Wednesday, December 3, 2008

Symmetrical effects of amphetamine and alpha-flupenthixol on conditioned punishment and conditioned reinforcement: contrasts with midazolam

Killcross, A.S., Everitt, B.J., & Robbins, T.W. (1997). Symmetrical effects of amphetamine and alpha-flupenthixol on conditioned punishment and conditioned reinforcement: contrasts with midazolam. Psychopharmacology, 129, 141-152.

There is evidence to suggest that forebrain dopaminergic systems are likely to be involved in both appetitive and aversive motivation. These authors studied the effects of dopamine (DA) agents on conditioned punishment (aversive learning) and conditioned reinforcement (appetitive learning) paradigms using DA agonists and antagonists injected systemically. In conditioned punishment, a Pavlovian CS predicting punishment is added to an instrumental bar-pressing paradigm, but only on one of the bars. Normal animals will adjust their bar-pressing away from this lever. (Note: These authors, however, implemented a punishment procedure by presenting a CS and shock upon bar-press, rather than a conditioned punishment procedure which would only present the CS upon bar-press). In conditioned reinforcement, a CS predicting reward is added to the instrumental bar-pressing paradigm on one of the bars. Animals will naturally come to favor this bar paired with the appetitive CS.

DA agonists increased the effect of a punishing CS, causing the animals to further decrease their bar pressing. DA agonists also enhanced the effect of an appetitive CS, increasing bar pressing. DA antagonists, on the other hand, decreased the effect of a punishing CS. They also reduced the effect of an appetitive CS. Thus, it appears dopaminergic agents modulate the behavioral impact of both appetitively and aversively motivated conditioned stimuli on instrumental performance. Systemic benzodiazepene administration was also explored with results showing a selective impact on aversively-motivated stimuli (i.e. no effect on the appetitive CS).

Saturday, November 29, 2008

The Value of Believing in Free Will

Vohs, K.D. & Schooler, J.W. (2008). The Value of Believing in Free Will. Psychological Science, 19, 1, 49-54.

This study found that weakening people's belief in free-will increased ignoble behaviors, specifically cheating. In the first experiment, a passive cheating paradigm was explored in which a computer "glitch" allowed the correct answer to a question to be flashed onto the screen unless the participant explicitly suppressed it. The experimental group was read a statement encouraging a belief in determinism, while the control condition was read an unrelated statement. Those in the experimental group showed weaker free will beliefs and more frequent cheating.

In the second experiment, an active cheating paradigm was explored. After reading either a pro-free-will statement or an anti-free-will statement, participants were left in the room on the "honor system" and told to reward themselves for their number of correct responses. In this experiment, as in the previous one, participants were under the impression that their anonymity was preserved. Results were similar with the determinism condition showing weaker free will beliefs and higher than average cheating. Thus, people's beliefs regarding their sense of control and self-agency may have social implications.

Saturday, November 22, 2008

Different lateral amygdala outputs mediate reactions and actions elicited by a fear-arousing stimulus

Amorapanth, P., LeDoux, J.E., & Nader, K. (2000). Different lateral amygdala outputs mediate reactions and actions elicited by a fear-arousing stimulus. Nature Neuroscience, 3, 1, 74-79.

One common reaction to threat is elicitation of unlearned species-typical defense reactions. Another is the ability to take novel actions in threatening situations, which may also prove advantageous. In escape-from-fear (EFF) tasks, animals come to learn that an arbitrary response (e.g. stepping into the adjoining chamber) terminates a CS which predicts shock. Authors placed lesions throughout the fear circuit to see try to elucidate function. Lateral amygdala (LA) is believed to be the sensory interface where CS information enters the amygdala; lesions here block acquisition of both conditioned freezing responses, as expected, but also block acquisition of the CS's reinforcement of a new response in the EFF task. Central nucleus (CE) lesions block expression of hard-wired motoric output (i.e. freezing itself), but not the EFF. Basal nucleus (B) lesions had no effect on conditioned freezing, but did block the EFF. By way of interactions between the B and striatal circuits, reinforcement in the amygdala may come to reinforce novel motor responses. Thus, it may be that activation of LA by a CS triggers a reactive response output system via the CE and an active output system via the B.

