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Born in West Virginia in 1980, The Neurocritic embarked upon a roadtrip across America at the age of thirteen with his mother. She abandoned him when they reached San Francisco and The Neurocritic descended into a spiral of drug abuse and prostitution. At fifteen, The Neurocritic's psychiatrist encouraged him to start writing as a form of therapy.
In the last post, we learned that the Editor-in-Chief of the Journal of Affective Disorders has published 165 papers in the journal, 155 of these since becoming editor in 1996. Excluding commentaries and editorials, that makes for a grand total of 142 articles thus far during his tenure as editor.The two major themes of Dr. Hagop Akiskal's papers are (1) the bipolar spectrum, and (2) temperament as the basis of mood, behavior and personality (e.g., Lara et al., 2006). Clearly, I cannot begin to summarize the content of these papers, but I will give some background material on the bipolar spectrum and "soft" bipolar (Akiskal & Pinto, 1999 - not published in JAD).Bipolar disorder, one of the most serious mental illnesses, is marked by periodic bouts of depression and mania (Bipolar I) or by depression and hypomania (Bipolar II). Given that depression often presents as the initial polarity, bipolar is frequently misdiagnosed as major depressive disorder (MDD), with disastrous consequences.1 The rigid categories of DSM-IV, however, may not capture everyone who displays clinically significant symptoms of bipolar disorder. Ghaemi et al. (2002) have noted that:...limitations of the DSM-IV nosology may impede the diagnosis of BD, because the DSM-IV has rather broad criteria for MDD and narrow criteria for BD.According to Akiskal and Pinto, the evolving bipolar spectrum (circa 1999) includes:BIPOLAR I: FULL-BLOWN MANIABIPOLAR I½: DEPRESSION WITH PROTRACTED HYPOMANIABIPOLAR II: DEPRESSION WITH HYPOMANIABIPOLAR II½: CYCLOTHYMIC DEPRESSIONS [often labeled as borderline personality disorder]BIPOLAR III: ANTIDEPRESSANT-ASSOCIATED HYPOMANIABIPOLAR III½: BIPOLARITY MASKED—AND UNMASKED—BY STIMULANT ABUSEBIPOLAR IV: HYPERTHYMIC DEPRESSION - "patients with clinical depression that occurs later in life and superimposed on a lifelong hyperthymic temperament."Each of the diagnostic categories was illustrated by a clinical case report. Cyclothymia is included in DSM-IV: "A history of hypomanic episodes with periods of depression that do not meet criteria for major depressive episodes. There is a low-grade cycling of mood which appears to the observer as a personality trait, and interferes with functioning." Hyperthymia, however, is not a diagnosis but an affective temperament "characterized by exuberant, upbeat, overenergetic, and overconfident lifelong traits." More specifically (Akiskal & Pinto, 1999):The attributes of a hyperthymic temperament are not episode-bound and constitute part of the habitual long-term functioning of the individual. Patients are typically men in their 50s whose lifelong drive, ambition, high energy, confidence, and extroverted interpersonal skills helped them to advance in life, to achieve successes in a variety of business domains or political life.Arnold Schwarzenegger comes to mind [if he had started having depressive episodes several years ago]. In fact, the case study of bipolar IV was presented as a highly successful, 53 year old married lawyer with three other families in different countries.Do powerful, philandering, middle-aged men who become depressed in their 50s really need their own special diagnosis??There are critics, of course... In his critique of the spectrum, Paris (2009) called it "bipolar imperialism" and said: "Until further research clarifies the boundaries of bipolarity, we should be conservative about extending its scope." It seems that no one is safe any more. Recurrent depression? Bipolar. Anxious and depressed? Most certainly bipolar.But the worse frontier of all has to be Bipolar Type VI: Dementia (Ng et al., 2008)! This paper presents "selected" case histories of 10 elderly patients from the California/Mexico border and Brazil. These patients presented with "late-onset mood and related behavioral symptomatology and cognitive decline without past history of clear-cut bipolar disorder." In other words: dementia (caused by neurodegenerative disease), with classic symptoms such as:Having hallucinations, arguments, striking out, and violent behaviorHaving delusions, depression, agitationAre we surprised that mood stabilizers and atypical antipsychotics were said to be beneficial??click on image for a larger viewAdapted from Table 1 (Ng et al., 2008). Clinical features and response to treatment in elderly patients with bipolar disorder type VI. [NOTE from The Neurocritic: atypical antipsychotics are in red, mood stabilizers are in blue.]Cases 1-5 are poor elderly Latino patients attending an adult day treatment center, and cases 6-10 are from private practice in a more affluent area of Brazil. Galantamine, donepezil, and rivastigmine are acetylcholinesterase inhibitors typically used to treat Alzheimer's disease [with limited effectiveness], while memantine blocks NMDA glutamate receptors. So why would the authors claim that the mood and behavioral problems had anything to do with bipolar disorder?Omitted from Table 1 (for space reasons and ease of presentation) are columns for premorbid temperament (as judged by family members) and family history. The temperaments were mostly cyclothymic or hyperthymic. Family histories included none (n=3), mood & anxiety (n=2), alcohol (n=2), and bipolar disorder (n=3). OK then, only 3 of the 10 patients had a family history of bipolar disorder. Again, what's the rationale for creating the new category of "bipolar type VI"?We present our perspective as an alternative to the more commonly held clinical–neurological view that agitation, impulsivity and related mood instability in Alzheimer's and other dementia patients merely represents frontal lobe dysfunction (Senanarong et al., 2004). A more sophisticated view in the literature argues that behavioral–cognitive syndrome in Alzheimer's disease is a prodromal stage, whereas in fronto-temperal dementia the behavioral disorder appears when the cognitive deficit ... Read more »
AKISKAL, H.; Pinto, O. (1999) THE EVOLVING BIPOLAR SPECTRUM Prototypes I, II, III, and IV. Psychiatric Clinics of North America, 22(3), 517-534. DOI: 10.1016/S0193-953X(05)70093-9
Ng, B., Camacho, A., Lara, D., Brunstein, M., Pinto, O., & Akiskal, H. (2008) A case series on the hypothesized connection between dementia and bipolar spectrum disorders: Bipolar type VI?. Journal of Affective Disorders, 107(1-3), 307-315. DOI: 10.1016/j.jad.2007.08.018
Is chocolate a legal "social drug" of abuse in the same category as nicotine, caffeine, and alcohol? Do you hang out at chocolate cafes with the purpose of becoming high or intoxicated? No? Have you heard of cancer-related deaths due to chocolate or driving under the influence of chocolate?And really, how much chocolate is considered "chocolate abuse"?1A new paper by Maremmani et al. (2011) addressed none of these questions, but asked 562 depressed Italian outpatients about their cigarette, coffee, and chocolate consumption. Why? Actually, it's not clear.Across all ages and cultures, mankind has always used substances in order to induce pleasurable sensations or desirable psychophysiological states. These substances, notably caffeine, tobacco, alcohol and chocolate, given their widely accepted recreational use, can be labeled ‘social drugs’.This passage appeared as Background in the Abstract and as the first two sentences of the Introduction: brief literature review. But we have no explanation of why cigarettes, coffee, and chocolate are assumed to be "social drugs". Are there no solitary smokers, drinkers, and eaters? Look at the large number of singletons staring at laptop screens at any Starbucks. However, cafe culture in Italy or France does allow for smoking, espresso sipping, and chocolate croissant nibbling all at the same time. Also, anti-smoking laws in other countries force smokers to congregate outside to smoke, which often turns into a social activity.But why look at the consumption of "social drugs" in people who are depressed? Aren't these individuals less inclined to be social? And aren't they likely to show anhedonia (loss of interest of pleasure) according to DSM IV criteria?2) markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation made by others)We're reminded that caffeine improves mood and cognitive performance, increases mental energy, and reduces fatigue, that nicotine increases attention and working memory, and that chocolate can also improve mood and even reduce stress. We're also reminded that psychiatric patients use more drugs than those in the general population:With regard to caffeine, in hospitalized psychiatric patients the prevalence of tolerance and intoxication is significantly higher than in the healthy population. The highest caffeine intake has been found in patients suffering from eating disorders (Ciapparelli et al., 2010) and schizophrenia (Rihs et al., 1996), the lowest in patients with anxiety disorders and major depression (Ciapparelli et al., 2010; Rihs et al., 1996).It's well known that the prevalence of smoking among individuals with schizophrenia is quite high (70-80%), higher than for those with other mental illnesses (Winterer, 2010). In fact, smoking is often considered a form of self-medication. So are cigarettes a "social drug" for smokers with schizophrenia?Finally, we have the case of chocolate, where Maremmani et al. (2011) issue a number of curious pronouncements:Lastly, the consumption of chocolate has shown interesting forms of linkage with psychiatric conditions. The correlation most often studied is that with depression: it has been observed that the craving for the rewards given by chocolate intensifies when depressive mood is induced... More severe depressive symptoms have been associated with higher chocolate consumption (Rose et al., 2010). Self-labeled ‘chocolate addicts’ do not generally seem to suffer from eating disorders, but may constitute a population of psychologically vulnerable people with a high predisposition to depression and anxiety disorders (Dallard et al., 2001). More specifically, a craving for chocolate seems to be unusually high not only in cases of depressed mood, but also in conditions of emotional dysregulation, like anxious and irritable states. The capacity to find comfort in eating chocolate seems to be related to the biological mechanisms of emotional instability,2 so that the depression associated with a craving for chocolate turns out to be an efficient discriminator of hysteroid dysphoria3 and DSM-IV atypical depression (Parker and Crawford, 2007; Schuman et al., 1987).So of the three "social drugs", chocolate seems like the winner among depressives of any sort, especially those with the greatest emotional dysregulation (i.e., those with bipolar disorder).Then the introductory narrative inserts a non sequitur or three on illegal drugs of abuse (heroin and cocaine) and alcohol use in bipolar disorder, and "cyclothymic traits" in bipolar individuals, heroin addicts, and alcoholics. Furthermore........This reported bipolar connection, in our opinion, is not just valid at a clinical level. We have stressed the possible role of the bipolar spectrum in the pathogenesis of substance use disorders. In particular, our integrated model provides an explanation for why the bipolar spectrum is the psychic substrate for the development of a substance-resorting attitude...So let's blur the lines between alcoholics and coffee drinkers, schizophrenic smokers and chocolate-craving dysthymics, severe bipolar I disorder and mild cyclothymia, shall we? Then what?The 562 depressed Italian outpatients were initially given one of four DSM-IV-TR diagnoses:192 patients with a Major Depressive Episode, 212 with Major Depression, Recurrent, 119 with Bipolar Depression, and 39 with Depression NOS (“not otherwise specified”).The participants also filled out the Hypomania Checklist (HCL-32) and according to the dichotomous rating procedure, there were 306 non-bipolar and 256 bipolar depressive patients [vs. 119 bipolar depressives according to DSM-IV-TR]. This illustrates the expansionism of the "bipolar spectrum" project, which is a major goal of the senior author.Then we have the vague quantification of chocolate use:The social drug habit was recorded in terms of the use of tobacco, coffee and dark chocolate-based food (chocolate bars, hot chocolate, chocolate-containing ice cream, biscuits or cakes). We classified smoking habits by division into 3 ascending ranks: total non-smokers, past regular users and current regular users and considered one cigarette as a “unit”. As to coffee, we distinguished between regular consumption (at least one coffee a day) and sporadic or no use [one cup was considered a unit]. What was considered a chocolate "unit"? The paper doesn't say.To reiterate: the goals of the study were to prove that the notion of "bipolar" should be expanded, and that those on the "bipolar spectrum" are more likely to abuse substances of any sort.And did the results support these ideas? Well, 44.5% of the DSM-IV-TR bipolar depressives were current smokers, and 43.4% of the HCL-32 bipolar depressives were current smokers. However, the statistics were only significant in the latter case, because the comparison was between only two groups, instead of between four groups. Even better are the number of cigarettes smoked daily: 10.66 for the DSM bipolars [vs. 8.13 for the other groups combined], and 10.45 for the HCL bipolars [vs. 7.51 for the non-bipolars]. The stats were nonsignificant in the first case (p=.33) and highly significant in the second case (p=.0003).In contrast, there were no differences in chocolate consumptio... Read more »
Maremmani I, Perugi G, Rovai L, Maremmani AG, Pacini M, Canonico PL, Carbonato P, Mencacci C, Muscettola G, Pani L.... (2011) Are "social drugs" (tobacco, coffee and chocolate) related to the bipolar spectrum?. Journal of affective disorders. PMID: 21605911
