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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
Case Report: novel treatment initiated by the patient to treat her symptoms of ocular neuromyotonia, or spontaneous spasms of the extraocular muscles.
As part of the Christmas 2010 issue of BMJ, Weston et al. (2010) reported the case of a 68 yr old woman with intermittent diplopia, or double vision. A cataract on her left eye was removed, which improved her vision.... Read more »
The Seductive Allure of Neuroscience ExplanationsThe previous post, Voodoo Correlations: Two Years Later, was a retrospective on the neuroimaging methods paper that was widely discussed in the blogosphere before it was considered "officially" published (Vul et al., 2009). The article, a controversial critique of the statistical analyses used by fMRI investigators in social neuroscience, made its initial appearance on Ed Vul's website once it was accepted by Perspectives in Psychological Sciences. This caused considerable consternation among the criticized authors and the journal editor (Ed Diener).Now, as part of the November 2010 issue of the journal (Diener's last as editor), six invited articles on Neuroimaging: Voodoo, New Phrenology, or Scientific Breakthrough? appear in a Special Section on fMRI (Diener, 2010). I was pleased to see that one of the articles addressed The Appeal of the Brain in the Popular Press (Beck, 2010), since this has been a major theme of my blog for almost five years. However, I was disappointed that the word "blog" was not mentioned at all in Beck's article.This should have come as no surprise, given the journal's response to bloggers in May 2009. The Editor's Introduction is worth a mention for the issues it raises about peer review and publication in these modern times.PREPUBLICATION DISSEMINATIONAs soon as I accepted the Vul et al. article, I heard from researchers about it. People around the globe saw the article on the Internet, and replies soon appeared as well. Although my plan was to publish the article with commentary, the appearance of the article on the Internet meant that researchers read the article without the accompanying commentaries and replies that I had planned to publish with it.In some fields such as economics, it is standard practice to widely disseminate articles before they are published, whereas in much of psychology this has been discouraged. An argument in favor of dissemination is that it speeds scientific communication in a fast-paced world where journal publication is often woefully slow. An argument against dissemination of articles before publication is that readers do not have the opportunity to simultaneously see commentary and replies. ... In the Internet age, the issue of prepublication distribution becomes all the more important because an article can reach thousands of readers in a few hours. Given the ability of the Internet to communicate so broadly and quickly, we need greater discussion of this issue.In reply, I wrote:Bloggers have discussed this specific issue months ago. For example, as noted in Mind Hacks,The paper was accepted by a peer-reviewed journal before it was released to the public. The idea that something actually has to appear in print before anyone is allowed to discuss it seems to be a little outdated (in fact, was this ever the case?).And The Neurocritic opined that...[The aggrieved authors] are not keeping up with the way that scientific discourse is evolving. Citing "in press" articles in the normal academic channels is a frequent event; why should bloggers, some of whom are read more widely than the authors' original papers, refrain from such a practice? Is it the "read more widely" part?-from The paper formerly known as "Voodoo Correlations in Social Neuroscience", by The NeurocriticDiener originally solicited six commentaries on the Vul et al. paper for the May 2009 issue of the journal. Ironically, authors on two of the papers have serious blogs:Statistical Modeling, Causal Inference, and Social Science is a blog written by Andrew Gelman, a Professor of Statistics and Political Science at Columbia. He was one of the first to blog about the paper in Suspiciously high correlations in brain imaging studies, with a more detailed post a month later (More on the so-called voodoo correlations in neuroscience). Lindquist and Gelman (2009) applauded the discussion engendered by "pre-publication dissemination":Their article has in a short time given rise to a spirited debate about key statistical issues at the heart of most functional neuroimaging studies. The debate provides a useful opportunity to discuss core statistical issues in neuroimaging and ultimately provides a chance for the field to grow and move forward.  is the blog kept by Tal Yarkoni, a Post-Doc at the University of Colorado Boulder. He happens to be an expert in statistics for fMRI analysis, and another one of the authors invited to submit a paper for the Vul, Harris, Winkielman, and Pashler festschrift/verdammung (Yarkoni, 2009):In this article, I argue that Vul et al.'s primary conclusion is correct, but for different reasons than they suggest. I demonstrate that the primary cause of grossly inflated correlations in whole-brain fMRI analyses is not nonindependence, but the pernicious combination of small sample sizes and stringent alpha-correction levels. Far from defusing Vul et al.'s conclusions, the simulations presented suggest that the level of inflation may be even worse than Vul et al.'s empirical analysis would suggest. His blog started in October 2009, after the commentaries were published.The Appeal of the Brain in the Popular PressThat brings us back to the article by Diane Beck, an Assistant