Elzinga et al. (2004). These measures were included in a study by Kuo and Linehan (2009). They found that when patients with BPD were shown film clips likely to excite a negative emotional re- sponse, they showed a reduced basal RSA. However, their skin conductance responses did not differ from controls. What Porges has called the “vagal brake” was not opera- tive. These findings give support to the view that coordination between parasympathetic and sympathetic activity is impaired in BPD.
The developing evidence concerning ab- normalities of autonomic nervous system activity in BPD must be considered in the context of the autonomic system’s role in the larger functioning of the body’s neurol- ogy. The autonomic system is part of the emotional processing system involving a complex coordination of functions rang- ing from higher-order capabilities, includ- ing evaluation of outer and inner events, to the most primitive, such as regulation of the heartbeat. The whole system must be seen asanecology,witheachpartinfluencingthe activity of all other parts. The determinants of this state, then, are not only top down but bottom up, a reciprocity understood by Dar- win (1872/1934). He wrote: “When the heart is affected it reacts on the brain, and the state of the brain again reacts through the pneumo-gastric nerve in the heart, so that under any excitement there will be much mutual action and reaction between these two most important organs of the body” (p. 25).
Much investigation of the autonomic system has concerned the top-down influ- ences. The anterior cingulate cortex (ACC) has been a particular focus of research, and findings show that it is composed of four main areas, distinguished histologically (Vogt, 2005). A “cognitive” role has been identified for the dorsal ACC, whereas the rostral and ventral ACC have an “affective function.” The ventral ACC is particularly implicated in autonomic arousal (Critchley et al., 2005; Patterson et al., 2002; Williams, Gordon, et al., 2000). There is an interplay among ACC regions leading to coordinated output. Depending upon environmental re- quirements, dorsal, rostral, and ventral ACC activity is, at times, alternatively turned on and off, mirroring, at a higher level of the nervous system, Sherrington’s reciprocal inhibition (Drevets & Raichle, 1998; Lane et al., 1998).
Diminished activity in the ACC is one of the better validated findings in BPD, as noted in previous chapters. Since the autonomic system is crucially involved in fundamental attentional processes such as orienting and habituation, it is unsurprising that the ACC is implicated in the focusing of attention, which involves autonomic activa- tion, most prominently shown in skin and heart responses.
Damasio has put forward an influential theory that gives an explanation of poor de- cision making in people with damage to the orbitofrontal cortex (OFC). Central to the theory is what he calls “somatic markers,” which, in short, are
. . . a special instance of feelings gen- erated from secondary emotions. Those emotions and feelings have been con- nected, by learning, to predicted future outcomes of certain scenarios. When a negative somatic marker is juxta- posed to a particular future outcome the combination functions as an alarm bell. When a positive somatic marker is juxtaposed instead it becomes a beacon of incentive. This is the es- sence of the somatic-marker hypoth- esis . . . on occasion somatic markers may operate covertly (without com- ing to consciousness) and may utilize an “as if” loop. (Damasio, 1996, p. 174, italics in original)
Damasio and his colleagues devised a game that enables them to study decision making. They call it the Iowa Gambling Task (IGT; Bechara et al., 1994). In this game the participants are given four decks of cards and a loan of $2,000 facsimile U.S. bills, and asked to play so as to win the most money. Turning each card carries an immediate re- ward ($100 in decks A and B and $50 in decks C and D). Unpredictably, however, the turn- ing of some cards also carries a penalty (which is large in decks A and B and small in decks C and D). Playing mostly from decks A and B leads to an overall loss; playing from decks C and D leads to an overall gain. The players cannot predict when a penalty will occur, nor calculate with precision the net gain or loss from each deck. They also do not know how many cards must be turned before the end of the game (the game in fact ends after 100 card selections).
As the participants play this game, their skin conductance responses are monitored. All participants show a skin response before and after making a decision. As the game goes on, normal players begin to have a sense of the riskier choice. They start to generate anticipatory skin responses in the 5 seconds before choosing a card, leading to preferences for the good decks. The an- ticipatory skin responses are not accompa- nied by any conscious apprehension, which generally, but not always, follows later. The people with ventromedial prefrontal cortex damage do sometimes become consciously aware that the high reward cards are bad choices, but they fail to generate anticipato- ry skin conductance responses and continue to choose the cards disadvantageously (Be- chara et al., 2005).