Today is the Mental Health Blog Party sponsored by the American Psychological Association as part of Mental Health Month. A widely neglected part of mental health treatment is encouraging and maintaining good physical health. This is extremely difficult when some of the major drugs prescribed for serious mental illnesses (such as schizophrenia and bipolar disorder) produce substantial weight gain. The "second generation" or atypical antipsychotics can cause obesity and hence diabetes, hypertension, cardiovascular problems, high cholesterol, and stroke.Yesterday the BBC posted this headline:Mentally ill have reduced life expectancy, study findsBy Dominic Hughes Health correspondent, BBC NewsPeople suffering from serious mental illnesses like schizophrenia or bipolar disorder can have a life expectancy 10 to 15 years lower than the UK average.Researchers tracked the lives of more than 30,000 patients through the use of electronic medical records.They found that many were dying early from heart attack, stroke and cancer rather than suicide or violence.Mental health groups say vulnerable people need to be offered better care to prevent premature deaths.. . . "We need to improve the general health of people suffering from mental disorders by making sure they have access to healthcare of the same standard, quality and range as other people, and by developing effective screening programmes."The BBC article referred to a paper that was published today in PLoS ONE (Chang et al., 2011). The authors reviewed the electronic database of a major mental health care provider (the South London and Maudsley NHS Foundation Trust). The results were alarming (but not new, unfortunately):A total of 31,719 eligible people, aged 15 years or older, with SMI [serious mental illness] were analyzed. Among them, 1,370 died during 2007–09. Compared to national figures, all disorders were associated with substantially lower life expectancy: 8.0 to 14.6 life years lost for men and 9.8 to 17.5 life years lost for women. Highest reductions were found for men with schizophrenia (14.6 years lost) and women with schizoaffective disorders (17.5 years lost). click on image for a larger viewFigure 1 (Chang et al., 2011). Annual mortality risk (%) by age groups and diagnoses of mental illness, compared to England and Wales population in 2008.The figure above illustrates the 2008 population of England and Wales in the red bars for five different age group: 15-29, 30-44, 45-59, 60-74, and 75+. Those with substance use disorders are shown in maroon, schizoaffective disorder in green, bipolar disorder in purple, schizophrenia in aqua, and depression/recurrent depression in light brown.Mortality risk is increased for all psychiatric diagnoses, and is especially evident in the middle three age groups. Life expectancies were estimated using these data, and the resultsconfirmed substantially shortened life expectancies at birth for all serious mental disorder groups investigated compared to national norms. Largest reductions were found for men with schizophrenia, women with schizoaffective disorders, and both men and women with substance use disorders.Why might this be? The authors do not speculate beyond stating that the "underlying causes may be multiple." Certainly, one can imagine that medication-induced weight gain [and increased levels of smoking] among the SMI contributes to lowered life expectancies.To counteract these dismal statistics, a regular part of mental health treatment should include programs that promote better physical health. Smoking cessation and nutritionists and structured exercise classes in addition to standard psychiatric care and substance abuse treatment.A six month intervention pilot study in Maryland enrolled 63 overweight participants at psychiatric rehabilitation day programs (Daumit et al., 2010):Results: ... In total, 52 (82%) completed the study; others were discharged from psychiatric centers before completion of the study. Average attendance across all weight management sessions was 70% (87% on days participants attended the center) and 59% for physical activity classes (74% on days participants attended the center). From a baseline mean of 210.9 lbs (s.d. 43.9), average weight loss for 52 participants was 4.5 lb (s.d. 12.8) (P<0.014). On average, participants lost 1.9% of body weight. Mean waist circumference change was 3.1 cm (s.d. 5.6). Participants on average increased the distance on the 6-minute walk test by 8%.Conclusion: This pilot study documents the feasibility and preliminary efficacy of a behavioral weight-loss intervention in adults with serious mental illness who were attendees at psychiatric rehabilitation centers...Although a 2% loss of body weight may not seem like much, it's better than a 10% weight gain over the same time period. The medical profession is obligated to provide the means for improved physical health in persons with serious mental illnesses. When physical health is potentially compromised by psychiatric treatments such as atypical antipsychotics, action to improve the situation is even more urgent.ReferencesChang, C., Hayes, R., Perera, G., Broadbent, M., Fernandes, A., Lee, W., Hotopf, M., & Stewart, R. (2011). Life Expectancy at Birth for People with Serious Mental Illness and Other Major Disorders from a Secondary M... Read more »
Chang, C., Hayes, R., Perera, G., Broadbent, M., Fernandes, A., Lee, W., Hotopf, M., & Stewart, R. (2011) Life Expectancy at Birth for People with Serious Mental Illness and Other Major Disorders from a Secondary Mental Health Care Case Register in London. PLoS ONE, 6(5). DOI: 10.1371/journal.pone.0019590
Daumit, G., Dalcin, A., Jerome, G., Young, D., Charleston, J., Crum, R., Anthony, C., Hayes, J., McCarron, P., Khaykin, E.... (2010) A behavioral weight-loss intervention for persons with serious mental illness in psychiatric rehabilitation centers. International Journal of Obesity. DOI: 10.1038/ijo.2010.224
Depression, by h.koppdelaneyIs depression actually good for you?Experts now believe that mild to moderate depression may be good for us – and even help us live longer. Rebecca Hardy explains how to reap the benefitsWe constantly hear how depression is blighting our lives, but some experts have an interesting, if controversial, theory: depression can be "good for us", or at least a force for good in our lives.Is this the start of a new Negative Psychology1 movement? Let's all seek out personal tragedy, sadness, insomnia, and a profound sense of failure and hopelessness, because it's good for us!!Last year, author and blogger Jonah Lehrer had a lengthy (and controversial) essay in the New York Times Magazine on Depression's Upside. The main idea, that depression has cognitive and evolutionary advantages, was largely based on a review paper by Andrews and Thomson (2009). In it, they put forth the analytical rumination hypothesis: depression is an evolved response to complex problems, and focusing on them to the exclusion of everything else is beneficial.In response, The Neurocritic was motivated to write about Depression's Cognitive Downside:On the contrary, numerous papers have shown that impairments in cognitive processes such as executive control, attention, and memory persist after a depressed person has recovered (Andersson et al., 2010; Baune et al., 2010; Hammar et al., 2009). In actively depressed patients, Baune and colleagues (2010) found impairments in all domains tested: immediate memory, visuospatial construction, language, attention, and delayed memory. These deficits can contribute to lower social and occupational functioning and a diminished quality of life. In addition, depression can be associated with declines in problem solving abilities on neuropsychological tests such as the Wisconsin Card Sorting Test and the Tower of London test.Now, a new paper by von Helversen et al. (2011) has claimed that depression is good for decision making. Lehrer wrote about this study as support for the analytical rumination hypothesis in Does Depression Help Us Think Better?Here’s where things get interesting: depressed patients approximated the optimal strategy [for hiring the best applicant in a simulated job search] much more closely than non-depressed participants did. The main problem with healthy subjects is that they proved lazy, unwilling to search through enough applicants. Those with depression, on the other hand, were much more willing to keep on considering alternatives, which is why they performed far better on the task. While this study comes with many caveats, it remains an interesting demonstration that depression, at least in specific situations, seems to enhance our analytical skills, making us better at focusing on social dilemmas.Participants in the study were 37 inpatients diagnosed with major depression upon admission to the hospital (10 of whom were omitted "due to technical difficulties with the choice task"). The 27 remaining patients were classified as either "depressed" (n=15) or "recovered" (n=12) based on improved scores on the Patient Health Questionnaire (PHQ-D) between admission and testing (which was a mean of 6.25 days -- that seems like an incredibly rapid remission, which makes one wonder about the actual severity and why they were admitted in the first place). Only half of the patients, both depressed and recovered, were on antidepressants (none were on other medications), which seems unusual for patients who may have been suicidal. Perhaps the criteria for admission to the psych ward in Germany are different than they are in the U.S. and Canada. The still-depressed patients were in hospital an average of 4.20 days when they were tested (which was not significantly different from the recovered patients). It wasn't completely clear if any of the patients were already on antidepressants, or whether the pharmacological treatment started during hospitalization for those on meds.2 The paper did not state whether any of the depressed patients had another diagnosis, such as an anxiety disorder of any sort (co-morbidity is common).Mean scores on the Beck Depression Inventory (BDI) were higher in the Depressed group (29.13) than in the Recovered group (16.67) or the Control participants (6.63), who also differed from each other. BDI scores of 14–19 are considered mildly depressed, 20–28 moderately depressed, and 29–63 severely depressed. So patients in the Depressed group scored at the low end of severely depressed, the Recovered participants were mildly depressed, and the Controls (n=27) were not depressed at all.The task administered to all participants is called the "Secretary Problem":The sequential decision-making task consisted of playing 30 games of a secretary-type problem. Each game challenged participants to find the best candidate for a job out of a sequence of 40 applicants. The 40 applicants were presented one after another, in a random sequence. After an applicant was presented, participants needed to decide whether they would accept the applicant or not. If they accepted the applicant, the game concluded and the next game started. If they rejected the applicant, the next applicant was presented. Rejected applicants could not be chosen later in that game. Information about the current candidate included their relative ranking compared to the candidates that came before, but not their absolute ranking. Points were awarded based on the absolute ranking of the candidate chosen on each round. If a participant didn't make a choice until the end of the sequence, they were forced to accept the final candidate. So it seems that an indecisive person would be more likely to continue the search for a longer time...Results showed there was a trend in that direction (p=.08): search length was 23.37 for Depressed, 16.87 for Recovered, and 17.96 for Controls. Performance goals for each round (how good a candidate would have to be in order to be chosen) and the relative rank of candidates did not differ between groups. However, the number of points awarded for each game did differ (p=.02): 37.67 for Depressed, 35.50 for Recovered, and 35.17 for Controls. A computational model suggested that the Depressed group had higher internal thresholds for the first and second, but not the third threshold. A caveat from the authors:However, although we found that depressed participants had higher thresholds than did nondepressed participants, we did not find significant differences in the self-reported goals of participants. This suggests that differences in behavior may not result from participants’ conscious effort to perform well. Thus, increases in thresholds could be an artifact stemming from greater persistence and the inability to disengage from a task.What does this mean? That severely depressed inpatients should be given the task of selecting job candidates for Fortune 500 companies, while they are so impaired otherwise that they are unable to work or function socially? Is a very modest performance benefit in a laboratory sequential decision making task worth the pain and suffering of severe depression, along with its concomitant deficits in other cognitive domains?... Read more »
Baune, B., Miller, R., McAfoose, J., Johnson, M., Quirk, F., & Mitchell, D. (2010) The role of cognitive impairment in general functioning in major depression. Psychiatry Research. DOI: 10.1016/j.psychres.2008.12.001
von Helversen, B., Wilke, A., Johnson, T., Schmid, G., & Klapp, B. (2011) Performance benefits of depression: Sequential decision making in a healthy sample and a clinically depressed sample. Journal of Abnormal Psychology. DOI: 10.1037/a0023238
