From Towards a Science of Consciousness 3         Section III: Neural Correlates        CogNet Proceedings

First Steps toward a Theory of Mental Force:
PET Imaging of Systematic Cerebral Changes after Psychological Treatment of Obsessive-Compulsive Disorder

Jeffrey M. Schwartz

Obsessive-compulsive disorder (OCD) is a common neuropsychiatric condition, affecting approximately 2 percent of the general population (Jenike et al. 1998). It is characterized by bothersome intrusive thoughts and urges that frequently lead to dysfunctional repetitive behaviors such as excessive hand washing or ritualistic counting and checking. As the result of a concerted research effort over the past two decades there has emerged a growing consensus that brain circuitry contained within the orbital frontal cortex, anterior cingulate gyrus and the basal ganglia is intimately involved in the expression of the symptoms of OCD (for recent reviews see Schwartz 1997a and b, Jenike et al. 1998).

There are several aspects of OCD that make it a potentially rich source of information about the sorts of natural phenomena that occur at the mind-brain interface. First, because the neurobiology of this condition is reasonably well understood, and its symptom presentation fairly distinct and readily describable, studying OCD provides substantial information about how functional activity in the affected brain regions is experienced by humans. Second, the nature of this disease state is such that people who are affected by it are generally quite aware that the bothersome intrusive thoughts and urges with which they are suffering are inappropriate and adventitious in the literal sense i.e., the symptoms are experienced as unwanted and extraneous intrusions into consciousness, and have a quality that has classically been described in the clinical literature as "ego-dystonic" or "ego-alien" implying "foreign to one's experience of oneself as a psychological being" (Nehmiah and Uhde 1989). Because of this, sufferers from OCD can frequently give clear and graphic descriptions of how the symptoms are subjectively experienced and how those conscious experiences change with treatment. Third, there are now very effective treatments of OCD involving both pharmacological and cognitive-behavioral psychological approaches, which can be administered either in conjunction or separately. Of particular interest are the recent findings that each of these treatments independently cause similar changes in patterns of brain metabolism in patients who respond to them (Baxter et al. 1992, Schwartz et al. 1996). Thus it becomes possible to track how changes in brain metabolism in specific brain circuits relate to changes in the internal conscious experience of well-defined neuropsychiatric symptoms.

One aspect of the study of cerebral metabolism in OCD and how it changes in conjunction with drug-free psychological treatment seems particularly relevant to the those interested in the study of the mind-brain interface. This involves the use of cognitive training as a means of enabling people suffering from this condition to come to a new understanding of the relationship between their brain, their conscious experience, and their choice of behavioral responses to that experience. It is on that aspect of the study of OCD that this chapter will focus. But first, let's take a brief look at the behavioral pathophysiology of OCD.

OCD: Overview of Brain Mechanisms


The major function of the basal ganglia, a set of gray matter structures lying deep within each brain hemisphere, is the processing of circuitry in the cerebral cortex for the purpose of efficiently initiating and guiding environmentally relevant behaviors. There is a substantial clinical literature that suggests a link between obsessive-compulsive symptoms and basal ganglia neuropathology. For instance, there have been numerous reports in the clinical literature describing the onset of obsessions and compulsions after a wide variety of insults to the basal ganglia, including even moderate decreases in oxygen supply or damage secondary to exposure to neurotoxic agents. Especially interesting are the findings of Susan Swedo of the NIMH, whose group has demonstrated a relationship between OCD in children and autoimmune attack on the basal ganglia occurring as a complication of streptococcal infection.

Numerous studies of the behavioral genetics of OCD also implicate the basal ganglia. James Leckman and David Pauls of Yale University have demonstrated a significant familial association between OCD and Tourette's Disorder, a condition that manifests with multiple motor and vocal tics and very likely involves the basal ganglia in its core pathophysiology. Other work has demonstrated marked increases in a variety of motor tic disorders among family members of patients with OCD (see Piacentini 1997, Jenike et al. 1998 for review). Thus the notion that OCD is a disorder in which brain pathology is related to what are essentially "multiple mental tics" is one that has significant clinical support.

