The Neurocritic

Genomarketing!

2009-11-08T14:42:00.000-08:00

You've heard of Neuromarketing, which measures the neural activity of consumers (via fMRI or EEG) in response to various products or advertisements. Now, get ready for Genomarketing! The Neuroethics & Law Blog has alerted us to a recent paper by De Neve and Fowler (2009) reporting that people with a specific low efficiency variant of the gene for monoamine oxidase A are significantly more likely to have credit card debt. Monoamine oxidase A (MAO-A) is an enzyme that breaks down the monoamine neurotransmitters (dopamine, norepinephrine, epinephrine, and serotonin). Using data from the National Longitudinal Study of Adolescent Health, the authors found in that sample of 18-26 year olds,

Having one or both MAOA alleles of the low efficiency type raises the average likelihood of having credit card debt by 7.8% and 15.9% respectively. About half of [the U.S.] population has one or both MAOA alleles of the low type. Prior research has linked this genetic variation to lack of conscientiousness, impulsivity, and addictive behavior.

Is this the foreshadowing of a highly unethical marketing practice? Marketing based on MAO-A genotype, as determined from mailed-in credit card applications and payments? Credit card companies will have in-house labs to extract DNA from stamps and envelope flaps (Sinclair & McKechnie, 2000; Ng et al., 2007).¹ Taking it one step further, entire marketing campaigns will be tailored to specific markers in an individual’s genome.²

Is this what it’s coming to? Not so fast. Are there any limitations in the findings of De Neve and Fowler (2009)? There are many!! The paper reported:

Allele frequency for the low grouping is 41% and high grouping is 59% in our sample. In Wave III, subjects were asked “Do you have any credit card debt?" About 41% answered in the affirmative.

However, the ONLY question was asked was “Do you have credit card debt?” – not how much debt or anything else. And of course, the interactions between genes and environment are immense, despite what simplistic popular media notions might lead you to believe (see Neuroanthropology for a critique). Without getting into details (which are better left to other blogs), De Neve and Fowler also note that:

Model 2 includes a number of socio-economic factors that influence financial decision-making. Income and education may in fact mediate the relationship between the genes we have identified and credit card usage.

Finally, another recent paper (Beaver & Holtfreter, 2009) found that possessing the high efficiency MAO-A allele (opposite of the one discussed here) predicts involvement in fraudulent behaviors. But only if you hang around with the wrong crowd. Specifically,

Analysis of male participants from the National Longitudinal Study of Adolescent Health (J. R. Udry, 2003) revealed a statistically significant Gene × Environment interaction in which the high-MAOA activity allele increased the odds of fraudulent behaviors, but only among male participants with a high number of delinquent peers.

Fraudulent behavior was determined by two questions. Can you guess them?

(1) How many times during the past 12 months have you used someone else’s credit card or bank card without their permission or knowledge?

(2) How many times during the past 12 months have you deliberately written a bad check?

Ha! Beaver and Holtfreter discuss the contrast of careful and deliberate planning [high-activity alleles] vs. impulsive violence³ [which also has a link to low-activity alleles]:

Genetic imaging research examines whether different alleles of a particular polymorphism are associated with differences in brain structure and functioning. Results have revealed that respondents possessing the low-MAOA activity alleles have limbic volume reductions, decreased cingulate activation, and hyperactivity in the amygdala and hippocampus—differences that may begin to explain the link between MAOA and violence. However, the etiologies of serious violence and fraudulent behaviors may be dissimilar. For example, engaging in fraudulent behaviors may take more time and more planning than is typical of most other antisocial behaviors, which are relatively unplanned and impulsive.

Bernie Madoff vs. Phil Spector? Sort of.

Footnotes

¹ This would only work, of course, for those who still conduct such business the old fashioned way. And please note that the cited references use these techniques for legitimate purposes!!

² See also Please Complete a Genome Scan with Your Mortgage Application.

³ Just stating the obvious here, but having credit card debt in no way, shape, or form implies that one is violent.

