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Headache, by Robert Magginetti (Tranquility Base)In the last post we learned about Alice in Wonderland syndrome, a rare phenomenon involving distortions of visual perception and body image, most often caused by migraines. Although a specialty practice in headache might seem dull [so to speak] at first glance to those interested in behavioral neurology, unusual and colorfully-named types of headaches can make things more interesting. In Case Studies of Uncommon Headaches (2006), Dr. Randolph Evans reviews a number of these unfortunate ailments, which include exploding head syndrome, neck-tongue syndrome, red ear syndrome, and burning mouth syndrome. So let's begin with a hot ear.Case 6. My ear is red, hot, and burningA 54-year-old white woman was seen who had a 10-year history of episodes of a burning sensation of the left ear. The episodes are preceded by nausea and a hot feeling for approximately 15 seconds and then the left ear becomes visibly red for an average of approximately 1 hour, with a range of approximately 30 minutes to 2 hours. Approximately once every 2 years, she had a flurry of episodes occurring over approximately a 1-month period during which she averaged approximately five episodes, with a range of 1 to 6. There also was an 18-year history of migraine without aura occurring approximately once a year. ... A cerebral arteriogram revealed a proximal left internal carotid artery occlusion of uncertain cause after extensive testing. MRI scan at age 45 was normal. Neurologic examination was normal. A carotid ultrasound study demonstrated complete occlusion of the left internal carotid artery and a normal right.The diagnosis? Red Ear Syndrome, first described by Lance (1994) in the aptly-titled article, The mystery of one red ear. Following a plea to colleagues to "lend me your ear," Lance (1996) subsequently reported on 12 cases. He concluded that RES:may be associated with irritation of the third cervical root [nerve in the neck], temporomandibular joint [jaw] dysfunction, or thalamic [pain] syndrome. It may also occur without obvious structural cause in response to touch or heat. The condition may be an example of the ABC (Angry Back-firing C-nociceptor) syndrome with the increase in ear temperature being caused by the antidromic ["backwards"] release of vasodilator peptides [calcitonin gene-related peptide and substance P].It can also occur in association with migraines, glossopharyngeal and trigeminal neuralgia, upper cervical spine pathology, and herpes zoster [shingles]. The GABA analogue and anti-seizure medication gabapentin can be helpful in preventing RES.By the way, the girl in the picture above [who is not Case 6] says her red ear doesn't hurt, and that she doesn't get headaches.Case 7. My mouth is burningA 49-year-old woman was referred by her primary care physician with a 1.5-year history of daily constant burning or numbness of the entirety of her tongue and the back of her throat. She also complains that the inside of her mouth is sensitive. She has had a dry mouth for the past year. ... Artificial saliva has not been helpful. She has tried a variety of pain pills without any help....Burning Mouth Syndrome1 most often afflicts middle-aged and older women. Causes include dry mouth (e.g., from medications or diabetes), nutritional deficiency, food allergies, fungal infection (candidiasis aka thrush), trigeminal small fiber neuropathy (nerve damage), and hormonal changes. Treatments range from estrogen-progesterone replacement therapy to nutritional supplements to switching prescription medications to addressing an underlying medical condition. I don't know if this syndrome can be considered a "headache" in the standard usage of the word, but then again I'm not a neurologist.Case 1. Noises in the nightA 43-year-old woman was seen with a 5-month history of a noise in her head. On an almost nightly basis, as she was falling asleep, she would hear a loud noise like "electrical current running" lasting a second. Sometimes her whole body would shake for a second afterwards. Very occasionally, she would have an associated flash of light. Frequently, a second episode of the loud noise occurred shortly after the first. She then could fall asleep without any problem.Exploding Head Syndrome (Pearce, 1988) is a bang-up way to be aroused from your nightly slumber. A small percentage (~10%) of sufferers see a flash of light, even fewer feel as if they've stopped breathing for a short time. It's more frightening than it is painful. Interestingly, Evans (2006) suggests that EHS might be caused by delay in the reduction of activity in the brainstem reticular formation as the patient transitions from wakefulness to sleep. In 1949, Moruzzi and Magoun were the first to recognize that stimulation of the brainstem reticular formation produces low-voltage fast activity in the EEG, characteristic of an alert and attentive behavioral state. So something might be neurologically amiss with the EHS patient's sleep-wake cycle, although Evans gave no direct evidence of this. And the explosion phenomenology is largely unexplained, as noted by Pearce (1988):The cause of the bomb-like noise remains a mystery: no known vascular or hydrodynamic changes in the brain, labyrinths, or cerebrospinal fluid would cause such a symptom, although a momentary (almost ictal) disinhibition of the cochlea or its central connections in the temporal lobes, or a sudden involuntary movement of the tympanum or tensor tympani, might be the explanation...Evans' other case studies recounted complaints of numb tongue (neck-tongue syndrome), painful scalp (nummular headache... Read more »
"Rare migraineurs have strange symptoms where the diagnosis may be lurking just down a rabbit hole" (Evans & Rolak, 2004).Alice in Wonderland syndrome is an unusual perceptual phenomenon most often caused by migraine headaches, but also seen in association with epilepsy and Epstein-Barr virus. The most well-known symptoms are: Alteration of body image: the sizes of parts of the body are perceived incorrectly. Alteration of visual perception: the sizes of external objects are perceived incorrectly.In their review, Evans and Rolak (2004) noted that:Patients are aware of the illusory nature of their perceptions and are sometimes reluctant to admit to them for fear of being thought insane. This sensation of formed body distortions, a type of metamorphopsia, appears to be caused by migrainous ischemia. Most authorities believe, based in part on direct electrical stimulation studies of the brain, that these body distortions ... arise primarily in the posterior parietal lobe, especially in the nondominant [right] hemisphere. Migrainous ischemia and irritability in this area produces the bodily distortions.Extensive [permanent] damage to the right parietal lobe can result in hemispatial neglect, where the patient ignores the contralateral (left) side of space, including the left side of the body. The visual illusions of metamorphopsia (as opposed to body distortions) have been associated with altered blood flow in the right temporo-occipital region (Heo et al., 2004).Vaughan Bell, primary author of the Mind Hacks blog, revealed that he experienced Alice in Wonderland syndrome as a child but grew out of it as an adult (see Three impossible things before breakfast). He linked to a Guardian article by journalist Rik Helmsley, who described his symptoms in detail:Floors either curved or dipped, and when I tried walking on them, it felt as though I was staggering on sponges. When I lay in bed and looked at my hands, my fingers stretched off half a mile into the distance...I graduated and took a job as a system administrator in a new town, but instead of going away, my symptoms just got worse. Everything was now distorted, all the time. Walking down the road, parked cars appeared the size of Corgi models, while I'd feel disproportionately tall. At work, my chair seemed enormous, while I seemed to have shrunk.The German expressionist artist Käthe Kollwitz may have suffered from AIWS, according to a recent article by Graeme Drysdale (2009). Kollwitz was known for her etchings, drawings, and woodcuts that portrayed graphic levels of suffering due to poverty, illness, and war. Her work often contained distorted depictions of hands and heads.Poverty, 1893-94 (or Misery), by Käthe KollwitzDrysdale's hypothesis is that Kollwitz's art was heavily influenced by AIWS symptoms caused by migraine or epilepsy:In her diary, Kollwitz self-described symptoms of Alice in Wonderland Syndrome during her childhood. She complained of episodes where objects appeared to grow larger or smaller and perceptual distortions where she felt she was diminishing in size. This may explain why Kollwitz’s artistic style appeared to shift from naturalism to expressionism, and why her artistic subjects are often shaped with large hands and faces. The distortion present in her visual art may have less to do with a deliberate emphasis of the artist’s feelings and more to do with her perceptual experience.Die Witwe I (The Widow I), 1922-3. Woodcut on paper.In her diary, she described frightening visual hallucinations:‘Then there was a horrible state I fell into when objects would begin to grow smaller. It was bad enough when they grew larger, but when they grew smaller it was horrifying’.So it's possible that the expressionistic distortions in the work of Käthe Kollwitz were brought on by Alice in Wonderland syndrome. To me that seems more plausible than psychoanalytic speculation on the role of "oral birth fantasies, sex fantasies and suppressed emotion."ReferencesDrysdale, G. (2009). Kaethe Kollwitz (1867-1945): the artist who may have suffered from Alice in Wonderland Syndrome. Journal of Medical Biography, 17 (2), 106-110 DOI: 10.1258/jmb.2008.008042Evans RW, Rolak LA. (2004). The Alice in Wonderland Syndrome. Headache 44:624-5.Heo K, Cho YJ, Lee SK, Park SA, Kim KS, Lee BI. (2004). Single-photon emission computed tomography in a patient with ictal metamorphopsia. Seizure 13:250-3.Johnny Depp as the Mad Hatter, in Tim Burton's adaptation of Alice in Wonderland.Alice: "If I had a world of my own, everything would be nonsense. Nothing would be what it is, because ever... Read more »
Drysdale, G. (2009) Kaethe Kollwitz (1867-1945): the artist who may have suffered from Alice in Wonderland Syndrome. Journal of Medical Biography, 17(2), 106-110. DOI: 10.1258/jmb.2008.008042
Figure 1. Schematic diagram of the radiofrequency ablation device, adapted from surgical oncology procedures to apply a focal high frequency alternating current to the region of the amygdala.Alternatively, a gamma knife-like TMS application, slyly incorporated into a metal detector, temporarily deactivates the amygdala when each customer enters the casino.Figure 2. Adjustable transcranial magnetic stimulation (TMS) helmet incorporated into a Metor 200 Walk-Thru Metal Detector.What was the inspiration for such ground-breaking technology?1 The revelation that two rare individuals with bilateral lesions of the amygdala2 did not care about losing large sums of money in a gambling task (De Martino et al., 2010). This comes as no surprise, really, since the same two patients (S.M. and A.P.) do not show fear in other contexts. Patient S.M. in particular has repeatedly demonstrated deficits in the perception of fear (reviewed in Adolphs, 2008). She's more likely to judge unfamiliar faces as trustworthy and approachable (Adolphs et al., 1998). Further, she fails to show a normal sense of distrust and "danger" (Tranel et al., 2006), and:Her interpersonal behaviour is notable for a somewhat coquettish and disinhibited style. She tends to be friendly with her examiners, with a familiar style of interaction that goes a little beyond what is typical in conventional Midwestern culture.In a related vein, her requirement for personal space is non-existent (Kennedy et al., 2009). On the other hand, she's impaired at making eye contact with people during conversations (Spezio et al., 2007). Although fearful facial expressions are a mystery, she can accurately judge fear from whole-body cues (Atkinson et al., 2007). Hmm. I find it puzzling when investigators publish a paper that stands in relative isolation from their previous work, as if the current result is so novel that it merits placement in a high-profile journal.So what does all this uncited work have to do with "loss aversion", the well-studied behavioral economic phenomenon3 probed in the current study? The authors proposed that "the amygdala computes a signal of prospective loss that is integrated with other information to guide behavioral choice" (De Martino et al., 2010). How does this fit with the collection of findings mentioned above? Granted, constraints of the short, high-impact journal article format prevent in-depth discussion and integration, but presenting so many punctate disconnected pieces just to up your number of glamor publications can be viewed as a disservice to the field. In my opinion, it's important to make connections between the different functions carried out by a particular brain structure (or network of structures), rather than treating the computations performed in a specific task as somehow uninformed by these other "computations".Adolphs et al. (2005) tied some of the disparate fear findings together when they linked S.M.'s lack of eye contact to her impaired recognition of fear from faces. But how does this connect with her propensity to throw money away in Vegas? More broadly, do pathological gamblers show amygdala-like deficits similar to S.M.? Probably not. Ultimately, the casinos don't care whether it's due to alterations in the striatum, the ventromedial prefrontal cortex, or the amygdala, they'd just like to attract customers with lowered loss aversion...Footnotes1 In case it's not completely obvious, these are fictional techniques.2 The cause of the amygdala damage was Urbach-Wiethe disease, a rare genetic disorder with less than 300 reported cases.3 To learn more about loss aversion in neurological patients, I refer the reader to this post in The Frontal Cortex.ReferencesAdolphs R. Fear, faces, and the human amygdala. (2008). Curr Opin Neurobiol. 18:166-72.Adolphs R, Tranel D, Damasio AR. (1998). The human amygdala in social judgment. Nature 393:470-4.Adolphs R, Gosselin F, Buchanan TW, Tranel D, Schyns P, Damasio AR. (2005). A mechanism for impaired fear recognition after amygdala damage. Nature 433:68-72.Atkinson AP, Heberlein AS, Adolphs R. (2007). Spared ability to recognise fear from static and moving whole-body cues following bilateral amygdala damage. Neuropsychologia 45:2772-82.De Martino, B., Camerer, C., & Adolphs, R. (2010). Amygdala damage eliminates monetary loss aversion. Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0910230107Kennedy DP, Gläscher J, Tyszka JM, Adolphs R. (2009). Personal space regulation by the human amygdala. Nat Neurosci. 12:1226-7.Spezio ML, Huang PY, Castelli F, Adolphs R. (2007). Amygdala damage impairs eye contact during conversations with real people. J Neurosci. 27:3994-7.Tranel D, Gullickson G, Koch M, Adolphs R. (2006). Altered experience of emotion following bilateral amygdala damage. Cogn Neuropsychiatry 11:219-32.