Professor in Psychology and Cognitive Neuroscience at the University of Illinois Urbana-Champaign. She examines the distorted media coverage of neuroimaging studies, and possible reasons for it (Beck, 2010):Since the advent of human neuroimaging, and of ... fMRI in particular, the popular press has shown an increasing interest in brain-related findings. In this article, I explore possible reasons behind this interest, including recent data suggesting that people find brain images and neuroscience language more convincing than results that make no reference to the brain (McCabe & Castel, 2008; Weisberg, Keil, Goodstein, Rawson, & Gray, 2008). I suggest that part of the allure of these data are the deceptively simply messages they afford, as well as general, but sometimes misguided, confidence in biological data. In addition to cataloging some misunderstandings by the press and public, I highlight the responsibilities of the research scientist in carefully conveying their work to the general public. While reading through the examples of poor media coverage, imagine the shock of recognition if you were to realize that you have written several trenchant blog posts criticizing these very articles. Yet all this work (and the writings of many others) is rendered invisible to the mainstream of the Association for Psychological Science.Why is blogging so non-existent in these circles? There's a large thriving community of science blogs. Go to ResearchBlogging.org and look under ... Read more »
Neurokitchen Design is the latest fad among the rich and famous, according to a poorly researched article in the Wall Street Journal:A Kitchen to Comfort Your SoulCombining psychology and neuroscience, Johnny Grey is an interior designer with a special recipeBy TARA LOADER WILKINSON'You can tell a lot about a person from their kitchen," says Johnny Grey, an award-winning interior designer specializing in "happy kitchens," a design philosophy that focuses on bringing emotional, physical and psychological well-being into kitchen planning.. . .Mr. Grey ... takes an unusual approach to interior design. He and his team spend up to 80 hours with clients, understanding what makes them tick, often going round for dinner and even staying over at their home. His aim? To create a domestic utopia tailored to their personality, using the principles of neuroscience, or the scientific study of the nervous system, to answer their emotional needs and subliminal desires, as well as building a seamlessly practical kitchen. It appears to work.However, Mr. Grey does not have an EEG lab to record the brain waves of his clients, as depicted in the image above. Nor does he have access to an MRI scanner, to my knowledge. For Mr. Grey to actually use the principles of neuroscience to design customized kitchens for his clients, he would need a method that records brain activity, whether it's electrical (EEG) or hemodynamic (fMRI).Is Neurokitchen Design the latest manifestation of explanatory neurophilia (Trout, 2008)?Credibility is a cherished currency in science, but its cues can be counterfeit. A novel series of experiments by Weisberg and her colleagues  show that non-expert consumers of behavioral explanations assign greater standing to explanations that contain neuroscientific details, even if these details provide no additional explanatory value. Here, we discuss the part that this ‘placebic’ information might play in producing a potentially misleading sense of intellectual fluency and, consequently, an unreliable sense of understanding.Even though it's likely that Grey's [pseudo]neuroscientific analysis provides no additional explanatory value, clients will pay more for a "scientifically designed" kitchen.A kitchen is a place where you prepare and clean upBut it's so more than that now..."A kitchen is no longer just for cooking. Often, the only time a couple will spend together awake, is in the kitchen," says the British architect [Grey], whose clients include Apple co-founder Steve Jobs, British singer Sting and millionaire publisher Felix Dennis.Isn't that nice! But as far as I can tell, the WSJ gets a number of details wrong in this paragraph, which nonetheless has the best quote of all:John Ziesel [Zeisel], a San Diego-based neuroscientist [sociologist] at the Salk Institute [I could find no listing for him there], meanwhile, is researching what he refers to as measurement-based design, which shows how spaces can shape our behavior. He uses everything from hormone studies, brain scans and targeted psychological experiments to foster his research. "A kitchen is a space loaded with emotional and behavioral cues," he says. "Neuroscience can help us understand what goes on behind the shiny surfaces and layout of kitchen cabinetry."Although they might seem to make strange bedfellows, the idea that neuroscience research can inform building design is not new. The Academy of Neuroscience for Architecture (ANFA) was founded in 2003.The Salk Institute in La Jolla, California, that architectural monument to science overlooking the Pacific Ocean, is indeed a focal point for ANFA. Jonas Salk himself enlisted architect Louis Kahn to design a research campus with lab space that would promote collaboration and creativity. The AFNA Board of Directors includes an impressive list of neuroscientists: Tom Albright, Michael Arbib, and Fred Gage to name but a few. Salk scientists Gage, Albright, and Terrence Sejnowski were on the original Advisory Board in 2003.In April 2004 the Dana Foundation presented a manifesto of sorts from ANFA founding president John P. Eberhard and freelance writer Brenda Patoine:Architecture with the Brain in MindA soaring cathedral, a brightly lit classroom, a