Фрагмент из статьи Neurofeedback and attachment disorder: Theory and practice

Фрагмент из статьи Neurofeedback and attachment disorder: Theory and practice (Глава 13 в книге Introduction to Quantitative EEG and Neurofeedback: Advanced Theory and Applications - by James R. Evans (Editor), Thomas H. Budzynski (Editor)).

Protocols

I enter the discussion of protocols with caution. Neurofeedback training is a dynamic, evolving process, engaged with a dynamic, emerging system: the brain in relation to itself; the brain in relation to another brain; the brain in relation to mind; and the developing mind in relation to the mind of another. Although all theory and most neurofeedback practice direct us to the right hemisphere with disorders of attachment, all protocols are designed for the individual, not for the diagnosis.

The experience to date in training those with attachment disorders, whether as children or adults, suggests that training at T4, P4, T4-P4, T4-F4 and T4-AF4 at reward frequencies from 10–13 Hz and lower, while inhibiting 0–6 Hz, are the most effective and generally well-tolerated protocols. I have encountered those who have met criteria for this disorder who have had difficulty with temporal lobe training but who did well at C4 and C4-P4. In these cases, it appeared that the contraindication for temporal lobe training may have been head injury at this or the contralateral site. In addition, there have been reports that some children with RAD, those that don’t respond well to right hemisphere training, will experience better results with a brief amount of C3-C4 protocol added to the right side training. (Personal conversation with Catherine Rule, 2004).

To date, most of the QEEG data related to RAD suggest that T6 and FZ might also be useful sites. T6 sits over the fusiform gyrus, the part of the brain that specializes in facial recognition and understanding of facial expression. Q findings may well reflect one of the central issues in the development of attachment disorder, i.e., the lack of reciprocal gaze and the interplay of faces that typify the attachment dance between mother and infant:

. . . excessive developmental cell death in specific groups of face processing neurons in the developing right fusiform gyrus, the area that decodes facial stimuli would be associated with . . . the psychopath’s mindblindness to fearful faces. (Schore, p. 300, 2003a)

In exploring this site to date, I have not found significant benefit over T4 and other T4 based bipolar protocols. But Schore and these Q findings suggest we more fully explore the potential of training at T6. The argument for T4 and, as we will see, for FPO2, is that they may provide a more geographically direct appeal 328 Neurofeedback and attachment disorder: Theory and practice to the regulation of the amygdala, and therefore provide more quieting of fear. FZ too has a geographical advantage. It sits above the anterior cingulate cortex (ACC), a structure that inhibits the amygdala. In most cases, rewarding FZ at 5–8 Hz or lower has significantly quieted fearfulness with the added benefit of easing the perseveration so typical of those with attachment problems.

It is important to note here that I have not found it necessary to use a QEEG to diagnose or address the symptoms and regulation issues of RAD. In the great majority of cases to date, training has been straightforward: right side, low-frequency reward, with over 150 sessions to be expected. I do recommend a “Q” in those cases where the patient does not stabilize, where you suspect seizure activity or brain injury, or when you see negative and unexpected effects from training. In this, I am not recommending against a QEEG, as many of these patients will have histories of confirmed or presumptive head injury and/or seizure. [^1] I am, instead, bowing to the pragmatics of cost and availability of QEEG, and reporting that I have not in my practice found it necessary to effectively treat the high arousal of these patients.

A. Negative effects

Using left hemisphere training is likely to evoke negative training effects in people who meet criteria for attachment disorder. This was brought home to me, early in my career, after several left side beta sessions with a young Aspergers patient. She liked how it made her feel: bold and confident. After several weeks of this training, she reluctantly confessed that she had begun a life of petty crime at her school, stealing both food and money. She had not done this before, and she was not drawn to doing it again—after we changed the training back to the right hemisphere. She recognized the sociopathic element in her and she felt, as I do, that this element was promoted by left hemisphere training.

In looking at training outcomes and phenomena, it is important not to be confounded by diagnosis. Aspergers, like autism and like RAD, is a severe disorder of affect regulation marked by heightened emotional arousal and requires most, if not all, training on the right hemisphere. RAD can be conceptualized as an “emotional autism.” I have seen similar effects in attempting to address left hemisphere deficits in the RAD population. When I tried training Sammy on the left side for his speech difficulties, he got sneaky and hurt the cat. A woman with a terrible and unresolved attachment history who had been warming up to her infant son, withdrew from him. I started to call these responses “left hemisphere effects.”