The aspect of cortical circuitry that has been particularly implicated in OCD pathophysiology involves the connections between the orbitofrontal cortex (OFC) and the caudate nucleus, the part of the basal ganglia that primarily processes input from the brain's frontal lobe. In 1987 our PET brain imaging group at UCLA found that metabolic activity in these two structures was increased in subjects with OCD. This finding has now been replicated in a series of subsequent studies by several other groups, with increased activity in the OFC and a closely associated structure called the anterior cingulate gyrus being consistently seen in symptomatic OCD patients. Of particular interest are the findings of Scott Rauch and Hans Breiter of Harvard University demonstrating acute increases in the activity of these structures in patients subjected to sudden exacerbation of their OCD symptoms (see Baxter 1995 for review of all these findings). There is now a significant consensus among neurobiologists that an impairment in the modulation of OFC and cingulate activity by the caudate nucleus is a key aspect in the pathophysiology of OCD.

Studies of cellular physiology in behaving monkeys (Rolls 1995) helps clarify possible mechanisms underlying these clinical findings. The group of E. T. Rolls of Oxford University investigated neuronal firing patterns in the OFC in monkeys trained to respond to various visual cues in order to receive juice as a reward. These experiments revealed several important aspects of OFC function. First, neurons in OFC change their firing pattern in response to visual cues depending on whether these cues are associated with rewarding or aversive stimuli. Seeing something associated with either reward or punishment triggers discrete patterns of neuronal firing in OFC. Further, OFC responses are very sensitive to the expectations the organism has concerning the stimuli to which it is exposed. For instance, if a monkey comes to expect that a blue light is associated with receiving juice, but no juice is delivered after the blue light appears, bursts of neuronal firing will occur in OFC. These cellular responses, which can be understood as an "error detection" mechanism, can underlie an internal sense in an organism that "something is wrong" in the environment, and are conducive to the acquisition of adaptive behavioral changes. Cellular responses of this kind are also seen in the anterior cingulate gyrus.

Thus, a malfunction of these structures can impair an organism's capacity to recognize that stimuli that once were behaviorally meaningful no longer are. This helps explain why primates, including humans, with damage to the frontal lobe often demonstrate much slower and less effective forms of behavioral adaptation when confronting changed environmental circumstances, frequently associated with repetitive inappropriate behavioral responses.

In contrast to the kinds of perseverative behaviors that are performed as the result of a failure of OFC and anterior cingulate to generate appropriate "error detection" signals, OCD symptoms can be understood as behavioral perseverations associated with a persistent internal sense that "something is wrong," which is inappropriately generated by a pathological hyperactivity of these structures. The cognitive foundation of our approach to treating OCD at UCLA Medical Center relies on enhancing the patients' insight into the fact that their adventitious thoughts and urges are caused by "false brain messages"-and then helping them utilize that insight to change the choices they make when selecting behavioral responses to those internal experiences. When this results in significant clinical improvement due to the performance of more adaptive behavioral responses, there are associated significant alterations in their patterns of brain metabolism in the OFC anterior cingulate and caudate. Before presenting that data I will briefly overview the method of the psychological treatment.

Mindful Awareness and the Impartial Spectator


In behavioral approaches to the psychological treatment of OCD patients learn to perform adaptive behaviors instead of pathological ones in response to the intrusive thoughts and urges that comprise the core symptoms of OCD. To successfully complete therapy patients must tolerate and effectively re-direct their responses to the acutely uncomfortable feeling states that arise as a result of OCD pathophysiology. There is now substantial evidence that the acquisition of specific cognitive skills by patients enables them to perform behavioral therapy techniques more effectively by increasing their ability to manage the intensely uncomfortable feelings that arise during treatment (Tallis 1995).