dim maze of hospital corridors: Most of us associate certain emotions, energy levels, and even mental states with the various spaces in which we spend our lives. What underlies these responses? How important are they? Architects and neuroscientists now beginning to grapple with those questions are coming up with discoveries that have important implications for how we design spaces as diverse as neonatal care units, schools, and residences for people with Alzheimer’s disease. The beneﬁts of collaboration between brain science and architecture are sure to increase, writes architect John Eberhard, founding president of the new Academy of Neuroscience for Architecture. Some research even suggests that certain designed environments encourage the proliferation of new brain cells.Five years later, the Institution of Engineering and Technology was more circumspect in its analysis of the trend:Architecture and neuroscienceEmpirical evidence demonstrating how buildings affect the function and structure of our brains is still thin on the ground. Fred Gage, a neuroscientist at the Salk Institute in La Jolla, California, says that, while architects have plenty of intuitions, the key will be to construct experiments to test the influence of the spatial environment on the brain. Despite the founding of the Academy of Neuroscience for Architecture (ANFA) in San Diego in 2003 - of which Gage is a director and past-president - “we have not yet accomplished as much as we aspired to,” he says. However, neuroscience has taught us much about how our brains construct our sense of place and how certain environments might stimulate the growth of new neurons.Fortunately, the Architects for Functional Neurogenesis special interest group seems to have escaped unscathed.NEXT UP: How hippocampal place cells have influenced Frank Gehry.Reference... Read more »
Trout, J. (2008) Seduction without cause: uncovering explanatory neurophilia. Trends in Cognitive Sciences, 12(8), 281-282. DOI: 10.1016/j.tics.2008.05.004
Fig 1A (modified from Blauwblomme et al., 2010). Top: coronal and lateral representation of the stereotaxic implantation scheme. Bottom: reflex seizure showing ictal onset in the right insula and secondary spreading in the hippocampus.Reflex epilepsy is a rare neurological condition in which seizures are triggered by a specific type of sensory input (Xue & Ritaccio, 2006). The most common reflex seizures are induced by light, but other reported triggers have included reading, Mah-Jong, music, the voice of a specific television performer,1 bathing, orgasm, and eating.The present case involved a 28 year old woman who had refractory partial seizures triggered by eating, which were preceded by an unpleasant taste in her mouth. Strawberry syrup ingestion was noted to be the easiest way to induce seizures. Nine years earlier, she had surgery to remove a vascular malformation from the right frontal operculum/insular cortex. This region contains gustatory cortex encoding for taste. Because of the uncontrolled nature of her seizures, the surgical team implanted intracranial electrodes to determine the focus of abnormal EEG activity.Two reflex seizures to strawberry syrup intake were recorded, which started with loss of consciousness, followed by facial flushing, oro-alimentary automatisms, repeated swallowing and sialorrhoea [excessive salivation], and ended with postictal confusion and amnesia. From a visual analysis of SEEG (Fig. 1A), seizures began in the anterior inferior portion of the insula with a high-amplitude spike followed by a low-voltage high-frequency discharge with secondary spreading to the hippocampus and then to the temporal neocortex. In the early ictal state, fast gamma band activity (30-120 Hz) showed increased power in the anterior inferior portion of the insula, accompanied by decreased power in the hippocampus.Functional MRI was also performed during strawberry syrup intake to map gustatory cortex, and another session recorded simultaneous resting state fMRI/EEG activity.Fig. 1C (modified from Blauwblomme et al., 2010). Overlay of fMRI and SEEG results. Left: crosshairs on the dorsolateral fronto-parietal region. Right: crosshairs on the anterior insula. The authors reported three major findings from the fMRI/EEG mapping (see Fig 1C): The dorsolateral anterior parietal cortex showed pre-ictal γ [gamma] power decrease (red) and belonged to the fMRI gustatory network (yellow). In the vicinity, the dorsolateral posterior frontal cortex showed preictal γ power increase (magenta) and interictal fMRI/EEG activations (green). Early ictal γ power increase (cyan) showed up in the inferior/middle part of the anterior insula, which also responded to taste fMRI (yellow). A preictal increase in γ power (magenta) was observed in the upper part of the anterior insula. Hippocampus showed early ictal decrease in γ activity (blue).The surgical team identified the specific region of the insula that was the problematic seizure focus (the middle short gyrus), and removed it. Two years later, the patient remains seizure-free, and presumably can enjoy strawberry syrup once again.Footnote1 The identity of said performer was revealed to be Mary Hart, host of Entertainment Tonight. From Science News (Vol. 140, No. 3, p. 45):...the woman had seizures only while watching "Entertainment Tonight."Systematic testing ruled out all but one of the cast members -- cohost Mary Hart, whose voice pattern consistently caused the seizures. [Dr. Venkat] Ramani prescribed anticonvulsant drugs and advised the patient not to watch the program. In the two years since, she has remained "relatively seizure free," he reports.ReferencesBlauwblomme, T., Kahane, P., Minotti, L., Grouiller, F., Krainik, A., Vercueil, L., Chabardes, S., Hoffmann, D., & David, O. (2010). Multimodal imaging reveals the role of γ activity in eating-reflex seizures. Journal of Neurology, Neurosurgery & Psychiatry DOI: 10.1136/jnnp.2010.212696Xue LY, Ritaccio AL. (2006). Reflex seizures and reflex epilepsy. Am J Electroneurodiagnostic Technol. 46:39-48.The Jam Lady
