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I’m trying to become a critically reflective researcher, a captain who sits at the helm and steers the research ship (rather than functioning more like the ship’s rudder, careening left and right at the whims of the ship itself).
I would like to publish more of our existing data and, moving forward, develop an efficient method of publishing data in a way that eliminates back-log. I would like to use methods and measures that have even greater ecological validity and that will allow us to answer questions that are important and fundable. I would like to apply for funding to cover FMRI scanning costs so that I can answer questions about neural circuits and train students to do so too. And, based on subsequent reflection, one addition: I would like to pursue answers to questions that align with my clinical, cognitive, and social interests. In a recent phone conference, Jeff Birk, Sarah Cavanagh, Maryna Raskin, Phil Opitz, and I were talking about a manuscript stemming from our work on emotion regulation among people who do versus don’t have a history of recurrent depression. I noticed that we’re on version 11 of this paper and when I went back to look up some study-related detail, it was dated 2012. So, we talked about it a bit and all agreed that our democratic approach of having all authors read and comment on every draft simply wasn’t working. After that conversation, Sarah went off and did some sleuthing and found several interesting and helpful posts like this one and this one that led her to construct a work flow that the group subsequently honed by email, shown next.
The work flow that follows is meant to reflect the steps to be taken after data have been collected and it’s time to figure out what interesting discoveries we’ve made. DENTAL DRAFT: FA sends dental draft, everyone comments, this time with thorough in-line edits to the writing. And perhaps this plan or something close to it is totally obvious to anyone who happens to be reading this, but it was a welcome epiphany for me.
Lately I’ve been finding myself thinking a lot about how scattered, behind, and under-the-gun I feel, and how little direction my research program seems to have at the moment. Then it occurred to me: Researchers could similarly keep a weekly research log to record salient research moments. Expressive Writing: To what extent does writing about daily stressful events in a way that encourages reappraisal promote well-being and stress resistance? Post-Event Processing: What are the predictors and consequences of repetitively reflecting on negative aspects of socially evaluative situations after the fact? Selection, Optimization, and Compensation with Emotion Regulation (SOC-ER) Framework: What are the resources that impact the choice to use certain emotion regulation strategies and success in doing so? I am working now with five exceedingly talented graduate students, each of whom is working toward a Ph.D. In the past, even recent past, we have used functional magnetic resonance imaging (FMRI) to collect data that sheds light on the neural circuits that underlie the psychological processes we’re studying. The main goal for clinicians who look at neuroscience research on OCD is to ultimately find treatment that works.
One of the first lines of treatment for OCD from a psychosocial perspective is CBT, a treatment that focuses on the assertion that through cognitive and behavioral techniques, the emotional and psychological underpinnings of the disorder can be altered (Wilson et al, 2014; Olatunji et al, 2013). While many studies analyze CBT as a single therapy option, CBT can also be considered an overarching category that splits into two specific types of CBT: Cognitive therapy (CT) and Exposure and Ritual Prevention (ERP).
Cognitive therapy is a form of CBT that focuses on attempting to modify beliefs about the significance of intrusive thoughts (Olatunji et al, 2013). Therapy isn’t always the first or only treatment for OCD patients; medication has often been used either alone or in accordance with therapeutic treatments.
Another pharmaceutical option is clomipramine, a tricyclic antidepressant that has been shown to benefit OCD patients (Pittenger & Bloch, 2014). While medication and cognitive-behavioral therapies are the most commonly used treatments for OCD and other mental disorders, various studies are looking into what other ways OCD symptoms can be relieved. ECT, while widely used to treat OCD up until the 1980’s, has been found to be ineffective in treating OCD symptoms (Bais, Figee, & Denys, 2014).
While treatment options are still being investigated, there are many promising areas for OCD symptom relief.
Last blog we discussed the ways in which affective abilities are varied in obsessive-compulsive disorder patients, the affective chicken as it were. One strong cognitive difference between patients with obsessive-compulsive disorder and healthy controls is a diminished ability to make goal-directed decisions (Gillan, 2014).
Gillan et al wanted to see if this impairment was due to a disruption in the balance between goal-directed action control and habitual behaviors, such as compulsive behaviors (Gillan, 2014). Another difference for OCD patients comes in the form of conflict monitoring and error detection.
While there is a clear difference in the results (OCD patients tend to do worse at these tasks than controls), the actual neural process for OCD patients is unclear at present. OCD patients also differ in executive control, and are found to have a decrease in overall executive functioning abilities (Lewin et al, 2014). This evidence of cognitive variation, along with the evidence of affective variation, paints a complex picture of OCD, where it is still unclear whether affect or cognition is the true initial cause of the disorder.
The final blog will step away from the question of what makes up OCD, and will instead focus on a question more important to patients with the disorder itself: how can we treat this?
One potential cause of anxiety is the “failure or loss of reward” (Gray & McNaughton, 2000).
In the meantime, I have more crudely modeled anxiety simply as not fully consuming the anticipated rewards.
Throughout this series, I have discussed the different situations (both typical and atypical) in which we fail to demonstrate towards others what is often considered a fundamental human experience: empathy. I feel as though the act of feeling positive emotions in response to other person’s malaise is perceived as relatively abnormal.
Finally, people may feel some pleasure towards another person’s pain simply because they think they deserve it! Examining Schadenfreude from a neural perspective has been relatively untouched thus far, yet the investigations that do currently exist paint an interesting picture. While decreased activation of areas such as the insula and the ACC may adequately explain the other failures of empathy I’ve discussed, it is insufficient in defining the neural bases of Schadenfreude. A second study utilized the fertile realm of rival sports fans to further examine the neural correlates of Schadenfreude. Their fMRI analyses focused on again, the ventral striatum, as well as our old friends, the insula and ACC. Although a great deal more research must be conducted to make more definitive conclusions about the neural bases of Schadenfreude, a clear pattern has emerged via the extant literature. Ellis identified that to every event in our lives we hold a belief and that belief leads to a consequence.It was further identified that distorted beliefs can lead to maladaptive behaviour and in turn psychological abnormality.
