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Deconstructing the most sensationalistic recent findings in Human Brain Imaging, Cognitive Neuroscience, and Psychopharmacology

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  • August 11, 2009
  • 12:06 AM

A New Clitoral Homunculus?

by The Neurocritic in The Neurocritic

Homunculus image from Reinhard Blutner.OK kids, let's start today's lesson by viewing the G-Rated [i.e., genital-less] flash explanation of homunculus.The neuroanatomical definition of homunculus is a "distorted" representation of the sensorimotor body map (and its respective parts) overlaid upon primary somatosensory and primary motor cortices. The above figure illustrates the sensory homunculus, where each body part is placed onto the region of cortex that represents it, and the size of the body part is proportional to its cortical representation (and sensitivity). It's rare to see the genitals represented at all. And if they are present, they are inevitably male genitals. To remedy this puritanical and androcentric situation, Swiss scientists at University Hospital in Zurich conducted a highly stimulating study in 15 healthy women to map the somatosensory representation of the clitoris (Michels et al., 2009).The authors begin by reviewing the work of Wilder Penfield et al.:During the last 70 years the description of the sensory homunculus has been virtually a standard reference for various somatotopical studies (Penfield and Boldrey 1937; PDF). This map consists of a detailed description of the functional cortical representation of different body parts obtained via electrical stimulation during open brain surgery. In their findings they relied on reported sensations of different body parts after electrical stimulation of the cortex. Assessment of the exact location was generally difficult and sometimes led to conflicting results. The genital region was especially hard to assess due to difficulties with sense of shame.Recent studies have tried to map the somatosensory represenation of the human penis using neuroimaging methods, but there has been disagreement over whether it shows the classic medial representation seen in the figure above, or a more laterally located representation in the postcentral gyrus. For example, Kell et al. (2005) noted that......classical and [some] modern findings appear to be at odds with the principle of somatotopy, often assigning it to the cortex on the mesial wall. Using functional neuroimaging, we established a mediolateral sequence of somatosensory foot, penis, and lower abdominal wall representation on the contralateral postcentral gyrus in primary sensory cortex and a bilateral secondary somatosensory representation in the parietal operculum.But there are no comparable fMRI studies of female genitalia. So how is such a study conducted, methodologically speaking? Electrical stimulation of the dorsal clitoral nerve was compared to electrical stimulation of the hallux (big toe). It was all very clinical, no sexual arousal involved. Here's the experimental protocol:Prior to the imaging session, two self-attaching surface disc electrodes (1 × 1 cm) were placed bilaterally next to the clitoris of the subjects so that we were able to stimulate the fibers of the dorsal clitoral nerve. Before the start of the experiment, electrical test stimulation was performed to ensure that subjects could feel the stimulation directly at the clitoris. In addition, the strength of electrical stimulation was adjusted to a subject-specific level, i.e. that stimulation was neither felt [as] painful nor elicited – in case of clitoris stimulation – any sexual arousal (see below). Functional imaging was performed in a block design with alternating rest and stimulation conditions, starting with a rest condition. ... In addition to the clitoris stimulation, we performed in eight of the recorded subjects a second experimental session, in which we applied electrical stimulation of the right hallux using the same type of electrodes, stimulation and scan paradigm.If you "see below" in the Methods you'll discover that after the fMRI session, participants rated their level of sexual arousal and discomfort on a visual analogue scale that ranged from -10 (unbearable pain or strong sexual arousal) to 10 (pleasure or no arousal at all/sleepiness). The median score for sexual arousal was zero with some variability [range: −7.5 to 8; −2 (25% percentile) and 2.5 (75% percentile)]. The median score for comfortableness was −2 [range: −7 to 9; −2.5 (25% percentile) and 0 (75% percentile)]. C'est la vie.The neuroimaging results revealed that compared to the rest blocks,Electrical clitoral stimulation produced significant activations predominantly in bilaterally prefrontal areas (BA 6, 8 and 45), the precentral, parietal and postcentral gyri, including S1 (BA 2 and 3; 40–70% probability) and S2 (BA 43 and ventral BA 40, 30–60% probability). In addition, distributed activations were also seen in the anterior and posterior parts of the insula and the putamen.Fig. 3 (Michels et al., 2009). Illustration of the random-effect group-activation pattern for the contrast ‘electrical clitoral stimulation versus rest’ (orange–yellow color code; p less than 0.02 uncorrected for multiple comparisons) and for the contrast ‘electrical hallux stimulation versus rest’ (green–blue color code; p less than 0.001 uncorrected for multiple comparisons) on a group average brain. A cluster extent threshold of p less than 0.05 is applied for both contrasts. Electrical clitoral stimulation elicited bilateral activations of lateral surface of S1 as indicated by the white circles.The major result was similar to the penile homuculus findings of Kell et al. (2005): a failure to replicate the original 1937 studies of Penfield and Boldrey. Although the statistical thresholds here for the clitoral stimulation were not stringent enough, the authors use this to their advantage:We found no evidence of clitoral representation in the mesial wall, even when using unconventionally low statistical thresholds. This finding is further substantiated by other recent cytoarchitectonic studies revealing that BA 2 does not reach the inter-hemispheric fissure and BA 3 and BA 1 reach the postcentral mesial wall with a probability of only 30% . Our results are also in good agreement with [neuroanatomical] studies on nonhuman primates. In conclusion, it appears that Michels et al. (2009) have indeed mapped out a new clitoral homunculus, to go along with the new penile homunculus. The standard somatosensory images should be revised accordingly.... Read more »

  • May 14, 2009
  • 08:40 PM

Suicide Rates in Greenland Are Highest During the Summer

by The Neurocritic in The Neurocritic

by: crdagainSeasonal affective disorder (SAD) is a cyclical depressive disorder that typically recurs every year during the shorter days and longer nights of late fall-early winter. Much of the research on SAD has focused on changes in the photoperiod and the accompanying effects on circadian rhythms during winter. So it might come as a surprise that in Greenland, the suicide rate peaks during the summer months of continuous sun (especially at the highest latitudes). However, the rate of homicides and the sales of beer do not show the same seasonal variation (Björkstén et al., 2009). Why might this be? Most suicides in Greenland are of the impulsive variety and are committed using violent methods. The authors' previous work observed the summer suicide spike (Björkstén et al., 2005), and now they wanted to determine whether homicides show the same seasonal pattern. They reviewed the evidence on serotonin, impulsivity, and violence, and hypothesized that altered serotonin turnover might be a common factor in both violent suicides and violent homicides (reasoning that increased serotonin turnover in spring and summer might enhance impulsiveness and aggression).How was this assessed? Northern Greenland (obviously) shows the greatest seasonal extremes in the amount of light and darkness. The country maintains good statistics, and the Inuit population is considered to be relatively homogeneous. Thus, Björkstén, Kripke, and Bjerregaard (2009) examined computerized records listing the causes of all deaths in Greenland during the time period of 1968-2002. To determine whether alcohol consumption played a role in the rates of suicides and murders, the pattern of beer purchases at a major chain store from July 2005 to June 2006 were used as a proxy ("Detailed sales data are secret for business reasons").The authors note some extremely tragic statistics:The suicide rate in Greenland increased during the 1970’s from a historically very low level to one of the highest levels in the world, 107 per 100,000 person-years in 1990-1994. The increase has been most pronounced among teenagers and young adults. A rapidly increasing suicide rate has been reported from other areas going through radical changes like in Eastern Europe after the fall of communism and among aboriginal people confronted with modern lifestyle.We have previously demonstrated that the vast majority of suicides in West Greenland are violent and peak in the summer when the Northern half of Greenland has constant day-light and the Southern half has extremely long days. Depression has, however, been reported uncommon and the majority of suicides seem impulsive rather than depressive.The overall homicide rate in Greenland has been reported much higher than that of the other Nordic countries. Homicides are almost exclusively impulsive and committed under the influence of alcohol...Continuing in a depressing vein, there were 1351 suicides (80.5 % were men) and 308 homicides during the 35 year period under study.Persons in upper teens and young adults were heavily over-represented among the suicide cases. Median age was 25 years...In 391 out of the 1351 cases (29%), the death certificate included a psychiatric diagnosis. In 214 cases (15.8%), there was a diagnosis of alcoholism or alcohol intoxication; two cases also had a diagnosis of psychosis. In only 52 cases (3.8%), there was a diagnosis of affective disorder, either unspecified or in the depressive state. In 104 cases, there was a diagnosis of psychosis. In addition to the 104 cases (7.7%), there were two with alcoholism and psychosis.However, affective disorders could have been underdiagnosed in the population... we don't really know for sure. What we do know is that violent methods of suicide were used in 95% of all cases (n=1286), with men using violent methods 97% of the time and women 86% of the time (the latter percentage in stark contrast to the general population outside of Greenland). Figure 3a below shows the seasonal variation in all suicide cases. The annual peak occurred on June 11th and the trough in November-January, and the effect of seasonality was significant (p... Read more »

  • July 8, 2013
  • 04:57 AM

A New Slant on Frontal Connectivity: the Frontal Aslant Tract

by The Neurocritic in The Neurocritic

The frontal aslant tract is shown in yellow (Fig 5, Catani et al., 2012). It's not every day that you hear about a newly described white matter pathway in the human brain. An interesting new study by a group of researchers in London and Chicago found a novel fiber tract implicated in verbal fluency impairments in patients with a lesser known neurodegenerative illness (Catani et al., 2013). This short fiber tract connects two different regions in the frontal lobe. It was recently identified using a combination of diffusion imaging and post-mortem dissection (Lawes et al., 2008; Catani et al., 2012; Thiebaut de Schotten et al., 2012). Dubbed the frontal aslant tract (FAT) by Catani and colleagues, it connects the posterior portion of the inferior frontal gyrus (IFG) to the supplementary motor area (SMA) and pre-SMA on the medial wall.1A number of experiments have already looked at the functional connectivity of these regions, during both resting state and task activation conditions. Statistically correlated fluctuations in the BOLD signal 2 are thought to reflect functional connectivity between two regions, but there is often no evidence that the two regions are directly connected anatomically. Therefore, in vivo structural MRI methods such as diffusion imaging can provide complementary data by visualizing white matter pathways to determine anatomical connections.The diffusion tractography results were then compared to blunt dissection of tracts from post-mortem brains, which helped to validate a method that some view as prone to limitations and potential artifacts.3 Fig. 10 (modified from Catani et al., 2012). Coronal slices of the ‘Digital Dejerine’ maps 4  and post-mortem blunt dissections of the corresponding tracts. E) The frontal aslant tract (FAT) connecting inferior and superior frontal gyri.A comparative study went further, showing that the results obtained from human tractography compared favorably to axonal tracing methods in monkeys (Thiebaut de Schotten et al., 2012).5  Fig. 6 (Thiebaut de Schotten et al., 2012). Reconstructions of the frontal aslant tract: comparison between post-mortem axonal tracing in monkey and human in vivo SD [Spherical Deconvolution] tractography shows simian-human similarities.However, one difference between this tract in monkeys and humans is that the FAT is lateralized in humans, being larger in the left hemisphere than in the right (Catani et al., 2012). In the left hemisphere, posterior IFG is part of Broca's area. This brings us back to the clinical importance of this basic neuoanatomical work.Verbal Fluency and the Frontal Aslant TractPrimary progressive aphasia (PPA) is a neurodegenerative disorder, the hallmark of which is the deterioration of specific speech and language functions. There are three variants, each with characteristic behavioral, neuroanatomical, and pathological features (Gorno-Tempini et al., 2011):Nonfluent/Agrammatic Variant PPA is characterized by halting, effortful speech with difficulties producing grammatical output and/or comprehending syntactically complex sentences. Word comprehension and object knowledge are intact. Atrophy in the left frontal cortex is apparent on MRI.Semantic Variant PPA is marked by impairments that include comprehending the meanings of words, naming objects and understanding their function. Motor speech production and grammatical output are spared. Atrophy is seen in the anterior temporal lobe.Logopenic Variant PPA involves word finding problems, phonological speech errors, and difficulties in repeating words and sentences. Word comprehension, object knowledge, and grammar are spared. Degeneration of left posterior temporal-parietal regions is observed.In the latest study by Catani et al. (2013), 35 patients with PPA and 29 controls participated in behavioral testing and MRI scanning. The tests included standard evaluations of language abilities including the Western Aphasia Battery, the Boston Naming Test, and the Peabody Picture Vocabulary Test. Tractography identified the frontal aslant tract and the uncinate fasciculus, which connects anterior temporal lobe regions to the IFG pars orbitalis and the orbitofrontal cortex. Quantitative measures included the number of streamlines (tract volume), fractional anisotropy, and radial diffusivity (measures of white matter integrity and axonal damage, respectively).Results indicated that patients with Nonfluent/Agrammatic PPA were impaired in a speech production task that required telling the story of Cinderella from a picture book. Poor performance in verbal fluency was associated with the extent of damage in the FAT, but grammatical deficits were not. In contrast, patients with Semantic Variant PPA showed deficits in semantic processing which correlated with degeneration in the uncinate fasciculus.What are the implications for the neuroanatomy of verbal fluency and speech output?...Patients with lesions of the pre-supplementary motor area present with various degrees of speech impairment from a total inability to initiate speech (i.e. mutism) to mild altered fluency. Our findings suggest that these medial regions of the frontal lobe could facilitate speech initiation through direct connection to the pars opercularis of the inferior frontal gyrus. Indirect support of this interpretation comes from the frequent observation of impaired fluency in patients with deep lesions in the frontal periventricular white matter. In these cases, a disconnection of the frontal aslant could explain the emergence of symptoms usually associated with frontal cortical damage. More broadly, characterizing the different pattern... Read more »