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Arrangement for psychotherapy fMRI studies using the couch of Sigmund Freud.[No not really, although the authors did stretch the implications of their findings in the Discussion...]Whether the proprietors of this blog want to admit it or not, neuropsychoanalysis appears to be a new field of study. What does psychoanalysis do to the brain? In a new Psychotherapy Research paper, Loughead et al. (2010) collected autobiographical relationship narratives from 16 healthy control participants free of any psychiatric or neurological ailments. These types of vignettes were used as stimuli because "people in psychotherapy spontaneously recall and tell stories about their relationships with other people..." A series of 14 one minute narratives was collected from each subject using the Relationships Anecdotes Paradigm (RAP) method, a structured interview designed to elicit descriptions of meaningful life events with another person. The participants then rated each episode on a 5-point Likert scale for positive and negative emotions.The investigators rated the narratives in another fashion to extract common themes. The core conflictual relationship theme (CCRT) method (Luborsky & Crits-Christoph, 1998) is a psychotherapy instrument used to measure patterns within interpersonal relationships:From a content analysis of the relationship narratives, it is possible to identify three kinds of relationship components: (a) wishes (wishes, intentions, goals of the individual or self); (b) responses from the other to the self; and (c) responses of the self to the other...The main CCRT relationship patterns are defined as the most repetitive relationship themes across an individual’s relationship narratives, usually those ranking first and second in frequency across the narratives. These main CCRTs have been a focus for the conduct of both psychotherapy and psychotherapy research (Luborsky & Crits-Christoph, 1998).Then a neuroimaging study was conducted with 11 of the participants (5 were ultimately tossed out for various reasons). It's notable that all subjects were free of psychiatric disorders, and none were in therapy. So the direct application of the results to psychotherapy practice is questionable. That said, what were the experimental procedures? For the narratives,The two most repetitive wishes (W), responses from others (RO), and responses of self (RS) were identified for each participant’s set of 14 narratives. These repetitive themes are hereafter referred to as the main CCRTs. Weighted scores were then assigned to each narrative based on the frequency with which the participant’s main CCRT themes appeared in her or his 14 narratives. For example, if a participant’s main RO was "hurt me" and it appeared in seven of 14 narratives, then each narrative containing the RO "hurt me" received a weighted score of 7....The weighted scores for the other elements were tallied up, and 3 narratives each were selected for the high and the low CCRT/emotion conditions [NOTE: these two factors could not be distinguished from each other]. In addition, narratives from one of the excluded participants served as the control, non-autobiographical relationship episodes:...The control episodes were selected to be similar to the personal condition in narrative structure, emotion, and CCRT content and yet have no autobiographical relevance to the participant.The three types of stimuli were presented in a block design: six 30-s blocks of personal narratives and six 30-s blocks of control narratives (half high, half low CCRT/emotion), with resting baseline thrown in for good measure. A sample CCRT narrative is shown below (click on image for a larger view).Figure I (Loughead et al. (2010). Sample CCRT relationship episode.The fMRI results came as no surprise to anyone: personal autobiographical memories activate the brain to a greater extent than someone else's memories. Wow!The network of frontal and parietal regions observed for the main effect of narrative type, which includes the anterior cingulate, precuneus/posterior cingulate, inferior frontal gyrus, inferior parietal lobule, and middle frontal gyri, is consistent with the existent neuroimaging literature on recall of autobiographical memories (Buckner & Carroll, 2007...).Figure II (Loughead et al. (2010). Brain images showing group main effect for narrative type (personal, control). Statistical parametric maps are displayed in radiological convention (left is right) standardized into Talairach space. ACC, anterior cingulate; Inf Front, inferior frontal gyrus; Mid Front, middle frontal gyrus; Inf Parietal; inferior parietal lobule. No voxels were above threshold for CCRT/emotion (high, low) main effect or the interaction.And there was absolutely no difference in brain activity elicited by the low CCRT and high CCRT conditions. So much for the CCRT method, at least in this non-psychiatric population. However, exploratory analyses showed correlations between BOLD signal and CCRT score in the left hippocampus, parahippocampal gyrus, and middle occipital gyrus. Not in the amygdala, however. The lack of main effect or interaction for the main variable of interest did not prevent the authors from speculating wildly:Our exploratory analysis suggests that narratives characterized by increasing amounts of the most repetitive (i.e., main CCRT patterns) are special from a neurobiological perspective... When narratives are high in CCRT content, this is somewhat akin to exposing, or reflecting back, the main CCRT themes to a patient (i.e., providing a transference interpretation). Thus, an area of further study suggested by these results is how exposure to the main CCRT themes (or transference interpretation) could modulate brain activation in the medial temporal and occipital lobes in treatment populations.Never mind that no psychotherapist was involved at all, since none of the participants were In Treatment. And what wild speculation would be complete without... MIRROR NEURONS!Memories, the self, and emotion have long been of interest to psychotherapy, and theory of mind/mentalization and the mirror neuron system have been proposed as specific mechanisms of psychotherapy process (Fonagy & Bateman 2006...). These results demonstrate that the essential psychotherapy activity of recall of autobiographical relationship episodes engages neural substrates for systems that have been identified by research as central for psychotherapy process.... Read more »
Loughead, J., Luborsky, L., Weingarten, C., Krause, E., German, R., Kirk, D., & Gur, R. (2010) Brain activation during autobiographical relationship episode narratives: A core conflictual relationship theme approach. Psychotherapy Research, 1-16. DOI: 10.1080/10503300903470735
Fig. 2 (Schaefer & Rotte, 2010). Example of a questionnaire used to form a semantic differential for one particular brand. Subjects had to rate the brands according to their relationships to 18 pairs of contrary adjectives.The nascent field of neuromarketing has grown tremendously in the last 5 years. Its goal is to use brain imaging techniques such as fMRI and EEG to gain hidden insights into consumer preferences. Commercial applications have far outstripped the peer-reviewed science necessary to validate their use. Google returns 322,000 hits for the term neuromarketing, whereas PubMed coughs up a sorry number - only 5 references! That doesn't stop large corporations from funneling millions of dollars into neuromarketing.A new study published by Schaefer & Rotte, 2010 combined the techniques of semantic differentials (rating products along a 7 point scale between 2 bipolar adjectives, as shown in Fig. 2) with fMRI. First, participants viewed 18 pictures of common pharaceutical brands, such as aspirin. They were asked to rate these stimuli on a 5-point-scale regarding their personal attractiveness. After the imaging session was over, they completed the semantic differential questionnaire. These ratings were used to analyze the fMRI data.Is this aspirin playful or serious?Fig. 3 (Schaefer & Rotte, 2010). Semantic space built by the results of the semantic differentials. Brands and concepts are displayed on a 2D schema (factors ‘social competence’ and ‘potency’; factors were orthogonal). Colored circles depict the different brands. [NOTE: click on the figure for a larger view, and you can see the adjectives used in the present study are depicted in light blue.]I knew next to nothing about semantic differentials before reading this paper, and that state of ignorance did not improve much when I finished reading. Some of the concepts were really murky and dependent on familiarity with the literature from 1957 and/or in German:...Although semantic differentials have been investigated for decades, the correct description of these factors remains an issue. Thus, different researchers have been using very different labels for the underlying factors. This is particularly true for the factor ‘evaluation’ (Osgood et al., 1957), which also has been described as ‘mother’ [in a psychoanalytic view (Hofstätter, 1957)] and more recently as ‘social competence’ (Dziobek and Hülser, 2007).The terms "evaluation", "mother", and "social competence" do not seem remotely equivalent. A book chapter by David Heise (1970) provided some clarity on the methodology:(2) Ratings on bipolar adjective scales tend to be correlated, and three basic dimensions of response account for most of the co-variation in ratings. The three dimensions, which have been labeled Evaluation, Potency, and Activity (EPA), have been verified and replicated in an impressive variety of studies.(3) Some adjective scales are almost pure measures of the EPA dimensions; for example, good-bad for Evaluation, powerful-powerless for Potency, and fast-slow for Activity. Using a few pure scales of this sort, one can obtain, with considerable economy, reliable measures of a person's overall response to something. Typically, a concept is rated on several pure scales associated with a single dimension, and the results are averaged to provide a single factor score for each dimension. Measurements of a concept on the EPA dimensions are referred to as the concept's profile.So why is a brand of aspirin rated on the dimension of seclusive--sociable? Because the results here were incorporated into a larger semantic space established in an earlier study. Principal component analysis reduced the dimensionality of the data to two main factors that accounted for 87% of the variance: ‘evaluation’ and ‘potency’. The authors didn't like ‘evaluation’ for some unexplained reason and instead used the term ‘social competence’ for a series of inanimate pharmaceuticals. [NOTE: Guess I'm not a marketer...]Moving on to the fMRI aspect of the experiment, it seems the authors wanted to relate the social competence of drug brands to neural activity in the medial prefrontal cortex (MPFC), which has been associated with self-referential processing and social cognition.Fig. 4A (Schaefer & Rotte, 2010). Contrasts of brands loading high on the factor ‘social competence’ compared with brands loading high on the factor ‘potency’. This contrast showed significant activation in the MPFC and the SFG (superior frontal gyrus).Oddly, the reverse contrast of high potency brands vs. high social competence brands did not produce any significant activity in the brain at all, which seems unexpected for a series of drugs. The high potency vs. low potency comparison revealed a reduction in SFG activity. To explain these results, the authors comitted the logical fallacy known as "reverse inference" by inferring the participants' mental state from the observed pattern of brain activity.fMRI enable us to link the factors driven out of the behavioral data with the activation of certain cortical areas. Since the functional meaning of those areas (the MPFC and the SFG) are known from previous studies, the results can tell us what the extracted factors are about. More in detail, the results suggest to mark the factor originally described as ‘evaluation’ now as being mainly characterized by social perceptions. Thus, the description ‘social competence’ for this factor seems to be much more appropriate. Hence, the fMRI results provide important improvements for the factorial model of semantic space, which would not have been possible by looking on the behavioral data alone.As for the SFG, they'd like to relate greater activity there to enhanced cognitive effort and working memory, but acknowledged this caveat:However, since the SFG has been related not only to working memory but also to a variety of different cognitive functions, these explanations remain speculative.Overall, I'm not sure how Bayer can target a new marketing campaign based on these results. The social competence of doctors recommending the aspirin, as in the classic commercial below? Comments, anyone?ReferencesHeise DR. (1970). The Semantic Differential and Attitude Research. Chapter 14 in Attitude Measurement.... Read more »