Thursday, October 23, 2008

Nonconscious mimicry as an automatic behavioral response to social exclusion

Lakin, J.L., Chartrand, T.L., & Arkin, R.M. (2008). I am too just like you: Nonconscious mimicry as an automatic behavioral response to social exclusion. Psychological Science, 19, 8, 816-822.

First, this study showed that following exclusion by a group, participants increased their nonconscious behavioral mimicry of a brand-new interaction partner, reinforcing the expectation that people should be motivated to engage in affiliative behaviors after exclusion. Second, the study attempted to see if this automatic behavior is carried out bluntly, or whether it is sensitive to other factors. Researchers found that individuals excluded by an in-group mimicked the behaviors of a subsequent interaction partner only if the partner was an in-group member (as opposed to an out-group member). Therefore, it appears that people are selective with their use of automatic mimicry, increasing employment of it with people who can potentially restore their status with the in-group. In this way, belongingness was seen as related to mimicry. (Other factors, such as mood, self-esteem, meaningful existence, and control did not appear to be as related.)

Thursday, October 9, 2008

Ethanol-conditioned flavor preferences compared with sugar- and fat-conditioned preferences in rats

Ackroff, K., Rozental, D., Scalfani, A. (2004). Ethanol-conditioned flavor preferences compared with sugar- and fat-conditioned preferences in rats. Physiology & Behavior, 81, 699-713.

Past studies in rats have suggested that the postingestive effects of various nutrients can condition strong flavor preferences. Research has been conducted on ethanol using oral conditioning (where the ethanol is mixed in with the flavoring, thus adding its own flavor to the mixture) and intragastic conditioning (where the ethanol is injected into the rat’s stomach after it ingests the flavoring, thus eliminating the ethanol’s flavor as a conditioning factor). However, the findings of these studies have been somewhat contradictory. Mehiel and Bolles (1988) found that rats equally preferred a flavor paired with ethanol and a flavor paired with sucrose, while Sherman et al. (1983) found that rats preferred a flavor paired with glucose to a flavor paired with ethanol. These studies different in terms of design, route of administration, and sugar used, but it is unclear which of these factors are responsible for the confliction. The present study examined this question in a series of four related experiments.

In the first experiment, sucrose and ethanol were compared to each other as well as to a control of water. These nutrients were each paired with a different flavor and administered through intragastric infusion. Unlimited access to alternating flavor/nutrient combinations was provided during a training period and then the amount of each combination consumed was measuring during a test in which the rats could choose between different combinations. The results were that (1) the rats preferred both sucrose- and ethanol-paired flavors to the water-paired flavor, (2) the rats strongly preferred the sucrose-paired flavor to the ethanol-paired flavor, and (3) the rats ingested more sucrose mixture than ethanol mixture during the training period.

The second experiment attempts to control for finding (3) in experiment one by adding the additional constraint that sucrose mixture consumption was limited to the previous day’s ethanol mixture consumption. Findings (1) and (2) did not change as a result.

In the third experiment, the oral conditioning method was used in place of intragastric infusion for nutrient administration. Once again, the findings did not change.

Finally, in the fourth experiment, ethanol was compared to fructose and corn oil using the intragastic infusions. Similar to the sucrose findings, the rats preferred these new sugars to ethanol, while still preferring ethanol to water.

This study supports the findings of Sherman et al. (1983) and eliminates training intakes, route of administration, and specific sugar/fat as explanations of Mehiel and Bolles’ (1988) contradictory findings. Something other than energy concentration affects the efficacy of ethanol as a reinforcer, making it less powerful than other sugars/fats.

Monday, October 6, 2008

Evidence for episodic memory in a Pavlovian conditioning procedure in rats

O'Brien, Jamus; Sutherland, Robert J. Evidence for episodic memory in a Pavlovian conditioning procedure in rats. Hippocampus. Vol 17(12) 2007, 1149-1152.