At UCLA we have developed a four-step cognitive-behavioral training method (see table 10.1) that is organized around the working hypothesis that the intrusive thoughts and urges of OCD are caused to a significant degree by a biomedical disease state (Schwartz 1997c). Because the cognitive aspect of this method accentuates the biomedical aspects of OCD symptom etiology, we use the term cognitive-biobehavioral to describe the overall treatment strategy. [Place table 10.1 here] What we are trying to achieve by this training is a deepening appreciation of the intimacy of the relationship between intrusive OCD thoughts and urges and what are basically "false brain messages" that can safely be ignored. The treatment goal, of course, is to learn to respond to these "false brain messages" in a new and much more adaptive way. This is done by applying techniques of behavioral refocusing in which functional activities are systematically performed in place of habitual OCD responses. These cognitive-behavioral treatment techniques enable patients to better manage the intense anxiety caused by OCD symptoms; this enhances their ability to perform consciously chosen adaptive behaviors rather than automaton like compulsive responses when besieged by the excruciatingly unpleasant thoughts and urges elicited by the brain biochemical abnormalities associated with OCD.

Table 10.1

Summary of the four steps of cognitive-biobehavioral self-treatment for obsessive-compulsive disorder (OCD). (From Schwartz 1997c)

  1. RE LABEL:
Recognize the intrusive obsessive thoughts and urges as a RESULT of OCD.

  1. RE ATTRIBUTE:

Realize that the intensity and intrusiveness of the thought or urge is CAUSED BY OCD; it is probably related to a brain biochemical imbalance.

REMEMBER: IT’S NOT ME, IT’S THE OCD

  1. RE FOCUS:

‘Work Around’ the OCD thoughts by focusing attention on something else for at least a few minutes, i.e., DO ANOTHER BEHAVIOR

  1. RE VALUE:

Do not take the OCD thought at ‘face value’. It is not significant in itself.

What we are trying to achieve by this training is a deepening appreciation of the intimacy of the relationship between intrusive OCD thoughts and urges and what are basically "false brain messages" that can safely be ignored. The treatment goal, of course, is to learn to respond to these "false brain messages" in a new and much more adaptive way. This is done by applying techniques of behavioral refocusing in which functional activities are systematically performed in place of habitual OCD responses. These cognitive-behavioral treatment techniques enable patients to better manage the intense anxiety caused by OCD symptoms; this enhances their ability to perform consciously chosen adaptive behaviors rather than automaton like compulsive responses when besieged by the excruciatingly unpleasant thoughts and urges elicited by the brain biochemical abnormalities associated with OCD.

One aspect of this training method has emerged as being of particular importance. As the concept that intrusive OCD symptoms are merely "false brain messages" becomes increasingly well integrated into the patient's cognitive framework, an important transition begins to take place. The nature of how the patient consciously experiences the uncomfortable feeling of an OCD symptom begins to change in a way that allows him/her to create a distance between the experience of self and the experience of the symptom. While it is true that this change in how the symptom is perceived is in some sense an accentuation of the "ego-dystonic" or "ego-alien" aspect of it, that is only one small component of the therapeutic process. The essence of this adaptive change in perspective is that the person with OCD becomes increasingly able to experience the intrusive symptom from the point of view of a clear-minded observer, and thus comes to see the symptom as merely the result of a malfunctioning mechanical process in the brain that, while unpleasant, is not of any great personal concern.

It is the ability to observe one's own internal sensations with the calm clarity of an external witness that is the most noteworthy aspect of this experience. Within the terminology of traditional Buddhist philosophy this sort of mental action is called mindfulness or mindful awareness (Silananda 1990). Noting the sense in which it involves clear observation by, as it were, "a man within," the Scottish philosopher Adam Smith (1976) described this sort of mental experience as the perspective of "the impartial spectator." Both of these descriptions are used during treatment to help clarify for patients how to use their new insight into the biomedical nature of OCD symptoms to create a distance between the symptom and their self-concept. Thus, for example, patients learn to stop making self-statements like, "I feel like I need to wash my hands again," and instead make statements of the type, "That nasty compulsive urge is bothering me again." This process, which requires profound and painstaking effort, can significantly enhance patients' abilities to manage the fears and anxieties associated with OCD symptoms, which enables them to more consistently alter their behavioral responses in increasingly adaptive ways.