Schaefer, M., & Rotte, M. (2010) Combining a semantic differential with fMRI to investigate brands as cultural symbols. Social Cognitive and Affective Neuroscience. DOI: 10.1093/scan/nsp055
A sense of agency is the feeling that you're initiating and controlling your own movements. This can go awry in schizophrenia, when individuals can experience delusions of control (Lafargue & Franck, 2009). In this state, the patient feels as if external forces are performing actions against his will. Loss of agency also occurs in alien hand syndrome, a rare and unusual neurological disorder in which the affected patient loses volitional control of one hand, which develops "a mind of its own."A recent fMRI study looked at the pattern of neural activation associated with a sense of agency in normal participants (Yomogida et al., 2009). To do this, they used a "violation-of-visual-feedback paradigm" as shown below in Fig. 1. Subjects played a video game in which they controlled the movement of a character using a joystick. In the control condition, audio feedback was provided when they hit one of the targets (tomato - "squish" or balloon - "pop"). In the agency violation condition, the computer program moved the character in a different direction than the subject intended. In the sensory-matching violation condition, either the wrong feedback sound was presented, or the correct feedback was presented at the wrong time. A separate "oddball" task did not involve a motor response but controlled for the infrequent occurrence of the violation conditions.Fig. 1 (Yomogida et al., 2009). Task paradigm of the agency and SM error task. On each trial, a target (red object) was presented in one of four locations on a screen. Subjects were asked to hit the target by controlling the character using a joystick. Three conditions were possible: control (C), agency violation (AGv), and sensory-matching violation (SMv). To determine the regions of activation related to agency violation, the AGv - SMv subtraction was performed. Significant activations were found in bilateral supplementary motor area (SMA), left lateral cerebellum, right posterior parietal cortex, and right lateral occipito-temporal cortex (in the vicinity of the extrastriate body area; see Downing et al., 2001).Adapted from Fig. 3 (Yomogida et al., 2009). Left: Activation areas specific to agency error. Right: Representative examples of activation profiles for control (C), sensory-matching violation (SMv), and agency violation (AGv) conditions. SMA: supplementary motor area, Cbll: left lateral cerebellum, rt. IPL: right inferior parietal lobule.A region of particular interest for alien hand syndrome (AHS) is the SMA, which is involved in the planning, initiation, and inhibition of motor responses. An older paper by Feinberg et al. (1992) identified two alien hand syndromes. One of these is associated with damage to the anterior corpus callosum, as happens in the classic "split brain" operation to sever the white matter connections between the two cerebral hemispheres (undertaken for seizure control). The more "alien" (or anarchic) of the syndromes involves damage to dorsomedial frontal cortex, including the SMA and the anterior cingulate.However, note in Fig. 3 above that the "activation" in SMA is actually manifest as a smaller reduction in activity for agency errors compared to sensory matching errors. What does this mean? The authors don't say.Activation of the cerebellum was linked to cerebellar abnormalities in schizophrenic patients who experience delusions of control. In contrast, the authors discounted the importance of occipito-temporal and posterior parietal regions for a sense of agency, since there was some increased activity in these areas for oddball errors, as well as agency errors. But in a recent brain stimulation study, Desmurget and colleagues (2009) implicated posterior parietal cortex in the intention to move:Stimulating the right inferior parietal regions triggered a strong intention and desire to move the contralateral hand, arm, or foot, whereas stimulating the left inferior parietal region provoked the intention to move the lips and to talk. When stimulation intensity was increased in parietal areas, participants believed they had really performed these movements, although no electromyographic activity was detected. Stimulation of the premotor region [which did not include SMA] triggered overt mouth and contralateral limb movements. Yet, patients firmly denied that they had moved. Conscious intention and motor awareness thus arise from increased parietal activity before movement execution.From The Learning Channel - creditsHere's a documentary about alien hand syndrome and the brain, circa 1993 (or maybe 1996). You'll have to sit through the melodramatic narration, the overwrought music, and the cheesy reenactments to watch interviews with afflicted patients and with Todd E. Feinberg, Joe Bogen, and Eran Zaidel.You can read more about alien hand and willed actions in these blogs posts:In search of the conscious willElectrical stimulation produces feelings of free willThe alien hand syndrome - caught on videoReferencesDesmurget M, Reilly K, Richard N, Szathmari A, Mottolese C, Sirigu A. (2009). Movement intention after parietal cortex stimulation in humans. Science 324:811-813.Downing PE, Jiang Y, Shuman M, Kanwisher N. (2001). A cortical area selective for visual processing of the human body. Science 293:2470-3.Feinberg TE, Schindler RJ, Flanagan NG, Haber LD. (1992). Two alien hand syndromes. Neurology 42:19-24. [PDF]Lafargue G, Franck N. (2009). ... Read more »
Dodonpa roller coaster, 170 feet tall, 106.9 mph. Located in Fuji-Q Highland amusement park in Japan.In case you didn't know, there's a reasonably sized literature on roller coaster headaches. An especially interesting case was reported by Fukutake and colleagues (2000) in Japan. A 24 year old woman frequently visited amusement parks, including Fuji-Q Highland -- home to 3 monster roller coasters (she rode each of them twice):One of these, the Fujiyama, is the world’s highest roller coaster at 259 feet. It has a drop of 230 feet at an angle of 65° and has the world’s fastest speed of 81 mph. There was no direct trauma to her head or loss of consciousness during the rides.The headache started when she was on her way home from the park. She went to the hospital when it persisted for 4 days.The woman’s headache was constant, mainly suboccipital, worse in the evening, and partially relieved by rest. ... Neurologic examination results were normal. Her pupils were equal and reactive to light, and there was no papilledema or retinal hemorrhages. Routine laboratory tests for blood and urine all were normal. Tension-type headache was initially diagnosed, and muscle relaxants were prescribed for 4 weeks with some benefit; the headaches fluctuated but were unrelieved.Two months later, MRI of the head ruled out an organic problem and showed bilateral subdural hematomas with neomembranes.Figure (Fukutake et al., 2000). T1-weighted MRI of the head showing bilateral subdural hematomas with neomembranes.The neurosurgeons removed the hematomas, and the patient's headaches resolved. She was completely symptom free 8 weeks later. The article doesn't mention whether she resumed riding roller coasters, however.But Are Pillow Fights More Dangerous Than Roller Coasters?Another paper compared head motions that occurred in 4 participants when they rode 3 different roller coasters at Six Flags, drove bumper cars, and had a pillow fight (Pfister et al., 2009). What are the implications for brain injury? they asked.The 18 mph (8.1 m/s) car crash simulation resulted in the highest measurements of linear acceleration, linear velocity, and rotational velocity of the head. The highest level of rotational acceleration was measured during the pillow fight. Interestingly, the pillow fight generated peak head accelerations and velocities greater than the 3 roller coaster rides. Despite the difference in the 3 roller coaster rides (ie, speed, turns, loops), they lead to similar head motions. It is important to note that variations in head motions were small between the roller coaster rides, pillow fight and 5 mph (2.2 m/s) car bumper hit.Mostly dismissive of the case study literature on roller coaster headaches, these authors ended on a pro-roller coaster note:Our current empirical data supports 2 scientific panels' opinions as well as previous results from a computational model. Specifically, head motions during roller coaster riding fall within the range of normal activities and are far below thresholds of TBI in normal individuals.ReferencesFukutake T, Mine S, Yamakami I, Yamaura A, & Hattori T (2000). Roller coaster headache and subdural hematoma. Neurology, 54 (1) PMID: 10636168Pfister, B., Chickola, L., & Smith, D. (2009). Head Motions While Riding Roller Coasters The American Journal of Forensic Medicine and Pathology, 30 (4), 339-345 DOI: 10.1097/PAF.0b013e318187e0c9