Obsessive compulsive disorder (OCD) is a mental illness characterized by unwanted and intrusive thoughts, feelings, or ideas (obsessions), and ritualized behaviors (compulsions) the individual feels driven to perform in order to alleviate the disturbing nature of the obsessions. It is a major anxiety disorder classified in Axis I of the DSM-IV, which can be disabling to those who suffer with it.The specific symptoms of OCD can include fear of contamination (from germs and physical contact with others) and resultant pathological cleaning rituals, fear of causing catastrophic harm to others, disturbing "impure thoughts" often of a sexual nature, and compulsive ordering, organization, and checking.Currently, major treatments for OCD include cognitive behavior therapy (CBT), considered to be......the most effective type of psychotherapy for this disorder. The patient is exposed many times to a situation that triggers the obsessive thoughts, and learns gradually to tolerate the anxiety and resist the urge to perform the compulsion. Medication and CBT together are considered to be better than either treatment alone at reducing symptoms.The most frequently prescribed drugs are the SSRI (selective serotonin reuptake inhibitor) antidepressants such as:Citalopram (Celexa)Fluoxetine (Prozac)Fluvoxamine (Luvox)Paroxetine (Paxil)Sertraline (Zoloft)Neuroanatomical circuit models of the underlying brain dysfunction have implicated fronto-striatal loops that control thoughts and actions. For example, OCD has been associated with overactivity in the orbitofrontal cortex (Menzies et al., 2008), overactive error monitoring processes in the anterior cingulate cortex (Fitzgerald et al., 2005), and reduced activation in dorsal prefrontal-striatal regions during planning (van den Heuvel et al., 2005) and task switching (Gu et al., 2008). In summary, OCD has been conceptualized as an impulse control disorder marked by a breakdown of high-level executive control over behavior.However, a new study by Koçak et al. (2011) has expanded the range of cognitive processes and brain regions that might be implicated in OCD. The authors proposed that since OCD patients are quite impaired at suppressing complex thoughts and intrusive images, they might also show deficits in suppressing very simple, neutral images and shapes.Participants in their fMRI experiment were 12 patients with OCD [eight were cleaners, three were checkers (one of the checkers also had contamination obsessions), and one had harming obsessions] and 12 age-matched controls. The tasks performed in the scanner involved forming a visual mental image of a geometric shape and then manipulating this visual image. Three of the tasks involved cognitive control over visual imagery (imagination, suppression, and erasing) and two were baseline tasks (free imagination, resting). Before the scanning session, participants studied the shape until they were able to draw it from memory.Fig. 1. (Koçak et al., 2011). The shape shown to the participants. The arrow (which did not appear on the paper used in the study) indicates the starting point of the erasing task. The participants were instructed to begin erasing the shape at the point indicated by the arrow and to continue until the shape completely disappeared.The instructions given to the participants for these tasks were as follows: 1. Imagination task: imagine the shape on the paper continuously until another command is given; 2. Suppression task: imagine the paper with the shape on it immediately after the command is given, and then immediately suppress the image of the shape (try to see the paper as blank) until another command is given; 3. Erasing task: imagine the paper with the shape on it, and then erase the shape by tracing its outline it until another command is given; 4. Free-imagination task; imagine whatever comes to mind and change it with any other intrusive image – a type of free-association task of mental images (this task was used as the baseline condition task); 5. Resting condition: rest while in the scanner.Since the tasks involved imagery alone and no overt responding, the only measures of performance were the participants' subjective evaluation of how well they were able to continually perform each task during the 25 sec blocks. The OCD group claimed they performed the suppression task better than controls, but we have no external way to validate this finding.Turning to the neuroimaging results, the major contrasts were the three active imagery tasks, each compared to the free-imagination baseline task. The group comparison across the three active tasks (which did not differ from each other) is shown below.Fig 3 (Koçak et al., 2011). The whole-brain result depicting significant activations related to the main effect of group (control > than OCD). Threshold at P < 0.05 (corrected for the whole brain). L: left; R: right; A: anterior; P: posterior; SFG: superior frontal gyrus; IPL: inferior parietal lobe; PCC: posterior cingulate cortex.Individuals with OCD showed less activation than controls in three regions in the right hemisphere: the superior frontal gyrus,1 the inferior parietal lobe, and the posterior cingulate cortex [part of the default mode network]. The right IPL is very important for visuospatial processing (Verden et al., 2010); OCD patients can exhibit visuospatial impairments. Furthermore, activations in both IPL and PCC have been observed in prior studies of visual imagery (Ganis et al., 2004). If the participants with OCD were less adept at imagining, manipulating and suppressing a geometric shape, perhaps this reflects a deficit in imagery that is much more basic than controlling the contents of thought.Although these results are very preliminary, the idea that obsessive thoughts could be associated with problems in the right parieta... Read more »
Koçak, O., Özpolat, A., Atbaşoğlu, C., & Çiçek, M. (2011) Cognitive control of a simple mental image in patients with obsessive–compulsive disorder. Brain and Cognition. DOI: 10.1016/j.bandc.2011.03.020
A study on electrophysiological recordings from single neurons in the dorsolateral prefrontal cortex of two monkeys trained to perform a visual target discrimination task (Lennert & Martinez-Trujillo, 2011) has supposedly given new hope to patients with a diverse array of neurological and psychiatric conditions, according to a press release:Filters That Reduce ‘brain Clutter’ IdentifiedScienceDaily (Apr. 19, 2011) — Until now, it has been assumed that people with conditions like ADHD, Tourette syndrome, obsessive compulsive disorder and schizophrenia -- all of whom characteristically report symptoms of "brain clutter" -- may suffer from anomalies in the brain's prefrontal cortex.Damage to this brain region is often associated with failure to focus on relevant things, loss of inhibitions, impulsivity and various kinds of inappropriate behaviour. So far, exactly what makes the prefrontal cortex so essential to these aspects of behaviour has remained elusive, hampering attempts to develop tools for diagnosing and treating these patients.But new research by Julio Martinez-Trujillo, a professor in McGill University's Department of Physiology and Canada Research Chair in Visual Neuroscience, has brought new hope to these patients. He believes the key to the "brain clutter" and impulsivity shown by individuals with dysfunctional prefrontal cortices lies in a malfunction of a specific type of brain cell. Martinez-Trujilo and his team have identified neurons in the dorsolateral sub-region of the primate prefrontal cortex that selectively filter out important from unimportant visual information. The key to the normal functioning of these "filter neurons" is their ability to, in the presence of visual clutter, selectively and strongly inhibit the unimportant information, giving the rest of the brain access to what is relevant.I am so flabbergasted by the number of misleading statements that I don't know where to begin. Let's take them in the order of occurrence."Until now" - This phrase implies that the study has refuted the assumption that ADHD, Tourette's, OCD, and schizophrenia are all associated with abnormalities in the prefrontal cortex (PFC). In fact, individuals with these disorders (and their PFCs) were not evaluated."brain clutter" - What does this mean? I'm not familiar with it as a technical term, nor how the phenomenon is manifest in all four of the above disorders. This issue is relatively minor."anomalies in the brain's prefrontal cortex" - The human PFC covers a large and diverse area of the brain.Fig. 1 (Fuster, 2002). Three views of the cerebral hemispheres with the areas of the prefrontal cortex numbered in accord with Brodmann’s cytoarcitectonic map.Neuroimaging findings in ADHD, Tourette's, OCD and schizophenia are not uniform, and the implicated subregions of PFC are not the same. For example, OCD has been associated with overactivity in the orbitofrontal cortex (Menzies et al., 2008) while schizophrenia is associated with altered activation of dorsolateral PFC (Volk & Lewis, 2010).1 This is highly relevant because as we'll see, the monkey neurons under investigation were in a specific region analogous to Brodmann area 46 in human dorsolateral PFC."Damage to this brain region" and the subsequent laundry list of altered behaviors - not all associated with damage to BA 46."brought new hope to these patients" - This is by far the most egregious falsehood of the entire press release. I find it to be utterly irresponsible.None of these claims were made in the paper itself, which examined firing rates of neurons in the principal sulcus of two rhesus macaque monkeys trained to perform a color-rank target discrimination task with moving random dot patterns.Figure adapted from the press release. The pinkish highlighted area of the brain is the principal sulcus region where neuron activity was recorded.The authors summarize the results below. You'll notice there's no mention of developing "tools for diagnosing and treating these patients" or bringing "new hope to these patients."Highlights► Interstimulus ordinal distance modulates attentional-filtering strength in monkeys ► Interstimulus ordinal distance modulates target selection by prefrontal neurons ► Varying suppression of distracters by dlPFC neurons determines attentional filtering ► Target enhancement by dlPFC neurons remains invariable with changes in performanceHere's the link for the original press release from McGill University. If you are so inclined:Contact: Katherine Gombay, Media Relations Office, McGill University - Tel.: 514 398-2189 Footnote1 I'm skipping the complexities of multiple fronto-striato-thalamic circuits.ReferencesFuster JM. (2002). Frontal lobe and cognitive development. J Neurocytol. 31:373-85.Lennert, T., & Martinez-Trujillo, J. (2011). Strength of Response Suppression to Distracter Stimuli Determines Attentional-Filtering Performance in Primate Prefrontal Neurons Neuron, 70 (1), 141-152 DOI: 10.1016/j.neuron.2011.02.041Menzies L, Chamberlain SR, Laird AR, Thelen SM, Sahakian BJ, Bullmore ET. (2008). Integrating evidence from neuroimaging and neuropsy... Read more »
Lennert, T., & Martinez-Trujillo, J. (2011) Strength of Response Suppression to Distracter Stimuli Determines Attentional-Filtering Performance in Primate Prefrontal Neurons. Neuron, 70(1), 141-152. DOI: 10.1016/j.neuron.2011.02.041
What is restless legs syndrome?Restless legs syndrome (RLS) is a neurological disorder characterized by throbbing, pulling, creeping, or other unpleasant sensations in the legs and an uncontrollable, and sometimes overwhelming, urge to move them. Symptoms occur primarily at night when a person is relaxing or at rest and can increase in severity during the night. Moving the legs relieves the discomfort. Often called paresthesias (abnormal sensations) or dysesthesias (unpleasant abnormal sensations), the sensations range in severity from uncomfortable to irritating to painful.RLS is a relatively common movement disorder that affects ~2.7% of the population (Earley & Silber, 2010). RLS might be related to dysfunction in basal ganglia circuits that use dopamine, which is needed to produce smooth, purposeful muscle activity and movement. Disruption of these BG circuits can produce involuntary movements. Thus, dopaminergic drugs such as pramipexole and ropinirole are often used for treatment, but these medications can produce unwanted side effects.A case study in the journal Sleep Medicine (Marin et al., 2011) reported on a patient who found his own method for the relief of his persistent RLS:Sexual intercourse and masturbation: Potential relief factors for restless legs syndrome?Restless legs syndrome (RLS) is a distressing neurologic condition characterized by urgency to move the legs usually associated with unpleasant sensations in the lower limbs. The symptoms are worst at night and at rest, and patients must move their legs or walk to get relief from their symptoms. Herein, we report a 41-year-old man with a history of severe RLS for 10 years causing him difficulty falling asleep and staying asleep. He fulfilled the four essential criteria established by the International RLS Study Group and he scored 32 in the International RLS Rating Scale. The patient reported that he would get complete relief from RLS symptoms, granting him a normal sleep following sexual intercourse or masturbation. Pramipexole was introduced 2 h before bedtime with significant improvement of RLS symptoms, but whenever he was without medication, he returned to sexual behavior to get relief from RLS symptoms.There are anecdotal reports that sexual activity and orgasm may relieve RLS symptoms, although in some cases sexual activity may worsen RLS. One may speculate that the release of orgasm-related dopamine and opioid may play a role in the relief of RLS symptoms. Additionally, there is a previous report of a RLS patient showing repetitive, rhythmic pelvic body movements resembling coital behavior at the wake–sleep transition.ReferencesEarley CJ, Silber MH. (2010). Restless legs syndrome: understanding its consequences and the need for better treatment. Sleep Med. 11:807-15.Marin, L., Felicio, A., & Prado, G. (2011). Sexual intercourse and masturbation: Potential relief factors for restless legs syndrome? Sleep Medicine, 12 (4) DOI: 10.1016/j.sleep.2011.01.001via New Scientist, Masturbation calms restless leg syndrome
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Marin, L., Felicio, A., & Prado, G. (2011) Sexual intercourse and masturbation: Potential relief factors for restless legs syndrome?. Sleep Medicine, 12(4), 422. DOI: 10.1016/j.sleep.2011.01.001