Catani M, Dell'acqua F, Vergani F, Malik F, Hodge H, Roy P, Valabregue R, & Thiebaut de Schotten M. (2012) Short frontal lobe connections of the human brain. Cortex; a journal devoted to the study of the nervous system and behavior, 48(2), 273-91. PMID: 22209688  

Catani M, Mesulam MM, Jakobsen E, Malik F, Matersteck A, Wieneke C, Thompson CK, Thiebaut de Schotten M, Dell'acqua F, Weintraub S.... (2013) A novel frontal pathway underlies verbal fluency in primary progressive aphasia. Brain : a journal of neurology. PMID: 23820597  

Gorno-Tempini ML, Hillis AE, Weintraub S, Kertesz A, Mendez M, Cappa SF, Ogar JM, Rohrer JD, Black S, Boeve BF.... (2011) Classification of primary progressive aphasia and its variants. Neurology, 76(11), 1006-14. PMID: 21325651  

Thiebaut de Schotten M, Dell'Acqua F, Valabregue R, & Catani M. (2012) Monkey to human comparative anatomy of the frontal lobe association tracts. Cortex; a journal devoted to the study of the nervous system and behavior, 48(1), 82-96. PMID: 22088488  

  • April 23, 2011
  • 05:26 AM

Irresponsible Press Release Gives False Hope to People With Tourette's, OCD, and Schizophrenia

by The Neurocritic in The Neurocritic

A study on electrophysiological recordings from single neurons in the dorsolateral prefrontal cortex of two monkeys trained to perform a visual target discrimination task (Lennert & Martinez-Trujillo, 2011) has supposedly given new hope to patients with a diverse array of neurological and psychiatric conditions, according to a press release:Filters That Reduce ‘brain Clutter’ IdentifiedScienceDaily (Apr. 19, 2011) — Until now, it has been assumed that people with conditions like ADHD, Tourette syndrome, obsessive compulsive disorder and schizophrenia -- all of whom characteristically report symptoms of "brain clutter" -- may suffer from anomalies in the brain's prefrontal cortex.Damage to this brain region is often associated with failure to focus on relevant things, loss of inhibitions, impulsivity and various kinds of inappropriate behaviour. So far, exactly what makes the prefrontal cortex so essential to these aspects of behaviour has remained elusive, hampering attempts to develop tools for diagnosing and treating these patients.But new research by Julio Martinez-Trujillo, a professor in McGill University's Department of Physiology and Canada Research Chair in Visual Neuroscience, has brought new hope to these patients. He believes the key to the "brain clutter" and impulsivity shown by individuals with dysfunctional prefrontal cortices lies in a malfunction of a specific type of brain cell. Martinez-Trujilo and his team have identified neurons in the dorsolateral sub-region of the primate prefrontal cortex that selectively filter out important from unimportant visual information. The key to the normal functioning of these "filter neurons" is their ability to, in the presence of visual clutter, selectively and strongly inhibit the unimportant information, giving the rest of the brain access to what is relevant.I am so flabbergasted by the number of misleading statements that I don't know where to begin. Let's take them in the order of occurrence."Until now" - This phrase implies that the study has refuted the assumption that ADHD, Tourette's, OCD, and schizophrenia are all associated with abnormalities in the prefrontal cortex (PFC). In fact, individuals with these disorders (and their PFCs) were not evaluated."brain clutter" - What does this mean? I'm not familiar with it as a technical term, nor how the phenomenon is manifest in all four of the above disorders. This issue is relatively minor."anomalies in the brain's prefrontal cortex" - The human PFC covers a large and diverse area of the brain.Fig. 1 (Fuster, 2002). Three views of the cerebral hemispheres with the areas of the prefrontal cortex numbered in accord with Brodmann’s cytoarcitectonic map.Neuroimaging findings in ADHD, Tourette's, OCD and schizophenia are not uniform, and the implicated subregions of PFC are not the same. For example, OCD has been associated with overactivity in the orbitofrontal cortex (Menzies et al., 2008) while schizophrenia is associated with altered activation of dorsolateral PFC (Volk & Lewis, 2010).1 This is highly relevant because as we'll see, the monkey neurons under investigation were in a specific region analogous to Brodmann area 46 in human dorsolateral PFC."Damage to this brain region" and the subsequent laundry list of altered behaviors - not all associated with damage to BA 46."brought new hope to these patients" - This is by far the most egregious falsehood of the entire press release. I find it to be utterly irresponsible.None of these claims were made in the paper itself, which examined firing rates of neurons in the principal sulcus of two rhesus macaque monkeys trained to perform a color-rank target discrimination task with moving random dot patterns.Figure adapted from the press release. The pinkish highlighted area of the brain is the principal sulcus region where neuron activity was recorded.The authors summarize the results below. You'll notice there's no mention of developing "tools for diagnosing and treating these patients" or bringing "new hope to these patients."Highlights► Interstimulus ordinal distance modulates attentional-filtering strength in monkeys ► Interstimulus ordinal distance modulates target selection by prefrontal neurons ► Varying suppression of distracters by dlPFC neurons determines attentional filtering ► Target enhancement by dlPFC neurons remains invariable with changes in performanceHere's the link for the original press release from McGill University. If you are so inclined:Contact: Katherine Gombay, Media Relations Office, McGill University - Tel.: 514 398-2189 Footnote1 I'm skipping the complexities of multiple fronto-striato-thalamic circuits.ReferencesFuster JM. (2002). Frontal lobe and cognitive development. J Neurocytol. 31:373-85.Lennert, T., & Martinez-Trujillo, J. (2011). Strength of Response Suppression to Distracter Stimuli Determines Attentional-Filtering Performance in Primate Prefrontal Neurons Neuron, 70 (1), 141-152 DOI: 10.1016/j.neuron.2011.02.041Menzies L, Chamberlain SR, Laird AR, Thelen SM, Sahakian BJ, Bullmore ET. (2008). Integrating evidence from neuroimaging and neuropsy... Read more »

  • January 15, 2009
  • 08:12 PM

Voodoo Schadenfreude

by The Neurocritic in The Neurocritic

Voodoo doll, by SickboyMost hip researchers in cognitive neuroscience and human brain imaging have already heard about the critical new journal article with the incendiary title: "Voodoo Correlations in Social Neuroscience" (Vul et al., in press - PDF). If you haven't, you can read a comprehensive summary here and a micro version here.Avenging Voodoo SchadenfreudeNature News ran a piece on the debate and the burgeoning backlash from an angry mob of researchers whose methods were derided as fatally flawed. Some of these authors (and perhaps some Nature editors) were miffed that bloggers wrote about the preprint when it was first made available to the public, as if that somehow violates the scientific method:The swift rebuttal was prompted by scientists' alarm at the speed with which the accusations have spread through the community. The provocative title — 'Voodoo correlations in social neuroscience' — and iconoclastic tone have attracted coverage on many blogs, including that of Newsweek. Those attacked say they have not had the chance to argue their case in the normal academic channels."I first heard about this when I got a call from a journalist," comments neuroscientist Tania Singer of the University of Zurich, Switzerland, whose papers on empathy are listed as examples of bad analytical practice. "I was shocked — this is not the way that scientific discourse should take place." Singer says she asked for a discussion with the authors when she received the questionnaire, to clarify the type of information needed, but got no reply.Based on the statements above, it would seem that Dr. Singer and her colleagues (Jabbi, Keysers, and Stephan) are not keeping up with the way that scientific discourse is evolving. [See Mind Hacks on this point as well.] 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? To their credit, however, they commented in blogs and publicized the link to a preliminary version of their detailed reply.....although calling it "summary information for the press" assumes that "the press" is extremely knowledgeable about neuroimaging methodology and statistical analysis.To learn more about the evolution of scientific discourse, let me briefly introduce you to the world of social media (e.g., FriendFeed, Facebook, and even Twitter). You can join the discussion at FriendFeed's Science 2.0 Room, which is "For people interested in Science 2.0 and Open Science, especially the use of online tools to do science in new ways." Although one needs a Facebook account to view these, Facebook groups include Neuroscience ROCKS (4,006 members), Neuroscience and Brain Studies (3,194 members), and Cognitive Neuroscience Society (2,147 members). Some social neuroscientists are, well, social enough to get it, because Columbia University Social Cognitive Affective Neuroscience Lab has a posse (79 fans, albeit inactive ones). And believe it or not, NIH now has Twitter feeds for press releases and funding announcements. As for individuals who are powerhouse resources on the future of scientific communication, I would recommend reading BoraZ (blog, Twitter), who is organizing the Jan. 16-18 ScienceOnline’09 conference, and Björn Brembs on scientific publishing and misuse of the Impact Factor.All is not puppies and flowers in the world of science social media, however. Proponents rarely acknowledge that many companies and institutions block access to these sites, so at present their usefulness is limited for many in the scientific community. A more obvious issue is that these sites can turn into an enormous time sink.Now back to Nature News and the voodoo backlash. In an ironic twist, one of the 'red listed' papers (Singer et al., 2006), published in Nature, was publicized as a study on Schadenfreude. Here's the Editor's Summary [which was covered by The Neurocritic three years ago]:I feel your painHumans have the capacity to empathize with the pain of others, but we don't empathize in all circumstances. An experiment on human volunteers playing an economic game looked at the conditional nature of our sympathy, and the results show that fairness of social interactions is key to the empathic neural response. Both men and women empathized with the pain of cooperative people. But if people are selfish, empathic responses were absent, at least in men. And it seems that physical harm might even be considered a good outcome — perhaps the first neuroscientific evidence for schadenfreude.Nature and Science have a long history of issuing overblown press releases that extrapolate the findings of a single, quite flawed [if you side with Vul et al.] neuroimaging paper to yield the revelation of deep truths about human social interactions (among other things). The Nature News piece, Brain imaging studies under fire (Abbott, 2009), continues:The article is scheduled for publication in September, alongside one or more replies. But the accused scientists are concerned that the impression now being established through media reports will be hard to shake after the nine-month delay. "We are not worried about our close colleagues, who will understand the arguments. We are worried that the whole enterprise of social neuroscience falls into disrepute," says neuroscientist Chris Frith of University College London, whose Nature paper [Singer et al., 2006] on response to perceived fairness was called into question. So media reports heavily promoted the field, and media reports will unduly tarnish the field.1NewScientist provides a clear instance of this, in what is surely a textbook exemplar of a pot-kettle moment.Doubts raised over brain scan findings14 January by Jim GilesSOME of the hottest results in the nascent field of social neuroscience, in which emotions and behavioural traits are linked to activity in a particular region of the brain, may be inflated and in some cases entirely spurious.But one doesn't have to look very far to find NewScientist headlines like these (I just searched the archives of this blog):Watching the brain 'switch off' self-awarenessDo games prime brain for violence?Starving is like ecstasy use for anorexia sufferersMirror neurons control erection response to pornSource of ‘optimism’ found in the brainSo the NS editorial below comes across as a wee bit hypocritical, even though it eventually acknowledges their own role in promoting "sexy-sounding" brain scan results.Editorial: What were the neuroscientists thinking?14 January 2009IT IS two centuries since the birth of Charles Darwin, but even now his advice can be spot on. The great man attempted a little neuroscience in The Expressions of the Emotions in Man and Animals, published in 1872, in which he discussed the link between facial expressions and the brain. "Our present subject is very obscure," Darwin warned in his book, "and it is always advisable to perceive clearly our ignorance." Modern-day neuroscience might benefit from adopting a similar stance. The field has produced some wonderful science, including endless technicolor images of the brain at work and headline-grabbing papers about the areas that "light up" when registering emotions. Researchers charted those sad spots that winked on in women mourning the end of a relationship, the areas that got fired up when thinking about infidelity, or those that surged in arachnophobes when they thought they were about to see a spider. The subjective subject of feelings seemed at last to be becoming objective. Now it seems that a good chunk of the papers in this field contain exaggerated claims, according to an analysis which suggests that "voodoo correlations" often inflate the link between brain areas and particular behaviours. Some of the resulting headlines appeared in New Scientist, so we have to eat a little humble pie and resolve that next time a sexy-sounding brain scan result appears we will strive to apply a little more scepticism to our coverage.Um, no joke guys.On the other hand, Sharon Begley at Newsweek is one science writer who hasn't been entirely convinced by the colorful brain images. On March 10, 2008, she wrote: Brain-imaging studies have proliferated so mindlessly (no pun intended) that neuroscientists should have to wear a badge pleading, “stop me before I scan again.” I mean, does it really add to the sum total of human knowledge to learn that the brain’s emotion regions become active when people listen to candidates for president? Or that the reward circuitry in the brains of drug addicts become active when they see drug paraphernalia?Therefore, her recent commentary on the brouhaha does not come across as an opinion that was invented yesterday:The 'Voodoo' Science of Brain Imaging If you are a fan of science news, then odds are you are also intrigued by brain imaging, the technique that produces those colorful pictures of brains “lit up” with activity, showing which regions are behind which behaviors, thoughts and emotions. So maybe you remember these recent hits... [gives many examples here] . . . the list goes on and on and on. And now a bombshell has fallen on dozens of such studies: according to a team of well-respected scientists, they amount to little more than voodoo science. The neuroscience blogosphere is crackling with—so far—glee over the upcoming paper, which rips apart an entire field: the use of brain imaging in social neuroscience.....Before concluding, I will state that I am not a complete neuroimaging nihilist. For examples of this view, see Coltheart, 2006 and especially van Orden and Paap, 1997 (as quoted by Coltheart):What has functional neuroimaging told us about the mind so far? Nothing, and it never will: the nature of cognition is such that this technique in principle cannot provide evidence about the nature of cognition.So no, I am not a Jerry Fodor Functionalist. I do believe that learning about human brain function is essential to learing about "the mind," that the latter can be reduced to the former, that fMRI can have something useful to say, and (more broadly, in case any anti-psychiatry types are listening) that psychiatric disorders are indeed caused by faulty brain function. But there's still a lot about fMRI as a technique that we don't really know. The best-practice statistical procedures for analyzing functional images is obviously a contentious issue; there is no consensus at this point. Our knowledge of what the BOLD signal is measuring, exactly, is not very clear either [see the recent announcement in J. Neurosci. that "BOLD Signals Do Not Always Reflect Neural Activity."] The critics among us2 are not trying to trash the entire field of social neuroscience (or neuroimaging in general). Some of us are taking concrete steps to open a dialogue and improve its methodology, while others are trying to rein in runaway interpretations.ADDENDUM: via Pieces of Me, I've just discovered the link to PsyBlog's detailed discussion of the Coltheart paper: Can Cognitive Neuroscience Tell Us Anything About the Mind?Footnote1 It isn't even necessary to quote the appropriate metaphorical expression here.2 By "us" I mean scientists: people who are students and post-docs and colleagues of esteemed investigators like Dr. Frith.ReferencesAbbott A (2009). News: Brain imaging studies under fire. Social neuroscientists criticized for exaggerating links between brain activity and emotions. Nature 457:245.Jabbi M, Keysers C, Singer T, Stephan KE. (in preparation). Rebuttal of "Voodoo Correlations in Social Neuroscience" by Vul et al. – summary information for the press. PDFSinger T, Seymour B, O'doherty JP, Stephan KE, Dolan RJ, Frith CD. (2006) Empathic neural responses are modulated by the perceived fairness of others. Nature 439:466-9.Vul E, Harris C, Winkielman P, Pashler H (2009). Voodoo Correlations in Social Neuroscience. Perspectives on Psychological Science, in press. PDF... Read more »