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Fig 1 (Firth et al., 2009). X ray pictures can easily detect an ingested coin. Position of coin on lateral view (left), relative to anterior (right) or posterior picture affects size of image on film.Every year, BMJ has a special Christmas issue with spoof articles and silly studies. Today's feature examines the relationship between the Dow Jones Industrial Average and the value of coins swallowed by children (Firth et al., 2009):Main outcome measures Total value of coins ingested and number of incidents of coins versus other objects swallowed, measured before and after the stock market crash of October 2008.The authors reviewed computerized records from the endoscopy suite at Massachusetts General Hospital:...we compiled data on all numismatic and sundry detritus acquired (NASDAQ composite index) from children’s gastrointestinal tracts by the paediatric gastroenterology service at our hospital between August 2006 and July 2009. ... We calculated the financial total swallowed and extracted as a fraction of the US$ or 100 cents (FTSE 100 index), and the ratio of patients with coins versus all those with foreign objects removed (pecuniary extraction ratio, PE ratio). We calculated the mean end-of-month closing value of the Dow Jones Industrial Average. We examined whether there was a change in the monthly mean NASDAQ, FTSE, and PE ratio before and after the collapse of the Dow Jones Industrial Average of October 2008.What did they find? There was no relationship between the value of the stock market and the value of coins swallowed by children, as one might intuitively expect from a population that has no idea that the Dow Jones Industrial Average even exists [except for maybe the 15 (!) year old]:The patients were aged 1 to 15 years. The NASDAQ composite index was 18. Eleven coins were retrieved from nine patients: three pennies (or cents), five nickels (1 nickel=5 cents), no dimes (1 dime=10 cents), and three quarters (1 quarter=25 cents), giving a total return on ingestment for the period, or FTSE 100 index, of $1.03. Seven other objects in seven children included an unsafe safety pin (open), a battery, a marble, a ballbearing, a magnet, a dentist’s guard, and a rubber doorstopper. The PE ratio was therefore 0.57 (9/16)....We found no change in the FTSE 100 index (2.3 v 3.1, P=0.77) or PE ratio (0.54 v 0.66, P=0.5) during a period of dramatic Dow Jones (12 537 v 8388, P less than 0.0001), despite the NASDAQ composite index remaining stable (0.4 v 0.5, P=0.75). In other words, despite a massive swing in the stock market there was no concomitant absolute or relative change in paediatric wealth intake against an unaltered background rate of foreign body ingestion.Nonetheless, the authors bemoan the paucity of gastropecuniary studies and call for further investigations in the numismedical field.Brain Blogger covers another article from the 2009 issue, Santa Claus: a public health pariah? in their post, Is a Slim Santa Claus Coming to Town? My personal favorite, though, is this announcement from BMJ editor Tony Delamothe: "Anaesthetists’ brains differ markedly from surgeons’. Who would have thought?"Classics from Christmases past include Are Surgeons Taller And Better Looking Than Other Doctors?, Sword Swallowing And Its Side Effects, Sneezing etiquette and the efficacy of masks, Sex, aggression, and humour: responses to unicycling, and Rage Against the Machine Syncope and the Texting Sign. Happy reading!ReferenceFirth, P., Zheng, H., & Biller, J. (2009). Ingested foreign bodies and societal wealth: three year observational study of swallowed coins. BMJ, 339 (dec04 1). DOI: 10.1136/bmj.b5066
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Firth, P., Zheng, H., & Biller, J. (2009) Ingested foreign bodies and societal wealth: three year observational study of swallowed coins. BMJ, 339(dec04 1). DOI: 10.1136/bmj.b5066
Help me, somebody help meI wonder where I amEverything's Gone Green----New OrderEdward Wild begins his comprehensive review on déjà vu in neurology with a definition from the unorthodox1 Dr. Vernon Neppe:V M Neppe proposed a definition of déjà vu in 1983 as “any subjectively inappropriate impression of familiarity of a present experience with an undefined past”. The definition is precisely worded and provides useful insights into the phenomenon.The word “any” is intended to convey aetiological neutrality, implying that the experience need not originate from any particular pathological entity, or indeed any cause at all.The “subjectively inappropriate” nature of déjà vu is critical to its understanding, as it implies insight into the unusual nature of the experience. The subject simultaneously seems to recognise a situation, yet knows that recognition to be impossible. Taking this further, the definition implies (though does not state) that the subject will try to explain the sense of familiarity and struggle to pinpoint its source but, frustratingly, cannot do so.The most commonly occurring instances of déjà vu in neurology are in people with temporal lobe epilepsy (Vignal et al., 2006). The famous neurologist John Hughlings-Jackson was the first to describe the "dreamy state" in 1888 (actual PDF!):The variety of epilepsy alluded to is one in which (1) the so-called "intellectual aura" (I call it "dreamy state") is a striking symptom. This is a very elaborate or "voluminous" mental state. One kind of it is "Reminiscence"; a feeling many people have had when apparently in good health... Along with this voluminous mental state, there is frequently a "crude sensation" ("warning") of (a) smell or (b) taste; (or, when there is no taste, there may be movements, chewing, tasting, spitting, implying (?) an epileptic discharge beginning in some part of the gustatory centres), or (c), the "epigastric" or some other "systemic" sensation. ...the "dreamy state" sometimes occurs without any of the crude sensations mentioned...Given the conflicting results of brain stimulation studies in epileptic patients (Mullan & Penfield, 1959;2 Halgren et al., 1978; Gloor et al., 1982; Bancaud et al., 1994), there has been a debate over which structures are most critical for eliciting the "dreamy state", and whether the spread of electrical discharge to temporal neocortex is necessary. Vignal et al. (2006) conclude thusly:In the dreamy state, the recalled memory can be recent or remote. The mechanism involved does not appear to be different for these two types, in that the discharge involves only the MTL structures [not temporal neocortex]. This permanent role for the hippocampus and amygdala tends to invalidate the model of memory consolidation proposed by Squire and Alvarez (1995)...Déjà vécu and visual memories involving recent and remote memories can be explained by the role of the amygdala, the hippocampus and rhinal cortex, whether right or left-sided, in the mechanisms of episodic autobiographical memory. The connections between these structures organize the content and the elaboration of the dreamy state for both remote childhood and recent memories.These authors also point out that there is a continuum between déjà vécu (the more encompassing term meaning having lived through something before) and visual memory, both of which can occur during spontaneous seizures.An interesting case study of déjà vu in a patient without temporal lobe epilepsy was reported by Kovacs et al. (2009). The patient, a 22 year old woman, was undergoing deep brain stimulation (DBS) to treat dystonia, a painful movement disorder involving involuntary muscle contractions and contorted posture. Due to a perinatal injury, she developed hemidystonia in her right arm. A stimulating electrode was implanted in the left internal globus pallidus (GPi), one of the output nuclei of the basal ganglia. Numerous papers have demonstrated that DBS in the GPi is effective in relieving the symptoms of dystonia.Fig. 1 (Kovacs et al., 2009). Localization of the stimulating electrode: (A) coronal MP-RAGE, (B) coronal FLAIR, (C) sagittal MP-RAGE. Visual inspection and application of the electronic version of the Schaltenbrand stereotactic atlas verified that the contact responsible for DV [déjà vu] was situated between the GPi and the underlying white matter. The electrode did not hit the mesial temporal structures.When stimulation at the deepest contact was turned on, the patient reported déjà vu phenomena:Preoperatively the patient had never experienced DV. Immediately after turning on the DV-inducing stimulation, she experienced an unusual and obscure feeling. In addition to discomfort and a slight disturbance, the subject had an intact sense of reality; she was able to observe what was going on around her and to maintain verbal and behavioral responsiveness. We defined this period as the standby state for DV (SSDV). The SSDV persisted until stimulation of contact 0 was turned off or the amplitude of stimulation was lowered below 2.7 V.During SSDV, she experienced impulse DV episodes lasting 4–5 seconds. On these occasions she felt that the situation seemed familiar. No visual or auditory illusions or hallucinations accompanied the DV. In addition, the patient felt neither the ability to predict the future nor unreality about current circumstances.A SPECT (single photon emission computed tomography) scan was performed during one of the DV stimulation sessions. Like its more expensive cousin PET (positron emission tomography), SPECT measures cerebral blood flow, albeit with lower spatial resolution than PET. Structures in the right medial temporal lobe (contralateral to the stimulating electrode) showed greater blood flow during DV (as did other regions):Compared with the baseline, SPECT during DV revealed right-sided hyperperfusion of the hippocampus, parahippocampal gyrus, fusiform gyrus, cerebellum, and temporal sup... Read more »
Facing a difficult surgery to remove that pesky medial sphenoid wing meningioma? Be sure your neurosurgeon looks at pictures of cute kittens and puppies before scrubbing up. Or so implies a goofy study by Sherman et al. (2009):Infantile physical morphology—marked by its “cuteness”—is thought to be a potent elicitor of caregiving, yet little is known about how cuteness may shape immediate behavior. To examine the function of cuteness and its role in caregiving, the authors tested whether perceiving cuteness can enhance behavioral carefulness, which would facilitate caring for a small, delicate child. In 2 experiments, viewing very cute images (puppies and kittens)—as opposed to slightly cute images (dogs and cats)—led to superior performance on a subsequent fine-motor dexterity task (the children’s game “Operation”). This suggests that the human sensitivity to those possessing cute features may be an adaptation that facilitates caring for delicate human young. [NOTE: and perhaps surgical patients.]"Operation"? But why?Standard laboratory dexterity tasks score performance as the number of objects successfully moved per second. Because cuteness may not make people faster (only more careful), we used a similar task that was not time dependent: the classic children’s game “Operation” (Hasbro, Pawtucket, RI), in which participants use tweezers to remove small objects (body parts) from confined spaces. This task is similar to standard fine-motor dexterity tasks, but performance can be quantified without reference to speed. Because positive actions directed toward a child likely require physical gentleness, we also used a grip-strength gauge as a measure of physical weakness/gentleness.In Experiment 1, participants were 40 female freshman at the University of Virginia who were assigned to one of two groups. The experiment involved playing Operation before and after looking at images of high cuteness (puppies and kittens) or low cuteness (dogs and cats). And as the authors predicted, subjects in the high cuteness condition showed greater improvement after viewing the pictures than did those in the low cuteness condition (p=.05).Experiment 2 did a better job of balancing the images on factors that were ignored in Exp. 1, such as interesting, enjoyable, and exciting. Male undergrads were included as well, to make sure the effect wasn't limited to cooing 18 year old girls. Again, participants in the high cuteness group showed greater improvement than those in the other group at the p=.05 level. The girls and the boys did not differ on this "cuteness effect."Why is this important?This is the first investigation to document that immediate shifts in carefulness—indexed here by fine-motor performance—can be elicited by cuteness cues. This suggests that two factors—the importance of physical contact in early mammalian development and the extremely delicate nature of human young—may have exerted evolutionary pressures favoring those who could respond to the presence of cues colloquially described as “cute” with increased carefulness.No overinterpretation of data here, nope, none at all... Move along, move along.Reference,Sherman, G., Haidt, J., & Coan, J. (2009). Viewing cute images increases behavioral carefulness. Emotion, 9 (2), 282-286 DOI: 10.1037/a0014904