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Blauwblomme, T., Kahane, P., Minotti, L., Grouiller, F., Krainik, A., Vercueil, L., Chabardes, S., Hoffmann, D., & David, O. (2010) Multimodal imaging reveals the role of activity in eating-reflex seizures. Journal of Neurology, Neurosurgery . DOI: 10.1136/jnnp.2010.212696
With your hosts, V.S. Ramachandran and and E.L. Seckel (2010) of VH1's The Surreal Life: Medical Hypotheses....We proposed and provided the first experimental evidence for a dysfunctional MNS [mirror neuron system] in ASD [autism spectrum disorders] (Altschuler et al., 1997). ... Nonetheless evidence at this point is “compelling but not conclusive”.On the assumption that the MNS is not completely missing but “dormant”, could they be revived? We propose having the children look into a room with multiple mirrors at various angles to provide multiple allocentric views of themselves. Three neurotypical volunteers would stand inside the room and dance to a rhythm while the child dances in synchrony with them. This is different from conventional dance therapy in ASD in that our treatment specifically emphasizes synchronous dance movements mimicking others (as well as the simultaneous presence of multiple mirror refections) in order to optimally stimulate any residual MNS. Given the existence of tactile – sensory mirror neurons that fire when you merely watch someone else being touched, one could also deliver varying patterns of touch as the child watches. The use of multiple reflections makes it unavoidable that the child has to see itself [sic] stimulated. One may need to start with simple rhythms and progressively graduate to more complex ones incorporating more elaborate gestures. The subjects could be tested for lasting improvement in behavioral scores which might spill over into more useful domains such as social interactions.MTV is planning to air its own version of this hot new treatment modality, Mirror Neuron Live.ReferencesAltschuler EL, Vankov A, Wang V, Ramachandran VS, Pineda JA. Person See, Person Do: human cortical electrophysiological correlates of monkey see monkey do cells. In: Poster session presented at the 27th annual meeting of the society for neuroscience. LA: New Orleans; 1997.Ramachandran, V., & Seckel, E. (2010). Synchronized dance therapy to stimulate mirror neurons in autism Medical Hypotheses DOI: 10.1016/j.mehy.2010.10.047VS Ramachandran's Modest Proposal: The neurons that shaped civilization.
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Ramachandran, V., & Seckel, E. (2010) Synchronized dance therapy to stimulate mirror neurons in autism. Medical Hypotheses. DOI: 10.1016/j.mehy.2010.10.047
Most everything you've read about the Doctors Prescribing 'Tetris Therapy' study is wrong. That ridiculous headline, courtesy of "fair and balanced" Fox News, is the most egregious lie I could find [if you have other favorites, please leave links in the comments]. Press stories frequently distort research findings, but sometimes the authors themselves shoulder the most blame (Holmes et al., 2010). Misuse of the words "trauma" "flashback" "cognitive vaccine" and "PTSD" are at fault here.The experiment in question is interesting as a memory study. It demonstrated that playing a visuospatial video game (Tetris) 30 min after a disturbing film can lessen intrusive visual memories, but playing a verbal trivia game (Pub Quiz) can have the opposite effect (Holmes et al., 2010). According to Baddeley (1992), this occurs because of two modality-specific working memory systems: the visuospatial sketchpad for visual working memory and the phonological loop for verbal working memory. Tetris interferes with the former, while Pub Quiz interferes with the latter.Sixty participants (18–60 yrs old; mean age=27 yrs; 30 females) took part in Experiment 1. They were carefully screened for trauma history, mood, trait anxiety and depression. Potential subjects were excluded if they had ever been treated for mental illness of any kind. So this is a group of healthy controls -- not depressed, not anxious, minimal exposure to trauma, and no PTSD. They were a happy bunch, with mean scores on the Beck Depression Inventory (BDI) of 5.7-6.2.1The participants were divided into three groups for the different treatment conditions, illustrated below.Figure 1 (from Holmes et al., 2010). Experiment 1 study design overview. Participants completed the trauma film paradigm, a well established experimental analog for PTSD. All participants viewed a traumatic film followed by a 30-min structured break. Participants were then allocated to one of three experimental conditions [Tetris vs. no-task control vs. Pub Quiz] which they completed for 10 min. Afterwards participants in the computer game conditions rated their enjoyment of the game. Flashbacks (involuntary memories) were monitored for 1 week using an intrusion diary. After 1 week, diary compliance was checked and a test of voluntary memory (recognition memory test) for the trauma film was administered.What is the "trauma film paradigm"?The 21-min film [previously used in 22] contained 15 clips of traumatic content including fatal road traffic accidents and graphic scenes of human surgery. Following that link leads you to this description (and a series of other studies):Participants were shown a 13 min film of real-life footage of