Edward Vul, Christine Harris, Piotr Winkielman, . (2009) Voodoo Correlations in Social Neuroscience. Perspectives on Psychological Science.

  • April 20, 2009
  • 09:06 AM

Neural Correlates of Admiration and Compassion and Envy and Schadenfreude

by The Neurocritic in The Neurocritic

In light of all the sensationalistic press coverage about a journal article that wasn't publicly available last week, it's worth taking a moment to look at the actual experiment. Of course, the savvy skeptics know by now that the paper in question (Immordino-Yang et al., 2009) has absolutely nothing to do with Twitter (see Recommended Reading below for a recap). Instead, the authors conducted a neuroimaging study to examine the brain's response to stories designed to elicit the emotions of admiration and compassion. To do this, the participants (n=13) first watched a series of mini-documentary narratives about real people (who were not celebrities). Each of the 50 narratives was 60-90 sec long, and incorporated audio, video, and still images to convey stories categorized as:1. Admiration for virtue (AV), which involved people performing highly virtuous, morally admirable acts. The narratives emphasized the virtuous and morally admirable nature of the protagonist, such as dedication to an important cause despite difficult obstacles, and did not include displays of notable skill.2. Admiration for skill (AS), which involved people adeptly performing rare and difficult feats, e.g., an athletic or musical performance, with both physical and cognitive components. No physically or socially painful acts were shown, and the skillful feats, although amazing, did not imply a virtuous protagonist or reveal a virtuous act.3. Compassion for social pain (CSP), which involved people in states of grief, despair, social rejection, or other difficult psychological circumstances. No physical pain was evident in these narratives, and the troubling circumstances were discerned from the descriptions, rather than being apparent in the images shown.4. Compassion for physical pain (CPP), which involved people sustaining a physical injury. The injuries were caused by sports and other mishaps and had no moral or social implications. The injuries were not the result of malevolence, and the participants were reassured that the injuries had no long-term implications....5. Control narratives, which involved comparable living, mentally competent people engaged in or discussing how they felt about typical activities under commonplace social circumstances. These circumstances were engaging but not emotion provoking.After each of the narratives, the subjects were asked to discuss how they felt about the protagonist's situation. This part of the study took 2 hrs, and was conducted outside the scanner. For the fMRI portion of the protocol, 5 sec recaps of all 50 scenarios were presented, and the task was to:induce in themselves for each story, as strongly as possible, a similar emotional state to the one they had experienced during the preparation session and to push a button to indicate the strength of the emotion they achieved in the scanner (from 1 to 4...). Participants were asked to report candidly on the strength of their current feelings in the scanner, rather than on the strength of feeling they remembered from the preparation session.OK, so the subjects were first asked to remember how they felt 2 hrs ago, then try to duplicate that feeling, and then report on how they feel now (rather than before). So there's a memory component and a decision component (i.e., to not confuse past feelings with the present). Each trial was sorted post hoc on the strength of the reported emotion, and only the effective trials were included in the analysis.The comparisons of interest were pain (compassion) vs. non-pain (admiration), and emotional responses to other peoples’ social/psychological conditions (AV, CSP) vs. to their physical conditions (AS, CPP). One of the first issues discussed is the recruitment of homeostatic mechanisms when experiencing these social emotions:It is well known that basic emotions such as fear, sadness, and happiness and limited social emotions such as moral indignation engage neural systems concerned with sensing and regulating body function with varying patterns, and it has been hypothesized that among those systems, the insula plays an especially prominent role. It is also known that engagement of social emotions and the consequent feeling for another’s social/psychological situation are described by poets and lay people alike in visceral and bodily terms and in terms of their heightening effect on one’s own self-awareness or consciousness.Basically, people may have visceral responses to the circumstances of others. How do these responses differ across physical vs. psychological situations? For example, admiring a gymnast's skill on the balance beam vs. admiring a student's charity work with Habitat for Humanity? Or feeling compassion for a single mother who loses her job vs. feeling compassion for one who sprains her ankle? Although it's not mentioned in the paper, this idea draws on Antonio Damasio's somatic marker hypothesis (e.g., Damasio, 1996). Perhaps this omission occurred because two of the main regions implicated -- the ventromedial prefrontal cortex (VMPFC) and the amygdala -- were not discussed in the paper [however VMPFC is difficult to image using fMRI because of susceptibility artifacts]. The somatic marker hypothesis is succinctly described by the title of one of Damasio's books: The Feeling of What Happens: Body and Emotion in the Making of Consciousness (1999).Other components in the somatic marker circuit include the insular cortex, a region implicated in interoceptive awareness of bodily states (Craig, 2009), and somatosensory cortices responsive to external stimuli. Because activity in the anterior insula features primarily in the Twitter-warped distortion of the story, I'll start here with the authors' third hypothesis:3. that activation in the anterior insula would peak and dissipate more quickly for CPP than for CSP or varieties of admiration.In a way, this is a trivial prediction, because one can evaluate the sprained ankle narrative more quickly than the job loss scenario. In fact, I will argue below that simple behavioral response time might be a more precise measure of how long it takes to generate the emotion in question than is the hemodynamic response (blood flow changes, measured by the BOLD signal in fMRI) in the insular cortex. One reason for this is because of the significant delay (5-6 sec at least) between initial neural firing and the peak of the hemodynamic response, which is estimated using a procedure that is not trivial for something as complex as an emotional response (for a more detailed discussion of this issue, I recommend this PPT file from Jodi Culham's excellent fMRI 4 Newbies site).Let's start with a simpler example. The figure below shows the averaged hemodynamic response function (HRF) in the primary visual cortex to a series of flashes. The HRF peaks at ~5 sec after the flash, whereas neurons in primary visual cortex fire within 50 msec and drop off shortly thereafter. Thus, the hemodynamic response to even a simple sensory stimulus lags behind neuronal firing by 5 sec.Fig. 2 (Calhoun et al., 1998). Time courses from four regions in the calcarine cortex (Pl-P4) and the averaged response (CIRQ). Amplitude units are normalized to a maximum of one and a baseline of zero.The next example shows the HRFs in occipital regions and the insula while subjects viewed rotating objects. The precise details aren't important here, but note the peak latency for the HRF in the insula is around 6-8 sec, with the later peak for novel objects (compared to repeated objects).Fig 2C (Weigelt et al., 2007). Event-related deconvolved BOLD fMRI responses (GLM parameter estimates averaged across trials and subjects for all voxels in each ROI) reported against time for each of the experimental conditions.That brings us back to Immordino-Yang et al. and the emotional narratives. In the figure below, note that the HRF time course does peak earlier for the CPP condition compared to the others, as predicted. However, the CSP condition rises at the same time, albeit with a later (very broad) peak.Fig. 3 (Immordino-Yang et al., 2009). Event-related averages for the time courses of admiration and compassion in the anterior insula, with standard errors. Units are percentage change in BOLD signal and time in seconds; time courses are not corrected for hemodynamic delay. For display purposes, BOLD data have been linearly interpolated to 1-s resolution. The volume of interest is displayed in pink. Conditions: AV (green): admiration for virtue; AS (yellow): admiration for skill; CSP (blue): compassion for social pain; CPP (red): compassion for physical pain. Note the rapid rise and dissipation of CPP versus the slower and more sustained rise of CSP, AV, and AS.It's critical to note that the onset of a felt emotion is not as easy to determine as the onset of a visual object. Although more detailed methods are in the Supplementary Materials not available as of this writing, it seems that respiration and heart rate data were obtained in 7 of the 13 subjects to help with this. I would say these psychophysiological responses, in concert with the participants' own reaction times for rating their subjective responses, would provide a more accurate measure of how long it takes to feel an emotion than the fMRI data. It's hard to know what an insular HRF of 6 sec vs. 10 sec means when watching a fast-paced movie or reading the CNN news crawl or yes, spending too much time on Twitter. Nonetheless, on the basis of these imprecise latency measures, the authors speculate:If replicated, this finding could have important implications for the role of culture and education in the development and operation of social and moral systems; in order for emotions about the psychological situations of others to be induced and experienced, additional time may be needed for the introspective processing of culturally shaped social knowledge. The rapidity and parallel processing of attention-requiring information, which hallmark the digital age, might reduce the frequency of full experience of such emotions, with potentially negative consequences.And there's your "Twitter is evil" angle.I'll leave you with this final thought: where's the line between admiration and envy, between compassion and schadenfreude? There actually is a recent paper on the Neural Correlates of Envy and Schadenfreude (Takahashi et al., 2009), and for now I'll refer you to this nice summary in Pure Pedantry.Recommended Twitter Reading:Social media threats hyped by science reporting, not science (Ars Technica)Experts say new scientific evidence helpfully justifies massive pre-existing moral prejudice. (Bad Science)For the last time: that "Twitter is Evil" paper is not about Twitter! (Bioephemera)Is Twitter evil? (Cosmic Log at MSNBC - despite the ridiculous headline, it's one of the few popular science articles to talk about the actual study... it even included a figure from the paper)The Neurology of Twitter (The Neurocritic proposes an actual fMRI study of Twitter, complete with predicted results)The Neurology of Twitter, Part 2 (Yet another recap of the media circus, with a time line of certain events)ReferencesCraig AD. How do you feel--now? The anterior insula and human awareness. (2009). Nat Rev Neurosci. 10:59-70.Damasio AR. (1996). The somatic marker hypothesis and the possible functions of the prefrontal cortex. Philos Trans R Soc Lond B Biol Sci. 351:1413-20.Mary Helen Immordino-Yang, Andrea McColl, Hanna Damasio, and Antonio Damasio. (2009). Neural correlates of admiration and compassion. Proceedings of the National Academy of Sciences.... Read more »

Mary Helen Immordino-Yang, Andrea McColl, Hanna Damasio, and Antonio Damasio. (2009) Neural correlates of admiration and compassion. Proceedings of the National Academy of Sciences.