Effects of Cognitive Behavioral Treatment on Cerebral


Systematic changes in cerebral glucose metabolism accompany the clinical improvements achieved using this method of cognitive-biobehavioral therapy (Schwartz et al. 1996). We investigated cerebral metabolic rate changes in eighteen drug-free subjects studied with PET scans before and after ten weeks of out-patient treatment. Twelve of them demonstrated clinically significant decreases in OCD symptom severity during the treatment period, and six did not. There were two main findings in this study:

1. Bilateral decreases in caudate nucleus metabolism, divided by ipsilateral hemisphere metabolism (Cd/hem), were seen in responders to treatment compared to nonresponders. This finding was more robust on the right (p = .003) than on the left (p = .02). (See figure 10.1.) [Place figure 10.1 here]

2. There were significant correlations of metabolic activity prior to treatment between the orbital cortex and the caudate nucleus, cingulate gyrus, and thalamus on the right. After effective treatment these correlations decreased significantly. (See table 10.2.)

Table 10.2

Normalized region of interest correlations (r) before and after treatment, for behavior treatment responders (n=12). (Modified from Schwartz et al., 1996)

//

left Orbit to left Caudate

.46 -.01
right Orbit to right Caudate

.74** .28
left Orbit to left Cingulate .11 .58*
right Orbit to right Cingulate

.87**** .22
left Orbit to left Thalamus

.34 .05
right Orbit to right Thalamus .81*** .14
left Caudate to left Thalamus .66* .36
right Caudate to right Thalamus. .69* .41
//

Note: significance (one-tailed) of individual pre- and post-treatment correlations—

*p<.05

**p<.01

***p<.001

****p<.0005

= significant (p<0.05) difference in pre- to post-treatment correlation.

Assessing the Data of Inner Experience


The philosophical position known as epiphenomenalism views conscious experience as the result, but not the cause, of physical activity in the cerebrum. However, the issue of the role of interpretation in the response to brain activity, specifically the question of what meaning and/or value the human mind places on the internal experience of any particular electro-chemical event in the cerebrum, does not seem to be adequately addressed by this view. This is especially so insofar as it involves the relationship between any particular act of understanding and/or valuing of the internal experience that arises in association with a given brain signal, the type and quality of behavior that follows it, and the nature of subsequent brain signals. Because OCD is a condition in which data concerning all three of these factors can currently be acquired, it provides an excellent vehicle for investigating how changes in the valuation one places on the inner experience of an electro-chemical brain event relates to subsequent behaviors and brain events.

The Austrian economist Ludwig von Mises stated that, "Valuing is man's emotional reaction to the various states of his environment, both that of the external world and that of the physiological conditions of his own body" (Mises 1978). It is a major task of both economists and the psychotherapists (among a wide variety of other investigators) to discern coherent relationships between the way people value their experience and the kinds of choices and actions they subsequently make. Given recent technological advances in the fields of brain imaging, it is now also possible to acquire data concerning brain events occurring in conjunction with these events. Has the use of brain imaging to study the pathophysiology and psychological treatment of OCD taught us anything useful about possible relationships between these various factors?

Let us attempt the beginnings of an answer to this question by examining the therapeutic process in the case of a man with typical OCD. (The clinical aspects of this case will, to save space, be markedly abbreviated. See Schwartz 1997c for details) At the outset of treatment this man is besieged by very intrusive and persistent thoughts and urges associated with a gnawing gut-level feeling of dread that his hands are contaminated with germs. This almost invariably leads to hand washing of such severity that it causes the skin to become red, raw and chapped. Although he knows that his concerns about germ contamination are excessive to the point of being nonsensical, the gnawing anxiety associated with the obsessive thoughts of possible contamination is so intense he almost invariably succumbs to it with bouts of hand washing. A large body of research data is consistent with the statement that the intrusive gnawing fear that "something is wrong" with his hands (e.g., they are "contaminated by germs") is caused by an error-detection circuit that is "locked in gear" as the result of faulty circuitry connecting his caudate nucleus, anterior cingulate and orbital cortex. When we explain this to the man, and give him associated instructional materials, emotional support and time, he comes to readily understand it. This learning process comprises the first two steps, Relabel and Reattribute, of the Four Step Method (see table 10.1) that is used as part of the treatment process.