Along with EXPLAINING the Irrational Thinking (a-b-c model) from Ellis, you SHOULD also EXPLAIN the Cognitive Triad and Illogical Thinking theory from Beck (1967). Beck suggested that negative thoughts underlie mental disorders, but wanted to know why people get depressed? The following handouts and worksheets are from my Tips and Tools for the Therapeutic Toolbox series by mental heath publisher, PESI. For book recommendations for clinicians as well as clients, see my recommended Bibliography page. Visit me on Facebook at my new Tips and Tools Facebook Page where we can share resources with one another! Although PESI is a Continuing Education Provider for mental health professionals, anyone interested in mental health and self help can sign up and benefit from these practical life skills web casts (and the books below) that are geared towards therapists to help clients.
The following psychotherapy resources are some examples of psychoeducational materials such as free therapy handouts and therapy worksheets that therapists can use and download for use with their clients. Since they are self-explanatory as stand alone resources, really anyone interested in self help can enjoy these various materials.
Life skills are the common everyday skills you need to manage your life effectively and cope with life challenges. Below are some sample free therapy handouts, therapy worksheets, self-help quizzes and therapeutic group activities. This book is another treasure chest of hands-on and easy-to-use handouts, activities, worksheets, mini-lessons and quizzes that help clients develop effective life skills. For the public I offer personal development plans, stress management techniques, positive thinking strategies, practical life skill strategies, and more. For counselors I offer psycho education strategies, counseling skills, social media for mental health professionals, making counseling groups innovative, and more.
Epidemiologic and clinical studies have consistently revealed remarkable results indicating that the prevalence of cigarette smoking is markedly elevated in patients suffering from mental illness.
It has been speculated that individuals with schizophrenic disorders may be utilizing nicotine administered through tobacco smoking to remediate clinical and cognitive deficits.
A population-based study recently published by Lasser and colleagues7 examined smoking prevalence in various psychiatric patient groups using the National Comorbidity Study (NCS) database.
There has been an increasing understanding of both the neurobiology of schizophrenia and nicotine addiction in the past 20 years. Mesolimbic DA (reward pathway) neurons are of particular importance since these neurons project from the ventral tegmental area (VTA) in the midbrain to anterior limbic forebrain structures such as the nucleus accumbens and cingulate cortex, and may mediate the rewarding effects of nicotine since they have presynaptic nAChRs. There is little evidence that smoking can significantly influence the positive and negative symptoms of schizophrenia. However, recent prospective studies found no evidence for significant changes in psychotic symptoms with smoking abstinence in schizophrenic patients, suggesting the safety of smoking cessation in this population.
Cigarette smoking may reduce neuroleptic-induced parkinsonism25 and worsen symptoms of tardive dyskinesia,26 but these studies have been of cross-sectional designs.
Our research group has found that switching schizophrenic smokers from typical antipsychotic agents to clozapine leads to reductions in self-reported cigarette smoking, especially in heavier smokers.33 Similar findings were reported by McEvoy and colleagues,34,36 who found that the degree of reduction may be dependent on clozapine plasma levels. The use of atypical agents and improvements in psychosocial and medical care probably affords an enhanced quality of life to individuals with schizophrenia. Once patients achieve smoking abstinence, it becomes crucial to employ cognitive-behavioral coping skills techniques to reduce the likelihood of a relapse.18,55,59 Skills such as drug refusal and coping with cravings are especially important for schizophrenic patients, as they are often in environments with other smokers and peer pressure to smoke is strong. Standard Food and Drug Administration-approved smoking cessation pharmacotherapies like NTP17,18 and sustained-release bupropion19,23,24 appear to be safe and efficacious in schizophrenic patients during the course of controlled studies. When using the NTP, patients should be cautioned not to smoke while they are wearing the patch due to concerns about nicotine toxicity: symptoms include tremor, nausea, vomiting, dizziness, and, in very rare cases, seizures, arrhythmias, and death. For bupropion, controlled studies have started dosing at 150 mg PO daily with an increase to 150 mg BID by day 4 of treatment.
The high rates of comorbid smoking in schizophrenic patients may relate to abnormal biology of nicotinic receptor systems and central dopamine pathways associated with this disorder. In addition, motivation to quit smoking is often low in schizophrenic patients and efforts need to be undertaken to increase the awareness of both patients and their clinicians of the dangers of habitual tobacco smoking.
Furthermore, there is increasing evidence from controlled studies that certain pharmacologic agents (eg, atypical antipsychotic drugs, nicotine replacement, and bupropion), in combination with behavioral support (eg, psychoeducation, MET, relapse-prevention, and social skills training), promote smoking reduction and cessation, and that these agents can be used safely for the treatment of cigarette smoking and nicotine dependence in clinically stable patients with schizophrenic disorders.
E-newsletter Opt-inSent no more than 2–3 times each month, our E-Newsletter brings you recent findings and commentary from the psychiatric literature. We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. The cognitive problems experienced by people with schizophrenia not only impede recovery but also interfere with treatments designed to improve overall functioning.
Across diagnoses the defining feature of mental ill health is impairment in the ability to function, which often translates into difficulties in attaining personal objectives or achieving expected goals.
Lysaker and Dimaggio (2014) consider that problems in the sphere of metacognition affect the ability of people to make sense of their illness experience and compromise the integrity of their personal goals.