the aftermath of road traffic accidents (compiled by Steil, 1996). This film has been used extensively in studies using the trauma film paradigm (e.g. Brewin and Saunders, 2001, Hagenaars et al., 2008, Halligan et al., 2002, Holmes et al., 2004, Holmes et al., 2006, Holmes and Steel, 2004 and Stuart et al., 2006). It consists of five separate scenes each introduced by a short commentary providing context for the scene.To begin with, actual trauma isn't forewarned or contextualized in advance. It's surprising and shocking. Granted, ethical considerations require informing the participants at the time of recruitment, but this imposes even more limits as a model of real trauma.Going back to the string of references, the first citation (Steil, 1996) indicates the author studied "Posttraumatic intrusions after road traffic accidents" (not merely watching a road traffic accident film). Nonetheless, let's quickly review some of the other papers, with an eye on the terminology used by the respective authors. Brewin and Saunders (2001) looked at "intrusive memories for a stressful film". Hagenaars et al. (2008) reported on "the development of intrusions after an aversive film". In 2004, Holmes et al. studied "intrusive memory development". Notice that "traumatic" and "flashbacks" aren't yet part of the lexicon. As time went on, Holmes et al., 2006 called it a "traumatic film" but hadn't yet transformed "intrusive memories" into "flashbacks". The language used to describe the experimental phenomena shapes the reader's willingness to view the film paradigm as a proxy for real trauma.What is a true flashback? Here's the relevant section of the DSM-IV Criteria for Posttraumatic Stress Disorder, which describes a flashback episode as a complex, multi-sensory experience and not just a visual memory:(3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur upon awakening or when intoxicated). Another element of these experimental designs can include ratings of how upset the participants were while viewing the gory film (Holmes et al., 2004):Participants rated their distress associated with viewing the film after it had ended. They also rated their level of depression, anger, happiness, and anxiety both pre- and postfilm. Eleven-point scales were used, with anchors of 0 (not at all) and 10 (extremely).In that study, ratings were 5.1 for a "no task" condition that did not involve a secondary task while watching the video. So these participants were not especially distressed. Furthermore, this unvalidated self-rating scale has no clinical relevance to PTSD. Eleven-point scales were also used to rate [non-clinical] levels of depression, anger, happiness, and anxiety both pre- and postfilm.Finally, to illustrate that the "trauma film paradigm" bears no relation to the lasting effects of real trauma that can cause PTSD is this ethical clarification (Holmes et al., 2004):With respect to the ethical issues of showing a film with traumatic content, ... Read more »
Holmes, E., James, E., Kilford, E., & Deeprose, C. (2010) Key Steps in Developing a Cognitive Vaccine against Traumatic Flashbacks: Visuospatial Tetris versus Verbal Pub Quiz. PLoS ONE, 5(11). DOI: 10.1371/journal.pone.0013706
"The more a delusion is investigated, the more understandable and less bizarre it becomes, often interwoven with the very individual patterns of experiencing relationships, adversities and suffering, and finally, for every delusional content, as bizarre and remote as it may appear, there may be a cultural niche, in which the same content may be considered legitimate and reasonable."-Pfeifer (1999), Demonic Attributions in Nondelusional Disorders.What is psychopathology? According to Wikipedia,Psychopathology is the study of mental illness, mental distress and abnormal, maladaptive behavior. The term is most commonly used within psychiatry where pathology refers to disease processes. Abnormal psychology is a similar term used more frequently in the non-medical field of psychology.But what is "abnormal, maladaptive behavior"? That's such an enormously complicated question that I wouldn't know where to begin. In fact, as a non-clinician I think it would be rather pompous of me to try and define the parameters of what is (and is not) pathological. For that I refer the reader to the ICD-10 or the Diagnostic and Statistical Manual of Mental Disorders (DSM), both voluminous (and imperfect) attempts to diagnose mental illness based on signs and symptoms. As most of you know, the DSM-IV is currently in the process of being revised. The DSM-5 will be the controversial new revision, with a (delayed) publication date of May 2013.The National Institute of Mental Health (NIMH) in the U.S. is starting to take a different approach to the classification of psychiatric disorders, one that incorporates dimensions of observable behavior as well as neurobiological measures. The aim of the Research Domain Criteria (RDoC) project......is to define basic dimensions of functioning (such as fear circuitry or working memory) to be studied across multiple levels of analysis, from genes to neural circuits to behaviors, cutting across disorders as traditionally defined. The RDoC draft outlines some problems with the present DSM approach:However, in antedating contemporary neuroscience research, the current diagnostic system is not informed by recent breakthroughs in genetics and molecular, cellular and systems neuroscience. Indeed, it would have been surprising if the clusters of complex behaviors identified clinically were to map on a one-to-one basis onto specific genes or neurobiological systems. As it turns out, most genetic findings and neural circuit maps appear either to link to many different currently