This sums up the basic conclusion of a new study on political orientation and brain structure by Ryota Kanai, Tom Feilden, Colin Firth and Geraint Rees in the journal Current Biology. Yes, that Colin Firth...Colin Firth's Speech during the 2011 Academy Awards. Firth won Best Actor for The King's Speech.Why are Colin Firth and Tom Feilden, both listed with BBC Radio 4 affiliations, authors on this paper? Let's go back to Tuesday, 28 December 2010 and two pieces that appeared on the BBC website.Politics: Brain or background?Science correspondent Tom Feilden: "What started out as a bit of fun has turned into quite a significant piece of science."Scientific research commissioned by this programme on behalf of our guest editor, Colin Firth, has shown a strong correlation between the structure of a person's brain and their political views. You can also listen to a brief audio clip of Feilden discussing the study at the link above. Firth actually commissioned Professor Geraint Rees at University College London to obtain structural MRI scans from two diametrically opposed politicians: conservative MP Alan Duncan (a member of the Conservative Party) and liberal MP Stephen Pound (a member of the Labour Party).Feilden then asks a question that is unanswerable from studying brain structure in adults: "Are political beliefs learnt, the product of experiences in our environment, or 'hard wired' in the brain?" Since a comparison of n=1 liberal versus n=1 conservative is not scientifically valid, Rees went back to a database of MRI scans from UCL students and asked these participants about their political beliefs. Feilden then discussed the results before the paper had been formally submitted for publication [according to the journal website, the paper was received by Current Biology on 11 January, 2011]. Briefly, he said that the gray matter of the anterior cingulate cortex was thicker among the liberal or left wing participants while the amygdala was much larger in those who identified as conservative or right wing."But is it cause and effect?" asks an interviewer. Rightfully so. Correlation does not equal causation. Then there's the claim that the structural brain variation means the political differences are "hard wired". The observed anatomical differences mean no such thing. Any experience will change the brain in some way, and repeated patterns of behavior, whether it's learning to juggle or voting conservative due to a certain set of core beliefs, can alter the brain. Nonetheless, we have the following headlineAre political beliefs hard-wired?Tom Feilden| 08:10 UK time, Tuesday, 28 December 2010"Give me the child until he's seven and I'll give you the man."It's clear from their motto that the Jesuits are firmly in the acquired camp when it comes to whether our political beliefs and values are learned or hard wired from birth: the product of experience rather than genetics.But is that true? ...along with the eventual admission:Although the results do show that political belief is reflected in the physical structure of the brain it's not clear which comes first. Whether the structure of the brain shapes political belief or political belief leads to the differential development of brain structure.All right, that was a media stunt, you say -- but how about the peer reviewed paper (Kanai et al., 2011)?A total of 90 healthy middle-class to upper-class participants (mean age = 23.5 yrs) underwent MRI scanning and [later?] filled out a very brief questionnaire on their political views:Participants were asked to indicate their political orientation on a five-point scale of very liberal (1), liberal (2), middle-of-the-road (3), conservative (4), and very conservative (5). ... Because none of the participants reported the scale corresponding to very conservative, the analyses were conducted using the scales of 1, 2, 3, and 4.If I'm not mistaken, no special effort was made to recruit very conservative participants, because the study was conceived after the MRIs were obtained.As reported by Feilden, being liberal was associated with a larger anterior cingulate whereas being conservative was associated with a larger right amygdala1 (see Figure 1 below).Figure 1 (Kanai et al., 2011). Individual Differences in Political Attitudes and Brain Structure. (A) Regions of the anterior cingulate where gray matter volume showed a correlation with political attitudes are shown overlaid on a T1-weighted MRI... A statistical threshold of p < 0.05, corrected for multiple comparisons, is used for display purposes. The correlation (left) between political attitudes and gray matter volume (right) averaged across the region of interest (error bars represent 1 standard error of the mean, and the displayed correlation and p values refer to the statistical parametric map presented on the right) is shown. (B) The right amygdala also showed a significant negative correlation between political attitudes and gray matter volume. Display conventions and warnings about overinterpreting the correlational plot (left) are identical to those for (A).The results were based on measurements of gray matter density in these two specific structures. How were they chosen? First, the anterior cingulate was selected based on the finding of Amodio et al. (2007) that......the amplitude of event-related potentials reflecting neural activity associated with conflict monitoring in the anterior cingulate cortex (ACC) is greater for liberals compared to conservatives. Thus, stronger liberalism is associated with increased sensitivity to cues for altering a habitual response pattern and with brain activity in anterior cingulate cortex.I had issues with this interpretation of the Amodio et al. study in 2007, which I will summarize here. One problem was attributing the observed results to political viewpoint and not to other factors. The study used EEG recordings, specifically event-related potentials. The ERP brain waves reflect electrophysiological activity recorded remotely from the scalp. While it's great for determining the temporal parameters of neural activity, it's not so great at determining where the activity is located in the brain.One brain wave of inter... Read more »
Ryota Kanai, Tom Feilden, Colin Firth, Geraint Rees. (2011) Political Orientations Are Correlated with Brain Structure in Young Adults. Current Biology. info:/10.1016/j.cub.2011.03.017
From Rolling Stone MagazineAn excerpt from Simon-Baron Cohen's new book, Zero Degrees of Empathy: a New Theory of Human Cruelty, appeared as The science of empathy in the Guardian. Overall, the writing revealed him to be unempathetic in some respects, particularly with regard to people with borderline personality disorder1 (BPD):Unempathic acts are simply the tail end of a bell curve, found in every population on the planet. If we want to replace the term "evil" with the term "empathy", we have to understand empathy closely. The key idea is that we all lie somewhere on an empathy spectrum. People said to be "evil" or cruel are simply at one extreme of the empathy spectrum. We can all be lined up along this spectrum of individual differences, based on how much empathy we have. At one end of this spectrum we find "zero degrees of empathy".. . .Zero degrees of empathy does not strike at random in the population. There are at least three well-defined routes to getting to this end-point: borderline, psychopathic, and borderline personality disorders. I group these as zero-negative because they have nothing positive to recommend them. They are unequivocally bad for the sufferer and for those around them. Of course these are not all the sub-types that exist. Indeed, alcohol, fatigue and depression are just a few examples of states that can temporarily reduce one's empathy, and schizophrenia is another example of a medical condition that can reduce one's empathy.This comes after an introduction that recounts a childhood memory: when his father told him that the Nazis turned Jewish people into lampshades and soap. So people with BPD are "evil", "zero-negative" and have "zero degrees of empathy" (similar to the Nazis). This is quite a stunning characterization, in fact one that is not borne out by the literature. For example, one study showed that individuals with BPD are actually better than controls on a test of empathy designed by Baron-Cohen himself (Fertuck et al., 2009).2 That would be the Reading the Mind in the Eyes Test (RMET), "a measure of the capacity to discriminate the mental state of others from expressions in the eye region of the face." The study showed that:The BPD group performed significantly better than the HC group on the RMET, particularly for the Total Score and Neutral emotional valences. Effect sizes were in the large range for the Total Score and for Neutral RMET performance. The results could not be accounted for by demographics, co-occurring Axis I or II conditions, medication status, abuse history, or emotional state. However, depression severity partially mediated the relationship between RMET and BPD status.The authors concluded that this enhancement of facial emotion recognition abilities (or "enhanced sensitivity to the mental states of others") is what can get BPD persons in trouble socially. Consistent with this finding, another study found a double dissociation between two different types of empathy in BPD (Harari et al., 2010). Emotional empathy was slightly enhanced, whereas cognitive empathy was significantly impaired relative to controls.Fig. 1 (Preißler et al., 2010). (A) a significant group-by-type (interaction) effect [F(1,40) = 6.375, P = 0.016]. The HC group had significantly higher scores (*) in the cognitive empathy scale, whereas there was an opposite trend is observed in the BPD group. Cognitive empathy, or the ability to take another person's perspective, is closely related to (or even synonymous with) theory of mind. On the other hand, emotional or affective empathy is "emotional contagion" - the ability to mirror an emotional response observed in another person and to experience it vicariously. The literature on emotional empathy in BPD isn't entirely consistent, however. Although Preißler and colleagues (2010) reported preserved (but not enhanced) performance on the RMET, they observed an impairment on the “Movie for the Assessment of Social Cognition” (MASC) in the BPD participants.In his book, Baron-Cohen also provides a case study from another population with "zero degrees of empathy" -- the psychopath:Paul's career of criminal behaviour had begun when he was as young as 13, when he had set fire to the school gym and sat in a tree across a field to watch it burn. He was expelled and from there went to three more schools, each time being expelled for aggression – starting fights in the playground, attacking a teacher who asked him to be quiet and even jumping on someone's head when they wouldn't let him join the football team.Paul [currently in jail for murder] is clearly not the kind of guy you want to live near. Many would not hesitate to describe him as "evil". He is a psychopath – a Type P – though to give him the proper diagnostic label, he has antisocial personality disorder. He earns this label because he shows "a pervasive pattern of disregard for and violation of the rights of others that begins in childhood or adolescence, and continues into adulthood".This sounds similar to the description of Cpl. Jeremy Morlock in The Kill Team, a recent article in Rolling Stone on the American soldiers in Afghanistan who killed innocent civilians and mutilated their corpses. [NOTE: I am not linking directly to this article because it contains very graphic and disturbing photographs. You'll find them within the online magazine if you want to see them.] According to Rolling Stone:Before the military found itself short of troops in Afghanistan and Iraq, Morlock was the kind of bad-news kid who the Army might have passed on. He grew up not far from Sarah Palin in Wasilla, Alaska; his sister hung out with Bristol, and Morlock played hockey against Track. Back in those days, it seemed like he was constantly in trouble: getting drunk and into fights, driving without a license, leaving the scene of a serious car accident.But it gets worse and escalates, just like with Paul: he committed the serious crime of spousal abuse only one month before being deployed. Unfortunately, he was only charged with "disorderly conduct" and then sent off to Afghanistan anyway:Even after he joined the Army, Morlock continued to get into trouble. In 2009, a month before he deployed to Afghanistan, he was charged with disorderly conduct after burning his wife with a cigarette. After h... Read more »
Fertuck, E., Jekal, A., Song, I., Wyman, B., Morris, M., Wilson, S., Brodsky, B., & Stanley, B. (2009) Enhanced ‘Reading the Mind in the Eyes’ in borderline personality disorder compared to healthy controls. Psychological Medicine, 39(12), 1979. DOI: 10.1017/S003329170900600X
Harari, H., Shamay-Tsoory, S., Ravid, M., & Levkovitz, Y. (2010) Double dissociation between cognitive and affective empathy in borderline personality disorder. Psychiatry Research, 175(3), 277-279. DOI: 10.1016/j.psychres.2009.03.002
An article from January is making the rounds again. One in nextgov's exposé-like series on America's Broken Warriors, it highlighted the fact that 20% of U.S. active duty troops are on psychotropic medications. While this may not be a good thing, the article was filled with erroneous information about specific psych meds and general scare-mongering from antipsychiatry "experts" pitching their books. Let's take a look.Military's drug policy threatens troops' health, doctors sayBy Bob Brewin 01/18/2011Army leaders are increasingly concerned about the growing use and abuse of prescription drugs by soldiers, but a Nextgov investigation shows a U.S. Central Command policy that allows troops a 90- or 180-day supply of highly addictive psychotropic drugs before they deploy to combat contributes to the problem. The CENTCOM Central Nervous System Drug formulary includes drugs like Valium and Xanax, used to treat depression, as well as the antipsychotic Seroquel, originally developed to treat schizophrenia, bipolar disorders, mania and depression.1. Valium (diazepam) and Xanax (alprazolam) are not used to treat depression. These sedative-hypnotic benzodiazepine medications are primarily used to treat anxiety disorders.2. The atypical antipsychotic Seroquel (quetiapine) was originally developed to treat schizophrenia, although now it is prescribed for bipolar disorder and major depression. Off-label usage of quetiapine, including as a sleep aid, is controversial and I won't be discussing it further here. That topic could easily take up several posts of its own.The article continues:A June 2010 internal report from the Defense Department's Pharmacoeconomic Center at Fort Sam Houston in San Antonio showed that 213,972, or 20 percent of the 1.1 million active-duty troops surveyed, were taking some form of psychotropic drug: antidepressants, antipsychotics, sedative hypnotics, or other controlled substances. Dr. Grace Jackson, a former Navy psychiatrist, told Nextgov she resigned her commission in 2002 "out of conscience, because I did not want to be a pill pusher." She believes psychotropic drugs have so many inherent dangers that "the CENTCOM CNS formulary is destroying the force," she said.Here we see Dr. Jackson's antipsychiatry agenda first established. All psych drugs are bad. Also note that Dr. Jackson resigned in 2002, before the war in Iraq began on March 20, 2003. So she doesn't have first hand experience with current prescribing practices or the effects of these medications on troops in Iraq and Afghanistan, which is what the article is about.We also have quotes from one of the leading