A different approach is to consider metacognition as the cognitive function responsible for insight (David et al., 2012). Self-related cognitive processes have been extensively linked to metacognition and considered important in influencing psychotic symptom development and maintenance. Self-related concepts feature implicitly in another prominent theory of psychotic symptoms development. It is well established that people with schizophrenia have a number of thinking biases which influence the development and maintenance of key psychotic symptoms such as delusions. Most definitions described above consider metacognition as the function responsible for regulating thoughts, emotions and beliefs. Awareness of cognitive problems can be thought of as a form of metacognitive knowledge that can effectively guide the deployment of cognitive resources to a specific task. It is possible to consider metacognitive knowledge and regulation as a hierarchy of mental processes referring to cognitive operations with some of these processes being more complex than others (Table 1). For the purpose of this paper we define metacognition as the process that regulates learning and information processing via metacognitive knowledge and regulation processes. Given that people with schizophrenia have poor recovery outcomes, it is surprising that little research has concentrated on how gains made in therapy through CR or other therapies transfers into functional gains.
Methods such as problem based learning (PBL) allow learners to acquire knowledge by exposure to problems.
With learning being the vehicle of change in most psychological therapies it is perhaps surprising that metacognition has only recently started to feature in CR descriptions. Without suggesting that anyone has done anything wrong in any way, I’m wondering if there might be a better process we could use to move this thing forward in a more efficient way? Frankly, the fact that manuscripts can move slowly in my lab in part stems directly from my unspoken desire to make them perfect. It was about the writing process and the tantalizing idea that the process could change in ways that would make research lives better for everyone.
In addition to this process being subject to the vagaries of everyone’s unique scheduling challenges, this approach didn’t ultimately respect the idea that position on the byline should be meaningful.
I had been going along wanting everyone to have a voice, everyone to have the opportunity to contribute their ideas and make the manuscript as good (perfect?) as it could possibly be before clicking “Submit.” But the fact is that there are better ways to ensure that everyone contributes and that the manuscript benefits from everyone’s unique perspective.
No matter how close to perfection the work seems to be when finally we click “Submit,” nobody else will see it as such. Writing this is my attempt to rein things in, to exert some top-down control over a bottom-up work life.
Brookfield’s book, “Becoming a Critically Reflective Teacher,” as part of a book group through our Center for Enhancing Learning and Teaching at Tufts (awesome center). This would enable a researcher to consider whether and how that salient moment should impact next research steps.
How do people compensate when their emotion regulation strategy choice fails to change one’s emotions as intended? Army Natick Soldier Research, Development, and Engineering Center contract, the focus of which, stated very broadly, is to support cognition and emotion in the contextualized soldier. Many of the trainees in my lab would like to be trained to use FMRI to answer questions in this domain. This is a common therapy for many different mental and emotional disorders including various anxiety disorders.
While this treatment has shown positive results in terms of treating OCD symptoms, the more frequently and initially utilized treatment for OCD is instead Exposure and Ritual Prevention (Olatuji et al, 2013). This form of CBT has also been shown to be effective for treating OCD symptoms, and some studies have not found a significant difference between the two types of CBT in terms of effectiveness of OCD treatment (Olatuji et al, 2013). The most customary pharmacological treatments for OCD are selective serotonin reuptake inhibitors (SSRIs) (Pittenger & Bloch, 2014). Many areas for treatment, including therapy, medication, and neuromodulation options, show beneficial effects for treating obsessive-compulsive disorder. Now let’s discuss some of the other cognitive differences seen within OCD, the “cognitive egg”. Some researchers, such as Gillan et al in their 2014 paper, discuss how the inability to control compulsive actions can be seen as an inability to make goal-directed decisions, where, for example, instead of deciding to leave the house by flipping the light switch once in order to reach their goal of making it to work on time, some patients with OCD will decide to flip the switch numerous times in accordance to their compulsion. They found that obsessive-compulsive disorder patients showed decision making that suggests they based decisions on the temporally present expected value, instead of taking into account other possibilities (would it have been better to choose the other option?) (Gillan, 2014).
You are asked to say what color the font of the word is, when your automatic instinct is to read the word itself.
Some found hyperactivity in the medial frontal cortical (MFC) regions during conflict, while others found reduced activity in the MFC, while still others found no difference (Stern & Taylor, 2014).
More specifically, the capacity to switch tasks, which includes executive functions such as attention and decision-making, has been theorized as a possible explanation for obsessions and compulsions (Stern & Taylor, 2014). However, it is clear that both affective brain regions, such as the orbitofronto-striatal system, and cognitive brain regions such as the OFC, frontal-parietal network, and MFC, are involved in the complexity that is obsessive-compulsive disorder (Kashyap et al, 2013). Neuropsychological functioning in obsessive-compulsive disorder: are executive functions the key defecit?
As a result, my focus is one the role of the dopaminergic pathways, especially the rolls of the OFC and striatum in the reward system.
Their model of anxiety focuses on the role of the hippocampus, and they propose it compares anticipated state and current state and that anxiety comes from a mismatch of these (see “conflict generation” in figure).
I hope over this series of posts I have given the reader a plausible explanation that some OCD behaviors may be linked to a malfunction of the reward system, which in turn causes anxiety, which in turn may trigger behaviors to relieve this anxiety.

For this last post, I plan to end with a bang and examine what I consider to be the ultimate failure of empathy: the experience of feeling actual pleasure at others’ misfortunes.
One major contributor is an environment of competition (hence, I’m guessing, the joy displayed by the Survivor contestant below). As I’ve mentioned several times during this blog series, failures of empathy are often demonstrated neurally by decreased activation of certain brain regions, notably the insula and the anterior cingulate cortex (ACC).
Remember: this failure of empathy is not simply not feeling empathy for another person, an act of omission, but also involves an act of commission, or feeling actual pleasure at another’s pain.
Results indicated that high ventral activity occurred while participants watched successes of their favored team, and that pleasures ratings correlated with this activity– a logical result. The neural foundation of this concept may very well be the intersection of inactivation of areas typically involved in empathic concern (e.g. These women appear to have contracted the flu virus during the first trimester of pregnancy and this has led to poor neural development and schizophreniaSecondly Syphilis is a sexually transmitted disease that has been known to cause brain damage and therefore can be shown to lead to abnormality. One problem with the biological Approach is that the premise lays no blame with the individual.