Several requirements have been proposed for establishing episodic memory in nonlinguistic species. Clayton et al. (2003) suggest that episodic memory competence requires integrated representations of “what", "where", and "when” content that can be flexibly updated as more information is gathered. Tests of episodic memory should be novel and unexpected, exceed the capacity of short-term memory (Dere et al., 2006), be unsolvable by familiarity judgments (Gallistel, 1990), and involve memories formed in unique one-trial learning episodes (Morris, 2001). In this article, O’Brien and Sutherland design and run an experiment that attempts to meet these requirements while testing for the flexible and integrated representations required for episodic memory.

In this experiment, twenty-two male Long-Evans rats were run through three experimental phases. In Phase 1, rats were given time to explore two different “contexts” (boxes A and B). These boxes were Plexiglas modular test chambers with steel grid floors. Box A had black colored walls and was scented with Quatzyl-D-Plus, while box B was white and scented with Clinicide. Each rat visited Box A on three successive mornings and Box B on three successive evenings. In Phase 2, rats were exposed to a single immediate shock in a “chimerical” box that was half black, half white, and unscented. For half the rats, this occurred in the morning and for the other half, it occurred in the evening; this is the study’s independent variable. In Phase 3, during mid-day, rats were placed in one of the contexts from Phase 1 (either Box A or Box B). Fear responses (this study’s dependent variable) were then measured by timing conditioned “freezing” behavior.

A repeated measure ANOVA was conducted on the percent of time spent freezing during Phase 3, and it was predicted that rats placed in the context congruent to the time of day of their shock would exhibit more freezing than rats placed in the incongruent context. (For example, if a rat was in Box A in the morning and Box B in the evening during Phase 1 and received its shock in the morning during Phase 2, then the congruent context would be Box A and the incongruent context would be Box B.) The results were a significant relationship in the direction predicted (F(1,20) = 45.0, P < 0.001).

These findings support the idea that rats acquire memories laden with temporal context (or “when” content), such as the time of day, which is an important requirement of establishing episodic memory competence. Further studies could continue this line of research by establishing evidence for rats generating “what” and “where” content, and by exploring the nature of rats’ temporal cues – possibly endogenous circadian oscillators (Gallistel, 1990) or the age of granule cells in the dentate gyrus of the hippocampus (Aimone et al., 2006).

Friday, September 19, 2008

Modifying shyness-related behavior through symptom misattribution

Brodt, S.E. & Zimbardo, P.G. (1981). Modifying shyness-related behavior through symptom misattribution. Journal of Personality and Social Psychology, 41, 437-449.

In response to anxiety-evoking stimuli, people develop a complex constellation of reactions. Over time, a general categorical label may come to link these components together and serve as a central explanation. For some people, this label may undergo further transformation from its original situational attribution to a broader usage that includes the person's disposition (personal causality). For example, a person may immediately invoke the label "I am afraid of men" which in turn may kick off a response chain and impose constraints upon it, creating self-fulfilling prophecies. The authors of this study wanted to weaken the 3-part link between perceived symptoms of arousal, the corresponding dispositional label, and resultant behaviors by intervening with symptom misattribution.

In this experiment with 46 college women, the dispositional label studied was shyness -- an excessive self-focus in which potential rejection by other people and social anxiety are salient cognitions. Seeking to redirect the arousal from an anxiety-laden source (being alone with a member of the opposite sex) to a nonpsychological source, the researchers exposed all the groups to intense noise and led the "shy misattribution" group to believe that common side effects of noise bombardment was heart-pounding and increased pulse, symptoms normally associated with their social anxiety. Another group, the "shy comparison" group were led to believe the noise only caused dry mouth. Another "non-shy" group, unlike the other groups did not score high on shyness ratings, were given the same story as the "shy misattribution group". Results showed that shy women, when given an alternative explanation for their social anxiety, were able to overcome normal limitations of their shyness, talking significantly more, acting more assertive, and showing a stronger affiliative preference than the comparison group. Thus, misattribution demonstrates the power of social cognitions in controlling behavior.

Monday, September 15, 2008

Hippocampal involvement in contextual modulaton of fear extinction

Ji, J. & Maren, S. (2007). Hippocampal involvement in contextual modulaton of fear extinction. Hippocampus, 17, 749-758.