antipsychiatry advocates, Dr. Peter Breggin:Dr. Peter Breggin, an Ithaca, N.Y., psychiatrist who testified before a House Veterans Affairs Committee last September on the relationship between medication and veterans' suicides, said flatly, "You should not send troops into combat on psychotropic drugs." Medications on the CENTCOM CNS formulary can cause loss of judgment and self-control and could result in increased violence and suicidal impulses, Breggin said.Dr. Breggin's credibility as an expert witness has been repeatedly questioned, however. I agree that mentally ill troops should not be sent into combat, but will also point out that untreated and unmedicated psychiatric disorders in a war zone can cause increases in violence and suicidal behavior.Back to Dr. Jackson:Jackson, the former Navy psychiatrist, now has a civilian practice in Greensboro, N.C. She said at least one drug on the CENTCOM formulary -- Depakote, an anticonvulsant, which military doctors prescribe for mood control -- carries serious physical risks for troops.Really? Depakote (valproic acid) is an antiseizure medication also used to treat bipolar disorder. I would like to see statistics on how frequently it's prescribed for "mood control" in soldiers without bipolar disorder.1 Depakote is toxic to certain cells, including hair cells in the ears, and can lead to hearing loss. Troops in a howitzer battery who already run the risk of hearing loss should not take Depakote, she said.3. Depakote is certainly not without its adverse effects, but hearing loss is an extremely rare side effect.2 In a study of 21 patients taking valproic acid (VPA) to control seizures, there were no differences in hearing thresholds between 125 and 16,000 Hz compared to age- and sex-matched controls (Incecik et al., 2007). In addition, there was no relationship between duration or dosage of drug and hearing levels.The medication also can cause what she calls "cognitive toxicity," also known as Depakote dementia, impairing a person's ability to think and make decisions. Jackson said that while Depakote has been investigated as an adjunct therapy for cancer, its use has been limited due to the drug's effects on cognition.4. Contrary to the notion of "Depakote dementia", VPA has been recognized for its potential to treat Alzheimer's disease (Nalivaeva et al., 2009; Zhang et al., 2010). VPA is a histone deacetylase (HDAC) inhibitor that might be able to prevent amyloid-beta aggregation in Alzheimer's disease by increasing the expression of clusterin, or apolipoprotein J (Nuutinen et al., 2010). This would in turn prevent the accumulation of amyloid plaques, a pathological feature in the brains of those with Alzheimer's.While it's possible that VPA could produce impairments in some cognitive domains, proper studies are difficult because you have to control for the length of illness in untreated patients (since cognitive deficits can be caused by the disorder itself). One such report on currently medicated (n=33) and currently unmedicated (n=32) patients with bipolar depression failed to find group difference in visual memory and sustained attention (Holmes et al., 2008). Unfortunately, this study collapsed across patients on lithium and valproic acid. Further, the groups weren't matched on age, sex, and depression scores. Finally, the medicated patients were more depressed, which might be expected to worsen performance on its own.A double-blind cross-over design in healthy controls administered a relatively high dose of VPA for two weeks (800 mg the first week, 1,000 mg the second). There were no changes in memory, concentration, perceptual speed, motor speed, and subjective ratings relative to placebo (Trimble & Thompson, 1981). The drug did, however, slow response times in a category decision task. A review of the literature on cognition and anticonvulsants concluded: "Overall, deficits are subtle, especially in the therapeutic range" for valproic acid (Goldberg & Burdick, 2001). Not exactly a ringing endorsement for cognitive toxicity and Depakote dementia.On to the next drug:The antidepressant Wellbutrin, also on the CENTCOM formulary, likely poses a long-term risk of Parkinson's disease, especially for older troops, said Jackson, author of Drug-Induced Dementia: A Perfect Crime (AuthorHouse, 2009).5. I found no published, peer-reviewed evidence that the antidepressant Wellbutrin (bupropion) increases the long-term risk of developing Parkinson's disease. [Guess we'll have to buy her book ... Read more »
Holmes MK, Erickson K, Luckenbaugh DA, Drevets WC, Bain EE, Cannon DM, Snow J, Sahakian BJ, Manji HK, & Zarate CA Jr. (2008) A comparison of cognitive functioning in medicated and unmedicated subjects with bipolar depression. Bipolar disorders, 10(7), 806-15. PMID: 19032712
Incecik F, Akoglu E, Sangün O, Melek I, & Duman T. (2007) Effects of valproic acid on hearing in epileptic patients. International journal of pediatric otorhinolaryngology, 71(4), 611-4. PMID: 17270285
Thompson PJ, & Trimble MR. (1981) Sodium valproate and cognitive functioning in normal volunteers. British journal of clinical pharmacology, 12(6), 819-24. PMID: 6803819
Fun With Behavior Therapy from the 70s, Part 2In our next installment of food-based behavior therapies to treat phobias in adults, we have a case report of combined exposure/M&M treatment (Kroll, 1975). First is a description of the client's fear of dogs:The client was a 22-yr-old female graduate student with a strong fear and avoidance of dogs. She had been told by her parents that a large brown dog had knocked her over when she was a child, but she did not remember the incident nor did she attribute her fear to it. She could not remember any time in her life when she was not afraid of dogs. The intensity of her fear was unaffected by size or breed of dog. If she was alone and saw a dog approaching her, she became highly anxious and walked away very rapidly or, if possible, crossed the street to avoid an encounter. When leaving her house and seeing a dog, she either exited through the back door or waited until the dog left before walking outside. If she was walking with another person and unavoidably encountered a dog, she became intensely anxious and held onto the other person tightly while attempting to put the person between her and the dog.Next is description of the treatment, which included voluntary food deprivation. Notice, however, that the client did not agree to 24 hrs without food:The client was instructed not to eat anything for 12-hr prior to the treatment session. It was originally planned that she would undergo 24-hr food deprivation, but she did not think she could go without eating longer than 12-hr. Because among her favorite foods M & M's were most preferred, I decided on using them to inhibit anxiety. She was told that they would have greater reward value than any other food and would therefore increase the probability of successfully inhibiting anxiety elicited by a feared object. And here we have evidence of the therapist's condescending attitude:Since I had told her of other cases in which food was used as an anxiety inhibitor, she was receptive to the use of M & M's. (It should be noted that she was unaware of the client populations with whom M & M's are typically used.)So the client bought a large bag of M&M's and went to an animal shelter, accompanied by the therapist. From the very beginning, the therapeutic value of the M&M's is not really clear, given the calming presence of the therapist:Upon entering the room in which the dogs were caged, the client's initial response was fear. She made no attempt, however, to leave the room. Starting at a distance of about seven feet--the farthest away in the room that one could stand from the animals--I walked with the client around the room as far as possible from the cages while feeding her M & M's. ... At the end of the session which lasted approximately 2-hr, she reported feeling relaxed in the presence of the dogs. She expressed confidence that she could encounter dogs without fear or need to avoid them.It's scientifically proven! M&M'S® can cure phobias in a single 2 hr session! However, that laughable conclusion was even questioned by the author at the conclusion of the article:The possibility exists that, instead of the feeding, or perhaps in addition to it, graduated exposure or therapist-client interaction or modeling were responsible, singly or in complex interaction for the client's improvement. As control observations were not made, one cannot rule out the possibility that the feeding was superfluous.To end on a serious note, one application of this approach to behavior therapy is not a laughing matter at all, as noted in a comment on my last post by Michelle Dawson, author of The Autism Crisis blog:Not phobias, but extreme food deprivation has been used as an early autism treatment, with very young children.You can find a 1970s use of extreme food deprivation at UCLA reported in this book. Lovaas' reported recommendation was 36hrs of food and liquid deprivation for a 4yr old. The purpose was to make the child "hungry and desperate enough to do anything for food." Instead the child got very sick, threw up bile, and was too tired and listless to work for his food.Another book reports in passing the use of routine food deprivation as autism treatment by Lovaas at UCLA, within the most famous autism study ever.To my knowledge there has never been any criticism of this kind of practice published in any journal.I highly recommend her three part series on Autism Advocacy and Aversives: part one, part two, part three.ReferenceKroll, H. (1975). Rapid treatment of dog phobia by a feeding procedure Journal of Behavior Therapy and Experimental Psychiatry, 6 (4), 325-326 DOI: 10.1016/0005-7916(75)90071-3
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Kroll, H. (1975) Rapid treatment of dog phobia by a feeding procedure. Journal of Behavior Therapy and Experimental Psychiatry, 6(4), 325-326. DOI: 10.1016/0005-7916(75)90071-3
Fun With Behavior Therapy from the 70s, Part 1In 1973, Bryntwick and Solyom published a paper on a new method of behavior therapy for elevator phobia, which involved depriving their clients of food and water for 24 hours. The rationale for their unorthodox approach was as follows:Fear habits in the animal laboratory have been diminished by first depriving the subject of food and then rewarding him with it in the fear provoking situation (Masserman, 1943; Wolpe, 1958). To apply this technique to clinical subjects has generally been considered "unthinkable". The present report illustrates the clinical effectiveness in the treatment of two elevator phobic subjects.Apparently, both of the patients voluntarily agreed to forgo eating and drinking for one day. Here is the background information on the two elevator phobic subjects, one of whom had good reason to be phobic (in my view):Mr. B.M., a 32-yr-old businessman, had suffered from an elevator phobia for about 5 yr. He attributed his fear to two occasions within a 2-week period when he was trapped in an elevator for a few minutes. Since then he would climb 16 floors rather than take an elevator. Several times daily he climbed three flights of stairs to his office. On a 0-4 point scale, he rated his fear of elevators as 4, corresponding to "terrifying panic attacks if avoidance impossible". No other obvious psychopathology was apparent...Mr. W.H., a 19-yr-old student, had suffered from travel and claustrophobia for approximately 3 yr. He was markedly obsessive, being very orderly, meticulous and hesitant, with a tendency to ruminate. One manifestation of his claustrophobia was avoidance of elevators. He also rated his elevator phobia at 4...As for treatment, both patients had failed "aversion relief therapy" for elevator phobia, so the authors found it appropriate to use feeding as a counter-conditioner in vivo.Each patient, after agreeing to the new procedure, was instructed not to eat or drink for 24 hr prior to the treatment session. After that deprivation the patient was led to an elevator where he found a table attractively arranged with his most preferred foods. For the next 35 rain he sat eating his dinner while the elevator moved up and down. At the end of the session, the patient was encouraged to take self-service elevators in as many different buildings as possible.Both patients reported minimal anxiety and for the first time did not avoid taking elevators.Possible scenario for the elevator exposure dining experience.Unfortunately, Mr. W.H. had a relapse after being the victim of a cruel prank:One week after the first session, however, Mr. W.H. was riding in an elevator when the building superintendent, also in the elevator, stopped it with the comment, "I wonder if it will start again". Although the elevator was stopped for only 5 sec, Mr. W.H.'s anxiety rose to its original intensity.No matter, all was not lost. Two weeks later a booster session eliminated his elevator phobia once again. Both patients were reportedly "phobia free" two years later.Not everyone in the behavior therapy community was pleased with this approach, however. Rosen and Orenstein (1974) were quite critical of the treatment, and nearly called the food deprivation aspect a farce:...There appears to be no evidence to support the position that such deprivation significantly adds to the effectiveness of a treatment program based on in vivo exposure alone. The first author’s own experience with an “elevator phobic” suggests that avoidance of elevators can be eliminated in a single in vivo session without recourse to theoretical “counter-conditioners”. The client spent 45 min riding in the elevator of an eight story building sometimes accompanied by the therapist and sometimes on her own. During the session there were large reductions in her self-reported anxiety. Four days later the client rode in the same elevator on her own. She has since ridden in other elevators demonstrating what could be called a “generalization of treatment effects”. This particular patient missed out on the elevator fine dining experience, though...ReferencesBryntwick, S. & Solyom, L. (1973). A brief treatment of elevator phobia. Journal of Behavior Therapy and Experimental Psychiatry, 4 (4), 355-356 DOI: 10.1016/0005-7916(73)90008-6Rosen, G. & Orenstein, H. (1974). A critical comment on the use of food deprivation in the “Brief treatment of elevator phobia”. Journal of Behavior Therapy and Experimental Psychiatry, 5 (3-4) DOI: 10.1016/0005-7916(74)90087-1Elevator - What Could Possibly Go Wrong?