This preliminary data led me to think that the left hemisphere of these individuals belonged in jail. Scheming replaces cause-and-effect; coldness replaces warmth. In all of these cases I was rewarding in the beta range, and these effects may have been driven as much by frequency as by site. There is emerging clinical data that claims we can train the left hemisphere as needed, at much lower frequencies, and not encounter negative reactions. But the caution remains. I have seen similar problematic outcomes with interhemispheric homologous site protocols, regardless of the reward frequency. Even patients without a presumptive history for RAD have exhibited flatness, coolness, rigidity, anger, and lack of empathy with overuse of these protocols. Unlike those with RAD who would not notice these effects, and wouldn’t mind them if they did, many of these patients have recognized them and have subsequently stopped or limited the duration of interhemispheric training. I have found these effects training interhemispherically at all homologous sites from the sensory motor strip to the prefrontal poles. To date, I have not seen them with interhemispheric training posterior to the central strip, but I look for them.

Interhemispheric protocols seem to be particularly helpful in conditions such as migraine. When these conditions occur in those with attachment disorder and they must be addressed, the practitioner is cautioned to pay close attention to the effects that interhemispheric protocols have on the patient’s capacity for interpersonal connection, and adjust training duration accordingly. In my experience so far, as little as 3 minutes of interhemispheric training can stabilize the brain against migraine without negatively affecting attachment.

B. Alpha–theta training

In addition to these concerns about left hemisphere and interhemispheric protocols, I want to add a note of caution about the use of alpha–theta training with this population. A case in point is a young woman who spent the first year of her life in a poor and understaffed third world orphanage. She was adopted at age one. She had her first serious emotional breakdown after visiting the orphanage as a young adult. She had had many problems growing up, including many on the symptom list for RAD, and came to me directly from a long-term psychiatric hospitalization. She was diagnosed with ADHD, post-traumatic stress disorder, bipolar illness, learning disability, and alcoholism. Even with this highly presumptive history and symptom formation, she had never been diagnosed with attachment disorder.

She stabilized quickly with eyes-open, right hemisphere training. Within 3 months of training two to three times a week, she was off lithium, out of a day treatment program, back at work part-time, and headed back to college. At about this juncture in the training, which was now integrated into meaningful talk therapy, she said something that could become a neurofeedback koan: “I have never been more myself and never known less who I am.” As her right hemisphere organized, her identity was emerging. Without the internalized mother, however, she lacked a mirror, and found herself hard to recognize. Part of my function as her therapist was to become “the mirror,” the attuned other, who could reflect her, back to her.

She was doing well when we decided to see if we could deepen her recovery through the introduction of alpha–theta training. She had tried some sessions several months earlier, and reported only that she heard moaning or chanting. This time she had done six sessions over a weekend. At the end of this time, she refused to do neurofeedback in any form. She had always come to her sessions beautifully dressed and well groomed. Her appearance was an important issue for her. After this long weekend, she arrived slightly disheveled. She did not like how she felt, which was difficult for her to describe, and she was angry and withdrawn from me. The struggle to regain our therapeutic alliance lasted weeks.

One day she told me that her dog was sick. Her only ongoing and secure attachment was with her dog; she loved him. This was a crisis. I asked her about his illness, and she told me that she hadn’t been feeding him regularly! She also told me that she hadn’t had the garbage collected for two months, since that weekend of alpha–theta training. I was struck by the enormity of emotional replay that she was engaged in. It seemed as though alpha–theta training had left her in a place that she knew as an infant. She seemed to be back at the orphanage; a place filled with garbage, where innocent and powerless children went hungry, where no mother cared for her.

Another patient with a history of profound neglect, poverty and trauma initially felt some relief with alpha–theta training, but kept her visualizations tightly controlled and scripted. She was unable to abandon herself to state, out of fear.