They found a concordance rate of 46% in MZ twins  and a 20% concordance rate in DZ (fraternal) twins. They claim that abnormal behaviour is learned through experience, and even if something has a physical or biological predisposition, the behaviour is maintained by environmental reinforcement. It is suggested that through classical conditioning people can learn to associate an unconditioned response with a neutral stimulus.
Here is a video I made for PESI to introduce my books and offer some practical tips and tools you can use with your clients.
Although the following links are no substitute for therapy, they can reinforce important life skills concepts and can provide structure and practice between sessions.
Since we are not born with instruction manuals about life, and formal schooling focuses much more on academics than personal adjustment, learning life skills is essential to developing our emotional intelligence, resilience, work-life balance, and much more. Visit back soon as more links are added to help you fill up your mental health life skills and therapy toolbox!
George is director of the Program for Research in Smokers with Mental Illness (PRISM), Connecticut Mental Health Center, and assistant professor of psychiatry in the Department of Psychiatry at Yale University School of Medicine, both in New Haven, Connecticut.
R01-DA-13672, R01-DA-14039, and K12-DA-00167 and a NARSAD Young Investigator Award granted to Dr.
The prevalence of smoking in schizophrenia, as in other mental disorders, is higher than in the general population. In schizophrenic populations alone, rates of cigarette smoking approach 90%, in comparison to 25% in the general United States population.1,2 Clinicians are well aware that tobacco smoking poses dangerous health risks such as cardiovascular disease and lung cancer.
Indeed, a growing number of studies have found evidence that there may be biological and psychosocial factors which may explain these high rates of smoking comorbidity in schizophrenic patients, and that based on such knowledge, effective pharmacologic and behavioral treatments can be developed for the treatment of nicotine addiction in schizophrenia. This study is one of the few that have controlled for important confounding variables such as age, sex, treatment with psychotropic medication, alcohol and caffeine use, and socioeconomic status.
This method probably gives a more accurate estimate of smoking prevalence in individuals with psychiatric disorders than data from surveys of clinical samples. Nicotine’s stimulation of presynaptic nAChRs on these neurons increases transmitter release and metabolism.
These are the same subcortical DA pathways that are implicated in the expression of the positive symptoms of schizophrenia. Such an increase in circulating levels would be expected to increase the likelihood of extrapyramidal symptoms and other antipsychotic drug side effects (sedation, anticholinergic side effects),16 but evidence for an increase in antipsychotic side effects has not been demonstrated in controlled smoking cessation studies.17-19 Nonetheless, adjustment of antipsychotic drug in schizophrenic patients who quit smoking may need to be considered, as well as close monitoring of plasma antipsychotic levels and extrapyramidal symptoms. Several cross-sectional studies have examined the effects of cigarette smoking on psychotic symptoms in schizophrenic patients,4,20,21 with inconsistent results. It is notable that patients typically know very little about the dangers of smoking on their health, so education about the health risks related to tobacco smoking is an important first step in working with patients to motivate them to quit smoking. This treatment is done in a group setting, and we work from a social skills training model which encourages schizophrenic patients to practice skills which help facilitate social interaction and trust of fellow group attendees and therapists.
In our research clinic, we have not encountered nicotine toxicity to be a significant problem, but patients are told that if they must smoke they should remove the patch and wait 1–2 hours before resuming smoking. A summary of pharmacologic and behavioral treatment that have been evaluated in controlled studies of nicotine addiction is listed in Table 2.
Hence, these patients may self-medicate clinical and cognitive deficits associated with schizophrenia that are nicotine-responsive. Psychoeducation, motivational enhancement, and relapse-prevention techniques are the mainstays of behavioral treatment for nicotine addiction in patients with schizophrenia. While there is little evidence from controlled clinical studies that smoking cessation produces a deterioration of clinical function (eg, positive and negative symptoms) in stabilized patients, clinicians should not attempt to persuade patients to quit smoking when they are clinically unstable since the likelihood of success is low. Level of functioning, severity of illness, and smoking status among chronic psychiatric patients. Nicotinic enhancement of fast excitatory synaptic transmission in CNS by presynaptic receptors. Haloperidol dosing requirements: the contributions of smoking and nonlinear pharmacokinetics. Clozapine serum concentrations are lower in smoking than in non-smoking schizophrenic patients. Individual changes in clozapine levels after smoking cessation: results and a predictive model. Nicotine transdermal patch and atypical antipsychotic medications for smoking cessation in schizophrenia. Cigarette smoking in schizophrenia: relationship to psychopathology and medication side effects. A pilot trial of bupropion added to cognitive behavioral therapy for smoking cessation in schizophrenia. Effects of sustained-release bupropion and supportive group therapy on cigarette consumption in patients with schizophrenia.
A comparison of smoking behaviours between patients treated with clozapine and depot neuroleptics.
Acute feasibility and safety of a smoking reduction strategy for smokers with schizophrenia. 5-HT(2A) and D(2) receptor blockade increases cortical DA release via 5-HT(1A) receptor activation: a possible mechanism of atypical antipsychotic-induced cortical dopamine release. Premature deaths in schizophrenia and affective disorders: an analysis of survival curves and variables affecting the shortened survival.
Mortality in psychiatric patients, with a specific focus on cancer mortality associated with schizophrenia.
Comorbidity of mental disorders with alcohol and other drug abuse: results from the Epidemiologic Catchment Area (ECA) study.
Schizophrenia and nicotine use: report of a pilot smoking cessation program and review of neurobiological and clinical issues. Would smokers with schizophrenia benefit from a more flexible approach to smoking treatment? This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience.