Responding to an extinguished CS is susceptible to many recovery effects. The first is renewal, in which changing the context favors recall of extinguished fear memory. Examination of its several forms (ABA, AAB, ABC) led researchers to postulate that following extinction the meaning of the CS becomes ambiguous and requires context to disambiguate; inhibitory association is "gated" so that its activation requires the simultaneous presence of the CS and the extinction context. The second is spontaneous recovery, or the return of conditional responding with the passage of time. Studies suggest that renewal and spontaneous recovery appear to result from a similar control mechanism, rather than simply erasure of the original fear memory. Therefore, some see SR as another renewal effect that occurs outside of the "temporal extinction context". Third is reinstatement, in which the extinguished response returns after extinction if the animal is merely exposed to the US alone in a distinct context. This, likewise, appears to be a context-dependent process.

These all suggest that extinction involves new learning, and that this learning is especially sensitive to context. The hippocampus, mPFC, and amygdala have been implicated in this learning. One model holds that when the animal is tested within the extinction context, hippocampus drives mPFC inhibition of LA. When animals are presented with an extinguished CS outside of the extinction context, the hippocampus may inhibit mPFC activation and thus promote excitation in the LA to renew extinguished fear under these conditions. Another model posits direct projection from hippocampus to LA subserving contextual modulation of extinction.

Tuesday, September 9, 2008

Switching on and off fear by distinct neuronal circuits

Herry, C. et al. (2008). Switching on and off fear by distinct neuronal circuits. Nature, 454, 600-605.

Whereas firing of amygdala neurons is necessary for retrieval of conditioned fear memories, extinction of these fear memories is thought to be controlled by constraining this neural activity by local inhibitory circuitry (under the influence of mPFC). However, fear extinction is known to be a fragile behavioral state, readily influenced by context, i.e. changing context can result in spontaneous recovery. This raises the question of whether there are specialized circuits driving behavioral transitions in opposite directions, namely fear-on and fear-off. This paper showed that neurons in the BA could be divided into distinct functional classes: those exhibiting selective increases in CS+ evoked spike firing during and after fear conditioning (fear neurons) and those exhibiting selective increases in CS+ evoked spike firing during extinction (extinction neurons). Further, close analysis revealed that these two groups were not only functionally different but also differentially connected, with (1) fear neurons selectively receiving input from the hippocampus, and (2) extinction neurons being reciprocally connected to the mPFC while fear neurons only projected unidirectionally to the mPFC. This would indicate that co-localized within the same nucleus, two discrete neuronal circuits exist, intermingled in a salt-and-pepper-like manner. Their close anatomical proximity may serve to facilitate local interactions, although these mechanisms remain unexplored. Taken together with evidence showing emotional perseveration (persistent lack of state change) concomitant with inactivation of the BA, results suggest that the BA is unlikely to be associated with the storage, retrieval, or expression of conditioned fear and extinction memories, but is more likely to mediate context-dependent behavioral transitions between low and high fear states.

Monday, September 8, 2008

mPFC neurons signal memory for fear extinction

Milad, M.R. & Quirk, G.J. (7 November 2002). Neurons in the medial prefrontal cortex signal memory for fear extinction. Nature, 420, 70-74.

Extinction is a process thought to form a new memory that inhibits the once-learned conditioned response. This paper suggests that consolidation of extinction learning potentiates activity in the infralimbic cortex (IL) of the mPFC which inhibits fear during subsequent encounters with fear stimuli. Electrophysiological recording showed that IL activity remained unresponsive during the conditioning phase and also during extinction training on Day 1. However, by Day 2, activity in the IL in response to tone was present from the start of the extinction phase. Further, stimulation of the IL paired with tone presentation resulted in less freezing behavior and also accelerated extinction learning. Therefore, enhanced extinction learning could be mediated directly by the stimulation or indirectly by the behavioral feedback of decrease freezing. Since the BLA sends excitatory projections to IL, it is possible that these inputs serve to potentiate IL neurons during the consolidation of extinction. The IL is then likely to inhibit expression of fear behavior via its projections to intercalated (ITC) cells in the CE, dampening the output of the amygdala. Pairing reminder stimuli with activation of the ventral mPFC through transcranial magnetic stimulation (TMS) might help strengthen extinction of fear in clinical settings.