recognized syndromes or to distinct subgroups within syndromes. If we assume that the clinical syndromes based on subjective symptoms are unique and unitary disorders, we undercut the power of biology to identify illnesses linked to pathophysiology and we limit the development of more specific treatments. ... To date, there has been general consensus that the science is not yet well enough developed to permit neuroscience-based classification. However, at some point, it is necessary to instantiate such approaches if the field is ever to reach the point where advances in genomics, pathophysiology, and behavioral science can inform diagnosis in a meaningful way.There is no absolute timeline of when these advances might occur. Instead of providing an immediate replacement for DSM and its clinical diagnoses, RDoC is a long-term project to help the research community by defining more biologically based organizational principles for various psychopathologies:RDoC will follow three guiding principles, all diverging from current diagnostic approaches. First, RDoC is conceived as a dimensional system (reflecting, e.g., circuit-level measurements, behavioral activity, etc.) spanning the range from normal to abnormal. ... Second, RDoC is agnostic about current disorder categories. The intent is to generate classifications stemming from basic behavioral neuroscience. Rather than starting with an illness definition and seeking its neurobiological underpinnings, RDoC begins with current understandings of behavior-brain relationships and links them to clinical phenomena. Third, RDoC will use several different levels of analysis in defining constructs for study (e.g., imaging, physiological activity, behavior, and self-reports of symptoms).What are the biological mechanisms driving abnormalities in the observed behaviors ("constructs") of e.g. fearfulness, reward sensitivity, attention, and self-representation? As shown in the matrix below, five major domains have been proposed to group the behavioral constructs, which can be evaluated at six levels of analysis.The basic idea is that these domains and constructs can go awry in any number of disorders. For instance, if you type "altered reward processing" into PubMed, among the 80 entries are studies in pediatric bipolar disorder, drug addiction, autism, schizophrenia, obesity, pathological gambling, mania, ADHD, and antisocial personality disorder. What are the neural correlates of altered reward processing? Is there a common mechanism across the various diagnostic categories listed above? Are many of the genes that predispose one to altered reward processing shared across disorders?Another problem that RDoC aims to address is extensive co-morbidity in many of the current diagnostic categories. A prime example is the complex construct of borderline personality disorder (BPD), marked by affective instability, unstable interpersonal relationships, and self-destructive behavior. NIMH notes that about 85 percent of people with BPD also meet the diagnostic criteria for another disorder, including:61 percent also have at least one anxiety disorder, most commonly a specific phobia, or social phobia49 percent have an impulse-control disorder, most commonly intermittent explosive disorder38 percent have a substance abuse or dependence disorder, most commonly alcohol abuse or dependence34 percent have a mood disorder, most commonly dysthymia (mild, chronic depression), or major depression.Here, one can view the diagnostic category of BPD as a collection of symptoms (or disorders) that can vary across individuals. The same can be said of schizophrenia. How do alterations in the underlying biological mechanisms drive various manifestations of mental disorders (Sanislow et al., 2010)?...any given disorder can be marked by disruptions among multiple mechanisms, and one particular mechanism may contribute to the psychopathology of a large number of disorders. Thus, the same mechanisms can be implicated in “different” disorders, whereas multiple mechanisms can be implicated in “one” disorder.Is Big Pharma abandoning psychiatry? (see Mind Hacks)The leaders of NIMH have expressed the opinion that the DSM and ICD have hindered the development of new treatments (Insel et al., 2010). Given the limited effectiveness of many pharmaceutical interventions, it is patently obvious that a new approa... Read more »
Sanislow CA, Pine DS, Quinn KJ, Kozak MJ, Garvey MA, Heinssen RK, Wang PS, & Cuthbert BN. (2010) Developing constructs for psychopathology research: Research domain criteria. Journal of abnormal psychology. PMID: 20939653
Celebrity SPECT scan from rehab patientCelebrity Rehab is an American TV reality show on VH1 that exploits the addictions of the rich and C- or D-List famous.“I thought REAL doctors talked to patients in offices behind closed doors.”-Lindsay Lohan [who reportedly turned down six figures to appear 0n the show]Privacy? Confidentiality? Those rights don't apply to the alcoholic and drug-addicted characters who appear on television and other public media outlets as a form of entertainment. How many of you professional psychology and mental health and cog neuro and pharmaceutical types have taken training courses such as the CITI Course in The Protection of Human Research Subjects? All of you?Medical Ethics do not apply to Dr. Drew, the star and chief physician of the Celebrity Addiction franchise:In 2009 [Dr. Drew] Pinsky drew criticism from experts for publicly offering professional opinions of celebrities he has never met or personally examined, based on media accounts, and has also drawn the ire of some of those celebrities.In contradistinction, proper clinicians who make media appearances take