Scam Journals Uncovered by Improbable Research

Improbable Research has recently reported on some unbelievably brash copyright violations by a set of scam journals:

Strange academic journals: Scam?

We have discovered what may be the world’s strangest collection of academic journals. Published by a shadowy entity, it suggests — at first glance, anyway — some kind of scam. But is there a scam, or not? If there is, what’s the point of it? If there’s not, same question. Maybe you can help us find the answers.

One journal is named Psychology. All its articles have been previously published in reputable journals, some almost a decade ago — but nowhere is that mentioned.

The abstract for one of the articles (PDF) is shown below.



It's absolutely identical to an article already published in the Journal of Personality and Social Psychology:

DeWall CN, Twenge JM, Gitter SA, Baumeister RF (2009). It's the thought that counts: The role of hostile cognition in shaping aggressive responses to social exclusion. J Pers Soc Psychol. 96:45-59 [request PDF].

Since two of the plagiarized articles were stolen from JPSP, I contacted both editors, Dr. Charles M. Judd and Dr. Jeffry A. Simpson. Dr. Simpson wrote back right away, advising me to contact the American Psychological Association, which holds the copyrights to all APA journals. I did send an email to the Copyright and Permission office and am waiting to hear back.

Since...

3. Permission is Not Required for the Following:

• A maximum of three figures or tables from a journal article or book chapter
• Single text extracts of less than 400 words
• Series of text extracts that total less than 800 words

No formal requests to APA or the author are required for the items in this clause.

...I'm reproducing the abstract below [it's 148 words long].


Click on image for a larger view and compare to abstract above.

Some other lovely tidbits from the Improbable Research post:

The publisher, Scientific Research Publishing, has other journals, as well. Some of them ... also appear to follow the “publish things that were already published, but don’t mention that” principle.

On the organization’s web site, we found barely any identifying or location information. The contact page says “Name: Scientific Research Publishing, Inc. USA” and lists an email address — but we have not found any such corporation in the USA, and email sent to that address has produced no reply. The web site is registered to an organization in Wuhan, China.

Some quick Googling of "Scientific Research Publishing, Inc." turned up a link to the professional activities of Dr. Dharma P. Agrawal, which include:

• Editorial Board Member, International Journal of Communications, Network and System Sciences (IJCNS), published by “Scientific Research Publishing,” Scientific Research Publishing, Inc. 5005 Paseo Segovia, Irvine, CA.

That's interesting, because 5005 Paseo Segovia, Irvine, CA is a private single-family residence that was last sold for $685,000 on 9/22/2008.

Let's conclude with a bit of irony from Scientific Research themselves:

For Authors

Submitted papers should not have been previously published nor be currently under consideration for publication elsewhere. Paper submission will be handled electronically through the PSYCH online system. All papers are refereed through a peer review process.

They also had the nerve to print 'Copyright © 2009 SciRes.' on every page of the purloined PDFs.

There's a little more sleuthing in this October 2009 thread in the JREF Forum [James Randi Educational Foundation]. I'll post more information if/when it arrives. Stay tuned.

via @noahWG.

UPDATE: The APA Permissions Office was already aware of the copyright violation, and they are currently looking into it.

Christmas Cheer from BMJ

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!

Reference

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

It Seems Like I've Been Here Before

Help me, somebody help me
I wonder where I am

Everything's Gone Green
----New Order

Edward 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 superior pole, and left-sided hyperperfusion of the cerebellum, operculum, insula, lingual gyrus, precuneus, and middle temporal gyrus. Hypoperfusion appeared bilaterally in the precentral and postcentral gyri, as well as in the frontal (especially supplementary motor cortex) and parietal areas.

Since no other cases of déjà vu have been reported in patients undergoing similar DBS, Kovacs and colleagues speculated that atypical neuroanatomy might have contributed to the phenomenon in this individual. An MRI prior to surgery showed right hemisphere dominance for language. In addition, they speculated on a possible functional relationship between the hippocampus and the contralateral basal ganglia, based on studies in rats. But overall, the authors admit they can't explain the pathophysiology of this unique DBS-evoked déjà vu.


Footnote

¹ Unorthodox, to say the least. Check out "vortex pluralism" -- his bizarre hypothesis to solve the mind-body problem.