A young patient who was diagnosed with dissociative identity disorder, and whose mother had suffered the same diagnosis, repeatedly tried alpha–theta training but, each time, pulled the electrodes off within minutes, in a state of indescribable, uninhabitable fear. Although not strictly or solely attachment disordered, both of these women had suffered absolute abandonment as infants. They were, I think, both attempting to shut down access to the unbearable state of “no mother.” It is unlikely that alpha–theta training creates a de novo state. The experience one has is probably one already known to the brain/mind, and recalled in this deep state training. If this speculation proves to be accurate, then we might assume that states of bliss and oneness, often reported by those training in alpha–theta, relate to early blissful fusion experiences between mother and infant. My adult adoptee had had no such experience nor had the two women who were raised in homes that echoed with the psychological absence of their mothers, and with all the chaos that ensues from neglect. They did not, as it were, have this default position. Secure attachment in the first 2 years may then be a critical factor in alpha–theta outcomes.

At the same time, I recognize that many colleagues report successful alpha– theta training with people who have poor attachment histories. These differing outcomes pose an interesting question. Might it be the case that the history and expectation of trainer has both subtle and powerful effects on outcomes? Might it be that the density of “no mother” in the experience of the trainer, coupled with that of the trainee, is powerful enough to overwhelm a positive outcome? Since so much of what we are observing and experiencing in the alpha–theta training seems to be occurring in the realm of subtle energies, this seems a credible hypothesis. This is a topic for further study and speculation elsewhere. For now, these cases should serve as a caution. Alpha–theta training may not be indicated for this population.

C. FPO2 training

LeDoux (1996) agrees with Schore about the importance of the prefrontal cortex in quieting fear. “Humans with prefrontal damage become oblivious to social and emotional cues and some exhibit sociopathic behavior. This area receives inputs from sensory processing systems…and is also intimately connected with the amygdala and the anterior cingulate region” (LeDoux, p. 278, 1996). According to LeDoux, the amygdala has two primary pathways: one thalamic and one cortical. Information about external stimuli reaches the amygdala by way of the direct pathways to the thalamus (low road) as well as by the pathways from the thalamus to the cortex to the amygdala. The direct thalamo–amygdala path is a shorter and thus a faster transmission route… However, because the direct pathway bypasses the cortex, it is unable to benefit from cortical processing…This can be very helpful in dangerous situations. However, its utility requires that the cortical pathway be able to override the direct pathway. (LeDoux, p. 164, 1996)

He uses the example of walking along a wilderness path and seeing a snake. The amygdala activates the prefrontal cortex and we flee or freeze, before we have time to process that this snake is in fact a rope left behind by a careless hiker. The correct identification is an example of the cortical override. As we have seen, a well-functioning RO C allows this override function. Without it, our wilderness explorer will continue to react to the rope as if it were a snake. Even when he knows better, it is difficult to communicate the reality to the non-verbal and powerful amygdala. We see this kind of “kindling” as a central to post-traumatic stress disorder, but it is a liability in all fear-based disorders.

In 1998, I began to explore the efficacy of training the prefrontal cortex at the site that I named FPO2. This site is off the 10–20 system and lies in the corner of the right eye, beneath the ridge of the orbital socket, where the eyebrow and the bridge of the nose meet. This is the endpoint of amygdala’s projection, and seems to be as close to the amygdala as we can get on the cranium. I began the exploration at 8–11 Hz with a 2–7 inhibit, and presently train at frequencies as low as 3–6 Hz and lower, generally with a 0–6 Hz inhibit. The hope was to exploit the limited afferent pathways to the amygdala, to quiet its reactivity. Clinical anecdotal evidence now abounds that training FPO2 reduces fear, and appears to impact fear memory. When FPO2 training is effective, people no longer believe or act on their post-traumatic impulses.

One colleague told me the following story. Several years before our encounter, he had been badly injured when a drunk driver, traveling in the wrong lane, 332 Neurofeedback and attachment disorder: Theory and practice crashed headlong into his car. He had been so traumatized by this accident that he had avoided taking that route ever since, even though this made his commute considerable longer. Two days after I trained him briefly at FPO2, he was driving home late and saw the headlights of a car coming directly at him on the wrong side of the highway. He swerved, pulled off and avoided the collision. He was amazed both at how calm he had been and that his old fear had not ignited. He had responded to the fear-inducing stimuli appropriately, but the event apparently did not create a post-traumatic kindling of the amygdala, a part of the brain quite prone to this terrible cascade.