  • January 22, 2009
  • 08:49 PM

When I Get That Feeling, I Need Sexual Sweating

by The Neurocritic in The Neurocritic

Did you know that male "sexual sweat" differs from ordinary sweat? Apparently so, according to a new paper in the Journal of Neuroscience (Zhou & Chen, 2008). Curiously, the article did not cite any references for this, nor did it specify the chemical composition of sexual sweat. Nonetheless, the results of an fMRI experiment suggested that the orbitofrontal cortex and the fusiform region in 20 female participants responded differently when smelling the two substances. How was such a study conducted, you might ask?And here the fun begins...Sweat collection. From 2 d before the experiment until the end of the experiment, 20 heterosexual male donors in a larger study refrained from using deodorant/antiperspirant/scented products, and used scent-free shampoo/conditioner, soap, and lotion provided by the experimenter. They reported to have experience with watching sexually explicit videos, and signed informed consent before participation. Subjects kept a 4" x 4" pad (rayon/polyester for maximum absorbance) in each armpit while they watched 20-min-long video segments intended to produce the emotions of sexual arousal (sexual intercourse between heterosexual couples) and neutrality (educational documentaries), respectively. ... Over the course of the 20 min video segments, donors experienced greater arousal (measured by skin conductance) while watching erotic videos than while watching neutral videos... Three healthy, male nonsmokers (aged 26, 29, and 29 years) were subsequently selected for the current study mainly because of their higher level of the self-reported sexual arousal.How were the female participants selected?We recruited only women for their superior sense of smell and sensitivity to emotional signals. Twenty right-handed females (mean age = 23.4 years) were selected from a group of 42 women on the basis that they reported to have no rhinal disorders or neurological diseases, and that they showed superior olfactory sensitivity to PSP [the putative sex pheromone androstadienone] and PEA [phenyl ethyl alcohol]. They either were in a heterosexual relationship or had been in one within the previous year. They were not on hormone contraceptives, and were tested during the periovulatory phase of their menstrual cycles. ... Subjects were informed that the study was on brain activations to natural compounds. They were blind to the nature of the smells used in the experiment.The scanning was performed while the women were inhaling......the sweat of sexual arousal in comparison with two other social chemosensory compounds (PSP and the sweat of neutrality) and a nonsocial smell [phenyl ethyl alcohol (PEA)].The sweat of neutrality. The sweat of sexual arousal! [plus the two others.] The subjects rated the four inhalants (presented 10 times each) on intensity and pleasantness, as shown below. And the smell of sexual sweat was not particularly pleasant...Figure 1. Mean intensity and pleasantness ratings. There are four types of olfactory stimuli, and SE bars are shown. For intensity, 1 refers to no smell, 2 little smell, 3 moderate smell, 4 quite a bit smell, and 5 strong smell. For pleasantness, 1 refers to very unpleasant, 2 unpleasant, 3 neutral, 4 pleasant, and 5 very pleasant. Sex, Sexual sweat; Neutral, neutral sweat. Sexual sweat and PSP were perceived to be more intense than neutral sweat; PEA was perceived to be more pleasant than sexual sweat and neutral sweat.At the end of the experiment, the participants gave verbal descriptions of the smells. Only one characterized sexual sweat as "sweaty/human." So the women were not [consciously] aware that the odor was obtained from sexually aroused men.The right hypothalamus showed increased activity to sexual sweat relative to alcohol, but so did androstadienone and neutral sweat. The two brain regions that responded more to sexual sweat than to the other odors are illustrated below. The right orbitofrontal cortex is an olfactory region, but the right fusiform gyrus is a high-level visual region. The authors say their fusiform region1 falls in the vicinity of the fusiform face area (FFA) and fusiform body area (FBA). Hmm.Figure 3. a. Coronal view showing an area in the right orbitofrontal cortex (33, 40, –1) activated in the omnibus ANCOVA F test (svc, p less than 0.005). d. Sagittal view showing a region in the right fusiform gyrus (35, –51, –7) activated in the omnibus ANCOVA F test (uncorrected p less than 0.0005, cluster size = 49 mm3).The authors took a giant leap when speculating about visual imagery of faces and bodies:The Talairach coordinates of the fusiform region identified in our experiment fall in the range of the coordinates for FFA and FBA. Such anatomical location likely reflects a recognition of the human quality in the sexual sweat, whose emotional nature may have also contributed to the activation. Considering its functional connectivity to the right hippocampus/ parahippocampal gyrus, the recognition may arise from implicitly associating the sexual sweat with humans based on past experience. The fact that most subjects did not perceive the sexual sweat as human related suggests that the effects we observed occurred at a subconscious level. Implicit face/body visual processing in response to a sexual chemosensory cue? But nothing specific in the hypothalamus or amygdala? That's a hard one to swallow.Footnote1 The FFA and FBA have been dissociated with scanning at high resolution.ReferenceW. Zhou, D. Chen (2008). Encoding Human Sexual Chemosensory Cues in the Orbitofrontal and Fusiform Cortices Journal of Neuroscience, 28 (53), 14416-14421 DOI: 10.1523/JNEUROSCI.3148-08.2008Chemosensory communication of affect and motivation is ubiquitous among animals. In humans, emotional expressions are naturally associated with faces and voices. Whether chemical signals play a role as well has hardly been addressed. Here, we use functional magnetic resonance imaging to show that the right orbitofrontal cortex, right fusiform cortex, and right hypothalamus respond to airborne natural human sexual sweat, indicating that this particular chemosensory compound is encoded holistically in the brain. Our findings provide neural evidence that socioemotional meanings, including the sexual ones, are conveyed in the human sweat.... Read more »

  • March 19, 2009
  • 02:25 PM

Lie To Me on the Autobiographical Implicit Association Test

by The Neurocritic in The Neurocritic

Lie to Me - Season 1 - "Moral Waiver" - Monica Raymund as Ria Torrescourtesy Adam Taylor/FoxLie detection is all the rage with the new TV show based on Paul Ekman's work1 that uses "microexpressions" to detect deception.The use of brain imaging technologies as lie detectors, and the admissibility of data obtained in this fashion as evidence in a court of law, has a high media profile as well - most recently (and notoriously) because of a juvenile-sex-abuse case in San Diego, recounted by Wired Science. The Stanford Center for Law & the Biosciences Blog has sounded the alarm in their post, No Lie MRI being offered as evidence in court:The case is a child protection hearing being conducted in the juvenile court. In brief, and because the details of the case are sealed and of a sensitive nature, the issue is whether a minor has suffered sexual abuse at the hands of a custodial parent and should remain removed from the home. The parent has contracted No Lie MRI and apparently undergone a brain scan... The defense plans to claim the fMRI-based lie detection (or “truth verification”) technology is accurate and generally accepted within the relevant scientific community in part by narrowly defining the relevant community as only those who research and develop fMRI-based lie detection.The Neurocritic weighed in on the overblown nature of these claims three years ago, with Brain Scans and Lie Detection: True or False?, Would I Lie to You?, and More Lies... Damn Lies... But even better, check out the excellent Deception Blog for an updated overview of the field.Given the high cost and dubious accuracy of fMRI technologies -- as well as the questionable accuracy of older EEG and polygraph methods -- there has been some interest in developing faster, easier, more reliable lie detection methods. Ian Sample at the Guardian's Science Blog went with this futuristic headline about the potential use of pupillometry as a routine security screening measure:Homeland Security seeks Bladerunner-style lie detectorDo our eyes betray us when we lie? The US government hopes to find out. . .Under the Small Business Innovation Research programme, the department has asked tech companies to bid for contracts to kick-start research in the area. Such a system, if it works, would undoubtedly be useful at airports and other high-security points.Here's the original SBIR solicitation for applications, which were due in February 2008:TITLE: Assess Ability to use Eye Tracking and Pupil Dilation to Determine Intent to DeceiveDESCRIPTION: Recent government sponsored research is working to produce a new line of flexible physiological and behavioral sensor technologies that are to be available for homeland security applications. These sensors, which must be non-invasive in nature and protect the privacy of the individual(s) involved, will be used to support human centered/behavioral screening processes in a variety of high and low volume venues. Security screening is conducted to evaluate the risk of individuals entering transportation and other critical infrastructure and requires efficient, rapid and accurate examination of a person. Persons involved in or planning to be involved in possible malicious or deceitful acts will show various behavioral or physiological abnormalities. Much of the technology and publications to date have focused on detection of guilty individuals using electrodermal measures. Research into other psychophysiological measures or the mechanisms underlying deception is still in its early stages. Early research has shown that pupil size varies with changes in a person's cognitive processing load. Current but unproven studies suggest that a cognitive decision to deceive or practice deception will result in a increased pupil size due to the greater cognitive processing required in comparison to truthful recall. An assessment study to determine the correlation between Pupillometry (dilation and contraction of the pupil relative to observed stimulus or emotion) and intent to deceive is required.For the ultimate in low-cost methods for lie detection, computerized reaction time tasks take the cake. An article about one of these appeared last year in Psychological Science (Sartori et al., 2008). The task they used is a variant of the Implicit Association Test (IAT) franchise that pits competing response tendencies against each other. Without getting into a lengthy discussion of the IAT, and the debates between its proponents and detractors,2 the autobiographical IAT (aIAT) employed by Sartori et al. ......allows one to evaluate which of two contrasting autobiographical events is true for a given individual. This is accomplished by requiring the respondent to complete two critical blocks of categorization trials, each of which pairs a different potentially autobiographical event with true events. Because pairing of a truly autobiographical event with true events should facilitate responses, the specific pattern of response times (RTs) in the two blocks indicates which autobiographical event is true and which is false.The participants saw different types of sentences and had to classify them as true/false or guilty/innocent. Examples of the different stimuli are listed below.adapted from Table 2 (Sartori et al., 2008).The real trick was in the way these sentence types were matched to response keys. In a series of five blocks of trials, the subjects were told to respond to each sentence as rapidly as possible. Across five experiments (each of which had a different kind of "guilty knowledge"), the order was Block 1: logical discrimination (true/false) - Block 2: initial autobiographical information (guilty/innocent) - Block 3: initial double categorization (false/innocent and true/guilty) - Block 4: reversed autobiographical discrimination (false/true) - Block 5: reversed double categorization (true/innocent and false/guilty). The order of the critical blocks 3 and 5 was counterbalanced across participants (as was the order of 2 and 4, which counterbalanced the response mapping for autobiographical trials accordingly). The key measure was the comparison between RTs to the double categorization trials in Blocks 3 and 5 -- innocent participants were expected to be slower on the "conflict" trials in which true/guilty and false/innocent were matched to the same response key, while guilty participants (who always denied their crimes) were expected to show the opposite pattern, which would reveal they were lying about their innocence.For the mock crime of stealing a CD for example, the results looked like this for the pairings of true/guilty and true/innocent:Fig. 1C (Sartori et al., 2008). For Experiment 2, results are shown for the critical block associating true sentences with guilty sentences and for the critical block associating true sentences with innocent sentences.Because the tests were able to discriminate between true and false events with 91% accuracy, the authors concluded that "the aIAT is an accurate method of detecting concealed knowledge that outperforms currently available lie-detection techniques." However, a brand new paper by Verschuere et al. (2009) has demonstrated that it's easy to fake your results in this aIAT! Oops. What Verschurere and colleagues did was provide the participants with instructions on how to beat the test. Before performing the aIAT a second time, they were told to slow down their responses in the true/guilty mapping condition. And the results for the faking version of the aIAT classified the majority of guilty liars as innocent. Imposing a response deadline, so the subjects had to respond within 1200 msec, did not alter the results.So there you have it. An extremely easy method for faking your results on the aIAT. In the past, The Neurocritic has taken the Human or Alien? test and the Dead or Alive? test. Turns out I'm neither human nor alien, and neither dead nor alive. Read those posts, and then try the tests yourselves.Footnotes1 However, as noted recently by World of Psychology, a paper by Bond (2008) questioned whether Ekman et al. (1991, 1999) omitted data unfavorable to their previously reported lie detection success rate of 73% in some federal agents. 2 The sadly defunct blog Mixing Memory was particularly critical of the IAT:The IAT isn't the only test of implicit "attitudes." . . . However, the IAT is the most popular, and has received a great deal of attention in the popular press, due in large part to a public relations campaign by its authors and the NSF and NIMH. In my mind, giving the IAT so much publicity is the most irresponsible thing I've seen in psychology since I began studying it... While the IAT has been publicized (by its authors!) as a measure of implicit attitudes, and even more, as a measure of implicit prejudice, there is no real evidence that it measures attitudes, much less prejudices. In fact, it's not at all clear what it measures, though the fact that its psychometric properties are pretty well defined at least implies that it measures something. On top of that, the IAT (like all of the other implicit tests) has serious methodological flaws that are currently being discussed in the literature. It's just irresponsible to publicize work, and claim that it does something very particular, when the work is still in the early stages and it's not at all clear what it's actually doing (read paper, or this one, for discussions of some of the problems with the IAT and other measures, including whether they actually measure "attitudes").ReferencesSartori, G., Agosta, S., Zogmaister, C., Ferrara, S.D., & Castiello, U. (2008). How to accurately assess autobiographical events. Psychological Science 19:772–780.Verschuere, B., Prati, V., & Houwer, J. (2009). Cheating the Lie Detector: Faking in the Autobiographical Implicit Association Test. Psychological Science DOI: 10.1111/j.1467-9280.2009.02308.x.Lie to Me - Season 1 - "Moral Waiver" - Kelli Williams as Gillian Foster and Tim Roth as Cal Lightmancourtesy Adam Taylor/Fox... Read more »