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Sherman, G., Haidt, J., & Coan, J. (2009) Viewing cute images increases behavioral carefulness. Emotion, 9(2), 282-286. DOI: 10.1037/a0014904
No more pain (no more pain)No more pain (no more pain)No drama (no more drama in my life, no ones gonna make me hurt again)No more in my lifeNo More Drama-----Mary J. BligeWomen who are victims of intimate partner violence (IPV) can suffer from post-traumatic stress disorder (PTSD), cognitive impairments (Twamley et al., 2009), and alterations in brain activity when anticipating aversive or threatening events (Simmons et al., 2008).In a neuroimaging study, 15 women with IPV-related PTSD were compared to 15 non-traumatized control women in a task that cued the presentation of either positive or aversive images (Simmons et al., 2008). The authors hypothesized that the women with PTSD would show exaggerated neural responses in the insula in anticipation of negative stimuli. This brain region is implicated in interoceptive awareness of bodily states (Craig, 2009), and is responsive to scenes and expressions of disgust (Stark et al., 2007).Figure 1 (Simmons et al., 2008). Anticipation Task. The fMRI task combined a continuous performance task with the interspersed presentation of affective stimuli. Subjects were asked to press the left or right button on a touch pad on the basis of the shape on the screen. Subjects were instructed before the task that a switch from a blue to a green shape accompanied by a low tone would indicate that a positive image was going to appear on the screen. In contrast, a switch from a blue to a red shape accompanied by a high tone signaled an impending negative image.A priori regions of interest (ROIs) were selected in bilateral anterior insula and right anterior/middle insula. These ROIs showed greater activation in anticipation of negative vs. positive images in both groups. Furthermore, the PTSD group showed greater signal change than controls in the right anterior/middle insula, as shown below.Figure 3 (Simmons et al., 2008). Anticipation of negative images versus positive images leads to increased activation in bilateral anterior insula (A shows right-sided activation and B shows left-sided activation) and (C) right anterior/middle insula, which was significantly more active in IPV relative to NTC subjects. Additional connectivity analyses suggested that correlations between activation in the insular regions and the amygdala were weaker in the IPV-PTSD group. The authors speculate that:...the increased activation in anterior/middle insula observed in IPV subjects with PTSD, in particular on the left side, might represent a neural substrate linking emotional distress, anticipatory processing, and autonomic arousal, which can advance action planning to reduce exposure to the aversive stimuli. Therefore, the anterior/middle insula activation might be interpreted as a “warning signal” that is associated with the anticipation of aversive symptoms such as hyperarousal. This interpretation is supported by the strong functional connectivity between anterior/middle insula and amygdala observed in the current study...Hyperarousal takes its toll on cognition, however, as demonstrated in another experiment that assessed neuropsychological functioning in a group of women with IPV-PTSD, who showed slower cognitive processing speed than controls (Twamley et al., 2009):We speculate that the cognitive slowing seen in PTSD may be attributable to reduced attention due to a need to allocate resources to cope with psychological distress or unpleasant internal experiences. A goal for the future is to see whether appropriate clinical treatment ameliorates this deficit. Overall, however, the best strategy is to stop the violence before it occurs. WHO, CDC, and womenshealth.gov have information on the prevention of intimate partner violence. You can also call the National Domestic Violence Hotline. Feel free to list addition resources in the comments.ReferencesCraig AD. How do you feel--now? The anterior insula and human awareness. (2009). Nat Rev Neurosci. 10:59-70.SIMMONS, A., PAULUS, M., THORP, S., MATTHEWS, S., NORMAN, S., & STEIN, M. (2008). Functional Activation and Neural Networks in Women with Posttraumatic Stress Disorder Related to Intimate Partner Violence. Biological Psychiatry, 64 (8), 681-690. DOI: 10.1016/j.biopsych.2008.05.027Stark R, Zimmermann M, Kagerer S, Schienle A, Walter B, Weygandt M, Vaitl D. (2007). Hemodynamic brain correlates of disgust and fear ratings. Neuroimage 37:663-73.TWAMLEY, E., ALLARD, ... Read more »
SIMMONS, A., PAULUS, M., THORP, S., MATTHEWS, S., NORMAN, S., & STEIN, M. (2008) Functional Activation and Neural Networks in Women with Posttraumatic Stress Disorder Related to Intimate Partner Violence. Biological Psychiatry, 64(8), 681-690. DOI: 10.1016/j.biopsych.2008.05.027
TWAMLEY, E., ALLARD, C., THORP, S., NORMAN, S., HAMI CISSELL, S., HUGHES BERARDI, K., GRIMES, E., & STEIN, M. (2009) Cognitive impairment and functioning in PTSD related to intimate partner violence. Journal of the International Neuropsychological Society, 15(06), 879. DOI: 10.1017/S135561770999049X
Fig. 1 (Hakeem et al., 2009). Photomicrographs of VENs in the brain of the African elephant. A: VENs in frontoinsular cortex (area FI). Scale = 25 μm.Spindle neurons, or Von Economo neurons (VENs), are a unique type of large, bipolar neuron found in layers III and V in the anterior cingulate cortex and the frontoinsular cortex of humans. 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?). Primate cerebral cortex (generally) consists of six layers, and the VENs and other large pyramidal cells in layer V are projection neurons. VENs are also seen in humpback, fin, sperm, and killer whales (Hof & Van der Gucht, 2007).More recently, spindle neurons have been found in elephants (Hakeem et al., 2009) and cetaceans such as the bottlenose dolphin, Risso’s dolphin, and the beluga whale (Butti et al., 2009).Fig. 3 (Hakeem et al., 2009). VEN-containing regions of the elephant brain indicated on coronal section outlines. The locations of the sections are indicated by the vertical lines on the inset tracing of the medial aspect of the brain. The left hemisphere is on the left side of the figure. A: VENs in a dorsolateral [DL] frontal cortical area. B: VENs were present in subgenual [SG] anterior cingulate cortex (ACC)... C: Area FI [frontoinsular], in which VENs were abundantly present. Scale = 1 cm. DM = dorsomedial.In elephants, VENs are located not only in ACC and FI, but also in dorsolateral frontal cortex. In cetaceans they can also be found in frontopolar cortex, as in humpback whales (Hof & Van der Gucht, 2007). According to Hakeem and colleagues:The VEN morphology appears to have arisen independently in hominids, cetaceans, and elephants. The VEN specialization may parallel the emergence of very large brain size in these mammals. The evolution of large brain size may place a special premium on overcoming geometric constraints to maintain rapid transmission of crucial information, and this need may explain the independent emergence of the VENs in these species. There are a few mammals apart from hominids, cetaceans, and elephants that have brains somewhat larger than the apes. It would be interesting to determine whether or not these mammals, such as the giraffes and hippopotamuses, have VENs in parts of the brain corresponding to FI and ACC. If they are present, it would suggest that the VEN morphology may be primarily related to absolute brain size. If not, it would suggest that the VENs may be related to behavioral specializations common to hominids, whales, and elephants.That's the more measured interpretation, because the abstract says:The VEN morphology appears to have arisen independently in hominids, cetaceans, and elephants, and may reflect a specialization for the rapid transmission of crucial social information in very large brains.As of now, the projection targets of the layer V spindle neurons are unknown, but are speculated to include (Butti et al., 2009):...projections to subcortical regions, such as the amygdala, hypothalamus, and periaqueductal gray, to which the ACC and FI/AI are known to project in primates. Altogether, VENs may be involved in the integration of emotions, vocalization control, facial expression, or social conduct as well as regulation of autonomic visceral, olfactory, and gustatory functions.Interestingly, another recent paper looked at convergent patterns of adaptive evolution in elephant and human ancestries (Goodman et al., 2009) -- see The Convergent Brains of Humans and Elephants.ReferencesButti, C., Sherwood, C., Hakeem, A., Allman, J., & Hof, P. (2009). Total number and volume of Von Economo neurons in the cerebral cortex of cetaceans The Journal of Comparative Neurology, 515 (2), 243-259 DOI: 10.1002/cne.22055Goodman, M., Sterner, K., Islam, M., Uddin, M., Sherwood, C., Hof, P., Hou, Z., Lipovich, L., Jia, H., Grossman, L., & Wildman, D. (2009). Phylogenomic analyses reveal convergent patterns of adaptive evolution in elephant and human ancestries. Proceedings of the National Academy of Sciences 106:20824-20829.Hakeem, A., Sherwood, C., Bonar, C., Butti, C., Hof, P., & Allman, J. (2009). Von Economo Neurons in the Elephant Brain The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology, 292 (2), 242-248 DOI: 10.1002/ar.20829Hof PR, Van Der Gucht E. (2007). Structure of the cerebral cortex of the humpback whale, Megaptera novaeangliae (Cetacea, Mysticeti, Balaenopteridae). Anatom Rec Part A, 290:1-31.Nimchinsky EA, Gilissen E, Allm... Read more »
Butti, C., Sherwood, C., Hakeem, A., Allman, J., & Hof, P. (2009) Total number and volume of Von Economo neurons in the cerebral cortex of cetaceans. The Journal of Comparative Neurology, 515(2), 243-259. DOI: 10.1002/cne.22055
At least it sounds pretty horrible...Dide-Botcazo Syndrome, or "top of the basilar" syndrome, is a rare clinical condition caused by bilateral occlusion of the posterior cerebral arteries (labelled below in red).The arteries of the base of the brain.A case report by Cappellari et al., 2009 describes a 72 year old man who had a major stroke affecting the territories of both posterior cerebral arteries, resulting in damage to L and R occipital cortex, R thalamus, and R medial temporal lobe (see below).Fig. 2 (Cappellari et al., 2009). MRI-DWI [diffusion weighted imaging] demonstrates areas of altered signal in bilateral occipital regions, right thalamus and right mesial temporal lobe [MTL, critical for memory], suggesting an ischemic origin [caused by decreased blood supply]. NOTE: R side of brain on L side of scan.Shortly thereafter, some of the ischemic areas started hemorrhaging (huge white areas in the CT scan below).Fig. 3 (Cappellari et al., 2009). Brain CT demonstrates a hemorrhagic transformation of the left temporal and occipital ischemic lesions.The resulting behavioral syndrome consisted of cortical blindness from the extensive damage to visual cortex, with anosognosia (denial or unawareness) for blindness, amnesia (from MTL damage), and topographical disorientation thrown in for good measure:Stable neurological picture, several days after onset, was characterized by persistent cortical blindness with absence of awareness of blindness, confabulation and spatial disorientation, recent memory disturbance, apathy, inertia and left hemiparesis [weakness].Along with all the other sensory and cognitive deficits, it seems like the co-occurrence of apathy and inertia was a good thing...ReferenceCappellari, M., Tomelleri, G., Matteo, A., Carletti, M., Magalini, A., Bovi, P., & Moretto, G. (2009). Dide-Botcazo syndrome due to bilateral occlusion of posterior cerebral artery Neurological Sciences DOI: 10.1007/s10072-009-0179-7