Hence there has been a proliferation of new therapies to treat cognitive problems with the hope that improvements will benefit future intervention and recovery outcomes.
People with schizophrenia are often (but not always) at the most severe end of the functional disability spectrum and these difficulties, once established, tend to last a long time and affect all aspects of their life.
Difficulties in these mental functions become evident when individuals are engaged in processes requiring an understanding of their own and other people's mental processes but also when this information is required to be mastered for social use. People with psychosis have negative beliefs about themselves and display unhelpful coping strategies toward their psychotic symptoms (Pickup and Frith, 2001).
These biases are targeted by psychological interventions such as Cognitive Behavioral Therapy for psychosis (CBTp) (Wykes et al., 2008) and specifically by Metacognitive Training (MCT) (see this issue [insert issue references]). An alternative, but not opposing, view characterizes metacognition as the process that regulates learning and information processing. This knowledge is essential for individuals to access the relevant resources required for maximal efficiency (Flavell, 1979). This framework may be useful in the context of therapy to identify competence levels at the beginning of an intervention and to consider progression milestones in mastering metacognitive skills. Metacognition requires some of the processes measured as executive functioning but is a wider concept involving decision making (see further explanatory examples in the discussion). Unlike in mental health, the field of education has stressed the importance of promoting transferable skills and evidence now exists for the mechanisms that may facilitate their acquisition and usage. Learners seek information that would reduce their uncertainty and self-guide their learning on the basis of problem demands.
Education reviews suggest that metacognitive skills can guide strategic learning by explicitly teaching strategies and knowledge use, and ensuring that learners use monitoring processes to implement and review their performance (Education Endowment Foundation, 2013). Here personal recovery-based goals are set with the client and these goals are ones that can be related to cognitive problems. In principle, the first author should contribute the most to the manuscript, followed by the second author, third, and so on.
Having said that, you have probably intuited that this post does *not* address the putative topic of this blog, “Emotion on the Brain.” You’re right.
In this book, Brookfield provides thoughtful suggestions about how to be critical about one’s teaching in a way that promises to improve the experience of both learning and teaching. I am also working with three exceedingly talented undergraduate students, all three of whom are completing senior honors thesis projects in the EBBL this year.
Most of the projects that the graduate and undergraduate students in the EBBL are working on are funded by this contract and, thus, should and do address questions in the realm cognition and emotion. For OCD specifically, CBT has been found to be largely effective for treating OCD symptoms compared to patient controls (Olatuji et al, 2013). While fluvoxamine was the first SSRI to be shown with beneficial effects for OCD patients, there has not been evidence of any significant difference of effectiveness between different SSRIs, and the difference between them is mainly individual side effects and patient preference (Pittenger & Bloch, 2014). TMS to the OFC has shown positive, yet temporary, results for OCD symptoms, and could be a promising technique after further studies (Bais et al, 2014).
Cognitive-behavioral therapy for obsessive-compulsive disorder: a meta-analysis of treatment outcome and moderators.
A new model for the initiation of treatment for obsessive-compulsive disorder: an exploratory study.
They highlighted that this is similar to patients with lesions to the OFC, suggesting that perhaps that region is significant for OCD decision-making (Gillan, 2014).
This error detection can be seen cognitively during tasks where there’s a mismatch between what the person normally would do and what is required (Stern & Taylor, 2014).
Other areas found to differ include the parietal cortex, the temporal cortex, and the striatum (Stern & Taylor, 2014). Studies during cognitive switching tasks have found that OCD patients show reduced activity in the frontal-parietal network (FPN), indicated in executive function and task control, as well as reduced activity in the OFC, temporal cortex, and others (Stern & Taylor, 2014).
Counterfactual processing of economic action-outcome alternatives in obsessive-compulsive disorder: further evidence of impaired goal-directed behavior.
Neuropsychological functioning in youth with obsessive compulsive disorder: an examination of executive function and memory impairment. However, given feedback I’ve received from earlier posts and a presentation I made in class, I feel compelled to address a different topic. It is my hypothesis that the anxious behavior is a result of a malfunction in processing rewards. I’ve marked one of the agents as having OCD by reducing the amount of reward it is able to consume at each food location. I can imagine that other behaviors, such as washing or hoarding, are also linked to a lack of reward and the anxiety that stems from this mismatch. Brain corticostriatal systems and the major clinical symptom dimensions of obsessive-compulsive disorder. Proton magnetic resonance spectroscopy in obsessive-compulsvie disorder: Evidence for reduced neuronal integrity in the anterior cingulated. The Germans call it ‘Schadenfreude’—literally “harm-joy.” I would argue that this experience isn’t so atypical, though, if you think about it. Think about it: if you are in a zero sum situation with another individual or entity, a misfortune for them may represent a beneficial situation for you, and thus, it logically follows that you may experience a bit of pleasure. Let me give you an example: Jimmy Swaggart is a television evangelist known very well for public derision and exposing other people’s sins, especially those sexual in nature. These areas are typically engaged not only when people experience pain and sorrow themselves, but also when they observe others in pain and sorrow.
Importantly, though, high ventral activity was also found when participants watched the failures of their rival team, which was also correlated with pleasure ratings. This is much greater than the 1% in the normal population.Family and twin studies have been carried out to assess the importance of genetics in abnormality.
The biological approach suggests that there is a physical cause for abnormality therefore if we diagnose someone as having a mental 'illness' then it is true to say that the individual should receive treatment and support for their illness, but this is not always the case as some people believe that the individual is to blame for their abnormal behaviour (cognitivists).2.