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Rosen, G. (1974) A critical comment on the use of food deprivation in the “Brief treatment of elevator phobia”. Journal of Behavior Therapy and Experimental Psychiatry, 5(3-4), 313. DOI: 10.1016/0005-7916(74)90087-1
Semantic dementia is a neurodegenerative disorder in the general class of frontotemporal lobar degeneration. Atrophy occurs bilaterally in the anterior temporal lobes, with the left hemisphere affected to a greater extent (Lambon Ralph & Patterson, 2008). Patients gradually lose semantic memory abilities (e.g., memory for word meanings and conceptual knowledge). Alterations in personality, interests, and tastes can be observed in some patients. A unique case study documented an increasing interest in polka music with the progression of semantic dementia (Boeve & Geda, 2001):A man exhibited typical features of semantic dementia (Neary et al., 1998), with onset at age 52. At age 55, he became infatuated with polka music. He would sit in his car in the garage and listen to polka on the radio or on cassettes, often for as long as 12 to 18 hours. Whereas some may argue that enjoying polka music is in itself pathologic, we view this patient’s new appreciation of polka similar to that recently described with pop music in two patients with frontotemporal dementia (Geroldi et al., 2000). Thus, heterogeneity in musical taste is yet one more dimension bridging semantic dementia and frontotemporal dementia.The progression of atrophy in the temporal lobes is shown below. The relative preservation of the frontal lobes is noteworthy.Figure (Boeve & Geda, 2001). Representative T1-weighted coronal MRI at ages 53 (top row) and 55 (bottom row) are shown. Note progressive atrophy of the left amygdala and temporal cortex, and although a definitive causal relationship cannot be made, the right amygdala and temporal cortex atrophy has evolved in concert with the patient’s polka music obsession.Roll Out the Barrel. . .Chorus:Roll out the barrel, we'll have a barrel of funRoll out the barrel, we've got the blues on the runZing boom tararrel, ring out a song of good cheerNow's the time to roll the barrel, for the gang's all here- lyrics courtesy of NIEHS, National Institutes of Health, Department of Health & Human Servicesvia @UCSDCogNeuroReferencesBoeve BF, Geda YE (2001). Polka music and semantic dementia. Neurology, 57 (8) PMID: 11673594Geroldi C, Metitieri T, Binetti G, Zanetti O, Trabucchi M, Frisoni G. (2000). Pop music and frontotemporal dementia. Neurology 55: 1935–1936.Lambon Ralph MA, Patterson K. (2008). Generalization and Differentiation in Semantic Memory: Insights from Semantic Dementia. Ann NY Acad Sci. 1124:61-76.Neary D, Snowden J, Gustafson L, et al. (1998). Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria. Neurology 51: 1546–1554."Beer Barrel Polka": Myron Floren on accordionBobby Burgess and Lawrence Welk dance with Cissy King
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ROMANTIC LOVE WAS INVENTED TO MANIPULATE WOMEN-Jenny Holzer, TruismsDoes romantic love manipulate women into providing free domestic labor and sexual favors for men? Some feminist views of romantic love [and the institution of marriage] portray it as controlling and oppressive (Burns, 2000):‘STOP HUMAN SACRIFICE. END MARRIAGE NOW.’ ‘IT STARTS WHEN YOU SINK IN HIS ARMS AND ENDS WITH YOUR ARMS IN HIS SINK.’ From a feminist perspective, romantic love was, and is, seen to obscure or disguise gender inequality and women’s oppression in intimate heterosexual relationships.But some in the men's movement see romantic love as dangerous for men as well as women, because it prevents men from being vulnerable (Bloodwood, 2003):...historically, romantic love has been a highly gendered but workable deal in which men provide women with social status and material goods while women provide men with sex/affective labour. Thus romantic relationships not only reinforce women’s second class status but also reinforce men’s lack of sex/affective autonomy, so that romantic love is equally dangerous for women and for men.Furthermore, romantic love is often portrayed as a relatively recent construct that is specific to Western societies. A cross-cultural study by Jankowiak and Fischer (1992) claimed that:The anthropological study of romantic (or passionate) love is virtually nonexistent due to the widespread belief that romantic love is unique to Euro-American culture. This belief is by no means confined to anthropology. The historian Philippe Aries (1962), for example, argues that affection was of secondary importance to more utilitarian ambitions throughout much of European history.However, their own analysis of the ethnographic literature found that romantic love (however ill-defined) could be observed in 147 out of 166 societies, including 77% in Sub-Saharan Africa and 94% in East Eurasia (Jankowiak & Fischer, 1992). Likewise, evolutionary anthropologist Helen Fisher and colleagues suggest that romantic love evolved as one of three motivational brain systems for mating, reproduction, and parenting (Fisher et al., 2002).The biological concept that romantic love (or attraction) is an emotional/motivational system in the human brain has prompted some neuroimaging investigators to search for its elusive neural correlates. How do you measure long-term intense romantic love in an fMRI experiment? Researchers have adopted the practical (yet flawed) strategy of examining the hemodynamic response to viewing pictures of a partner with whom participants were "madly in love".Previous studies on the "neural correlates of romantic love" have focused on recently attached heterosexuals from the UK (Bartels & Zeki, 2000) or US (Aron et al., 2005). One of the main findings from these studies is that the expected dopamine/reward areas [including ventral tegmental area (VTA), substantia nigra (SN), and caudate nucleus] showed greater activation when looking at the pictures of the partner, compared to pictures of a close friend or neutral acquaintance. And in the previous post on Posterior Hippocampus and Sexual Frequency, we saw a similar response in a specifically recruited group of participants still "madly in love" after 21 years of marriage (Acevedo et al., 2011).So are the "neural correlates of romantic love" the same in non-Western, non-heterosexual participants? Two recent papers attempted to spread the love to include diverse "others" (Xu et al., 2010; Zeki & Romaya, 2010). Is the simple act of asking if the Chinese and teh gays are "just like us" when it comes to love offensive? I'll let you be the judge.Although the original study of Bartels and Zeki (2000) recruited an ethnically and culturally diverse group of subjects, all were heterosexual. Zeki and Romaya (2010) wanted to extend this work to include romantically involved gay participants. This time, they included 12 females (6 in straight and 6 in lesbian relationships) and 12 males (6 in straight and 6 in gay relationships) in their fMRI experiment. I won't belabor the methods [and the critiques thereof] here, but will refer the reader to Posterior Hippocampus and Sexual Frequency.1Fig. 2 (Zeki & Romaya, 2010). Illustration of the t statistic for the contrast Loved > Neutral showing selected activations superimposed over averaged anatomical sections. Random effects analysis with 24 subjects. Background threshold p uncorrected < 0.001. (A) Medial sagittal plane (x = 0) showing activations in the tegmentum [VTA], hypothalamus and [cerebellar] vermis. (B) Sagittal plane x = −12 (LH) showing activation in the caudate head, anterior cingulate and parietal cortex. (C) Horizontal plane z = −30; right cerebellum. (D) Horizontal plane z = −9; mid insula, left hemisphere. As for differences between the groups, there were none: no main or interactive effects of gender or sexual orientation. The results were the same for gay and straight, male and female participants [but remember that the numbers were very low, n=6 for each of the four cells]. So this particular [underpowered] study suggests that "the romantic love brain circuit" (i.e., familiarity, attention, memory, reward, etc. activity associated with looking at your partner's face) is not restricted to heterosexuals. Did they really expect anything different? Actually not, Zeki and Romaya predicted a null effect.However, the authors themselves note the difficulties inherent in their entire endeavor:We begin by emphasizing that any study of so complex and overpowering a sentiment as love is fraught with difficulties. Chief among these is that the sentiment itself involves many components – erotic, emotional, and cognitive – that are almost impossible to isolate from the overall sentiment of love. ... While acknowledging this difficulty, we tried as best we could to circumvent it, by applying a uniform criterion – that of a loved face – for studying the brain's love system. Another problem is the difficulty of controlling the mental processes that occur when subjects view their lovers' faces. The only way to address this is through the statistical methods we have used to analyze our results. We have employed a random effects analysis using the summary st... Read more »
Xu, X., Aron, A., Brown, L., Cao, G., Feng, T., & Weng, X. (2011) Reward and motivation systems: A brain mapping study of early-stage intense romantic love in Chinese participants. Human Brain Mapping, 32(2), 249-257. DOI: 10.1002/hbm.21017
Zeki, S., & Romaya, J. (2010) The Brain Reaction to Viewing Faces of Opposite- and Same-Sex Romantic Partners. PLoS ONE, 5(12). DOI: 10.1371/journal.pone.0015802
Fig. 2D (Acevedo et al., 2011). Image and scatter plot illustrating greater response to the Partner (vs. a highly familiar acquaintance) in the region of the posterior hippocampus is associated with higher sexual frequency.Now there's an unexpected correlation suitable for Valentine's Day. How romantic! Actually, it is romantic because the neuroimaging study by Acevedo et al. (2011) is entitled "Neural correlates of long-term intense romantic love." How do you quantify long-term intense romantic love in an fMRI experiment?Well, what the study really examined is the brain's hemodynamic response to viewing pictures of a spouse with whom participants were still "madly in love" after an average of 21 years. Over the course of the experiment, subjects repeatedly viewed four different digital photos: Partner, Close Friend (CF), Highly Familiar "Neutral" acquaintance (HFN), and a Low-Familiar Neutral acquaintance (LFN). Specifically,The protocol implemented a block design of two 12-min sessions each consisting of six sets of four 30-s tasks in an alternating fashion, followed by stimulus ratings. Each session included two alternating images (starting image counterbalanced), interspersed with a count-back task. Duplicating procedures of Aron et al. (2005), Session 1 displayed Partner and HFN images. For the additional control comparisons, Session 2 displayed CF and LFN images. Participants were instructed to think about experiences with each stimulus person, nonsexual in nature.Yeah, it might be a problem if the participants remembered bouts of sex when they viewed their partners... Fig. 2D shows that activation in a tiny area of the left posterior hippocampus correlated with sexual frequency. The two outliers who had sex every day (or nearly every day)1 could be driving the correlation -- they certainly had a greater number of memories to choose from, and to suppress. In humans, activity in the posterior hippocampus is sensitive to the familiarity of stimuli that have behavioral relevance (Strange et al., 1999), and is associated with memory for repeated stimuli (Poppenk et al., 2010).How do Acevedo et al. (2011) interpret this correlation?Although little is known about the posterior hippocampal region [NOTE: untrue], some studies have shown increased activation in this area in association with hunger and food craving (LaBar et al., 2001; Pelchat et al., 2004), with particularly greater activity shown in obese individuals (Bragulat et al., 2010).Craving, eh? Not memory? Although the authors would like to think they controlled for familiarity with the Close Friend contrast, it seems to me nearly impossible that a co-worker, sibling, cousin, or friend could fulfill all familiarity criteria except romantic relationship. Furthermore, most of the analyses focused on comparisons between Partner vs. Highly Familiar Neutral 2 to match their previous paper (Aron et al., 2005) on the early stages of romantic love (1-17 months in duration).I could go on about the analysis methods, and whether reporting the single voxel with highest activity is appropriate [see Voodoo Correlations]. Or I could go on about the subject selection criteria: the 17 heterosexual participants (10 women, 7 men, ages 39-67 yrs, married 10-29 yrs) had an annual household income ranging from $100,000-$200,000 (perhaps not representative of the general population).But what about the main findings? Am I just being a cynic when it comes to love? It's true, some of the expected dopamine/reward areas [ventral tegmental area (VTA) and substantia nigra (SN)] showed greater activation when looking at the long-term Partner, which was very much like what was