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Cappellari, M., Tomelleri, G., Matteo, A., Carletti, M., Magalini, A., Bovi, P., & Moretto, G. (2009) Dide-Botcazo syndrome due to bilateral occlusion of posterior cerebral artery. Neurological Sciences. DOI: 10.1007/s10072-009-0179-7
Cognitive empathy, or the ability to take another person's perspective, is closely related to (or even synonymous with) theory of mind,...the ability to attribute mental states—beliefs, intents, desires, pretending, knowledge, etc.—to oneself and others and to understand that others have beliefs, desires and intentions that are different from one's own.On the other hand, emotional or affective empathy is "emotional contagion" - the ability to mirror an emotional response observed in another person and to experience it vicariously. Dr. Simone Shamay-Tsoory and colleagues (2009a) have developed a model that distinguishes between the two types of empathy, which are represented by separate neuroanatomical systems (see figure below).Fig. 6 (Shamay-Tsoory et al., 2009a). Two separate systems for emotional and cognitive based empathy. Behaviourally, emotional empathy involves personal distress, empathic concern and emotion recognition. Anatomically the IFG [inferior frontal gyrus] appears to be responsible for emotional empathy. ... Cognitive empathy, on the other hand, involves perspective taking, the fantasy scale and theory of mind and is mediated by the VM [ventromedial prefrontal cortex].Individuals with bipolar disorder can show deficits in social cognition and emotion regulation even in the euthymic (remitted) state (Green et al., 2007). These observation led Shamay-Tsoory et al. (2009b) to examine cognitive and emotional empathy in 19 euthymic patients with bipolar disorder and 20 matched control participants:The cognitive and affective aspects of empathic abilities were assessed using the Interpersonal Reactive Index. The Interpersonal Reactive Index includes four seven-item subscales, each tapping a different aspect of empathy: (a) the perspective taking subscale, which measures the reported tendency to adopt spontaneously the psychological point of view of others; (b) the fantasy subscale, measuring the tendency to imaginatively transpose oneself into fictional situations; (c) the empathic concern scale, measuring the tendency to experience feelings of sympathy and compassion for others; and (d) the personal distress scale assesses the tendency to experience distress and discomfort in response to others’ observed distress.The perspective-taking subscale was used as a measure of cognitive empathy, and the personal distress scale was used as a measure of emotional empathy. To assess theory of mind, the ability to detect faux pas was examined using a set of stories developed by Baron-Cohen et al. (1999). For example:James bought Richard a toy airplane for his birthday. A few months later, they were playing with it, and James accidentally dropped it. "Don't worry" said Richard, "I never liked it anyway. Someone gave it to me for my birthday."Questions after each faux pas and control passage assessed story comprehension, false belief (i.e., the speaker had a mistaken belief and not malicious intent), faux pas detection, and specific identification of the faux pas. Also tested were recognition of emotional expressions from the eyes, cognitive flexibility, and spatial planning abilities.The results indicated that the participants with bipolar disorder had lower scores than controls for cognitive empathy, but higher scores for emotional empathy.Figure 1 (Shamay-Tsoory et al. (2009b). Participant Empathy Scores.A similar effect was observed in the faux pas task, with the patients impaired on cognitive understanding, but not in affective understanding or in recognition of the faux pas. This agrees with prior studies on theory of mind in bipolar disorder (Malhi et al., 2008; Montag et al., 2009). On the other hand, the bipolar individuals showed completely intact performance on recognizing emotion in the eyes and in the spatial planning task. However, they had difficulty in set shifting and reversal learning in the cognitive flexibility task. And greater difficulty with reversal learning was associated with lower cognitive empathy scores, suggesting that cognitive inflexibility contributes to the deficiency in taking another's perspective.What does this mean?The present study results suggest that [the likelihood to engage in the process of reflecting on the viewpoint of others] is impaired in bipolar disorder. On the second affective scale, personal distress, the bipolar disorder group actually scored significantly higher than healthy comparison subjects... This indicates a greater tendency to have self-oriented feelings of anxiety and discomfort in response to tense interpersonal settings........[Their] exaggerated emotional response to others may be expressed in a dysfunctional empathic emotional overreaction (or “hyper empathy”).This notion is consistent with the “simulation” theory, according to which individuals impersonate others’ emotional mental states, using their own mental state. Thus, it may be hypothesized that bipolar disorder patients tend to engage in the “oversimulation” of others’ emotions, as reflected in high affective empathy, and as a result, they tend to misinterpret others’ mental states, which is reflected in impaired cognitive empathy and theory of mind.What are the brain systems that mediate such difficulties in those with bipolar disorder? Returning to the model in Figure 6 (above), Shamay-Tsoory et al. (2009a) associated emotional empathy with the inferior frontal gyrus (IFG) and cognitive empathy with ventromedial prefrontal cortex (VM). How did they determine such a clear dissociation? This was from another experiment that administered the same set of tests to a different population: neurological patients with fairly discrete lesions in each of those brain areas.Fig. 2 (Shamay-Tsoory et al., 2009a). Group and task (cognitive versus emotional empathy) interactions. Significant interaction between group and empathy type. Patients with VM lesions were impaired in cognitive empathy compared to the healthy controls (HC), patients with posterior lesions (PC) and patients with IFG lesions whereas patients with IFG lesions wer... Read more »
Shamay-Tsoory, S., Aharon-Peretz, J., & Perry, D. (2009) Two systems for empathy: a double dissociation between emotional and cognitive empathy in inferior frontal gyrus versus ventromedial prefrontal lesions. Brain, 132(3), 617-627. DOI: 10.1093/brain/awn279
Shamay-Tsoory, S., Harari, H., Szepsenwol, O., & Levkovitz, Y. (2009) Neuropsychological Evidence of Impaired Cognitive Empathy in Euthymic Bipolar Disorder. Journal of Neuropsychiatry, 21(1), 59-67. DOI: 10.1176/appi.neuropsych.21.1.59
The Ventricles of the Brain (Ross & Wilson)You can always count on the journal Medical Hypotheses (published by Elsevier) for a good laugh. The Editor-in-Chief (Bruce G. Charlton) accepts all sorts of completely speculative crackpot articles. Who can forget the classic, Is there an association between the use of heeled footwear and schizophrenia? [see The Journal of Truly, Truly Outrageous Medical Hypotheses.] Or the crowd favorite, Ejaculation as a potential treatment of nasal congestion in mature males? [see More Truly, Truly Outrageous Medical Hypotheses.]The latest masterwork (Hendrie & Pickles, 2009) contends that major depression is an evolutionary adaptation triggered by damage to one's reproductive potential, which in turn causes the release of a yet-to-be-discovered nasty substance into the third ventricle:...depression is an evolutionary adaptation that emerged where displaced dominants needed to make a transition to lower social status and that is now triggered, in those individuals that have this adaptation, by damage to reproductive potential from any source. The behavioural cluster associated with depression includes adoption of a hunched posture, avoidance of eye contact, loss of appetite for food and sex and sleep disruption. This behavioural cluster serves to reduce an individuals’ attack provoking stimuli and so facilitates this social change. When viewed in this context, it becomes clear that many of the brain areas that mediate these behaviours (e.g. the pineal, hypothalamus and amygdala, whose main output, the stria terminalis passes through) all lie in close physical proximity to the third ventricle. In consequence, it is proposed that depression has its origins within this ventricle. Disruption of circadian rhythms, appetite for sex and food and fear/defence responses would all ensue if structures that border the third ventricle, or whose main connections pass through it, were damaged. Therefore, it is hypothesised that the behavioural expression of this adaptation is mediated by a single or pulsatile release of a yet to be identified noxious factor into the ventricular space.Where did these ideas come from?? Like most everyone else, Hendrie and Pickles (2009) are not satisfied with the current crop of antidepressants or with the monoamine hypothesis of depression (Hirschfeld, 2000), which is incomplete at best. Then they take a giant leap and make up one of those evo psych just-so stories:...damage to reproductive potential is now the key stimulus that triggers depression in those modern humans that have this adaptation, rather than loss of status per se.This analysis accounts for why it is life events such as the death of a spouse or a child that are major causes of depression.How about the death of a sister or a grandmother or an uncle? Or a beloved pet? Do these tragic events damage the reproductive potential of those who are prone to depression in such circumstances?And why is the third ventricle so important?...many of the brain areas mediating the behavioural cluster associated with depression are in close physical proximity to the third ventricle. For example, the pineal is involved with the regulation of sleep/wake cycles, the hypothalamus regulates appetite for food and sex and the amygdala, whose main output, the stria terminalis passes through the third ventricle has an influence on social affiliation as well as fear and defensive behaviours. Hence, it is proposed that this may well be the site where the behavioural expressions of depression are initiated.Fig. 3 (Hendrie & Pickles, 2009). Functions of structures closely associated with the third ventricle. The table shows those structures that directly border the third ventricle and those that are connected to it via structures that pass through. The function of the behavioural cluster associated with depression is to reduce the emission of attack provoking stimuli. This is achieved through increased defensiveness, decreased motivation to engage in consummatory behaviours and sleep disturbance, so that there are activity peaks at times when other individuals are inactive. The damage produced by the release of a noxious substance into the CSF [cerebrospinal fluid] is not under precise control...Uh huh. And how are we supposed to identify this unknown toxin released into the CSF in order to develop new treatments? They come up with two ideas:The first is to try and identify the proposed substance that is causing the damage with a view to blocking its action or preventing its’ release. This would however be technically difficult as it relies on obtaining samples of CSF from the third ventricle at a precise time, to catch the pulse or pulses. As this would probably not be possible in humans, animal models will be of importance...The second approach is to develop treatments that target the damage and so reverse its effects. Given that for purely statistical reasons, it is mostly glial cells that are affected, as may also be reflected in alterations to peripheral measures, growth factors such as BDNF and GDNF could be of benefit. ... Nonetheless, treatment using this approach will always be vulnerable to a second or subsequent release of the causative agent and hence the identification of that remains the real prize.Any takers? What a wonderful project for a graduate student!ReferencesHendrie, C., & Pickles, A. (2009). Depression as an evolutionary adaptation: Anatomical organisation around the third ventricle. Medical Hypotheses DOI: ... Read more »