  • March 20, 2011
  • 06:30 PM

On M&M'S® and Dog Phobia

by The Neurocritic in The Neurocritic

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

... Read more »

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  

  • October 26, 2009
  • 06:37 AM

Unusual Changes in Sexuality: Case Studies in Neurology

by The Neurocritic in The Neurocritic

Fig. 1 (Currier et al., 1971). Scalp EEG showing sharp wave activity from left anterior temporal region.In the last post we learned a bit about hypergraphia, a compulsion to write that sometimes occurs in those with temporal lobe epilepsy (TLE). According to the late behavioral neurologist Norman Geschwind (reprinted in 2009; also see Devinsky & Schachter, 2009), hypergraphia is one in a cluster of interictal [between seizure] personality traits in some TLE patients1 which can also include religiosity, hypermorality, aggressiveness, clinginess, increased emotionality, and sexual changes (mostly hyposexuality but also other alterations):Hyposexuality is the most common, but other kinds of sexual changes do occur. ... In England, Davies and Morgenstern went out and found, among the temporal lobe epileptics, several other patients who were transvestites. ... I’m sure that the great majority of transvestites don’t have temporal lobe epilepsy, but it’s interesting that for whatever reason it can cause this. Although I’ve seen many women with temporal lobe epilepsy, someone called to my attention a phenomenon that I hadn’t observed before. The last four women I have seen have all been bisexual, which again is a rather striking finding.Sexual behavior preceding (auras) or during (automatisms) seizures is another story. The EEG traces in Fig. 1 above are from an epilepsy patient who experienced "sexual seizures" during which she engaged in somewhat purposeless "pseudointercourse" behavior, with no memory for the event afterward. Although the general consensus is that sexual automatisms are usually associated with seizure foci in the temporal lobes (Mascia et al., 2005), an influential earlier paper insisted the origin of "sexual seizures" was in the frontal lobes (Spencer et al., 1983).Changes in sexuality can also occur after strokes or due to brain tumors. Neurophilosopher Patricia Churchland drew attention to one of these case reports in a New Scientist article on free will and criminal responsibility:In 2003, the Archives of Neurology carried a startling clinical report [Burns & Swerdlow, 2003]. A middle-aged Virginian man with no history of any misdemeanour began to stash child pornography and sexually molest his 8-year-old stepdaughter. Placed in the court system, his sexual behaviour became increasingly compulsive. Eventually, after repeatedly complaining of headaches and vertigo, he was sent for a brain scan. It showed a large but benign tumour in the frontal area of his brain, invading the septum and hypothalmus - regions known to regulate sexual behaviour.After removal of the tumour, his sexual interests returned to normal. Months later, his sexual focus on young girls rekindled, and a new scan revealed that bits of tissue missed in the surgery had grown into a sizeable tumour. Surgery once again restored his behavioural profile to "normal".Figure 1 (Burns & Swerdlow, 2003). MRI scans at the time of initial neurologic evaluation: T1 sagittal (A), contrast-enhanced coronal (B), and contrast-enhanced axial (C) views. In A and B, the tumor mass extends superiorly from the olfactory groove, displacing the right orbitofrontal cortex and distorting the dorsolateral prefrontal cortex.This case raises the issues of diminished capacity and criminal responsibility. The man knew what he was doing was wrong -- intact capacity and moral knowledge -- but he could not inhibit his inappropriate sexual behavior. It's hard to argue against the finding of diminished responsibility when staring at a gigantic brain tumor. But many other examples of impulsive sexual offenses (Langevin, 2006) aren't nearly as obvious (e.g. after head injuries when the damage might not be visible on an MRI scan). How does society deal with them?A key factor is a change in behavior...Multidirectional disorders of sexual drive in a case of brain tumourThe next report is from Poland (Lesniak et al., 1972 -- before the days of MRI or even CT scans). This case history is even more disturbing and involves greater criminal offenses than the patient of Burns and Swerdlow (2003).A description and analysis of various disorders of sexual impulse are presented. They occurred gradually between the ages of 56 and 60 years in a man previously in good health. The disorders were as follows: harlotry, incestuous intercourse with his under-age daughter [used physical violence and threatened to kill her if she told], sodomy, hetero- and homosexual pedophilia, masochism [he demanded that his wife beat him with a club] with some symptoms of sadism, coprolalia and exhibitionism. [Also bestiality with cows and calves.] Pedophilia and exhibitionism [he fancied wearing a red ribbon around his exposed penis] were the counts of the man’s indictment. After twice-repeated forensic and psychiatric examination and observation, sexual psychopathy and male climacteric were also recognized; and the defendant was acknowledged to be responsible. In the course of further examination, the psychoorganic syndrome with symptoms of moria was recognized clinically. Further specialist examinations, especially by X-ray (pneumoencephalography) showed the presence of neoplasm (probably benign glioma or meningioma) situated at the basal paracentral part of the right forehead lobe [right orbitofrontal cortex again]. Its presence being acknowledged, the defendant was found irresponsible; due precautions and eventual neurosurgical treatment were proposed. It has been stressed that the appearance of the above disorders, especially in view of the age of the subject, must lead one to suspect an organic origin.During the trial (reminiscent of the proceedings against serial child killer and cannibal Albert Fish), expert witnesses for the prosecution found nothing organically wrong, and declared the defendant “at the moment of committing the criminal acts he was charged with, had retained the ability to recognize the significance of these acts, whereas his ability to control his acts had been slightly restricted”. The defendant was found guilty, the defense appealed and a retrial was granted. He was placed under observation for 2 months at the Psychiatric Clinic in Cracow, when the authors became involved in his case:The neurological examination revealed a considerable bilateral impairment of smell [a tell-tale sign of bilateral orbitofrontal damage] and a marked inequality of the reflexes of... Read more »

  • March 15, 2009
  • 12:52 AM

I Know What You Sweated Last Summer

by The Neurocritic in The Neurocritic

From the authors who first brought you "sexual sweat" (Zhou & Chen, 2008)...Be afraid... be very afraid and prepare yourself for the sequel: "FEARFUL SWEAT" (Zhou & Chen, 2009)!!!In case you didn't know that "sexual sweat" (collected from men watching porn) differs from ordinary sweat, the results of an fMRI experiment suggested that the orbitofrontal cortex and the fusiform region in 20 female participants responded differently when smelling the two substances (Zhou & Chen, 2008). However, we don't know anything specific about the unique chemical composition of sweat obtained from sexually aroused men, and why it resulted in differential brain activity in women who could not identify the odor as "sweaty/human" (see When I Get That Feeling, I Need Sexual Sweating).Nonetheless, in the present study Zhou and Chen (2009) wanted to determine the effects of another putative chemosensory signal on the perception of emotional expressions in faces. Specifically, as they explain below......we conducted two experiments focused on the effect of a fear-related chemosignal (sweat collected from donors viewing horror videos) in an emotion-identification task. We used the same type of olfactory stimuli (emotional sweat collected on gauze pads and gauze pads with no sweat) throughout, but varied the effectiveness of the visual input by varying the ambiguity of the facial emotions (from somewhat happy to ambiguous to somewhat fearful). Our manipulation of ambiguity was achieved through morphing between happy and fearful faces [as shown in Fig. 1a].Fig. 1a (Zhou & Chen, 2009). Examples of the morphed faces of two actors. For each actor, we selected seven morphs, ranging from somewhat happy to somewhat fearful. These faces were judged to be fearful 20% to 80% of the time in our pilot experiment, in the absence of any olfactory stimuli. Specifically, the Level 4 morph for each actor was the most ambiguous, judged to be fearful in the pilot study 45% to 55% of the time. And what about the olfactory stimuli obtained from the male sweat donors?On the day of each session, they wore next to their skin a new T-shirt (provided by the experimenter), to prevent odor contamination by their regular clothes. During each session, they kept a 4- x 4-in. pad (rayon-polyester blend for maximum absorbance) under each armpit while they watched each of three 20-min video segments intended to produce the emotions of fear (horror movies), happiness (slapstick comedies), and neutrality, respectively. Different videos were shown in each session. During the videos, participants’ heart rate was recorded... After watching each video, the donors rated how angry, fearful, happy, neutral, and sad they felt during the video, using a 100-mm visual analog scale. From each donor, we selected the pads worn during the 20-min videos that elicited the highest level of self-reported happy feelings and the highest level of self-reported fearful feelings. So the 48 young female subjects (mean age 19.6 years) viewed the various faces while exposed to different olfactory stimuli, and decided whether they were happy or fearful. Results indicated that on average they were significantly more likely to identify the most ambiguous morph as fearful when smelling the fearful sweat relative to the control condition (which, unfortunately, was a rayon-polyester pad with no sweat). Although the likelihood of identifying an ambiguous face as fearful did not differ between the happy sweat and control conditions, there was no direct statistical comparison between the two sweat conditions, which would seem to be a problem.adapted from Fig. 2b (Zhou & Chen, 2009). Nevertheless, there was some evidence that male horror movie sweat was able to bias the women towards viewing an ambiguous face as fearful, and this was not due to the pleasantness (or lack thereof) or intensity of the olfactory stimulus. I'd be curious to see how the "sweat of neutrality" and the "sweat of sexual arousal" [as identified by Zhou & Chen, 2008) in their earlier study] would influence emotion recognition judgments...ReferencesZhou W, Chen D. (2008). Encoding Human Sexual Chemosensory Cues in the Orbitofrontal and Fusiform Cortices. Journal of Neuroscience, 28 (53), 14416-14421.Zhou, W., & Chen, D. (2009). Fear-Related Chemosignals Modulate Recognition of Fear in Ambiguous Facial Expressions. Psychological Science, 20 (2), 177-183. DOI: 10.1111/j.1467-9280.2009.02263.xIntegrating emotional cues from different senses is critical for adaptive behavior. Much of the evidence on cross-modal perception of emotions has come from studies of vision and audition. This research has shown that an emotion signaled by one sense modulates how the same emotion is perceived in another sense, especially when the input to the latter sense is ambiguous. We tested whether olfaction causes similar sensory modulation of emotion perception. In two experiments, the chemosignal of fearful sweat biased women toward interpreting ambiguous expressions as more fearful, but had no effect when the facial emotion was more discernible. Our findings provide direct behavioral evidence that social chemosignals can communicate emotions and demonstrate that fear-related chemosignals modulate humans’ visual emotion perception in an emotion-specific way—an effect that has been hitherto unsuspected.Bonus! See sensory psychologist and olfactory specialist Avery Gilbert's take on these two studies in Basic Instinct: The Smell of Fear and Sex.TAG body spray for sick cats. "This spray is definitely not for me."... Read more »

  • August 30, 2010
  • 12:58 PM

Ketamine for Depression: Yay or Neigh?