great pains to avoid such unethical outbursts. As explained by Dr Petra Boynton:They tried to make me talk about rehab but I said ‘no, no, no’Yesterday I had over 25 emails and phone messages from journalists wanting me to comment on the mental state of several celebrities currently in the press with various drug/relationships problems. And I’ve said no to all of them.At the risk of sounding like a broken record here’s why psychologists (and other experts working with the media) can’t talk about celebrities.If we know the celeb in person (for example as their therapist or healthcare provider) we are breaking their confidence if we speak about them in public. If we do not know them personally we’re simply speculating about them if we were to comment.The same applies to case studies based on people who are not famous.In Season 3 Episode #6, ('Triggers') Dr. Drew takes former NBA star Dennis Rodman to see our favorite neurohuckster, Dr. Daniel G. Amen, for a SPECT scan. Amen claims he can diagnose all sorts of psychiatric and neurological ailments using SPECT (single photon emission computed tomography)1 procedures performed at his clinics.Drew Pinsky exacerbates the unprofessional circus-like atmosphere by making all sorts of unfounded dire predictions about the state of Rodman's brain.Dr. Drew voiceover: It's day 13, and despite nearly 2 weeks of intense treatment, Dennis has rigidly refused to identify as an alcoholic. It's clear to me there's much more going on here. Probably on an organic basis, both in terms of his personality functioning and possibly damage caused by the alcohol itself. I've arranged for Dennis to receive a brain scan to show him objective evidence of what I suspect is going on.Van arrives at the Amen Clinics in Newport Beach, CA and Rodman is placed in the scanner.Cue colorful images of Mr. Rodman's brain appearing on the monitor. All very scientific. Then Dr. Drew introduces him to Dr. Amen.Amen: "So, we did a study called SPECT that looks at how your brain works. And what we see on your scan here, there's some evidence of alcohol damage. When we see this bumpy appearance, I don't like that. I would worry that you could get something like Alzheimer's disease if you don't do a better job of taking care of your brain. Alcoholic dementia is the second most common cause of dementia in the country. The exciting thing is it can be better but without taking good care of it this is going to deteriorate and get worse."Rodman: "Uh... it doesn't matter. All right." (Gets up and leaves).Amen made some rather outrageous statements here. Even though he used the qualifying words something like, there is absolutely no evidence that alcoholism causes the amyloid plaques and neurofibrillary tangles of Alzheimer's disease. In fact, the pathologies are produced by entirely different mechanisms (Aho et al., 2009):In the present study, no statistically significant influence was observed for alcohol consumption on the extent of neuropathological lesions encountered in the three most common degenerative disorders. Our results indicate that alcohol-related dementia differs from VCI [vascular cognitive impairment], AD [Alzheimer's disease], and DLB [dementia with Lewy bodies]; i.e., it has a different etiology and pathogenesis.One meta-analysis even found that heavy drinkers did not have an increased risk of dementia of any kind,2 and regular drinkers had a reduced risk (Anstey et al., 2009).Then brain imaging non-expert Dr. Drew narrates...Dr. Drew voiceover: Dennis's scans were quite dramatic. In addition to there being an unusual pattern of temporal lobe dysfunction, which confirms my feelings about his personality, he also clearly has damage from alcohol.Dr. Drew (to Amen): "It makes me sad thinking about it... if he doesn't change."I see...Where in the temporal lobe did Dr. Drew find the confirmatory evidence of personality disorder? Anterior temporal lobes (semantic memory)? Posterior/inferior temporal regions, such as the fusiform gyrus (high-level vision)? Superior temporal plane (audition)? Region of the left posterior superior temporal gyrus (Wernicke's area for language comprehension)? Area MT/V5 (perception of motion)? The medial temporal lobe memory system? The amygdala and other portions of the limbic system? Yeah, maybe that, but Amen's "bumpy appearance" was located in ventral visual areas.... Read more »
Adinoff, B., & Devous, M. (2010) Scientifically Unfounded Claims in Diagnosing and Treating Patients. American Journal of Psychiatry, 167(5), 598-598. DOI: 10.1176/appi.ajp.2010.10020157
Charles Hamilton Hughes (1839-1916) was the founder and editor of The Alienist and Neurologist. The journal was published from 1880 until his death in 1916, making him the sole editor for all 37 volumes. Remittances for subscriptions ($5 for four issues per year) and "articles or photographs from subscribers or friends and material acceptable for publication" were sent to his address in St. Louis.What is an alienist?An "alienist" is "one who treats mental diseases; a mental pathologist; a 'mad doctor'," according to The Oxford English Dictionary. The OED also defines "alienation" as in this sense as "mental alienation; withdrawal, loss, or derangement of mental faculties; insanity." The insane were thought estranged (alienated) from their normal faculties. The root of "alienist" is the Latin "alienare," to make strange. The word "alienist" came across the Channel to England from France where "aliene" meant insane and an "alieniste" was one who cared for the mentally ill: a psychiatrist.What were Hughes's contributions to neurology and psychiatry? Notable excerpts from his obituary:By the Death of the Founder of the Alienist and Neurologist one of the great pupils of the famed American School of Psychiatry of Rush, Stedman, Brigham, Gait and Ray has passed away. He had imbibed to the full the critical, judicial, radical, yet logically conservative, spirit of this school.. . .In 1880 he founded the Alienist and Neurologist, which soon assumed and kept a prominent position among medical journals. From the beginning it was recognized as of authority by the British Journal of Mental Science, the French Annales Medicopsychologiques, the Berlin Allgemeine Zeitschrift fur Psychiatric, [etc.]