From a clinical perspective, what has the man learned: what is it that he now understands? The essence of his new knowledge is definitely not that his fear of being contaminated is a false cognition, because he already knew that to a significant degree when he appeared for treatment-in fact that's largely why he sought treatment. (To properly understand the clinical phenomena of OCD it is critical to remember that sufferers are still "in touch" with reality-the core problem is that their judgment gets overwhelmed by intense doubt, fear, and anxiety, which compulsions are a vain attempt to relieve. Indeed, compulsions tend to exacerbate the anxiety.) The essence of his new knowledge is that the reason his intrusive persistent thoughts and urges don't go away is that a biochemical imbalance in his brain results in his conscious mind being bombarded with a steady stream of "false error messages" or (as many patients prefer to call them) "false alarms." So what does that knowledge accomplish?

Well one thing it definitely does not accomplish is any meaningful change in the raw perception of the actual feelings of fear and anxiety-the gut is still churning and the gnawing sense that "your hands are dirty" is very definitely still present. That's almost certainly because the brain mechanisms underlying those inner experiences (the mechanisms upon which, to use the technical term, those experiences supervene) has not changed in any significant way. What has begun to change is the value the man now puts on those feelings and sensations. What he is beginning to do is learn how to control his emotional reactions to those feelings and sensations, by which I specifically mean the kinds of interpretations and meanings he attributes to them. At this point in treatment he basically feels the same-but he has changed in a critical way how he understands those feelings. With that change in understanding he has set the stage for making different choices about how to act on those feelings and sensations. Now, by consistently Refocusing his behavioral output onto healthful rather than pathological behaviors, while systematically Revaluing his inner experience of OCD symptoms on a regular basis (steps three and four in table 10.1), he can consciously establish new and much more adaptive response patterns to internal experiences that, prior to treatment, were almost always followed by nearly automatic pathological hand washing. And controlled scientific data now exist associating those new consciously chosen response patterns with statistically significant changes of energy use in the very brain circuitry that underlie his painful intrusive thoughts and urges, changes that bring with them a marked amelioration of the intensity and severity of his mental suffering.

How to Generate New Brain Circuits


From the perspective of a classically trained neurophysiologist there must exist new patterns of nervous system activity that are intimately related to the new understanding our man now has begun to attain regarding the unpleasant sensations his OCD pathology is bombarding him with-sensations that are, in all probability, causally linked to hyperactivity in brain circuitry involving the OFC, anterior cingulate and caudate nucleus. The key question from a philosophical perspective is what kind of process generates those new patterns of brain activity that arise in association with the man's new understanding. For an epiphenomenalist this question must be answered by statements that in essence "map out" or "specify a blueprint for" the kinds of neuronal process that lead to the new pattern of brain activity-no other type of answer is permissible given the constraints epiphenomenalism imposes with respect to the kinds of causal processes that effect changes in conscious activity. The epiphenomenalist position is that changes in the nervous system cause all changes in consciousness.

When asked to further specify what kind of process it is that relates a new moment of conscious understanding to the generation of new patterns of brain activity, the epiphenomenalist has no choice but to try to turn the question around and say that there was no new moment of understanding until the new brain patterns emerged-and when asked about what kind of process it is that causes those new brain patterns to emerge they will defer to some unknown future when the classically trained neurophysiologist will be able to answer that kind of question.

Fortunately, our man with OCD already has a good answer to that question, as he will proceed to demonstrate by exerting his will in order to endure and ultimately overcome his pain. Through a process that involves making the hard choices and performing the courageous actions that it takes to mindfully nurture and deepen his new understanding, he will begin to consciously alter his behavioral responses to his nasty OCD feelings-and in so doing he will systematically change the very brain circuitry that is causing his suffering.