by The Neurocritic in The Neurocritic

Venn diagram of psychoactive drugs [click for larger image]This post is part of a Nature Blog Focus on hallucinogenic drugs in medicine and mental health, inspired by a recent Nature Reviews Neuroscience paper, The neurobiology of psychedelic drugs: implications for the treatment of mood disorders, by Franz Vollenweider & Michael Kometer. This article will be available, open-access, until September 23. For more information on this Blog Focus, including a Table of Contents, please visit The Great Beyond.The secret history of psychedelic psychiatry is discussed over at Neurophilosophy. Neuroskeptic covers Serotonin, Psychedelics and Depression while Mind Hacks provides a personal look at yagé in Visions of a psychedelic future.Veterinary Anesthetic, Club Drug, or Antidepressant?Club drug "Special K" (aka ketamine) is stepping out of the laser light into the broad daylight of mainstream psychiatry with the publication of a new review article by Vollenweider and Kometer (2010). Long used to anesthetize animals (and children), ketamine was classified as a "dissociative anesthetic" by Domino et al. (1965) for its combined effects of sedation/analgesia and hallucinations. Domino (2010) recently revisited his classic paper, which reported on a study in 20 volunteers incarcerated at the Jackson Prison in Michigan:The first human was given ketamine in an intravenous subanesthetic dose on August 3, 1964. Guenter [Corssen, M.D.] and I gradually increased the dose from no effect, to conscious but “spaced out,” and finally to enough for general anesthesia. Our findings were remarkable! The overall incidence of side effects was about one out of three volunteers. Frank emergence delirium was minimal. Most of our subjects described strange experiences like a feeling of floating in outer space and having no feeling in their arms or legs. The ego death of the "K hole" can be a terrifying experience for some ("I ceased to exist") or transformative for others ("I witnessed myself as a part of the universal collective of strange energy")1. In their Nature Reviews Neuroscience opinion piece, Vollenweider and Kometer considered ketamine a psychedelic, along with the traditional hallucinogens such as LSD, psilocybin, and mescaline. They noted that both classes of drugs may have psychotherapeutic effects through actions on the excitatory glutamate neurotransmitter system.Ketamine is an antagonist of the glutamate NMDA receptor and is thought to work by blocking NMDA receptors on inhibitory GABA-containing interneurons, ultimately promoting glutamate release. In a scientific tour de force, Li and colleagues (2010) demonstrated that the mTOR (mammalian target of rapamycin) protein kinase pathway is rapidly activated by ketamine. This sets off a cascade of events including the formation of new synapses on dendritic spines. Using a combination of cellular, molecular, electrophysiological, behavioral, and phamacological techniques, ketamine was shown to exhibit antidepressant properties in animal models of depression and anxiety, perhaps via rapid induction of synaptic plasticity in the medial prefrontal cortex (PFC). Regions of the medial PFC in humans, particularly the ventral anterior cingulate cortex, have been implicated in the pathophysiology of major depression.Human clinical trials of ketamine as a rapidly acting antidepressant aren't especially new. A randomized, double-blind study in 2000 involved administration of saline or a single subanesthetic dose of ketamine (0.5 mg/kg intraveneously) to nine depressed patients, seven of whom completed the trial (Berman et al., 2000). Within 72 hrs, amelioration of depressive symptoms was observed. Half of the treated patients showed a 50% or greater improvement in depression scores. However, these therapeutic effects weren't very long-lasting, returning to baseline levels in 1-2 weeks. In a larger study, 18 patients with major depression participated in a similar double-blind cross-over design where they received the 0.5 mg/kg dose of ketamine and placebo one week apart (Zarate et al., 2006). The patients were rated at baseline and at 40, 80, 110, and 230 minutes and 1, 2, 3, and 7 days post-infusion on a number of clinical scales, including the Hamilton Depression Rating Scale (HDRS), the Brief Psychiatric Rating Scale (BPRS) positive symptoms subscale, and the Young Mania Rating Scale (YMRS).The primary outcome measure was change in HDRS score, shown in Figure 2 below (top graph). Significant improvements began at the 110 min time point. Scores declined further from 1-3 days and remained below placebo levels for 7 days. However, unusual experiences were noted at 40 min, with substantial increases in scores for psychosis-like and mania-like symptoms. Other adverse events associated with ketamine included......perceptual disturbances, confusion, elevations in blood pressure, euphoria, dizziness, and increased libido. ... The majority of these adverse effects ceased within 80 minutes after the infusion. In no case did euphoria [YMRS] or derealization/depersonalization [BPRS] persist beyond 110 minutes (Figure 2, middle and bottom graphs).Figure 2 (Zarate et al., 2006). Change in the 21-item HDRS, BPRS positive symptoms subscale, and YMRS scores over 1 week (n=18). Values are expressed as generalized least squares means and standard errors for the completer analysis. * indicates PSo here we have several research groups that say yay! to ketamine as an antidepressant. Are there any naysayers?Although the immediate onset of symptom amelioration gives ketamine a substantial advantage over traditional antidepressants (which take 4-6 weeks to work), there are definite limitations (Tsai, 2007). Drawbacks include the possibility of ketamine-induced psychosis (Javitt, 2010), limited duration of effectiveness (aan het Rot et al., 2010), potential long-term deleterious effects such as white matter abnormalities (Liao et al., 2010), and an inab... Read more »

  • September 14, 2009
  • 08:05 AM

Great and Desperate Cures for Addiction

by The Neurocritic in The Neurocritic

《Chinese Journal of Drug Dependence》1999-04Does anyone know what aerosol bioelectricity is?? And why it might be used to treat heroin addiction? The entire literature seems to be in Chinese. I came across that particular paper while searching for others, specifically reports on ablative psychosurgery1 for the treatment of opiate addiction in China (Gao et al., 2003 is the first in English). Hence, the title of the present post is a reference to the book by Elliot Valenstein, Great and Desperate Cures: The Rise and Decline of Psychosurgery and Other Radical Treatments for Mental Illness.Are there other "unusual" Chinese treatments for addiction, beyond what might be expected (e.g., acupuncture and traditional medicine)? Tetrodotoxin (TTX), a neurotoxin found in puffer fish, is a worthy runner up to aerosol bioelectricity. TTX inhibits action potentials by blocking voltage-dependent sodium channels. It has been tested as a treatment for severe cancer pain, which motivated Shi and colleagues (2009) to compare low dose TTX to placebo in abstinent addicts. After watching a heroin-related video, the group receiving TTX reported lower levels of craving and anxiety, without alterations in heart rate or blood pressure. However, these acute results were from a single session with no long-term follow up.Although Chinese treatments for internet addiction are getting all the headlines these days, drug addiction is actually a much more serious problem. In their review of the literature, Tang et al. (2006) inform us that:Historically, China has had extraordinarily high rates of opiate dependence. These rates declined drastically following the 1949 revolution; however, opiate abuse has re-emerged in the late 1980's and has spread quickly since then. ... The number of registered addicts in 2004 was 1.14 million (more than 75% of them heroin addicts), but the actual number is probably far higher. Opiate abuse contributes substantially to the spread of HIV/AIDS in China, with intravenous drug use the most prevalent route of transmission (51.2%). Currently, the main treatments for opiate dependence in China include short-term detoxification with opiate agonists or non-opiate agents, such as clonidine or lofexidine [alpha-2 adrenergic drugs that inhibit norepinephrine release]; Chinese herbal medicine and traditional non-medication treatments are also used. Methadone maintenance treatment (MMT) has not been officially approved by the Chinese government for widespread implementation, but some pilot studies are currently underway.Which brings us back to neurosurgery. But before discussing the results of Gao et al., a quick review. In the last post, we learned about a new and less desperate cure, the application of Deep Brain Stimulation for Severe Alcoholism. The target region in this small clinical trial (n=3) was the nucleus accumbens (NAcc), which has been called a "pleasure center" and "hedonic hot spot" that responds to food and pharmaceutical and financial and sexual rewards. The idea behind NAcc DBS was to reduce alcohol craving and "incentive sensitization" in severely impaired patients who had failed multiple treatments (Heinze et al., 2009). The researchers drew upon the experimental and theoretical work of Berridge and colleagues (2009) distinguishing between the "wanting" (incentive salience) and "liking" (hedonic impact) aspects of reward:Usually a brain ‘likes’ the rewards that it ‘wants’. But sometimes it may just ‘want’ them. Research has established that ‘liking’ and ‘wanting’ rewards are dissociable both psychologically and neurobiologically. By ‘wanting’, we mean incentive salience, a type of incentive motivation that promotes approach toward and consumption of rewards, and which has distinct psychological and neurobiological features."Liking" has been strongly linked to endogenous opioid systems in the NAcc and ventral pallidum [part of the globus pallidus] as shown below.2From Fig. 1 (Berridge et al., 2009). Forebrain hedonic hotspots in nucleus accumbens shell and in ventral pallidum where mu opioid agonist microinjections cause amplification of ‘liking’ reactions to sweetness. Red/yellow indicates greatest amplification of ‘liking’ for the sensory pleasure.In contrast, "wanting" has been most strongly associated with dopamine in the NAcc, but in reality......brain substrates for ‘wanting’ are more widely distributed and more easily activated than substrates for ‘liking’. Neurochemical ‘wanting’ mechanisms are more numerous and diverse in both neurochemical and neuroanatomical domains... In addition to opioid systems, dopamine and dopamine interactions with corticolimbic glutamate and other neurochemical systems activate incentive salience ‘wanting’. Pharmacological manipulations of some of those systems can readily alter ‘wanting’ without changing ‘liking’. For example, suppression of endogenous dopamine neurotransmission reduces ‘wanting’ but not ‘liking’.Addiction is conceived as a process by which drugs of abuse produce neural sensitization and compulsive "wanting" even in the absence of "liking". With this literature in mind, Gao et al. (2003) wished to:...explore a new way of treating drug addiction by ablating the NAcc... using stereotactic surgery, blocking the mesocorticolimbic dopamine circuit, alleviating craving for drugs and lowering the relapse rate after detoxification. On the basis of animal experiments, stereotactic surgery was performed in 28 patients by making a lesion in the NAcc bilaterally to treat opiate dr... Read more »

  • May 12, 2010
  • 08:10 AM


by The Neurocritic in The Neurocritic

"Head-wound Hank", from Geek Orthodox.The 19th century archive of The Lancet1 is filled with simply delightful case reports. Who can resist the allure of early plastic surgery failures, such as RHINOPLASTIC OPERATION, PERFORMED BY M. LISFRANC, FOLLOWED BY DEATH? Or how about a Case of Local Tubercular Deposit on the Surface of the Brain, presented by Robert Dunn, Esq.? Finally, the tragic History of a Case of Hydrophobia, treated at the Hotel Dieu at Paris, by an injection of water into the veins did not end well (through no fault of R. Magendie, of course):2 It results from the history of this case, that a disease, which exhibited all the characters of hydrophobia, ceased by the introduction of a pint* of warm water into the veins; that the patient survived this introduction eight days: that no accident appeared to follow from it; and that the death of the patient appears to have been caused by a local disease, which was wholly unconnected with the hydrophobia, and the new mode of treatment.* The pint of Paris contains 48 cubic inches. -ED.In 1828, Dr. Sewall (Professor of Anatomy in the Colombian College, D.C.) reported on two of his cases. They are not for the faint of heart. A warning for political incorrectness is also warranted here.CASE 1. In February 1827, W. Brown, a coloured man, aged fifty years, in encountering with another individual, received a severe blow on the right side of the head with a sharp spade. When Dr. Sewall arrived, which was only a few minutes after the accident, he found him bleeding profusely, and much exhausted from the loss of blood. Though not insensible, he had lost his reason, and did not know how he came by the injury. There was a deep wound dividing the integuments, the whole of the temporal muscle, penetrating the cavity of the cranium, and extending horizontally, from an inch above the external angular process of the frontal bone, through the parietal bone just above the squamous suture, forming a fissure of three inches in length. The lower portion of bone was considerably depressed, and the two edges separated about half an inch. Two branches of the temporal artery were taken up; when, on a more critical examination, it was ascertained that the dura mater was divided for an inch in extent...OK, so the patient really did have a 3 inch crack in his skull with brain matter oozing out. Mr. Brown was treated by Dr. Sewall ("dressings were applied"). When pus was coming from the gaping wound, there was swelling followed by sloughing (apparently). Then bits of brain were scooped away with a spatula. Lovely.Although he suffered from severe headaches, Mr. Brown was declared none the worse for the wear:For about ten days after the accident, the patient complained of constant, and sometimes of severe, pain in the head; and on one occasion was affected with a slight spasm of the muscles of the face, neck, and extremities. The wound healed, and in six weeks the patient was quite well. He subsequently followed his occupation, that of scavenger, and did not manifest any deviation in the functions either of body or mind from their ordinary healthy condition.The bar was probably set pretty low for what was considered an "ordinary healthy condition" for a "coloured" man who worked as a scavenger in 1827...The second case was of a five year old boy who was kicked in the head by a horse. No race was specified, so we'll assume he was white. More oozing and scooping of brain:CASE 2. September 18th, 1827, Lewis Poole, aged five years, while playing in the street, was kicked by a horse, and taken up in a state of insensibility. Dr. Sewall arrived a quarter of an hour after the accident, and found a semicircular wound in the integuments of the head, and, corresponding with this, a large fissure in the frontal and parietal bones, about three inches above the external angle of the right eye. Through this fissure a portion of brain protruded, somewhat larger than a walnut, and was composed both of cortical [gray] and medullary [white] matter, which were easily distinguished. This was so far separated from the parts beneath, as to be removed without any violence.Once again we're informed of the patient's full recovery, but only after much unpleasantness. He was bled to the point of unconsciousness initially and then given a powerful and toxic emetic for two weeks straight:Particular circumstances prevented the subsequent use of the lancet; but he was purged actively and daily for two weeks, and the pulse kept down by nauseating doses of the tartate of antimony. Extensive suppuration came on, with a copious discharge of pus; the wound gradually healed, and in about five weeks the child was quite well. He has since remained in perfect health.I wonder for how long that lasted, since Antimony Potassium Tartate is considered a dangerous good (.doc). Inhalation can cause irritation, sore throat, coughing, and shortness of breath. Eye or skin contact causes irritation, redness, and pain. Ironically, the recommended treatment after swallowing this compound is to induce vomiting immediately. The long-term consequences of antimony poisoning are not likely to be conducive to perfect health. Neurosurgical care has certainly come a long way since 1827.Footnotes1 Now on Facebook and Twitter! Keeping up with the 21st century.2 It probably wasn't his fault if the patient was really infected with the rabies virus (aka hydrophobia).ReferenceDr. Sewall (1828). CASES OF INJURY OF THE HEAD, ACCOMPANIED BY LOSS OF BRAIN. The Lancet, 10 (265) DOI: 10.1016/S0140-6736(02)98130-4
... Read more »