Neural mechanisms of extinction

Quirk, G.J. & Mueller, D. (2007). Neural mechanisms of extinction learning and retrieval. Neuropsychopharmacology Reviews, 1-17.

The simplest form of emotional regulation is extinction, is which conditioned responding to a stimulus decreases when the reinforcer is omitted. Exinction, like any learning process, occurs in 3 phases: acquisition, consolidation, and retrieval. Cannabinoid and opioid receptors appear to be implicated in the acquisition of extinction since anandamide and opioid antagonists impair within-session extinction of fear. Consolidation appears to depend on protein synthesis within the BLA, frequency bursting of the infralimbic region (IL) of the vmPFC shortly after extinction, and general involvement of the hippocampus, especially in tasks such as inhibitory avoidance and contextual fear. Retrieval of extinction memories involves the expression of inhibitory circuitry and is highly context-specific. Inhibition circuitry within the amygdala includes local inhibitory neurons within the BLA and CE, as well as islands of GABAergic neurons between these two sites known as the intercalated (ITC) cells. ITC cells could serve as a site of extinction memory since they inhibit CE output neurons and BLA neurons, acting as an off-switch for the amygdala. ITC cells receive strong projection from the IL mPFC, and IL activity is correlated with the extent of extinction retrieval. In fact, electrical stimulation of IL reduces conditioned fear and strengthens extinction memory. The prelimbic (PL) mPFC, on the other hand, excites fear expression and can augment fear expression via projections to the basal nucleus of the amygdala. Thus, the PFC can fully control overall fear expression. Individuals with PTSD show reduced vmPFC and hippocampal volume and activity, as well as increased amygdala activity. Stress may also impair extinction, since chronic stress is shown to decrease dendritic branching and spine count in hippocampus and mPFC, but increase it in BLA, which could be expected to increase conditioning and impair extinction. Pharmacological adjuncts to current extinction-based exposure therapies may accelerate and strengthen extinction. Among them D-cycloserine, yohimbine, sulpiride, and methylene blue show promise. Administration of glucocorticoids such as cortisol before exposure therapy may also help.

Sunday, September 7, 2008

Dopamine gates LTP in lateral amygdala

Bissiere, S., Humeau, Y., & Luthi, A. (June 2003). Dopamine gates LTP induction in lateral amygdala by suppressing feedforward inhibition. Nature Neuroscience, 6, 6, 587-591.

It has been known that both long-term potentiation (LTP) and concomitant activation of dopaminergic nerves to the amygdala underlie the acquisition of fear conditioning. In fact, dopamine is known to be released in the amygdala during stress and intra-amygdala injection of dopamine receptor antagonists prevents fear conditioning. This study investigated the mechanisms supporting this and showed how dopamine could modulate fear conditioning by modulating inhibitory synaptic transmission within the amygdala. Specifically, D2 dopamine receptors could enable the induction of LTP by suppressing feedforward inhibition from local inhibitory interneurons.

Friday, September 5, 2008

Neuronal Signalling of Fear Memory

Maren, S. & Quirk, G.J. (November 2004). Neuronal Signalling of Fear Memory. Nature Reviews Neuroscience, 5, 844-850.

Plasticity within the CNS is necessary for the representation of new information, and can range from synthesis and insertion of synaptic proteins to whole-brain synchronization of neuronal activity. Pavlovian fear conditioning is an especially interesting phenomenon since such fear memories are acquired rapidly and are long-lasting. Research first noticed conditioning-induced changes in the midbrain, thalamus, and cortex; however, it was unclear whether or not these were primary sites of plasticity or were simply downstream from other plastic sites. Eventually the lateral nucleus of the amygdala (LA), receiving direct projections from the auditory thalamus, was posited to be vital for auditory fear conditioning. The dorsal subdivision of the nucleus (LAd) seems to be the first site in the auditory pathway to show associative plasticity that is not fed forward passively from upstream sites, is not dependent on downstream sites, and is crucial for conditioned behavior. And LA neurons appear to drive plasticity at both thalamic and cortical levels.