Therefore allowing the individual to learn that avoiding situations will reduce the negative emotions. These free downloadable therapy handouts, worksheets, self help quizzes and life skills activities provide psychotherapeutic resources that ensure continued growth and personal development. Skill building through these free downloadable Cognitive Behavior Therapy worksheets and Communication handouts help your clients put to practice what they learn in the therapy session. Smoking is also associated with higher rates of medical morbidity, including cardiovascular and lung diseases, and with higher mortality in schizophrenic patients. In spite of the long-term health hazards associated with cigarette smoking, nicotine dependence has been difficult to treat in the schizophrenic population.
This article reviews the epidemiology, neurobiology, clinical impact, and approach to treatment for nicotine and tobacco addiction in patients with schizophrenic disorders. We briefly describe the pharmacologic effects of nicotine, and how these effects may link nicotine addiction with schizophrenia. Goff and colleagues20 found that schizophrenic smokers had higher total scores on the Brief Psychiatric Rating Scale than nonsmokers, and higher subscale scores for both positive and negative symptoms. Thus, an understanding of biological and psychosocial factors which render schizophrenic patients at high risk for developing nicotine addiction, as well as which contribute to their low intrinsic motivation to change smoking behaviors, are both critical to guiding efforts directed toward improving smoking cessation treatment in this population. Psychoeducation, in combination with classical motivational enhancement techniques (MET), can be combined to move patients through the stages of change56 toward abstinence. We have found that this combination of education, MET, and skills training can be quite effective for helping schizophrenic patients quit smoking and, with classic relapse-prevention skills training, remain abstinent. These findings have profound implications for understanding the neurobiology of schizophrenic disorders and for development of better treatments for nicotine addiction in this population, given that these patients appear to be at increased risk for developing smoking-related medical illnesses. Cognitive remediation therapy (CR) that relies on intensive task practice can support basic cognitive functioning but there is little evidence on how these therapies lead to transfer to real life skills. Functioning difficulties are further limited by reduced normative developmental experiences, such as fewer or disrupted years in education, loss of friends or a lack of opportunity to make them, arising as a result of mental health problems.
Pharmacological therapies designed to target symptoms have a limited impact on cognitive difficulties (Keefe et al., 2007). Since its first definition, many authors have contextualized this concept to specific approaches and adapted and elaborated on its original meaning. Limited insight and illness awareness have been associated with poor outcomes in people with psychosis (Frith, 2004) and changes in this function associated with clinical improvement (Corcoran and Frith, 2003).
Coping strategies may be controlled by metacognitive beliefs and difficulties in this domain may influence illness outcomes. This cognitive function is now widely referred to as theory of mind but can be seen as a metacognitive ability. This is not a new idea in psychology and has roots in Vygotsky's theories of learning potential but has been revisited more recently by Flavell (1979).
Individuals with a diagnosis of schizophrenia exhibit a mismatch between the subjective awareness and objective performance on cognitive tasks usually in the direction of under-estimating the problems (Cella et al., 2014). Studies conducted in the field of CR have highlighted the limited direct effect that enhancing cognition alone has on functioning suggesting that more complex mediating and moderating factors may be implicated in explaining the effects of the therapy (Wykes and Spaulding, 2011). Executive functioning, a concept akin to metacognitive regulation and monitoring, has been the focus of measurement which has demonstrated important links with clinical and functioning variables.
The effect of adopting this metacognitive approach to facilitate learning has tangible effects. For CR the primary target is cognition as changes are thought to exert an effect on functioning, however, there is limited knowledge on how the transfer from improved cognition to improved functioning may work. Metacognition is also applied in the context of CR as a process of recognizing the needs of a task and implementing the appropriate strategies and resources.

But it’s hard to set aside the very concrete thought that motivates striving for perfection, namely that if what we submit isn’t stellar, then people in the field (who I admire and respect!) might infer that the science coming out of my lab sucks (or, worse, they’ll make an internal attribution and infer that I suck at being a scientist). Files on my computer suggest that Phil sent version 1 of the paper to co-authors in September 2013, not too long after we finished collecting all of the data. No matter how hard we work to think and write clearly about the work we’re doing, to write the best manuscript we can, other smart people will come along and see it differently, point out flaws, and suggest improvements. This post is about emotions and brains only in the sense that I’m experiencing job-related emotions and they’re on my mind (in my brain?) so I’m writing about it. One of the things he suggested was that teachers keep a weekly teaching log to record salient teaching moments. My salient research moment was the realization that my research life is terrific in many ways, but it seems to be running me rather than the other way around.
On the ill-being side, studies in the lab have focused primarily on anxiety and depression. I’m also collaborating with several colleagues, some who are former trainees from my lab, to varying degrees of involvement on projects that are in various stages of development, from design to manuscript preparation. We primarily collect behavioral and autonomic psychophysiological dependent measures in mostly laboratory-based experimental paradigms in which one participant at a time views stimuli on a computer monitor and follows specific instructions that prompt the target psychological processes.
While there are studies that show these effects continue for some time after treatment ends, it is still less certain for how sustaining these alterations on OCD symptoms really are (Olatuji et al, 2013).
However, dosage does influence effectiveness, where SSRIs in higher doses are more effective for OCD than lower doses (Pittenger & Bloch, 2014). DBS has shown long-term effectiveness for OCD patients, with target areas including ventral striatum, nucleus accumbens, and other regions of the cortico-striato-thalamocortical circuit (Bais et al, 2014). They also found that OCD patients reacted more emotionally, consistent with affective differences discussed in my previous post.
These anxiety centers may be active during the anxious behavior but may not be the source of the disorder. First, it is consistent with my hypothesis that part of the problem may lay in the reward system. Other than this fractional reduction in reward processing, the two child agents are identical. Functional Neuroimaging and the Neuroanatomy of Obsessive-Compulsive Disorder. Psychiatric Clinics of North America, 23(3), 563–586. From rival sports fans to hated politicians, you must admit that you sometimes experience even a bit of pleasure from the misfortunes of whomever these individuals are in your own life. The affective aspect to Schadenfreude (though quite related to the social aspect of competition) is envy, which stems from perceptions of inferiority.