  • March 26, 2011
  • 07:04 PM

Pharmacological Misinformation Foisted on Unsuspecting Public

by The Neurocritic in The Neurocritic

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  

  • May 11, 2011
  • 02:59 PM

Revisiting Depression's Cognitive Downside

by The Neurocritic in The Neurocritic

Depression, by h.koppdelaneyIs depression actually good for you?Experts now believe that mild to moderate depression may be good for us – and even help us live longer. Rebecca Hardy explains how to reap the benefitsWe constantly hear how depression is blighting our lives, but some experts have an interesting, if controversial, theory: depression can be "good for us", or at least a force for good in our lives.Is this the start of a new Negative Psychology1 movement? Let's all seek out personal tragedy, sadness, insomnia, and a profound sense of failure and hopelessness, because it's good for us!!Last year, author and blogger Jonah Lehrer had a lengthy (and controversial) essay in the New York Times Magazine on Depression's Upside. The main idea, that depression has cognitive and evolutionary advantages, was largely based on a review paper by Andrews and Thomson (2009). In it, they put forth the analytical rumination hypothesis: depression is an evolved response to complex problems, and focusing on them to the exclusion of everything else is beneficial.In response, The Neurocritic was motivated to write about Depression's Cognitive Downside:On the contrary, numerous papers have shown that impairments in cognitive processes such as executive control, attention, and memory persist after a depressed person has recovered (Andersson et al., 2010; Baune et al., 2010; Hammar et al., 2009). In actively depressed patients, Baune and colleagues (2010) found impairments in all domains tested: immediate memory, visuospatial construction, language, attention, and delayed memory. These deficits can contribute to lower social and occupational functioning and a diminished quality of life. In addition, depression can be associated with declines in problem solving abilities on neuropsychological tests such as the Wisconsin Card Sorting Test and the Tower of London test.Now, a new paper by von Helversen et al. (2011) has claimed that depression is good for decision making. Lehrer wrote about this study as support for the analytical rumination hypothesis in Does Depression Help Us Think Better?Here’s where things get interesting: depressed patients approximated the optimal strategy [for hiring the best applicant in a simulated job search] much more closely than non-depressed participants did. The main problem with healthy subjects is that they proved lazy, unwilling to search through enough applicants. Those with depression, on the other hand, were much more willing to keep on considering alternatives, which is why they performed far better on the task. While this study comes with many caveats, it remains an interesting demonstration that depression, at least in specific situations, seems to enhance our analytical skills, making us better at focusing on social dilemmas.Participants in the study were 37 inpatients diagnosed with major depression upon admission to the hospital (10 of whom were omitted "due to technical difficulties with the choice task"). The 27 remaining patients were classified as either "depressed" (n=15) or "recovered" (n=12) based on improved scores on the Patient Health Questionnaire (PHQ-D) between admission and testing (which was a mean of 6.25 days -- that seems like an incredibly rapid remission, which makes one wonder about the actual severity and why they were admitted in the first place). Only half of the patients, both depressed and recovered, were on antidepressants (none were on other medications), which seems unusual for patients who may have been suicidal. Perhaps the criteria for admission to the psych ward in Germany are different than they are in the U.S. and Canada. The still-depressed patients were in hospital an average of 4.20 days when they were tested (which was not significantly different from the recovered patients). It wasn't completely clear if any of the patients were already on antidepressants, or whether the pharmacological treatment started during hospitalization for those on meds.2 The paper did not state whether any of the depressed patients had another diagnosis, such as an anxiety disorder of any sort (co-morbidity is common).Mean scores on the Beck Depression Inventory (BDI) were higher in the Depressed group (29.13) than in the Recovered group (16.67) or the Control participants (6.63), who also differed from each other. BDI scores of 14–19 are considered mildly depressed, 20–28 moderately depressed, and 29–63 severely depressed. So patients in the Depressed group scored at the low end of severely depressed, the Recovered participants were mildly depressed, and the Controls (n=27) were not depressed at all.The task administered to all participants is called the "Secretary Problem":The sequential decision-making task consisted of playing 30 games of a secretary-type problem. Each game challenged participants to find the best candidate for a job out of a sequence of 40 applicants. The 40 applicants were presented one after another, in a random sequence. After an applicant was presented, participants needed to decide whether they would accept the applicant or not. If they accepted the applicant, the game concluded and the next game started. If they rejected the applicant, the next applicant was presented. Rejected applicants could not be chosen later in that game. Information about the current candidate included their relative ranking compared to the candidates that came before, but not their absolute ranking. Points were awarded based on the absolute ranking of the candidate chosen on each round. If a participant didn't make a choice until the end of the sequence, they were forced to accept the final candidate. So it seems that an indecisive person would be more likely to continue the search for a longer time...Results showed there was a trend in that direction (p=.08): search length was 23.37 for Depressed, 16.87 for Recovered, and 17.96 for Controls. Performance goals for each round (how good a candidate would have to be in order to be chosen) and the relative rank of candidates did not differ between groups. However, the number of points awarded for each game did differ (p=.02): 37.67 for Depressed, 35.50 for Recovered, and 35.17 for Controls. A computational model suggested that the Depressed group had higher internal thresholds for the first and second, but not the third threshold. A caveat from the authors:However, although we found that depressed participants had higher thresholds than did nondepressed participants, we did not find significant differences in the self-reported goals of participants. This suggests that differences in behavior may not result from participants’ conscious effort to perform well. Thus, increases in thresholds could be an artifact stemming from greater persistence and the inability to disengage from a task.What does this mean? That severely depressed inpatients should be given the task of selecting job candidates for Fortune 500 companies, while they are so impaired otherwise that they are unable to work or function socially? Is a very modest performance benefit in a laboratory sequential decision making task worth the pain and suffering of severe depression, along with its concomitant deficits in other cognitive domains?... Read more »

  • September 9, 2009
  • 01:55 PM

Deep Brain Stimulation for Severe Alcoholism

by The Neurocritic in The Neurocritic

Deep brain stimulation (DBS) for treatment-refractory psychiatric disorders has been gaining in popularity. The procedure involves neurosurgery to implant stimulating electrodes aimed at a target region inside the brain. It works using the same sort of pacemaker-like device used for DBS in Parkinson's disease, which has been remarkably successful at alleviating symptoms. DBS as a treatment for neurological disorders such as Parkinson's, primary generalised dystonia, atypical tremor syndromes, cluster headache, phantom limb pain, and epilepsy has been mostly unobjectionable.However, the Neurological/Psychiatric Divide makes DBS for mental illnesses such as major depression and obsessive compulsive disorder more ethically problematic. A new paper in the Archives of General Psychiatry (Rabins et al., 2009)1 summarizes a consensus conference held on this and related issues (such as human subjects protection and the design of clinical trials). A list of 16 guidelines was issued, which included the following:2. Deep brain stimulation for disorders of MBT [Mood, Behavior, and Thought] is at an early proof-of-principle stage and must be considered investigational. Currently, no single target has been validated or demonstrated to be superior to others in any disorder of MBT. Therefore, it is premature to rule out the study of new implantation sites that have a good scientific rationale...3. The comparative efficacy and safety of DBS vs other treatments, including ablative surgery, should be studied further. Such studies are ethical and scientifically necessary.4. Given its history, neurosurgical intervention for disorders of MBT is a socially and culturally sensitive area of research and practice. Therefore, DBS for disorders of MBT should be studied in carefully designed trials and should be performed only at expert centers that are participating in such trials and that adhere to the highest scientific, clinical, and ethical standards.. . .12. The consent process should include discussion of what is and is not known about long-term consequences of DBS. Potential adverse outcomes include potentially limiting participation in future research, inability to use certain other treatments, and an inability to undergo certain tests. ... Additionally, the consent process should state explicitly that, even with positive outcomes, DBS for disorders of MBT is unlikely by itself to improve all aspects of the individual's mood, function, and interpersonal relationships: DBS is only one aspect of a comprehensive treatment program.The specific indications mentioned by Rabins and his 18 co-authors were major depression, obsessive-compulsive disorder, and Tourette syndrome. Severe alcohol dependence was not included as one of the disorders. DBS for alcoholism sounds rather drastic, doesn't it? Nonetheless, a German research group led by Hans-Jochen Heinze (et al., 2009) was not deterred. They recently reported results from 3 male patients2 with severe and refractory alcohol dependence as part of a small clinical trial that will ultimately include 10 patients.Inclusion criteria are: male gender, age 25–60 years, finished detoxification and subsequent period of abstinence of at least 2 weeks. Moreover, the patients are required to have demonstrated treatment failures of at least two inpatient programs of at least 6 month duration, failure of anti-craving substances (e.g., acamprosate, naltrexone), failure of community and self-help programs. ... Patients are excluded, if they meet any of the following criteria: seizures during the detoxification phase, high score on neuroticism scales, antisocial personality disorder, clinically significant impairments on a neuropsychological test battery Further exclusion criteria were circumscribed brain damage or marked atrophy on MRI, alcohol-related personality change, and use of additional addictive substances.The target region? The nucleus accumbens (NAcc), the “Universal Addiction Site” -- an oversimplification, they admit, but still, the NAcc is......a central place in orchestrating the events related to the “wanting” [Robinson & Berridge, 2008] of alcohol on the one hand and drug-induced neural sensitization on the other hand. Anatomically, the NAcc receives inputs from the prefrontal cortex on the one hand and limbic structures such as the hippocampus and amygdala on the other. This circuitry allows for the integration of contextual information arising from hippocampus and emotional information coming from the amygdala with cognitive information supplied by the PFC in the selection of goal-directed behaviors in general and behaviors related to drug “wanting” in particular, which is why the NAcc has been called a limbic-motor interface.Since anatomical information was not illustrated in the current paper, a figure from the earlier work of Schlaepfer et al., (2007) is presented below.The topographical location of the nucleus accumbens in relation to other brain structures on a horizontal plane 3 mm below the AC-PC plane (Schlaepfer et al., 2007).That protocol was designed to relieve anhedonia (inability to experience pleasure from normally pleasurable life events) in major depression. Why not stimulate the "pleasure center" when you're feeling blue? Extensive research in animals and humans has demonstrated "hedonic hot spots" (Pecina et al., 2006) [or "liking" of pleasant sensory experiences] in the NAcc that respond to food and pharmaceutical and financial and sexual rewards.But what are the procedures for targeting the same region to reduce reward and pleasure? Well, we don't know from reading Heinze et al. (2009): "Details regarding the stimulation protocols in the different patients can be found elsewhere" [insert citation of an in press paper that is not online yet]. Details on the "clinical aspects" are pretty sparse and the focus is on the "basic science aspects" (electrophysiological recording and cognitive task performance to assess action monitoring and the salience of drug-related cues).Was the DBS treatment effective? All patients had failed multiple detox treatments, withdrawal therapies, and drug trials (acamp... Read more »

Rabins, P. et al. (2009) Scientific and Ethical Issues Related to Deep Brain Stimulation for Disorders of Mood, Behavior, and Thought . Archives of General Psychiatry, 66(9), 931-937. info:/