Fear memories are useful to anticipate and respond to dangers within the environment. However, when signals for aversive events no longer predict those events, fear to those signals subsides. This is an inhibitory learning process known as extinction. It appears that although fear subsides after extinction, the fear memory is not erased. Extinction seems to be highly context dependent and sometimes short-lived. Fear responses can be spontaneously recovered over time. It seems biology has deemed it better to fear than not to fear. It is more likely that additional memories which interfere with pre-existing excitatory responses are learned in the extinction process. Again the amygdala seems to be essentially involved here. Further, the mPFC, which has an inhibitory influence on both the LA and the CE (the main output regions of the amygdala) through a rich network of inhibitory interneurons embedded in the amygdala, appears to be a major participant, and is perhaps modulated by context via hippocampus.

Emotion Circuits in the Brain

LeDoux, J.E. (2000). Emotion Circuits in the Brain. Annual Reviews in Neuroscience, 23, 155-184.

Emotion research was largely lost for some time in the wake of the cognitive revolution. However, people soon realized a purely cognitive view of the brain -- leaving out emotions, motivations, and the like -- is likely to paint an unrealistic view of real minds. Unfortunately, attempts to dig into emotions once again were hamstrung by the limbic system concept, a flawed and inadequate theory of the emotional brain: cognition does not only reside in the neocortex and emotions do not only reside within the limbic system (a moving target itself).

Emotion research began its official resurgence with a bottoms-up examination of fear conditioning, with a bulk of the work focused on the auditory modality. Research soon named amygdala as centrally important, a site where transmission of information about the CS and US converged and output projections controlled fear reactions. On the input side, CS sensory inputs terminate in the lateral amygdala (LA), coming from both the auditory thalamus and the auditory cortex, although plasticity seems to occur initially through the thalamic pathway. US information also seems to converge in the amygdala, receiving inputs from the spino-thalamic tract, cortical areas that process somatosensory stimuli including nociceptive stimuli, the parabrachial area, and the spinal cord. On the outbound side, the central nucleus of the amygdala (CE) projects to autonomic (hypothalamus) and defensive motoric (periaqueductal gray) centers. Methodologies used have largely been single unit recordings, long-term potentiation (LTP) studies, and pharmacological experiments which block LTP. Studies have focused on two types of fear learning: simple fear conditioning (a benign tone comes to evoke a fear response) and contextual fear conditioning (fear responsivity to environmental cues). Research agrees that the amygdala seems to be required for Pavlovian fear conditioning to occur, although the site of long-term fear memory storage is still unknown: it may very well exist in the amygdala, but it may also be distributed across multiple structures or transferred off to cortical areas over time. However, plasticity within the amygdala is probably not required for learning cognitive aspects of fear.

Human studies have echoed many of the results from animal literature. Additionally, they have found perceptual deficits of the emotional meaning of faces in patients with amygdalar damage. The amygdala also appears activated more strongly in the presence of fearful and angry faces than of happy ones. Further, when the activity of the amygdala during fear conditioning is cross-correlated with other regions of the brain, the strongest relations are seen in subcortical areas, emphasizing the importance of the direct thalamo-amygdala pathway in the human brain. Although a fear conditioning approach cannot account for all aspects of human fear and anxiety disorders, it may be especially elucidating for PTSD, panic disorders, and phobias. Difficulty in extinguishing fear memories witnessed in human disorders may also involve the medial prefrontal cortex circuitry.

Future research needs to integrate both cognition and emotion. How fear processing in the amygdala can influence perceptual, attentional, and memory functions of the cortex, and vice versa, is begging for additional research, although it is known that the amygdala does receive input from cortical sensory processing regions and projects back to these both directly and indirectly. How conscious emotional feelings are manifest is also relatively unexplored, although the models posit that feelings may arise from interactions between the amygdala and prefrontal working memory areas, sensory processing areas in cortex, long-term memory systems in the temportal lobe, and arousal systems which maintain global projections.