. Contributions to the Alienist and Neurologist were therefore widely quoted in Europe, even in circles hostile to America.The personal contributions of Dr. Hughes to psychiatry and neurology were varied, valuable and original. His discovery of the virile reflex1 was widely cited...However, an obituary in the Journal of Nervous and Mental Disease was less flattering:...He early maintained an interest in neurology in what was hardly more than a frontier trading post and where the existence of neurology was hardly dreamed of according of the canons of to-day. It was then a crude product but it was sincere and as he upheld it, it was a light in the wilderness. As St. Louis grew and began to feel itself this early lamp shone less brightly in contrast, but Dr. Hughes, although he may not have kept in touch with the latest advances, still maintained a vital interest and enthusiasm....He became widely known through the Alienist and Neurologist, which he founded in 1880 and which he made the medium for an open discussion of neurological and psychiatrical problems. It was received among European publications, though it never definitely stood for vigorous research and the vigorous pushing forward into, progressive lines which marks the neurology of to-day.Mental AlienationIn The Neurocritic's previous post on Arithmomania, Hughes was credited with an article on "Autopsychorhythmia," or repetition psycho-neurosis (Hughes, 1901). He was clear to distinguish this phenomenon from the related conditions of echolalia (automatic repetition of another's speech) and coprolalia (involuntary uttering of obscenities, which is seen in only 10% of patients with Tourette's syndrome).The constant repetition of a rhythmical movement in the mind, regardless of time or place or circumstance, and which an enfeebled volition cannot regulate to conform to the requirements of environment, characterises this symptom of brain overstrain and psycho-motor automatic impulse. Neuropathic and consequent psycho-motor neurasthenia appear to be at the bottom of this condition...There's an element of "nervous breakdown" and mental exhaustion in some of the case reports, particularly in the patients who made good recoveries. For instance,A gentleman of extensive business affairs who came to me on the verge of financial and business bankruptcy, but who is now after many years of health successful in a new but less harassing line of business, would continuously say to himself : "Too many irons in the fire, too many irons in the fire." His intellect was clear but his brain was jaded and unstable-in that stage of cerebrasthenia that so often precedes the final brain-break of insanity. The closing out and winding up of his business saved him for recuperation and another and less harassing and more successful career. Conversely, other patients remained mired in insanity:I have heard a chronic alcoholic repeat over and over through the day, "Little Bo-Peep, he lost his sheep, and doesn’t know where to find them," etc., and have known chronic lunatics who would repeat some long-ago-learned distich or rhyme or some insanely-constructed jingle of words in maudlin monotone, from the day’s beginning to the ending thereof, in all their waking hours, some of them ringing their peculiar song, like the dying swan, to the end of their unfortunate lives.He considered autopsychorhythmia to be a brain disease, which seems obvious to us today, but he apparently needed to distinguish the centrally located pathology from peripheral motor abnormalies:The pathological lesion of autopsychorhythmia is evidently in the mind area of the brain cortex.2 It is truly transcortical and not localised exclusively in the speech area. It is a psychical and not purely psychomotor involvement-a psychical lesion shown in peculiarity of psychomotor expression.Were there any treatments for such a malady? An 18 year old music student, a handsome and bright young lady, was prescribed a regimen of "rest, change of environment, cessation of study and piano practice, withdrawal from musical companionship, brain-tranquillising galvanisations, ether-menthol evaporating lotions to the head, chemical brain restraint, and pepsines and laxatives." Another charming young lady received "six weeks’ treatment with bromide of potassium, timely hypnotics, tonics, aloetic laxatives and gelsemium."Oh, by the way, The Alienist and Neurologist accepted advertising...Footnotes1 From Hughes (1891):In a previous communication on this subject (vide Alienist and Neurologist for January, 1891), I have called attention to the fact that in a perfectly healthy individual, whose spinal cord is entirely normal, especially in its genitospinal center, placed supine on a couch without headrest, nude about the loins, the sheath of the penis made tense by clasping the foreskin with the left index finger and thumb at about the place ... Read more »
HUGHES, C. (1901) AUTOPSYCHORHYTHMIA OR REPETITION PSYCHO-NEUROSIS. MORBID RHYTHMIC FORMS OF AUTOMATICITY AND RHYTHMIC FORMS OF MENTAL ALIENATION. The Lancet, 157(4051), 1124-1126. DOI: 10.1016/S0140-6736(01)89412-5
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