There is one particularly key point, both clinically and philosophically, to comprehend about what occurs at the interface of conscious experience and brain activity during the moments of therapeutic breakthrough in the course of our man's treatment-those very special moments always involve an ACTIVE process. For at the moment when the man with OCD summons the mental strength to exert his will and physically actualize his new understanding by adaptively changing his behavior, he will be overcoming tremendous biological forces that are operating in order to resist that change. And the force it takes to surmount that resistance is in no sense a manifestation of any passive or random process-indeed, that force represents the essence of what the words active and purposeful really mean.

Assuming that his new understanding about the "false brain messages" underlying his intense urge to wash his hands is itself related to new patterns of brain activity (which, however they are generated, I believe is a very fair assumption), a major difficulty still confronts our man: How does he focus his attention on the "true message" those new and still frail and developing circuits are sending to his consciousness when he is simultaneously being bombarded by intense, powerful, and extremely distracting "false messages" that are very much still being "transmitted" by his hyperactive cortical-basal ganglia circuitry. Where, in other words, does he find the energy to strengthen the "good message" signal in his fragile and still developing new circuitry? And further, how does he now activate motor circuitry that will take him away from rather than toward the bathroom sink-for movement toward the sink, and the initiation of further damaging hand washing has been his habitual motor response to the urge from the "false brain message" for many years now, and so that particular motor response itself will have a very well-developed brain circuitry associated with it, with its own associated drives and urges.

The answer to this question, as every good OCD therapist knows, is that he generates the energy to activate his new health giving and life affirming circuitry through the exertion of his will, and the power of his striving-a power that can generate a real and palpable force, which I propose to term mental force. It is just this mental force, directed in our OCD patient's case by focusing his attention on his new "good message," which will strengthen and enhance his new brain circuitry's "message transmitting" capacity.

Now without question this newly proposed term, mental force, represents a still largely hypothetical entity at the present moment. But there does seem to be a theoretical need for a force of this kind in nature. For once one acknowledges the clinical fact that in order to change one's behavior in the midst of a barrage of intense dreadful feelings produced by pathological OCD brain circuitry, one must utilize an active process; and further reflects on the type of mechanism it would require for such an active process to cause the kind of systematic energy use changes those pathological circuits have undergone in the data presented in figure 10.1 and table 10.2, one may well come to the conclusion that a mental force, or something very much like it, is a necessary condition to accomplish the task. Without such a force the demonstrated changes in cerebral energy use, which are statistically significant only for those OCD subjects who demonstrate clinically meaningful improvement, would have to be generated by a passive process-but that is plainly inconsistent with a very large amount of clinical data, most especially the verbal reports of patients who have undergone treatments of this type. To precipitously reject such verbal reports as an unimportant source of data is not only scientifically and methodologically unjustified, it reflects an ad hoc perspective adopted merely to protect a profoundly counter-intuitive way of thinking.

In the course of preparing this chapter I discussed its cental point-the very special, yet palpably familiar, force required to activate the newly forming healthy brain circuits that are called upon when one engages in cognitive-biobehavioral treatment-with the patients in my OCD therapy group. One group member commented by suggesting that it seemed to him that this force was the internal world equivalent of the kind of force that it takes "to make water run uphill" in the external world. This insight seems very germane, perhaps even precise, to me. For with the availability of brain imaging techniques that can quantitatively measure energy fluxes in the brains of freely acting humans, the possibility of quantitatively characterizing the mental force involved in altering those fluxes in the course of well-defined conscious processes becomes a real possibility. Much work remains to be done as we proceed on the path toward a science of consciousness.

Acknowledgments


This work was made possible by generous donations from the Charles and Lelah Hilton Family. Stimulating discussions with Dr. Henry P. Stapp, Dr. Ann Graybiel, and Dr. David Chalmers helped me formulate these ideas.

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