Tuesday, August 19, 2008

Our 100th Post!

Congratulations to all those who posted, i.e. Jeff and I. Maybe we can recruit some more people to join in! Stay tuned.

Wednesday, August 13, 2008

An Illustration of DBT

Linehan, M.M. (1998). An Illustration of Dialectical Behavior Therapy. In Session: Psychotherapy in Practice, 4, 2, 21-44.

In addition to providing illustrative transcripts from dialectical behavior therapy (DBT) sessions, the bulk of the read, this paper also summarizes DBT's theoretical perspective, its various treatment stages and targets, as well as treatment strategies. DBT was developed to treat clients meeting criteria for borderline personality disorder (BPD) whose behavioral patterns are commonly problematic and stressful for clients and therapists alike, not the least of which is suicidality. DBT theorizes that BPD individuals lack interpersonal, self-regulation, and distress-tolerance skills, and what skills they do possess are often undermined by behaviors which block the use of the capabilities the client does have. As such, outcomes are typically unpredictable, even for patients who resist the tempting urge to quit and remain in treatment.

DBT recommends splitting up therapy into different stages, each with unique goals. In Stage I, treatment tries to achieve self-control, with control over one's suicidal behaviors being most important. In Stage II, clients try to experience emotions without resistance and to form and maintain connections to people, places, and activities, even if they are somehow associated with past trauma. Stage III focuses on reducing residual problematic patterns that interfere with clients achieving other important goals. When successful, Stage IV achieves a lasting sense of completeness and the capacity for sustained joy.

DBT's treatment strategies include: (1) dialectical strategies which combine acceptance with change, synthesize opposites, and move the client from "either-or" thinking to "both-and" thinking; (2) core strategies of client validation and problem-solving; (3) communication strategies which balance warm responsiveness to the client's wishes with irreverence; and (4) case management strategies which help the therapist tackle the difficult problems of suicidality with team support and aim to ultimately teach the client how to effectively interact with their world, rather than teaching the environment how to interact with them.

Tuesday, August 12, 2008

Functional analytic psychotherapy

Kohlenberg, R.J. & Tsai, Mavis. Functional analytic psychotherapy. Journal of Psychotherapy Integration, 4, 175-201.

Functional analytic psychotherapy (FAP) is a radical behaviorist approach to psychotherapy. As such, it views everything we do as behavior and believes these behaviors are the result of contingencies of reinforcement we have experienced in past relationships. The therapy emphasizes the importance of the client-therapist relationship since it creates a functionally similar environment [to the "real world"] which can evoke problematic behavior (deemed CRB1's) that can then be observed and responded to with reinforcement, shaping, and interpretations. Improvements witnessed in-session (deemed CRB2's) can be praised and reinforced immediately, and the clinician's reinforcement can be assessed for effectiveness. Further, its emphasis on contextualism leads therapists to develop a comprehensive understanding of the meaning of a client's behaviors and forces practitioners to remain open-minded about an intervention's potential effectiveness given the context. As such, FAP commonly embraces and enhances concepts and techniques from different therapies, such as psychoanalysis and cognitive therapy. Practitioners of FAP are encouraged to tailor their use of therapeutic techniques depending on: what will evoke the client's problems in the session, whether the client's problems are rule-governed or contingency-shaped, and what will be naturally reinforcing of the client's target behaviors.

Tuesday, July 29, 2008

Acceptance and commitment therapy

Harris, R. (August 2006). Embracing your demons: an overview of acceptance and commitment therapy. Psychotherapy in Australia, 12, 4, 2-8.

Acceptance and Commitment Therapy (ACT) is one of the "third-wave" behavioral therapies which emphasizes mindfulness and is intended to be used with a broad range of clinical conditions. The goal of ACT is to create a rich and meaningful life, while accepting the pain that inevitably goes with it. Western psychology has typically operated under the "healthy normality" assumption which states that by their nature, humans are psychologically healthy. That is, they will naturally be happy and content, and suffering is seen as abnormal. However, research shows that psychiatric disorders are exceedingly commonplace, as is nonclinical psyshological suffering, despite our high standards of living. ACT assumes, rather, that psychological processes of a normal human mind are often destructive. They posit that there is a dark side of language and cognition which sits at the root of this suffering. We often struggle with our thoughts and feelings, hoping to change them, avoid them, ameliorate them, and get rid of suffering. In doing so, ACT points at that some of these tactics often create extra suffering for ourselves. These "emotional control strategies" commonly become costly, life-distorting, or harmful. In ACT, there is no attempt to reduce, change, avoid, suppress, or control these private experiences. Instead, mindfulness is encouraged.