² For more on these classic stimulation studies, check out Wilder Penfield, Neural Cartographer.

References

Bancaud J, Brunet-Bourgin F, Chauvel P, Halgren E. (1994). Anatomical origin of déjà vu and vivid ‘memories’ in human temporal lobe epilepsy. Brain 117:71–90.

Gloor P, Olivier A, Quesney LF, Andermann F, Horowitz S. (1982). The role of the limbic system in experiential phenomena of temporal lobe epilepsy. Ann Neurol 12:129–44.

Halgren E, Walter RD, Cherlow DG, Crandall PH. (1978). Mental phenomena evoked by electrical stimulation of the human hippocampal formation and amygdala. Brain 101:83–117.

Hughlings-Jackson J. (1888). On a particular variety of epilepsy (“intellectual aura”), one case with symptoms of organic brain disease. Brain 11:179–207

KOVACS, N., AUER, T., BALAS, I., KARADI, K., ZAMBO, K., SCHWARCZ, A., KLIVENYI, P., JOKEIT, H., HORVATH, K., & NAGY, F. (2009). Neuroimaging and cognitive changes during déjà vu. Epilepsy & Behavior, 14 (1), 190-196. DOI: 10.1016/j.yebeh.2008.08.017

Mullan S, Penfield W. (1959). Illusions of comparative interpretation and emotion: production by epileptic discharge and by electrical stimulation in the temporal cortex. AMA Arch Neurol Psychiatry 81:269–84.

Neppe V. (1983). The psychology of déjà vu: have I been here before? Witwatersrand University Press, Johannesburg.

Squire LR, Alvarez P. (1995). Retrograde amnesia and memory consolidation: a neurobiological perspective. Curr Opin Neurobiol 5:169–77.

Vignal JP, Maillard L, McGonigal A, Chauvel P. (2006). The dreamy state: hallucinations of autobiographic memory evoked by temporal lobe stimulations and seizures. Brain 130:88-99.

Wild E. (2005). Déjà vu in neurology. J Neurol. 252:1-7.

It seems like I've been here before
It seems like I've been here before
It seems like I've been here before
It seems like I've been here before.

----New Order

WATCH - Everything's Gone Green

Kittens in the Operating Room

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

Surprise Kitty

I warned you...

No More Drama

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 life

No More Drama
-----Mary J. Blige

Women 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.

References

Craig 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.2008.05.027

Stark 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, 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, 879-887. DOI: 10.1017/S135561770999049X

WATCH - No More Drama

Spindle Neurons in Elephants and Dolphins: Convergent Evolution in Large-Brained Mammals?

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.

References



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

Goodman, 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.20829

Hof 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, Allman JM, Perl DP, Erwin JM, Hof PR. (1999). A neuronal morphologic type unique to humans and great apes. Proc Natl Acad Sci 96:5268-73.


Fig. 5 (Hakeem et al., 2009). The phylogenetic distribution of the VENs. Species in which VENs have been observed are indicated by underlines; species which have been examined and found to possess no VENs are indicated by italics. Note that while the African and Indian elephants have VENs, they share this trait only with other large-brained groups (the cetaceans and humans/great apes) and not with their nearest relatives, the rock hyrax, manatee, giant elephant shrew, and tenrecs.

The Horror of Dide-Botcazo Syndrome

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...

Reference

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

Impaired Cognitive Empathy in Bipolar Disorder and in Patients with Ventromedial Prefrontal Lesions

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 were impaired in emotional empathy compared to the HC, VM and the PC group.

As with most things, though, the anatomical dissociation wasn't completely clean; there was some degree of overlap, as shown below.

Fig. 5 (Shamay-Tsoory et al., 2009a). Location and overlap of brain lesions according to emotional versus cognitive empathy impairment-groups. (A) Lesions of the emotional-empathy-impaired group (n=6). Four patients had an IFG damage involving [Brodmann] area 44, one had a VM damage and one had a PC damage. Chi-square analysis revealed that lesions involving area 44 were significantly more frequent in this group as compared to the non-impaired group. (B) Lesions of the cognitive-empathy-impaired group (n=7): five had VM damage involving area 10 and 11, one had an IFG damage and one had a PC damage. Chi-square analysis revealed that lesions involving area 10 and area 11 were significantly more frequent in this group as compared to the non-impaired group.