seen in the young lovers.Fig. 2A (Acevedo et al., 2011). Individuals self-reporting intense love for a long-term spouse show significant neural activation in dopamine-rich, reward regions of the VTA/SN in response to images of their partner vs a highly familiar acquaintance.Ultimately, the paper sends a positive message that in certain relationships, the exciting, obsessive, and rewarding period of intense romantic love can last for over 20 yrs, well beyond the typical and oft-cited (oprah.com)3 18 month to 3 year duration: IMPLICATIONSIndividuals in long-term romantic love showed patterns of neural activity similar to those in early-stage romantic love. These results support theories proposing that there might be mechanisms by which romantic love is sustained in some long-term relationships. For example, the self-expansion model suggests that continued expansion and novel, rewarding events with the beloved may promote increases in romantic love. Novel, rewarding experiences may use dopamine-rich systems (Schultz, 2001; Guitart-Masip et al., 2010) similar to those activated in this study.Beyond reporting relationship length (and sexual frequency), the participants filled out questionnaires including the Passionate Love Scale, the Love Attitudes Scale, the inclusion of other in the self (IOS) Scale, and the friendship-based love scale. All indicators suggested that the subjects were still "madly in love" with their partners. Did we really need neuroimaging to tell us that? Maybe...Footnotes1 The mean sexual frequency was 2.2 times a week.2 The HFN has been known about as long as the Partner, but is substantially less close than both the Partner and the Close Friend.3 If anyone can find a better reference for this than oprah.com or Tennov, D., 1979. Love and limerence. The Experience of Being in Love. Stein and Day, New York -- let me know.ReferencesAcevedo BP, Aron A, Fisher HE, & Brown LL (2011). Neural correlates of long-term intense romantic love. Social cognitive and affective neuroscience PMID: 21208991Aron A, Fisher H, Mashek DJ, St... Read more »
Acevedo BP, Aron A, Fisher HE, & Brown LL. (2011) Neural correlates of long-term intense romantic love. Social cognitive and affective neuroscience. PMID: 21208991
In the November 2010 issue of Perspectives in Psychological Sciences, a Special Section on "Neuroimaging: Voodoo, New Phrenology, or Scientific Breakthrough?" (Diener, 2010) looks back at the infamous paper by Vul et al. (2009) and forward into the future. In one of the articles, an extended analogy is made between modern neuroimaging and the phrenology of yore (Poldrack, 2010):Imagine that fMRI had been invented in the 1860s rather than the 1990s. Instead of being based on modern cognitive psychology, neuroimaging would instead be based on the faculty psychology of Thomas Reid and Dugald Steward, which provided the mental “faculties” that Gall and the phrenologists attempted to map onto the brain. Researchers would have presumably jumped from phrenology to fMRI and performed experiments manipulating the engagement of particular mental faculties or examining individual differences in the strength of the faculties. They almost certainly would have found brain regions that were reliably engaged when a particular faculty was engaged and potentially would also have found regions in which activity correlated with the strength of each faculty across subjects.Gall's ambition and vanity are now 'activation for judgment about self versus others', localized to medial prefrontal cortex. Friendly attachment/fidelity have been transformed into 'viewing a friend versus viewing a stranger', associated with right temporoparietal cortex.-- click on image for larger view--Table 1 (Poldrack, 2010). A Mapping of Gall's 27 Faculties to Potentially Related Neuroimaging Research.Although few today would hold that 19th century faculty psychology is an accurate description of the structure of the mind, we can likely all agree that if the phrenologists had created task manipulations to isolate their proposed faculties using fMRI, something would have “lit up.” What would the patterns of activation associated with these faculties have looked like? If we believe, as I think most would agree, that each of the phrenologists' putative faculties relies in actuality upon a combination of basic mental operations, then we would likely expect that the maps obtained for a given faculty would include a large set of activated regions that would tend to overlap across tasks meant to tap into different faculties. Regardless, one can be almost certain that Gall and his contemporaries would have taken these neuroimaging results as evidence for the biological reality of his proposed faculties. But we know better now, don't we? Because Neural Networks Debunk Phrenology!The studies show that network interactions among anatomically discrete brain regions underlie cognitive processing and dispel any phrenological notion that a given innate mental faculty is based solely in just one part of the brain.Does anyone really believe in phrenology any more? Who advocates such a view? Cognitive neuropsychologists? Single-unit neurophysiologists? OR has localization of function in discrete networks (rather than an individual structure or a bump on the head) become the new phrenology? I think the story goes like this: complex adaptive behavior is an emergent property of network interactions. This is certainly not a new idea (see any number of publications by Joaquin Fuster)...According to Poldrack (2010), neuroimaging research strategies have evolved from “where” (blobology or neophrenology) to “what” (characterize function of a specific brain region) to “fractionation” (determine whether different mental processes engage different brain regions). Ultimately, localization of function is still the final goal... as it was for the original phrenologists:Phrenology teaches us that in this life every act of the mind is performed through the instrumentality of the brain, and that peculiar states of this organ invariably accompany particular mental dispositions.-M.B. Sampson Esq. (1842)ReferencesDiener E (2010). Neuroimaging: Voodoo, New Phrenology, or Scientific Breakthrough? Introduction to Special Section on fMRI. Perspectives on Psychological Science 5:714-715.Poldrack, R. (2010). Mapping Mental Function to Brain Structure: How Can Cognitive Neuroimaging Succeed? Perspectives on Psychological Science, 5 (6), 753-761 DOI: 10.1177/1745691610388777Sampson MB (1842). PHRENOLOGY IN ITS APPLICATION TO THE TREATMENT OF CRIMINALS. The Lancet 37:639-643.Vul E, Harris C, Winkielman P, Pashler H (2009). Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social Cognition. Perspectives on Psychological Science 4:274-290.
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Poldrack, R. (2010) Mapping Mental Function to Brain Structure: How Can Cognitive Neuroimaging Succeed?. Perspectives on Psychological Science, 5(6), 753-761. DOI: 10.1177/1745691610388777
Diagram showing principal systems of association fibers in the human brain. The superior longitudinal fasciculus (SLF) is labeled at the center top (marked by purple arrows).New Scientist covered two journal articles by Rametti and colleagues (2010, 2011), a group of Spanish researchers and clinicians affiliated with Unidad Trastorno Identidad de Género [Gender Identity Disorder Unit]. Using the diffusion tensor imaging (DTI) method, they initially wanted to identify any sex differences in the white mater of the brains of non-transgendered male and female heterosexuals. Then the next step was a prediction that FTM (Female-to-Male) transsexuals would be more like males, while MTF (Male-to-Female) transsexuals would be more like females.Transsexual differences caught on brain scan12:16 26 January 2011 by Jessica HamzelouDifferences in the brain's white matter that clash with a person's genetic sex may hold the key to identifying transsexual people before puberty. Doctors could use this information to make a case for delaying puberty to improve the success of a sex change later.In 5 years of writing this blog, I have come across a multitude of news stories and press releases that make outrageous claims. Here's another one to add to the list. On the basis of two highly variable DTI studies in 36 pre-operative, pre-hormone treatment transgender individuals, now we're supposed to screen children for gender variant behavior and scan them at a young age, so their hormones can be altered before puberty?Returning to the structural imaging experiments, were there any hypotheses at the outset, or were these completely exploratory studies? The authors cite the work of Zhou et al. (1995) on postmortem staining of the bed nucleus of the stria terminalis (BST). This subcortical nucleus connects the amygdala to the septal nuclei, hypothalamus, and thalamus. BST has been shown to play a role in the sexual behavior of male rats. The size of this nucleus in MTF brains was similar to that in female controls, both being smaller than male controls.However, it's not possible to visualize the BST in living humans, so the authors went with DTI to look for cortical white matter changes. The participants in the first study were 18 FTM transgendered persons (before undergoing hormonal treatment), along with 24 male and 19 female heterosexual controls. The major findings in terms of sex differences between groups were located mainly in 3 fiber tracts:anterior and posterior parts of the right superior longitudinal fasciculus - contains connections between the frontal, parietal, occipital, and temporal lobes including language-related areas (Mori et al., 2008).forceps minor (anterior forceps) - fiber bundle connecting the lateral and medial surfaces of the frontal lobes, crossing the midline via the genu of the corpus callosum.corticospinal tract - connects the cerebral cortex and the spinal cord, contains mostly motor axons.In all 3 tracts, males showed higher fractional anisotropy (FA) than females. FA is a measure of local tissue properties including density, coherence, diameter, and myelination.Fig. 1 (Rametti et al., 2010). Sex differences in fractional anisotropy (FA). FA is lower in female than in male controls in the superior longitudinal fasciculus with a posterior (A) and anterior (B) predominance. Control females also show lower than control male FA values in the forceps minor (C) and the corticospinal tract (D). The group skeleton used for the between group contrast study is green. The red color shows the clusters of significantly decreased FA in female compared to male controls. The threshold for significance was set at p < 0.05 corrected for multiple comparisons.FTM individuals showed greater FA values in all 3 tracts than did the control females. They were similar to control males for anterior and posterior SLF and forceps minor, and in between control male and female FA values for the corticospinal tract.What does this mean? Basically, at this point, it's like reading tea leaves. We have no indication of other potential differences between the groups in cognitive, emotional, personality, or motor measures, in alcohol use, or in other psychiatric diagnoses. We do know that testosterone levels of the FTM participants were like those of control females, because they had yet to undergo hormone treatment.Moving right along to the second experiment, which compared MTF individuals to controls (Rametti et al., 2011)... The participants were 18 untreated MTF transsexuals (mean age = 25 yrs), 19 female (mean = 33 yrs) and 19 male controls (mean age = 32 yrs). Yes, the MTF individuals were significantly younger than controls [the human frontal lobe in particular is known to continue maturation processes into the 20's]. Procedures were similar to those used previously. Results in this study showed a greater number of differences in the white matter of male vs. female controls (again, with larger FA values for males): left and the right SLFforceps minorright inferior front-occipital fasciculus (IFOF)corticospinal tract left cingulumSo what's new in this list? Left SLF, Right IFOF, Left cingulum. This finding indicates that individual differences were observed between two groups of male and female control subjects [or else there were unreported methodological differences]. If normal sex differences in DTI studies include IFOF and cingulum here but not there, that presents a problem for comparison to the transgendered populations.Nonetheless, what did that comparison show? The MTF individuals showed FA values between those of male and female controls for all tracts (except for IFOF, where they did not differ from males).Fig. 2 (Rametti et al., 2011). Histograms showing the FA... Read more »
Rametti, G., Carrillo, B., Gómez-Gil, E., Junque, C., Segovia, S., Gomez, �., & Guillamon, A. (2011) White matter microstructure in female to male transsexuals before cross-sex hormonal treatment. A diffusion tensor imaging study. Journal of Psychiatric Research, 45(2), 199-204. DOI: 10.1016/j.jpsychires.2010.05.006
Rametti, G., Carrillo, B., Gómez-Gil, E., Junque, C., Zubiarre-Elorza, L., Segovia, S., Gomez, �., & Guillamon, A. (2010) The microstructure of white matter in male to female transsexuals before cross-sex hormonal treatment. A DTI study. Journal of Psychiatric Research. DOI: 10.1016/j.jpsychires.2010.11.007