Roberts and her colleagues, building on the work of Damasio and his colleagues, showed that the representation of the aversive event (i.e. choosing the bad card) in those with OFC damage is not entirely cut off from interchange with the environ- ment (Roberts et al., 2004). They studied the effect of unanticipated and anticipated responses to acoustic startles in patients with OFC damage. The patients showed intact physiology when the startle was not anticipated. Their faces showed more sur- prise than controls, and they reported more fear. On the other hand, when the startle was anticipated, they showed no anticipatory au- tonomic response, in this case, a decrease of heart rate.
These findings and those of the IGT are consistent with the idea that the represen- tation in the brain of the event involves au- tonomically mediated somatic changes that are aspects of the emotional effect of that event that give it its meaning. This meaning, which determines a response, cannot be ac- tivated by conscious, higher-order cognitive processes in those with OFC damage, but it can be activated by relatively unconscious, automatic processing. This latter situation resembles that of patients with BPD in whom the primitive registration of the aversive event is activated by means other than those of normal consciousness.
A deficiency in orbitofrontal function has been proposed as a likely determinant of BPD symptomatology, as outlined in previ- ous chapters. This proposal leads to the pre- diction that those with BPD will fare badly at the IGT. Haaland and Landrø (2007) tested this hypothesis, comparing the performance of 20 patients with BPD with 15 healthy con- trols. The patients with BPD made less ad- vantageous choices than the controls. The difference could not be explained by indi- cators of general cognitive function or by symptoms of depression.
The patterned skin sensations and marks that sometimes appear on the skin of those with BPD, as if “branded” by traumas, have no technical or medical name. They might appropriately be called stigmata, since the original meaning of the word stigma was “a mark upon the skin; . . . a brand” (Oxford English Dictionary, 1971). Charcot and Janet, however, used this term to designate a quite different group of symptoms that has no representational significance and that serves a defensive purpose. As noted previously, Janet gave the name of “accidents” to those clinical phenomena that are representations, on the body, of traumatic expe- rience. His case of Marie was an example. “Accidents” include stereotyped patterns of movements that appear from time to time as repetitions of a fragment of traumatic memory.
A study of these phenomena may lead to a better understanding of the BPD syndrome itself. The phenomena may provide evidence, in miniature, of the essential forms of the larger disorder. Scientific data about the phenomena are few. Inferences are necessarily made from pathological states, which might mirror, in certain respects, the autonomic abnormalities that are involved in their production. Brain damage, particu- larly prefrontal and especially orbitofrontal, seems likely to provide evidence that could be the basis of hypotheses directing future research.
The skin changes representing trauma are an intriguing subject, given the com- mon embryological origin of skin and brain. In the earliest stages of evolution, contact with the skin was the principal means of the organism’s feeling and knowing. The feel- ing and knowing of any event is represented in the nervous system on multiple levels. Such representations, in the Damasio the- sis, are encoded with “somatic markers” that provide the events with their mean- ing. This process depends upon the auto- nomic nervous system. The case vignettes of subjects with BPD given at the beginning of this chapter suggest that primitive rep- resentations of trauma, or more precisely, of fragments of the trauma, are activated by unconscious processes and that they are relatively inaccessible to higher-order con- scious mental processing, which retrieves higher-order representations. In the case of severe trauma, it may be that these high- er-order representations are not properly formed. This idea derives from the “dissolution model.”
It is not known how common are the patterned skin sensations and marks that ap- pear as if “branded” on the skin by trauma, analogous to the “burning in” of PTSD (Terr, 1988). They are only discovered by patient reports and not by the ordinary processes of psychiatric examination. If they are not particularly common, it may be because the situation that was their origin is also not particularly common. The incidents re- counted earlier suggest that this is one of massive trauma inflicted on a highly vulner- able personality, someone young and lack- ing the “buffer” of resilience provided by a maturely developed sense of self. It might be supposed that in these circumstances, an event creating an emotional response of great severity and intensity, leading to ter- ror, could cause a maximal disconnection between neural systems. At the same time, the more recently evolved functional “lev- els” would become deactivated, leading to a profound “dissolution” and a retreat down the hierarchy of consciousness. At this level the later evolved “distance receptors” of vi- sion and hearing would lose their domina- tion. The dominant experience would come from the more primitive receptors of touch and smell, and the trauma recorded in these terms. Registration of the event at higher levels would be impeded.
The data currently available (e.g., Kuo & Linehan, 2009) suggest that the disconnectedness of autonomic function in BPD is not only “vertical,” that is, between higher-order systems of monitoring and control and lower-order systems, but also “horizontal,” between excitatory and inhibitory mechanisms. This figuratively two-dimensional failure of coordination in neural functions that normally operate together may mirror the larger disconnectedness underlying the symptomatology of BPD.


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