It is plausible that the reward system of the brain, regions responding to appetitive or pleasurable stimuli, may be at work. For ACC and insula activity, higher activity was found when participants watched their favored team fail, which was correlated with pain ratings (again a logical result—remember that these regions are activated both when one feels pain and when one observes others in pain). Neural responses to in- group and out-group members’ suffering predict individual differences in costly helping. Ventricles are sacks of fluid in our brain, people with schizophrenia tend to have larger ventricles than the normal population.
A second criticism to the biological approach is that it relinquishes responsibility from the suffer. However it should be recognised that the concordance rate is not 100% in MZ twins, therefore this demonstrates that depression cannot be entirely down to genetics and other factors must be involved.
Stress management activities and techniques, counseling worksheets, counseling activities for individuals as well as group counseling sessions, all provide valuable life skills information and opportunities to practice new skills.
For those interested in group therapy activities, there is also a couple sheets here that are perfect for interactive group activities.
Schizophrenia is characterized by a constellation of clinical and cognitive deficits, and these patients may remediate such deficits by cigarette smoking. This may explain why most smokers report that the most satisfying cigarette of the day is the first one in the morning. Ziedonis and colleagues21 found increased positive symptoms, and reduced negative symptoms that varied by amount smoked.
A summary of patient and treatment factors which predict successful nicotine addiction treatment outcomes17-19,55,57 in patients with schizophrenia is presented in Table 1. These may be particularly marked in people with schizophrenia as the disorder starts early and so there is less chance of learning or practicing skills important for future achievements. The main developments have been in the sphere of pedagogy and the concept has driven much of the innovation in learning and teaching over the past 20 years (Education Endowment Foundation, 2013). Despite a shared sense amongst clinicians that this may be an important domain to target there are no specific interventions for this domain. A study by Morrison and Wells (Morrison and Wells, 2003) reinforced this idea by suggesting that people who experience hallucinations, but do not develop schizophrenia, have higher levels of cognitive control compared to people with schizophrenia.
According to Frith psychotic phenomena, such as thought insertions or delusions of control, are dependent on the inability to correctly represent intentions and actions or to exert monitoring and control over cognitive operations (Frith, 2004). Here the components of metacognition are: monitoring (evaluation of cognitive functioning), control or regulation (directing and evaluating cognitive and behavioral performance), and knowledge (understanding task difficulty and the resources required). Research in this area has also demonstrated the importance of the learning environment for generalization and transfer.
Here we will describe how we think metacognition should be used as part of CR to maximize transfer and functional gains.
The second school adopts a strategy approach, which suggests that intensive practice should be supplemented by explicit training of strategies and approaches to the tasks (Cella et al., 2012). This is referred to as metacognitive regulation which is generally divided into three sub-processes—planning, monitoring and evaluation.
More than two years and ten drafts later, submission is still just a dot on a distant horizon. As pointed out by Maryna, this cascading level of contribution means that the authors in the middle of the byline, who are essentially getting the least amount of credit, should also do the least amount of actual work on the paper. This enables a teacher to consider whether and how that salient moment should impact next teaching steps. So, I’m going to start with a log – blog, really – that describes my research life and what I’d like to achieve next. This has generated and will continue to generate, useful knowledge that advances the field. DBS has also shown fewer side effects for patients, although DBS is more evasive than the other stimulation techniques (Bais et al, 2014). If any agent does not consume as much reward as anticipated at any location, then anxiety begins to mount.
Decision-making impairment in obsessive-compulsive disorder as measured by the Iowa Gambling Task.
I’ll just say this: I always love when a scandal befalls Georgetown University, whom I despise (as my alma mater is GW), but I will begrudgingly admit that these hostile feelings probably (maybe, possibly) stem from the fact that Georgetown is perceived to be a better school than GW. While participants partook in this, the experimenters measured fMRI activity and subjective ratings of pain, pleasure, and anger.
Importantly, again, high insula and ACC activity was also found when participants watched the successes of their rival team. Us versus them: Social identity shapes neural responses to   intergroup competition and harm. When your gain is my pain and your pain  is my gain: neural correlates of envy and Schadenfreude. Genetic and environmental factors may also play a role in the high comorbid rates of smoking in schizophrenia.
Hall and colleagues4 found that schizophrenics who were former smokers had fewer negative symptoms than current schizophrenic smokers.
It is hypothesized that these therapies achieve higher transfer by improving metacognition.
Society further limits opportunities through discrimination and stigma which prevent testing or practicing skills. Psychological and behavioral interventions have more successfully been developed to fill this gap. In the domain of psychopathology the concept has received a high level of attention as problems in metacognition are thought to be implicated in a large number of higher level mental functions including self-reflection, introspection and behavior implementation. This stresses the importance of metacognitive control and appraisal of psychotic experiences as a factor contributing to transition to schizophrenia and illness prognosis. Similarly, other proponents have elaborated on this idea and proposed that psychotic symptoms may result from problems in source monitoring (Keefe et al., 1999) through as the difficulty in distinguishing between the origins of self-generated and externally generated stimuli.
This has prompted a number of studies specifically investigating the contribution that regulation and knowledge may have to functioning in people with schizophrenia. Knowledge is learnt only as part of a unique context and it is less likely to generalize if the learning and the everyday life application contexts are different. More recently, the connection between an individual's metacognition and learning and especially how it can be boosted has been investigated.
However, mediation models of improving functioning suggest that the variance accounted for by improved cognitive performance alone is only 15%, leaving as much as 85% of variance unexplained.
In the planning stage individuals bring to mind all the relevant information to complete a task and organize the stages into the necessary sequence for the task. Granted, it’s a monster data set, one that stems from a laboratory session for which data were collected from July 2010 to August 2012, a year of every-four-months longitudinal follow-up surveys, and an MRI session, the last of which was run in May 2013. Doing so promises a steadier flow of manuscripts being published, ideally in no more than three drafts.