Hendrie, C., & Pickles, A. (2009) Depression as an evolutionary adaptation: Anatomical organisation around the third ventricle. Medical Hypotheses. DOI: 10.1016/j.mehy.2009.10.026
Internet addiction is a murky and controversial disorder that is the subject of intense debate over whether it should be included in the new DSM-V. Here are the proposed diagnostic criteria as developed by Dr. Kimberly Young:Do you feel preoccupied with the Internet (think about previous online activity or anticipate next online session)?Do you feel the need to use the Internet with increasing amounts of time in order to achieve satisfaction?Have you repeatedly made unsuccessful efforts to control, cut back, or stop Internet use?Do you feel restless, moody, depressed, or irritable when attempting to cut down or stop Internet use?Do you stay on-line longer than originally intended?Have you jeopardized or risked the loss of significant relationship, job, educational or career opportunity because of the Internet?Have you lied to family members, therapist, or others to conceal the extent of involvement with the Internet?Do you use the Internet as a way of escaping from problems or of relieving a dysphoric mood (e.g., feelings of helplessness, guilt, anxiety, depression)? Answering "yes" to five or more questions may mean you suffer from Internet addiction over a six month period and when not better accounted for by a manic episode.You can rate your own level of addiction by taking the Internet Addiction Test (sponsored by The Center for Internet Addiction, of course).Dr. Young was featured in a recent article, along with Dr. Vaughan Bell (of Mind Hacks fame) taking the contrary position:Internet addiction: New-age diagnosis or symptom of age-old problem?. . .Kimberly Young, director of the online resource The Center for Internet Addiction, says that internet addiction may not yet be clearly defined, but you know it when you see it.. . .Young: “The internet has inherent value and utility, and there are many good things about it, but there is this dark side.”Or is there? Not according to Vaughan Bell, a visiting research fellow with the Department of Clinical Neuroscience, Institute of Psychiatry at King's College London in the United Kingdom. Bell has argued that the internet is not an activity, and therefore internet addiction is a flawed idea (J Ment Health 2007;16:445-57).“Fundamentally, the internet is a medium of communication,” says Bell, who claims that one can no more be addicted to the internet than to radio waves. “The concept itself doesn’t make sense.”Bell acknowledges that some people use the internet and other technologies to excess, but believes they do so to avoid dealing with underlying problems, such as depression or social anxiety disorder, which have well-established treatments.Other prolific bloggers who are noted opponents of the IA diagnosis include Dr. Shock and Dr. John Grohol.1 On the other hand, internet addiction is accepted as a major a problem in several Asian countries, including China and South Korea. Some of you might be familiar with the stories of [alleged] abusive and illegal clinics in China. With this as background, it was inevitable that someone would do a neuroimaging study of individuals with IA, and it was a group in Shanghai that was the first to do so (Zhou et al., 2009).In their study, 18 teenagers (2 females and 16 males, mean age = 17.23 ± 2.6) with IA were compared to 15 age-matched control participants. Structural MRIs were performed and quantified using voxel-based morphometry (VBM):VBM is a neuroimaging analysis technique that allows investigation of focal differences in brain anatomy, using the statistical approach of so-called statistical parametric mapping. ... VBM registers every brain to a template, which gets rid of most of the large differences in brain anatomy among people. Then the brain images are smoothed so that each voxel represents the average of itself and its neighbors. Finally, the image volume is compared across brains at every voxel.The paper was very light on analytic methods and mum on important details about possible co-morbid psychiatric diagnoses in the kids with IA. As noted by Vaughan, depression and social phobia -- along with bipolar disorder, obsessive-compulsive disorder, various addictions, and other impulse control disorders -- could compel one to spend more time on the internet for gambling, gaming, chatting, porn-watching, etc.With all these caveats in mind, the results are shown below....the VBM of the MRI data illustrated that the IA group had lower GMD [gray matter density] in the left anterior cingulate cortex (ACC), left posterior cingulate cortex (PCC), left insula, and left lingulate gyrus. No significant difference was found in the white matter change between the two groups.Fig. 1 (Zhou et al., 2009). Regions of decreased GM shown on the template in the left anterior cingulate cortex (A), left posterior cingulate cortex (B), left insula (C), and left lingual gyrus (D) in IA subjects compared with the controls.Most of the changes look pretty small, so it's hard to know what to make of them. On top of that, some of the regions seem mislabeled (the posterior cingulate in particular looks way off). And the findings only demonstrate correlation, not causation.So in the end we have no idea if "internet addiction" shrinks tiny bits of your brain...Footnote1 Blogging and social media are not addictive at all. Right?ReferenceZhou, Y., Lin, F., Du, Y., Qin, L., Zhao, Z., Xu, J., & Lei, H. (2009). Gray matter abnormalities in Internet addiction: A voxel-based morphometry study. ... Read more »
Zhou, Y., Lin, F., Du, Y., Qin, L., Zhao, Z., Xu, J., & Lei, H. (2009) Gray matter abnormalities in Internet addiction: A voxel-based morphometry study. European Journal of Radiology. DOI: 10.1016/j.ejrad.2009.10.025
Contour Drawing Rating Scale (Thompson & Gray, 1995) - established as a reliable and valid measure of body size perception.Anorexia nervosa, an obsessive and unrelenting quest for thinness, is one of the most deadly psychiatric disorders. The documented mortality rate ranges from 3.3% to 18% in different studies (Herzog et al., 2000), and those with the disorder are ten times more likely to die from their illness than a comparable healthy population. A severe distortion of body image is a cardinal feature of anorexia:Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight.An excellent recent review covered the alterations in widespread neural circuits observed in those with anorexia, along with abnormalities in the neurotransmitters serotonin and dopamine (Kaye et al., 2009):New brain imaging technology provides insights into ventral and dorsal neural circuit dysfunction — perhaps related to altered serotonin and dopamine metabolism — that contributes to the puzzling symptoms found in people with eating disorders. For example, altered insula activity could explain interoceptive dysfunction, and altered striatal activity might shed light on altered reward modulation in people with anorexia nervosa.Another angle to examine is the reason for such pervasive distortions of self-image. Are there literally changes in visual cortex function that correlate with this symptom?But first, a few words on some confusing neuroanatomical terminology. The striatum is a subcortical structure that consists of the caudate nucleus and the putamen. As mentioned above, the striatum is involved in reward processing (among other things). On the other hand, the primary visual cortex, or V1 (at the back of the occipital lobe) is sometimes referred to as striate cortex. Higher levels of visual cortex beyond V1 are known as extrastriate cortex. And there is where our story begins.In 2001, an fMRI study demonstrated that a specific region in extrastriate cortex, in the lateral occipitotemporal cortex, showed selective responses to pictures of bodies and body parts relative to other types of visual stimuli (Downing et al., 2001). The authors dubbed this region the "extrastriate body area" (EBA). An earlier study in epileptic patients (McCarthy et al., 1999) found regions that showed selective responses to hands, relative to faces and objects (they didn't test other body parts). Instead of using fMRI, McCarthy and colleagues recorded from electrode grids placed directly on the cortical surface for the purpose of monitoring for seizures, prior to surgical resection of the epileptogenic tissue. They observed a specific electrophysiological response, which was evoked 230 msec after the subjects viewed pictures of hands.So the question arises, are there neuroanatomical and functional changes in the extrastriate body area of individuals with anorexia? Suchan et al. (2009) quantified the structural MRIs of 15 women with anorexia and 15 healthy control women. They also localized the EBA using functional MRI -- participants viewed the stimuli used in the study of Downing et al. (freely available for download). The participants also completed the Contour Drawing Rating Scale, and the scores were compared to those given by 10 independent female raters who viewed photos of the subjects.Not surprisingly, the women with anorexia (BMI=16.0, see images of Christian Bale in Anorexia, Insomnia, and Paranoia for an example) overestimated their body size. Conversely, the healthy women (BM=22.0) underestimated their body size. And using a whole-brain voxel-based morphometric analysis, gray matter density was indeed reduced in the left EBA of the anorexic participants.Fig. 2 (Suchan et al. (2009). Activation of the extrastriate body area (EBA) localizer scans from healthy age matched controls (blue), women with anorexia nervosa (AN; green) and reduction of gray matter in the EBA of the AN group (white). Overlap between EBA activation of healthy, age matched controls and AN is coloured in light-blue.Of course, whether the neuroanatomical change is a cause or an effect of the disease is unknown, as acknowledged by the authors:Although the present study is the first to demonstrate focused gray matter volume reduction in the EBA, several open questions remain. First, the causality is unclear. Future studies using a longitudinal design should focus on the question of whether the EBA volume reductions precede the onset of the AN and therefore might be of etiological relevance or whether they are a result of the disorder.Nevertheless, preliminary evidence supports a role for visual perceptual deficits contributing to body image distortion in anorexia nervosa.I'll leave you with the music video for Tunic (Song for Karen) by Sonic Youth. It's a weirdly arty but touching depiction of Karen Carpenter's struggle with anorexia and bulimia, with Kim Gordon as Karen.dreaming, dreaming of a girl like mehey what are you waiting for - feeding, feeding meI feel like I'm disappearing - getting smaller every daybut I look in the mirror - I'm bigger in every wayTunic (Song for Karen) ------Sonic YouthReferencesDowning PE, Jiang Y, Shuman M, Kanwisher N. (2001). A cortical area selective for visual processing of the human body. Science 293:2470-3.Herzog DB, Greenwood DN, Dorer DJ, Flores AT, Ekeblad... Read more »