  • November 15, 2009
  • 12:19 AM

I Feel Your Pain, I REALLY Do: Synaesthesia for Another's Pain

by The Neurocritic in The Neurocritic

"I feel your pain"Empathy for another person's pain is a hot topic of study in the glamorous field of social cognitive neuroscience. The capacity for empathy supposedly involves mirror neurons, those media darlings of The Young, [The Not-So-Young], and The Neuro:A mirror neuron is a neuron that fires both when an animal acts and when the animal observes the same action performed by another. Thus, the neuron "mirrors" the behavior of the other, as though the observer were itself acting.These magical cells have even inspired famous neuroscientists to utter ridiculous hyperbole:The mirror neurons, it would seem, dissolve the barrier between self and others. I call them "empathy neurons" or "Dalai Llama neurons".-- MIRROR EURONS AND THE BRAIN IN THE VAT by V.S. Ramachandran Synesthesia for pain, a newly described syndrome, goes one step further (Fitzgibbon et al., 2009):In synaesthesia for pain a person not only empathises with another's pain but experiences the observed or imagined pain as if it was their own. Neural mechanisms potentially involved in synaesthesia for pain include “mirror systems”: neural systems active both when observing an action, or experiencing an emotion or sensation and when executing the same action, or personally experiencing the same emotion or sensation. For example, we may know that someone is in pain in part because observation activates similar neural networks as if we were experiencing that pain ourselves. We propose that synaesthesia for pain may be the result of painful and/or traumatic experiences causing disinhibition in the mirror system underlying empathy for pain.And what is synesthesia, exactly? According to Edward M. Hubbard's website, SYNESTHESIA can be defined unusual conscious experience, in which stimulation of one sensory modality leads to a sensory experience in a second, unstimulated sensory modality. For example, seeing letters might lead some people to see colors. Others report that the days of the week or months of the year are arranged like a map in space. Still others report that hearing voices or music cause them to see colors, or that hearing words makes them taste fact, almost any sensory modality can be involved in synesthesia.One of the more common forms of synesthesia (illustrated above) is grapheme-color synesthesia, where numbers and letters are consistently associated with specific colors (Ward et al., 2005). A more unusual form is lexical-gustatory synesthesia, in which spoken and written words elicit specific taste sensations that remain constant (Ward & Simner, 2003). For instance, Tony Blair tastes like desiccated coconut.According to the recent review of the literature by Fitzgibbon et al. (2009), amputees with phantom limb pain comprise the vast majority of those with synaesthesia for pain:Known Characteristics of Synaesthesia for Pain in a Sample of Amputees with Phantom PainBrought on by viewing others in pain and/or observing pain on the television and in movies.Brought on both when observed pain matches that of the amputated site and/or any general painBrought on regardless of the identity of the observed person in pain, i.e. can be a loved one or a stranger.The experience is similar to the experiences of phantom pain, for example, described as a short sudden ‘electric shock’.Experienced in the phantom limb and/or stump.The researchers propose that:pain experiences may cause disinhibition of mechanisms underlying empathy for pain, resulting in synaesthesia for pain. This proposal is supported by studies that have found mirror activity to be involved in the pain matrix (e.g. Ochsner et al., 2008 and Singer et al., 2004); however, the specific processes that weaken these inhibitory mechanisms are unclear...Ultimately, in synaesthesia for pain, "there is no self–other distinction in the observation of pain in another person."ReferencesFitzgibbon, B., Giummarra, M., Georgiou-Karistianis, N., Enticott, P., & Bradshaw, J. (2009). Shared pain: From empathy to synaesthesia. Neuroscience & Biobehavioral Reviews DOI: 10.1016/j.neubiorev.2009.10.007Ward J, Simner J. (2003). Lexical-gustatory synaesthesia: linguistic and conceptual factors. Cognition 89:237-61.Ward J, Simner J, Auyeung V. (2005). A comparison of lexical-gustatory and grapheme-colour synaesthesia. Cognitive Neuropsychology 22:28-41.
... Read more »

Fitzgibbon, B., Giummarra, M., Georgiou-Karistianis, N., Enticott, P., & Bradshaw, J. (2009) Shared pain: From empathy to synaesthesia. Neuroscience . DOI: 10.1016/j.neubiorev.2009.10.007  

  • May 10, 2012
  • 08:22 AM

Spindle Neurons in Macaques?

by The Neurocritic in The Neurocritic

Spindle neurons, or Von Economo neurons (VENs), are a unique type of large, bipolar neuron found primarily in layer Vb in the anterior cingulate cortex and the frontoinsular cortex of humans.1 In 1999, Nimchinsky and colleagues discovered that among the 28 nonhuman primate species they examined, only great apes had VENs [see Spindle Neurons: The Next New Thing?].Spindle neurons are also seen in humpback, fin, sperm, and killer whales (Hof & Van der Gucht, 2007), elephants (Hakeem et al., 2009), and cetaceans such as the bottlenose dolphin, Risso’s dolphin, and the beluga whale (Butti et al., 2009).Because VENs are only found in large-brained, highly evolved social species, and are potentially implicated in certain neurological and psychiatric disorders, their hypothesized functions include empathy, conscious awareness, and self-referential processing. A 2011 review by Allman and colleagues reiterated that only great apes (bonobos, chimpanzees, gorillas, orangutans) have VENs and suggested they......may be a specialization related to very large brain size. The large size and simple dendritic structure of these projection neurons suggest that they rapidly send basic information from FI [frontoinsular cortex] and LA [limbic anterior area] to other parts of the brain, while slower neighboring pyramids send more detailed information. Selective destruction of VENs in early stages of frontotemporal dementia (FTD) implies that they are involved in empathy, social awareness, and self-control, consistent with evidence from functional imaging.VENs: Not Only for Great Apes Any More!But now, a new study has identified these special neurons in the insular cortex of macaque monkeys (Evrard et al., 2012).Figure 1 (Evrard et al., 2012). The Von Economo Neuron Is Present in Layer 5b in a Restricted Portion of the Agranular Anterior Insula in the Macaque Monkey (A) High-magnification photomicrographs demonstrating the identical morphology of the macaque and human VENs. Scale bar represents 25 μm.Why weren't they found in the earlier studies that looked for them?Three reasons: (1) they're a lot smaller in monkeys; (2) they're more fragile in monkeys; and (3) they're confined to a more limited anatomical region.First, the large human VENs unambiguously stand out at low microscope magnifications. Searching for relatively smaller VENs among the densely packed cell population in layer 5 in the monkey required the highest microscope magnification, which would be unusual for anyone accustomed to examining the more obvious VENs in hominids. Second, the cytoskeletal matrix of the small monkey VENs might be more fragile during histological processing than that of the larger human VENs. ... Third, in the major prior study, the number of VENs in humans and great apes was counted in consecutive sections that were apparently spaced at 1 mm intervals ... such a sampling paradigm would likely have been inadequate for the identification of VENs within the small VEN-containing region of the ventral AAI that measures ∼2 × 2 × 1 mm3 in macaques.The authors pointed out a major advantage of their new discovery, namely that more invasive studies are now possible (i.e., you can't do single cell neurophysiology in dolphins or bonobos).But wait... are they really VENs?The morphology, size, laminar distribution, and proportional distribution of the monkey VEN suggest that it is at least a primal anatomical homolog of the human VEN. Allman, Hof, and colleagues might have something more to say on the matter, based on their earlier findings (e.g., Allman et al., 2011):The VENs are illustrated at higher magnification in Figure 3, which shows that they have very similar morphology in the great apes and humans. In primates, the VENs are present in FI only in great apes and humans. This is the same taxonomic distribution as was found for the VENs in LA, which suggests that the VENs emerged as a specialized neuron type in the common ancestor of great apes and humans. Figure 3 (Allman et al., 2011). VENs in area FI of humans and great apes.The new paper concedes that:The presence of VENs in the macaque does not discredit prior evidence for a crucial role of the VENs and AIC in the emergence of self-awareness and social cognition in humans (Craig, 2009; Allman et al., 2011). VENs in humans appear to be disproportionally slightly larger than in macaques (see above); they may also have an enhanced immunopositivity (and perhaps gene expression) for proteins that are typically involved in homeostasis, which perhaps favors higher interoceptive sensitivity. Are they confined to the anterior insula in macaques? No, VENs were also found in the ACC, but that will be reported separately (a lesson for all you junior scientists).Now that they've been found in monkeys [and can be studied physiologically], will spindle neurons finally catch up with their more glamorous elder cousins, the mirror neurons? Are they really the next new thing? Six years ago, I pondered these points:Somehow, the "spindle neuron" meme hasn't caught on like the "mirror neuron" meme. Is it because spindle neurons have been only been described anatomically (not physiologically), while the reverse is true for mirror neurons? Anatomically speaking, do we know much about mirror neurons? Evrard, Forro, and Logothetis are all over it:...invasive studies of their organization, hodology, and physiology could provide significant insights into the evolutionary basis for self-awareness and empathy in humans. Regarding the latter, it would be particularly interesting to examine whether the VENs share functional similarities with the “mirror” neurons of the ventral premotor cortex (Gallese et al., 2004).Finally, a commentary in Neuron by Critchley and Seth (2012) wonders if studies of the macaque insula will reveal the neural mechanisms of self-referen... Read more »

  • August 2, 2011
  • 05:00 AM

The Man Who Mistook a Harmonica for a Cash Register

by The Neurocritic in The Neurocritic

One of the most famous books written by Oliver Sacks, popular author and beloved behavioral neurologist, is The Man Who Mistook His Wife for a Hat. One of the chapters describes the case of a patient with visual agnosia, or the inability to recognize objects.Below is a conversation between Sacks and Dr. P, the patient with visual agnosia.I showed him the cover [of a National Geographic Magazine], an unbroken expanse of Sahara dunes.'What do you see here?' I asked.'I see a river,' he said. 'And a little guest-house with its terrace on the water. People are dining out on the terrace. I see coloured parasols here and there.' He was looking, if it was 'looking', right off the cover into mid-air and confabulating nonexistent features, as if the absence of features in the actual picture had driven him to imagine the river and the terrace and the colored parasols.I must have looked aghast, but he seemed to think he had done rather well. There was a hint of a smile on his face. He also appeared to have decided that the examination was over and started to look around for his hat He reached out his hand and took hold of his wife's head, tried to lift it off, to put it on. He had apparently mistaken his wife for a hat! His wife looked as if she was used to such things.Visual agnosia is caused by an acquired brain injury to high-level object processing areas in lateral occipital and ventral temporal cortices. Primary and secondary visual regions are spared, meaning that basic visual responses are not compromised. Language and naming are intact, as is the ability to identify objects through other modalities (e.g., auditory, tactile).A case study published in Neuron (Konen et al., 2011) describes a patient similar to Dr. P. Patient SM is a right-handed, 36 year old male who sustained a closed head injury in an automobile accident at the age of 18. He recovered after the accident but was left with visual agnosia and prosopagnosia, an impairment in recognizing faces. The damaged area of his brain was fairly circumscribed1 and smaller in size than in many other patients with visual agnosia:The lesion was situated within LOC, anterior to hV4 and dorsolateral to VO1/2, and was confined to a circumscribed region in the posterior part of the lateral fusiform gyrus in the RH [right hemisphere]. Typically, this region responds more to intact objects than scrambled objects and damage to this circumscribed area is likely the principle etiology of SM's object agnosia.Figure 4 (modified from Konen et al., 2011). Lesion Site of SM in Anatomical Space. (C) Axial view of the lesion site marked in green. The slices were cut along the temporal poles for enlarged representation of occipitotemporal cortex.In addition, detailed topographic mapping of visual cortex was conducted using fMRI in SM and controls. Responses in early cortical areas (prior to the lesioned fusiform gyrus in the feedforward processing stream) were intact in SM.Figure 1 (Konen et al., 2011). Topographically Organized Areas and Lesion Site in SM (A) and Control Subject C1 (B). Flattened surface reconstructions of early and ventral visual cortex. The color code indicates the phase of the fMRI response and region of visual field to which underlying neurons responded best. Retinotopic mapping revealed regular patterns of phase reversals in both hemispheres of SM that were similar to healthy subjects such as C1. SM's lesion is shown in black, located anterior to hV4 and dorsolateral to VO1/2. LH = left hemisphere; RH = right hemisphere.Conversely, the hemodynamic response to object presentation was reduced in the area surrounding the lesion, as expected. But the most remarkable and surprising aspect of the study is that reductions in object-related responses were also observed in the corresponding region of SM's intact left hemisphere. How might this be explained?...while the RH lesion might be primary, this lesion has remote and widespread consequences, with functional inhibition of homologous regions in the structurally intact hemisphere. Such a pattern raises the question whether the observed brain-behavior correspondence serves as the neural underpinning of the impairment or whether reconceptualizing SM's agnosia in terms of disruption to an interconnected more distributed neural system might be a better characterization of SM's pattern and of agnosia more generally.The authors discuss their findings in the video below, where Marlene Behrmann mentions that SM mistook a picture of a harmonica for a cash register.Video Abstract (mp4)Highlights► Unilateral lesion of lateral fusiform gyrus in right hemisphere causes object agnosia ► Agnosic patient exhibits normal retinotopy and visual responsivity in visual cortex ► Object-responsive and object-selective responses are reduced in both hemispheres ► Cortical plasticity evident with reorganization of intermediate and higher-order areasFootnote1 The Methods section notes additional damage in the corpus callosum and left basal ganglia.ReferenceKonen, C., Behrmann, M., Nishimura, M., & Kastner, S. (2011). The Functional Neuroanatomy of Obj... Read more »

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