Nonetheless, such human lesion studies can demonstrate the importance of specific brain areas for the cognitive or emotional processes in question, thereby illuminating the underlying neural network abnormalities in psychiatric disorders.

References

Baron-Cohen S, O'Riordan M, Stone V, Jones R, Plaisted K. (1999). Recognition of faux pas by normally developing children and children with Asperger syndrome or high-functioning autism. J Autism Dev Disord. 29:407-18.

Green MJ, Cahill CM, Malhi GS. (2007). The cognitive and neurophysiological basis of emotion dysregulation in bipolar disorder. J Affect Disord. 103(1-3):29-42.

Malhi GS, Lagopoulos J, Das P, Moss K, Berk M, Coulston CM. (2008). A functional MRI study of Theory of Mind in euthymic bipolar disorder patients. Bipolar Disord. 10:943-56.

Montag C, Ehrlich A, Neuhaus K, Dziobek I, Heekeren HR, Heinz A, Gallinat J. (2009). Theory of mind impairments in euthymic bipolar patients. J Affect Disord. Sep 12. [Epub ahead of print].



Shamay-Tsoory, S., Aharon-Peretz, J., & Perry, D. (2009a). 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. (2009b). 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


Figure 2 (de Waal, 2008). The Russian doll model of empathy and imitation. Empathy (right) induces a similar emotional state in the subject and the object, with at its core the perception-action mechanism (PAM). The doll's outer layers, such as sympathetic concern and perspective-taking, build upon this hard-wired socio-affective basis. Sharing the same mechanism, the doll's imitation side (left) correlates with the empathy side. Here, the PAM underlies motor mimicry, coordination, shared goals, and true imitation. Even though the doll's outer layers depend on prefrontal functioning and an increasing self-other distinction, these outer layers remain connected to its inner core.

The Stanley Cup of Neuroscience

The brain of famous amnesic patient H.M. is being sectioned right now!



Watch it live at The Brain Observatory.

They are currently cutting the frontal lobe.

UPDATE (Dec. 3, 1:40PM): They've entered the temporal lobes.

UPDATE (Dec. 4, 1:35PM): Primary visual cortex has surfaced. The end is in sight!

UPDATE (Dec. 4, 11:11PM): They're almost finished!


Below is an MRI of H.M.'s brain when he was still alive.


Figure 1 (Corkin, 2002). Multiplanar views of 18 averaged T1-weighted MRI volumes showing preserved structures in H.M.’s MTL. This magnetic resonance imaging (MRI) scan was obtained on 15 December 1998. The images are based on data averaged over 18 runs; images were motion corrected using the first scan (out of the 18 axials) as a reference. The asterisk marks the intersection of the three viewing planes, just caudal to the left medial temporal lobe (MTL) resection, seen best in the transaxial view. Top left, sagittal view; bottom left, coronal view; bottom right, transaxial view; top right, surface rendering showing locations of transaxial and coronal planes. Abbreviations: CS, collateral sulcus; EC, entorhinal cortex; H, hippocampus; L, left; PH, parahippocampal gyrus; R, right.


Coda (from Corkin, 2002):

Prospects

H.M. is now 75 years old. His mobility is markedly reduced because of osteoporosis, another side effect of phenytoin (Dilantin). Although he is in relatively good health, plans are in place for the post-mortem examination of his brain when he dies. He and his court-appointed conservator have both signed his brain donation form, ensuring that the final chapter in his lifelong contribution to science will include a precise description of his brain and documentation of his lesion. His wish to help other people will have been fulfilled. Sadly, however, he will remain unaware of his fame and of the impact that his participation in research has had on scientific and medical communities internationally.

An impact he could never appreciate: Henry G. Molaison died a year ago today on Dec. 2, 2008 at the age of 82.

Noxious mystery substance released into the third ventricle is the cause of depression!

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!

References

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

Hirschfeld RM. (2000). History and evolution of the monoamine hypothesis of depression. J Clin Psychiatry 61 Suppl 6:4-6.