We’ve also managed to create a pretty serious back-log of data and we’re not moving all of these data toward publication. However, it is a limiting context that certainly does not echo the complexities of real-world emotions and their regulation. Reward is often associated with positive emotions, and anxiety is clearly a negative emotion. If anxiety passes a threshold, the agent returns to the last spot at which rewards were not fully realized and continues to attempt to acquire more reward. Next, participants read a second set of scenarios in which each of the three targets experienced a misfortune, and indicated their level of pleasure in response to these scenarios. This represents a related concept to Schadenfreude for which the Germans also have a word impossible to pronouce: Glu?ckschmerz, or pain at another’s success.
Not only is the devil (representing pleasure at others’ pain) present, but the angel (representing empathy) is also not there to counterbalance the impact of the devil. Preclinical and human laboratory studies have elucidated factors which may determine this comorbidity in schizophrenia, and recent treatments for both nicotine dependence (eg, nicotine replacement, bupropion) and schizophrenia (atypical antipsychotic drugs) may be useful for smoking reduction and cessation in this population. People with schizophrenia have metacognitive problems; these include poor self-awareness and difficulties in planning for complex tasks.
Cognitive Remediation (CR) was designed to target cognitive problems with the broader aim of improving functioning. Source monitoring can be seen as a metacognitive component providing agency information and facilitating the appraisal of events and life situations.
This concept coincides with executive function and is thought as the process that regulates and controls cognitive functions including working memory, attention, reasoning and information retrieval (Elliott, 2003). Executive function predicts supported and employment outcomes (Tan, 2009) and social functioning in people with schizophrenia receiving disability benefits (Tandberg et al., 2013).
This consideration stresses the importance of focussing on maximizing the opportunity for learners to acquire and maintain schemas that can be used in different situations. Notwithstanding the measurement problems in cognitive outcomes following remediation, we contend that some of this unexplained variance relates to skills learnt directly within CR that are immediately transferrable to everyday tasks and social relationships. In the monitoring phase the individual monitors actions as they are executed and adapts them if needed. And lack of reward is unlikely to be sufficient to produce the negative emotion of anxiety (though sadness is likely to result from a lack of reward). In the near future, I hope to model the role of the hippocampus in finding these mismatches using analogical comparisons.
Observations of this simulation reveal that any agent may begin to exhibit this behavior of returning to a spot to reinspect it. Results showed that ventral striatum activity, representing reward processing, increased only in response to the misfortune of the superior male, an envied target.
This paper reviews this evidence as well as research on why metacognition needs to be explicitly taught as part of cognitive treatments.
In people with schizophrenia the term metacognition is used by different proponents with diverse meanings and implications for outcomes and therapy. This process is often involved in tasks requiring the coordination of complex cognitive operations such as changing a plan in view of freshly gathered information, generating strategies, solving unexpected problems and organizing sequences of behaviors to accomplish a task.
This suggests that aspects of metacognition captured by executive functioning measures are important to symptom and functional outcomes. Providing practice in every possible environment where the schema may be needed is, however, impossible so the focus has shifted to which learning strategies may facilitate this transfer process.
In the evaluation stage the individual reconsiders the cognitive operations and evaluates their usefulness for similar future tasks. However, only the “OCD agent” will continuously exhibit this behavior and repeatedly return to the same spot.
Additionally, pleasure ratings, a behavioral measure of Schadenfreude, correlated with said ventral activity. The evidence is based on research on learning spanning from neuroscience to the field of education. CR is designed to provide intensive practice in both basic and high level cognitive functions and the evidence suggests that supplementing cognitive task practice with strategy use can achieve higher returns in terms of functional gains (Wykes et al., 2011).
Abstract explanations can supplement practice (Anderson et al., 1996) but more recently the research focus has been on cognitive control and how the allocation of cognitive resources may influence learning, transfer and usage of learnt material in everyday life (Tullis and Benjamin, 2011). So there is evidence that targeting metacognition can improve learning and recall and improves generalization to other tasks. Here CR changes metacognition and the cognitive tasks but it is mainly metacognition (indicated by the width of the line) which drives the effects on functional outcome.
In this post I will try to make the connection between poor reward consumption and anxious behavior exhibited in those with OCD.
Thus, this investigation served as initial evidence that the reward system may indeed be involved in the neural bases of Schadenfreude. The biological approach states that psychological abnormality has a physical cause this explanation does not consider the cognitions, learned behaviour or early psychosexual experiences.
This has prompted research into the mechanisms that may facilitate transfer of therapy gains into everyday life functional changes and can support recovery (Wykes et al., 2012).
This is achieved through explicit teaching of strategies for learning and generalization to other situations. Performance on cognitive tasks may also improve not just through task practice but through improvements in metacognition.
In the planning phase patients are encouraged to make plans formally before acting, to forecast possible difficulties in order to prevent problems. Swaggart made a very public and very humiliating confession, during which the pain was clearly visible on his face (see below). These types of metacognition are essential for successful task performance, in particular, for controlling effort, accuracy and efficient strategy use.
This paper will focus on the key role of metacognition in aiding transfer of therapy gains to everyday life.
This new model suggests that cognitive task improvement is not a mediator but is a third variable affected by the mediator (metacognition) and that therapy should target metacognition.
This includes non-cognitive factors such as, social anxiety, boredom and feeling low in mood. We consider metacognition vital for the transfer of therapeutic gains to everyday life tasks making it a therapy target that may yield greater gains compared to cognition alone for recovery interventions.
In the monitoring stage patients are encouraged to check the execution of the plan including making an assessment of the proficiency of the strategies used and flexibly adapt them to the situation.
In the evaluation phase, patients are encouraged to assess and review their performance and consider what went well and what could have been done differently.

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