ACT commonly employs six techniques: (1) Cognitive Defusion: Learning to perceive thoughts, images, emotions, and memories as what they are, not what they appear to be. (2) Acceptance: Allowing them to come and go without struggling with them. (3) Contact with the present moment: Awareness to the here and now experience with openness, interest, and receptiveness. (4) Observing the self: Accessing a transcendent sense of self, a continuity of consciousness which is changing. (5) Values: Discovering what is most important to one's true self. (6) Committed Action: Setting goals according to values and carrying them out responsibly.

Sunday, July 27, 2008

Relapse Prevention for Alcohol and Drug Problems

Witkiewitz, K. & Marlatt, G.A. (2004). Relapse Prevention for Alcohol and Drug Problems. American Psychologist, 59, 4, 224-235.

Relapse prevention (RP) is a cognitive-behavioral approach with the goal of identifying and preventing high-risk situations such as substance abuse, obsessive-compulsive behavior, sexual offending, obesity, and depression. Relapse is seen as both an outcome and as a transgression in the process of behavior change. An initial setback (lapse) may either translate into a return to the previous problematic behavior (relapse) or into the individual turning again towards positive change (prolapse). That individuals commonly experience lapses, and even relapses, is not contested. However, an understanding of this phenomenon continues to evolve.

Relapse is thought to be multi-determined, especially by self-efficacy, outcome expectancies, craving, motivation, coping, emotional states, and interpersonal factors. High self-efficacy, negative outcome expectancies, potent availability of coping skills following treatment, positive affect, and functional social support are expected to predict positive outcome. Craving has not historically been shown to serve as a strong predictor.

The article proposes a new reconceptualization of relapse as a multidimensional, complex system. Such a nonlinear dynamical system is believed to be able to best predict the data witnessed, which commonly includes cases where small changes introduced into the equation seem to have large effects. The model also introduces concepts of self-organization, feedback loops, timing/context effects, and interplay between tonic and phasic processes. The effectiveness and efficacy of RP for various goals is also discussed in the article.

(I, Doug Girard, am the author of this article, Relapse Prevention, and I release its content under the terms of the GNU Free Documentation License, Version 1.2 and later.)

Thursday, July 10, 2008

Theory-based research for understanding dynamic psychotherapy

Luborsky, L., Barber, J.P., & Crits-Christoph, P. (1990). Theory-based research for understanding the process of dynamic psychotherapy. Journal of Consulting and Clinical Psychology, 58, 3, 281-287.

This article reviews empirical support for 6 basic theoretical assumptions central to psychodynamic psychotherapy. (1) A therapeutic alliance must develop. The strength of therapeutic alliance (the collaborative and affective bond between therapist and client) is shown to predictive of positive outcomes. (2) Patients display transference. Trends from existing studies show central relationship patterns exist which are largely consistent over time and may be projected onto the therapist. (3) Accurate interpretations of transference by the clinician lead to increased benefits for the client. Findings are inconsistent on this point, specifically on the relation between increased number of transference interpretations and outcomes. Mediators may exist, such as how the patient responds to the interpretation. (4) The patient will benefit more from more accurate interpretations. Accurate interpretations correlate with "better" sessions. Accuracy of interpersonal aspects of interpretation predicted outcomes best. (5) Increased insight about themselves and their relationships with others leads to better outcomes. Gaining an understanding about the therapist and others is associated with outcomes. An understanding of self and parents does not seem to be as well correlated. (6) Improved patients show greater change in their transference patterns. Results are consistent with the theory that transference still exists but is under better control and mastery. Patients' expectations of how others will respond becomes less negative and their mental health improves.