A patient of mine, however, did suffer this exact cascade during FPO2 training. She has a history of severe emotional, physical, and sexual assault as a child in the context of profound parental absence. By the age of 30 she had suffered a stroke and had seizure and migraine, as well as severe PTSD. Within 3 minutes of FPO2 training she felt twitching in her face, a symptom that signaled the onset of seizure, and she was alarmed. We stopped the training and she did not go into seizure. Instead, over the next 2 weeks she regained memory of 9 years of her childhood that had not been available to her before that FPO2 training. We had, it appeared tapped directly into fear-based memory. Needless to say, our therapy was then turned to processing and integrating these memories.

This was a challenging epoch for her and I recently asked her, a year or so after this episode, whether she would ever train at FPO2 again. She said, “Oh, definitely. It was very rough, but it gave me a large part of my life back.” The scope of this chapter allows only a brief discussion of the role of the therapist, but this case study suggests how important therapeutic competence is when working at this level with neurofeedback. Neurofeedback practitioners must be present for what comes up, must recognize what they see, and then be able to work it through, interpersonally and therapeutically.

We don’t always trigger fear memory. In fact, in my experience to date, we usually do not. After training at FPO2, my young Aspergers patient reported her first “experience of moral compunction.” She read her stepfather’s face in response to her threatening behavior and felt, for the first time, that she “just could not do that to him.” FPO2 training softened the response of an RAD mother to her toddler, and he responded quickly and warmly to her new presence.

Perhaps the most profound case is that of a mother in her thirties with a history of incest, neglect, and physical abuse who became pregnant with her third child after the onset of training. Although she was a devoted mother who had already addressed a lot of her past in psychotherapy, her two older children suffered the effects of her history and their father’s with disregulation of their own. She had suffered severe post-partum depressions after both births. When fetal movement began in this pregnancy, she described the baby as “almost aggressive,” kicking her hard, doing somersaults, rarely quiet and then for only short periods. Such activity in pregnancy can be predictive of rapid cycling bipolar disorder in children (Papolos and Papolos, 2000).

I introduced FPO2 as a regular part of the mother’s training during the fifth month. During the training, she reported that the fetal movement quieted significantly, something it had not done at T4 earlier in the session. Over the next month, with FPO2, fetal movement became graceful and fluid. The mother reported that there was no more aggressive kicking, and no more somersaulting. She felt bonded to the baby in utero in a way that she had never known was possible.

After birth, her baby demonstrated remarkable levels of self-regulation. She didn’t fuss, she slept well, she was weaned easily from the breast, she didn’t use pacifiers or suck her fingers, and she rarely needed soothing. Her mother suffered no post-partum depression. The baby remains friendly and happy as her baseline mood, and she attracts people to her.

I can only begin to speculate on the method of action. It might be as straightforward as quieting the mother’s fear, and her high stress level quieted the baby. It is clear that the effect on fetal movement was specific to FPO2. It seems fair to assume some correlation between this level of fetal activity and hyper-arousal in the prenatal infant. It is the case that the amygdala comes on line in the fetal brain at 5 months in utero, the same time that fetal movement begins. Although we were training the mother to quiet her amygdala activity, perhaps this directly signaled the baby’s to quiet as well. It was a clear and undeniable in-session effect that deepened over the course of training in the next 4 months. We will only be able to know the effects of the training on this mother and baby as the child grows up. Even if the benefits were unequivocal, such a case would clearly have to be replicated and validated before we can know if there is widespread application of FPO2 in helping mothers to bond to their babies, and for the babies to achieve such levels of self-regulation. This I have to leave for the researchers.

Given the present levels of insecure attachment in the US, this is vital research. But maternal infant bonding is not only a priority in the US; it is or should be a priority worldwide. Neglected, abandoned and orphaned children are at great risk of attachment disorder, and the subsequent development of sociopathic personality. There are 35 million AIDS orphans alone. What does this portend for our common welfare?

[^1]: In personal conversation, Jay Gunkleman estimated 10% of this population will have seizure activity, and Ed Hamlin estimated a number as high as 20%. Sebern F. Fisher, M. A., BCIA 329