Bottom image adapted from Fig. 2 of Schumann et al. (2010). Neuroanatomy of the human amygdala postmortem. Nissl-stained section of amygdala nuclei.The amygdala is a subcortical structure located within the medial temporal lobes. It consists of a number of different nuclei, or collections of neurons delineated by commonalities in morphology and connectivity. The amygdala is best known for major roles in fear conditioning (Paré et al., 2004) and responding to emotional stimuli more generally (Phelps & LeDoux, 2005), but its functions extend beyond that.A new study by Bickart and colleagues (2010) examined the relationship between the overall size of the amygdala in a group of 58 volunteers and the number of people in each person's social network. The authors observed a direct correlation between the two: the larger the amygdala, the larger the social network. Why did they expect such a finding? The "social brain hypothesis" (Dunbar, 1998) is cited as providing general evidence in favor of increased brain size in more social animals. However, the major references that motivated the specific hypothesis about the amygdala are book chapters, which seemed rather weak and unscholarly to me.Predictably, a number of silly headlines appeared in the popular press...How to Win Friends: Have a Big Amygdala?Got a big social network? Then you probably have a large amygdala, according to a new study that found a connection between the size of this brain region and the number of social relationships a person has. The complexity of those relationships — as measured by the number of people who occupied multiple roles in a social network such as being simultaneously a friend and a co-worker — was also linked with amygdala size....and in blogs:The Twitter Spot in Your BrainHeavy Facebook users may have weighty amygdalasBut the worst headline of all (because it is patently false) is...Study: More Friends on Facebook Equals A Bigger Amygdala In Your BrainThe number of Facebook friends you have is correlated to the size of your amygdala, the center used to process the memory of your emotional reactions in your brain, according to a new study published in Nature Neuroscience. The volume of your amydala has been connected to the size of the circle of those you come in contact with even with nonhuman primate species before, so Kevin Bickart and his coauthors took the idea and tested it out on people who interact with people on Facebook.Does the Amygdala Have a Social Network?First of all, the size of the amygdala has absolutely nothing to do with Facebook or any other contemporary social networking site. The scale for quantifying social network size and complexity was taken from a 1997 paper on Social Ties and Susceptibility to the Common Cold (Cohen et al., 1997), which in turn cited a book chapter from 1991. There was no such thing as Facebook or Myspace in 1997, only Geocities (1994) and Tripod.com (1995). As for the history of online communities, The WELL was launched in 1985 as a bulletin board system and could be considered as a proto-social networking site.So who was included in Cohen et al.'s (1997) definition of a social network? One requirement was that the participant spoke to the individual in person or on the phone at least once every two weeks:The Social Network Index assesses participation in 12 types of social relationships. These include relationships with a spouse, parents, parents-in-law, children, other close family members, close neighbors, friends, workmates, schoolmates, fellow volunteers (eg, charity or community work), members of groups without religious affiliations (eg, social, recreational, or professional), and members of religious groups. One point is assigned for each type of relationship (possible score of 12)1 for which respondents indicate that they speak (in person or on the phone) to someone in that relationship at least once every 2 weeks. The total number of persons with whom they speak at least once every 2 weeks (number of network members) was also assessed.Results for the amygdalar correlations with social network size and complexity were nearly identical, so the authors focused on the former in the paper. Importantly, amygdala volume did not correlate with life satisfaction or the perceived quality of the relationships. Basically, you could have a large social network that is not of your own choosing. One participant could have a large family, many co-workers, intrusive neighbors, and few real friends, while another is gregarious and parties with different groups of friends every night of the week. This particular study does not distinguish between the two.Were any other parts of the brain correlated with social network size? No! [which I find hard to believe]. For the entire group of 58 participants, no significant results were observed in other subcortical regions (i.e., hippocampus [which served as a control region], brainstem, nucleus accumbens, ventral diencephalon, thalamus, caudate, putamen, and globus pallidus). An exploratory whole-brain analysis of cortical thickness did not reveal any correlations at conventional levels of significance.Are we supposed to believe that only one area of the brain is involved in maintaining social networks? I think not. Even within the article, subgroups of participants (i.e., males, all older subjects)2 showed correlations between hippocampal volume and social network characteristics. This makes intuitive sense, as a better memory might be helpful in keeping track of large numbers of people.What about cortical regions containing spindle neurons (Nimchinsky et al., 1999), a cell type unique to humans, great apes, humpback whales, elephants and dolphins? Spindle neurons (aka von Economo neurons) are found in the anterior cingulate cortex and frontoinsular cortex. Or how about orbitofrontal cortex, with a volume that correlates with social cognitive competence (Powell et al., 2010)? None of these regions were related to network size.What happens to people born without amygdalae due to Urbach-Wiethe disease, a rare genetic disorder? Does "the woman without ... Read more »
Freelance medical and science writer Rob Stepney noticed the rapid growth of "x" and "z"-named products included in the British National Formulary (BNF). So for the Christmas 2010 issue of BMJ (Stepney, 2010), he investigated this phenomenon:Of 1436 products added to the BNF between 1986 and 2005, more than a fifth had names that began with z or x or contained a prominent x or z within them. In 1986, only 19 branded drugs began with one of these letters. Over the next two decades, the number of brands beginning with a z increased by more than 400% (to 63) and those beginning with an x increased by 130% (to 16). In the same period, the overall content of the BNF grew by only 80%. Why did it happen? He first asks whether use of the voiced fricative “zuh” sound might be special in some way, but he quickly dismisses this possibility, along with the popularity of z in the Middle East.Instead, he speculates that x and z might have been perceived as making products stand out in a crowd:Reflecting their infrequent occurrence in English words, x and z count for 8 and 10 points in Scrabble, the highest values (along with j and q) in the game. So names that contain them are likely to seem special and be memorable. “If you meet them in running text, they stand out,” is the way one industry insider explained. Generally, they are also easy to pronounce.In my view, however, the rush to uniqueness resulted in an overcrowded field. The market became saturated with X and Z brand names, which can cause confusion.Fig 1 (Stepney, 2010). Number of drugs with a brand name beginning with z or x listed in March edition of BNF for each year. New formulations of existing brands and zinc related compounds have been excluded.For instance, the August 9, 2007 newsletter from the Institute for Safe Medication Practices discusses Progress with preventing name confusion errors and links to a document on the most problematic look-alike and sound-alike drug names of 2006-2007 (PDF). These include:ZYPREXA (olanzapine) and ZYRTEC (cetirizine)Name similarity has resulted in frequent mixups between Zyrtec, an antihistamine, and Zyprexa, an antipsychotic. Patients who receive Zyprexa in error have reported dizziness, sometimes leading to a related injury from a fall. Patients on Zyprexa for a mental illness have relapsed when given Zyrtec in error.Other frequently confused Z/X pairs:Zantac – XanaxZantac – ZyrtecZestril – ZyprexaZestril – ZetiaZocor – ZyrtecAt any rate, here's Stepney's (2010) conclusion:I suggest that this phenomenon arose because of the fast rate at which new products were being introduced, the fact that the difference between many “me too” drugs was more apparent than real, the immense rewards that were seen to accrue from innovative marketing, and the fact that the ploys available for use in the naming of drugs are so restricted.A full list of the drugs mentioned in the article can be viewed here.ReferenceStepney, R. (2010). A dose by any other name would not sell as sweet. BMJ, 341:c6895 DOI: 10.1136/bmj.c6895
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Crucifixion, by Francis Bacon (1933).Crucifixion (1933) (oil on canvas) was subsequently purchased by Sir Michael Sadler (who, other than friends or relations, was the first to buy a painting), and who also commissioned a second version, Crucifixion (1933) (chalk, gouache and pencil), and sent Bacon an x-ray photograph of his own skull, with a request that he paint a portrait from it. Bacon duly incorporated the x-ray directly into The Crucifixion (1933).A paper by an interdisciplinary team of Serbian radiologists, anatomists, artists, and pathologists examined how neuroradiological images have been used as a form of artistic expression (Marinković et al., 2010). They started by describing skull x-rays incorporated into the paintings of Francis Bacon and Diego Rivera, then gave examples of contemporary artists who transform computerized tomography (CT) and magnetic resonance images (MRI) into art. These works include Wooden Brain (The 3D MRI Cubes) by Neil Fraser and "Art and Science #1" by Marjorie Taylor, which can be seen at the The Museum of Scientifically Accurate Fabric Brain Art.I would add to the list any number of works by Damien Hirst, including this self-portrait:...which he incorporated into this album cover for See the Light by The Hours.Marinković and colleagues (2010) mentioned the commercialization of neuroradiology and colorized pictures of the brain by companies such as shutterstock, where you can subscribe for $249 a month and download stock photos of a "female doctor examining a brain cat scan" and "colorful brain model isolated on dark background" (much like this one).The authors also surveyed 12,673 artworks in books and Google images. They found that neuroradiological images were used in 29 works (1.01%) created by 31 artists (1.58% of 1,964 total).They wished to make their own contributions to this collection, and they did so with three pieces presented in the paper. In one of these, they...performed an x-ray of four post mortem hemispheres following the injuction of a radiopaque substance into their sulci and insertion of the copper wires around the corpus callosum and along the calcarine and parieto-occipital sulci. The radiograph of one of the hemispheres was then superimposed in Phototshop with the photograph of the subsequently made cast of the cerebral arteries.Radiological Image, by Marinković et al. (2010).Finally, they......made an inverse image of a colorized brain in a front view. this image was then superimposed with a photograph of illuminated optic fibers in the background.Cognitive Radiation, by Marinković et al. (2010).Anatomy and art intersect in a number of places, at the Mütter Museum in Philadelphia, the Morbid Anatomy website, the Bioephemera website by Jessica Parker, and Gunther von Hagens' BODY WORLDS (the Bioethics of which is discussed here), among many others. Portraits of the Mind: Visualizing the Brain from Antiquity to the 21st Century by Carl E. Schoonover is a popular new book that's currently out of stock at Amazon.Neuroradiology, and especially the development of beautiful colorized diffusion tensor images, has captured the minds of artists, designers, and the public.From the Human Connectome Project, an effort to map the white matter connectivity of the human brain.ReferenceMarinkovic, S., Stošic-Opincal, T., Štrbac, M., Tomic, I., Tomic, O., & Djordjevic, D. (2010). Neuroradiology and Art: A Review and Personal Contribution The Tohoku Journal of Experimental Medicine, 222 (4), 297-302. DOI: 10.1620/tjem.222.297"I think one of the things is that, if you are going to be a painter, you have got to decide that you are not going to be afraid of making a fool of ... Read more »
Marinkovic, S., Stošic-Opincal, T., Štrbac, M., Tomic, I., Tomic, O., & Djordjevic, D. (2010) Neuroradiology and Art: A Review and Personal Contribution. The Tohoku Journal of Experimental Medicine, 222(4), 297-302. DOI: 10.1620/tjem.222.297
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