Suchan, B., Busch, M., Schulte, D., Grönermeyer, D., Herpertz, S., & Vocks, S. (2010) Reduction of gray matter density in the extrastriate body area in women with anorexia nervosa. Behavioural Brain Research, 206(1), 63-67. DOI: 10.1016/j.bbr.2009.08.035
I've opened up these scarsI'll make you face thisI pulled myself so farI'll make you, face, this, now!---Linkin ParkDeliberate self-harm, or self-injury, is becoming increasingly recognized as a problem affecting adolescents and young adults. Rates are difficult to determine, as the behaviors are often concealed. One recent study tracked a group of 1400 Midwestern US high school students over a 5 year period (Muehlenkamp et al., 2009). Rates of non-suicidal self-injury (NSSI) over 2001-205 were as follows:Besides being associated with depression and eating disorders (especially among girls), the current psychiatric bible (DSM-IV-TR) includes self-injury as one of nine diagnostic criteria for Borderline Personality Disorder:Recurrent suicidal behavior, gestures, threats or self-injuring behavior such as cutting, interfering with the healing of scars (excoriation) or picking at oneself.Other criteria of BPD include:A pattern of unstable and intense interpersonal relationships characterized by alternating between extremes of idealization and devaluation.Identity disturbance: markedly and persistently unstable self-image or sense of self.Impulsivity in at least two areas that are potentially self-damaging (e.g., promiscuous sex, eating disorders, binge eating, substance abuse, reckless driving).Affective instability due to a marked reactivity of mood (e.g., intense episodic dysphoria, irritability or anxiety usually lasting a few hours and only rarely more than a few days).Although it's considered a very serious personality disorder, the diagnostic label is a controversial one, coming under fire from feminists (Shaw & Proctor, 2005) and from some psychiatrists, like Dinah at Shrink Rap (see Over The Border Line).Why Do Cutters Have Reduced Pain Perception?An earlier study by Schmahl et al. (2006) examined the Neural correlates of antinociception in borderline personality disorder during the administration of heat pain. Do borderline patients injure themselves to "feel" (or "feel more normal") OR to down-regulate the emotional components of pain? The results didn't really answer this question, but the authors gave two options:Limbic deactivation has been found to correlate with the degree of coping in aversive situations in general. . . . Thus, in view of these findings, self-inflicted pain may function to normalize neural activity in specific brain regions involved in emotional and cognitive processing. Alternatively, repeated self-injury could lead to an adaptation of pain thresholds and pain processing reflected in the current findings of elevated pain thresholds and disturbed prefrontal and limbic pain processing.A new fMRI study by Kraus et al. (2009) took a different approach and compared BPD patients and controls who listened to standardized scripts of self-injurious behavior while in the scanner. The procedure was as follows:Script-driven imagery was utilized to deliberately evoke emotional distress. The segments were Neutral (a woman on a shopping trip), Trigger (the woman watching a dispute between a mother and her child), Cognitive and Emotional Reactions (think about similar situations with your own mother), Self-Injurious Behavior (a typical act is described, from preparation to cutting itself), and Relaxation (presumably including the SI-induced decrease in aversive inner tension in BPD).For the between-group comparisons, the imaging data weren't particularly strong at revealing robust differences. The primary finding was reduced activity in left orbitofrontal cortex in the BPD patients during the Cognitive and Emotional Reaction phase, possibly reflecting dysregulation of emotional control. However, the most intriguing finding in my view was deactivation in mid-cingulate cortex during the Self-Injury script. Although the authors didn't plot this result, the coordinates for the deactivation overlap with regions of the anterior cingulate involved in the affective components of pain (Rainville et al., 1997).What's plotted below is the result of a coordinate-based meta-analysis of the neuroimaging literature on pain perception using the activation likelihood estimation (ALE) method. Articles on physical pain were identified in the BrainMap database (see Hypnosis and Pain Control for details). Of relevance for our current purposes is this midsaggital slice showing strong activation across studies of pain perception in a region of the anterior cingulate cortex that showed deactivation in the BPD patients during the self-injury script (the precise focus is indicated by the blue crosshairs). Although very preliminary, this finding may suggest that imagining an act of self-injury may downregulate the affective component of pain in individuals with borderline personality disorder.As always, there are limitations with such a pilot study. The authors even list them at the outset:Fixed-effects analyses limit the ability to generalize from the study sample to the larger population of patients with borderline personality disorder (BPD).Due to the study design, a single section of the script could not be repeatedly presented, thus possibly diminishing the effect size of our results.As no control script was used, it cannot be determined whether our findings are related to self-injurious behavior (SIB) per se or to BPD features in general.Nonetheless, Kraus et al. are continuing to expand on this work with fMRI studies that more closely mimic SIB than the present script design.References... Read more »
Kraus, A., Valerius, G., Seifritz, E., Ruf, M., Bremner, J., Bohus, M., & Schmahl, C. (2009) Script-driven imagery of self-injurious behavior in patients with borderline personality disorder: a pilot FMRI study. Acta Psychiatrica Scandinavica. DOI: 10.1111/j.1600-0447.2009.01417.x
Taken from Fig. 1 (Bewernick et al., 2009). Hamilton Depression Rating Scale (PDF) over time.Two and a half years ago, The Neurocritic wrote about the very early results of deep brain stimulation (DBS) in the nucleus accumbens for severe, refractory depression. You can read about the details of the procedure and its scientific motivation here:More About the Nucleus AccumbensNAcc Localization for DBSBriefly, the nucleus accumbens (NAcc) is considered one of the brain's PLEASURE CENTRES:When the cortex has received and processed a sensory stimulus indicating a reward, it sends a signal announcing this reward to a particular part of the midbrain–the ventral tegmental area (VTA)–whose activity then increases. The VTA then releases dopamine not only into the nucleus accumbens, but also into the septum, the amygdala, and the prefrontal cortex.The nucleus accumbens then activates the individual’s motor functions, while the prefrontal cortex focuses his or her attention.It makes sense as a DBS target region from the standpoint of 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" in the NAcc.The current paper by Bewernick et al., 2009 reports on the results from 10 patients who received NAcc-DBS for at least 12 months. These patients were severely ill and completely non-responsive to any other treatment. On average, they had been continuously depressed for 10 years, were completely unable to work, had been hospitalized numerous times, had failed over 20 medication treatment courses, were currently on 4 different drugs, had received over 20 electroconvulsive therapy (ECT) treatments, and 316 hours of therapy, all to no avail.The primary results are illustrated in Fig. 1 above. Half the patients (n=5) were considered "treatment responders" who experienced a 50% reduction of depressive symptom severity as assessed by the HDRS, and half did not respond. Anxiety scores also declined in the responders, and engagement in pleasant activities increased.There were some adverse events related to the surgical procedure (swollen eye in 6 patients, pain and dysphasia in 3), as well as transient adverse events related to stimulation parameter changes e.g., anxiety (n=3), hypomania, paresthesia, and agitation (all n=2). Nonetheless, the authors concluded on a positive note:DBS to the nucleus accumbens had clinically relevant antidepressant and antianhedonic effects in a patient population that was at least as treatment-resistant as those reported on in other studies of DBS in major depression (Lozano et al., 2008; Malone et al. 2009). The efficacy to adverse event ratio in this small group was favorable. Site-specific antianxiety effects also could be demonstrated.By targeting one site in a network of brain regions implicated in processing of affective stimuli, it was possible to manipulate anhedonia in particular. Additional studies with larger sample sizes and rigid selection criteria are needed to analyze effects of stimulation to different targets on specific symptoms and clinical phenotypes of depression. In the future, symptom-based DBS therapy, adapted to the individual needs of the patients, could be a plausible treatment option for severe TRD.ReferencesBewernick, B., Hurlemann, R., Matusch, A., Kayser, S., Grubert, C., Hadrysiewicz, B., Axmacher, N., Lemke, M., Cooper-Mahkorn, D., & Cohen, M. (2009). Nucleus Accumbens Deep Brain Stimulation Decreases Ratings of Depression and Anxiety in Treatment-Resistant Depression. Biological Psychiatry DOI: 10.1016/j.biopsych.2009.09.013Lozano AM, Mayberg HS, Giacobbe P, Hamani C, Craddock RC, Kennedy SH. (2008). Subcallosal cingulate gyrus deep brain stimulation for treatment-resistant depression. Biol Psychiatry 64:461-7.Malone DA Jr, Dougherty DD, Rezai AR, Carpenter LL, Friehs GM, Eskandar EN, Rauch SL, Rasmussen SA, Machado AG, Kubu CS, Tyrka AR, Price LH, Stypulkowski PH, Giftakis JE, Rise MT, Malloy PF, Salloway SP, Greenberg BD. (2009). Deep brain stimulation of the ventral capsule/ventral striatum for treatment-resistant depression. Biol Psychiatry 65:267-75.
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Bewernick, B., Hurlemann, R., Matusch, A., Kayser, S., Grubert, C., Hadrysiewicz, B., Axmacher, N., Lemke, M., Cooper-Mahkorn, D., & Cohen, M. (2009) Nucleus Accumbens Deep Brain Stimulation Decreases Ratings of Depression and Anxiety in Treatment-Resistant Depression. Biological Psychiatry. DOI: 10.1016/j.biopsych.2009.09.013
"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 as...an 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 foods...in 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.
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