References

Beaver, K., & Holtfreter, K. (2009). Biosocial Influences on Fraudulent Behaviors. The Journal of Genetic Psychology, 170 (2), 101-114. DOI: 10.3200/GNTP.170.2.101-114

De Neve, Jan-Emmanuel and Fowler, James H. The MAOA Gene Predicts Credit Card Debt (August, 18 2009). Available at SSRN: http://ssrn.com/abstract=1457224

Ng LK, Ng A, Cholette F, Davis C. (2007). Optimization of recovery of human DNA from envelope flaps using DNA IQ System for STR genotyping. Forensic Sci Int Genet. 1(3-4):283-6.

Sinclair K, McKechnie VM. (2000). DNA extraction from stamps and envelope flaps using QIAamp and QIAshredder. J Forensic Sci. 45(1):229-30.

A New Outlook

2009-11-06T02:39:00.000-08:00

"A New Outlook" is a multimedia installation by Bree Yenalavitch at...

...Project Room G3, an artist run project space found by Sojung Kwon started April 2009, that focuses on work which has a performative, temporal, and non-classical aesthetic. It is located at Angels Gate Cultural Center in San Pedro [in Southern California].

Bree Yenalavitch is a Los Angeles area artist working in multimedia. She received her BA from the University of California Santa Barbara in 2002 and MFA from Otis College of Art and Design in 2006. Her recent online project can be viewed at www.thebree.tv, where she presents the laboratory of Dr. Specialist - a great woman of science. Bree can also be seen in the Inauguration Show at Project Room G3, where viewers interacting with her participatory project will find their perspective has been rendered askew.

Everything in its Right Place

2009-11-06T01:50:00.000-08:00

Sarah Sze
Things Fall Apart
2001
"010101: Art in Technological Times"

Sarah Sze is a contemporary visual artist (and winner of a MacArthur Fellowship in 2003) who creates unique, site-specific sculptures and installations which make use of ordinary technological and scientific objects.

Sarah Sze
Everything in its Right Place

Even the details in Sarah Sze’s sculptures have details. All her installations are extraordinarily ambitious and are constructed with fastidious precision, consequently, her output is relatively small compared with many other artists. Everything in its Right Place, 2002–03, is one of her most important and most ambitious works.
...
The multitude of small parts in Sze’s Everything in its Right Place shifts us away from a panoramic spectatorship to inspection mode. The site-specificity of Sarah Sze’s work is best understood through the idea of environments created by overarching structures of collection and models, where narratives and nostalgias intersect as property and space, affecting us through the flickering effect of their soaring elegance and beauty.

And then we have the ever-optimistic Thom York of Radiohead, who has a different idea of the concept...

Everything, everything, everything, everything..
In its right place
In its right place
In its right place
In its right place

What, what is that you try to say?
What, what was that you tried to say?
Tried to say.. tried to say..
Tried to say.. tried to say.. tried to say...

Everything In Its Right Place
------Radiohead

Beating Heart - Scott Becker Multimedia

Werewolves of London, Ontario

2009-10-31T19:43:00.000-07:00

An American Werewolf in London

In the last post, we learned about the Psychopharmacology of Lycanthropy (and "endogenous lycanthropogens") from the April 1, 1992 issue of the Canadian Medical Association Journal (Davis et al., 1992). In a more serious review on clinical lycanthropy in the British Journal of Psychiatry Coll, O'Sullivan, and Browne (1985; PDF) began by stating:

Lycanthropy is the delusion in which an individual believes he has been transformed into an animal, traditionally a wolf. Descriptions of this syndrome are found in the earliest medical writings such as those of the Greek Paulus Aegineta in the seventh century A.D. (Adams, 1844). There is also a biblical description of the syndrome in the Book of Daniel. Nebuchadnezzar (605-562 B.C.), the king who rebuilt Babylon, succumbed to a lycanthropic state after suffering from an apparent depressive illness for seven years.

Nebuchadnezzar, by William Blake

In his 1621 magnum opus, The Anatomy of Melancholy, Robert Burton (aka Democritus Junior) explained it thusly (in Part 1):

Lycanthropia, which Avicenna calls cucubuth, others lupinam insaniam, or wolf-madness, when men run howling about graves and fields in the night, and will not be persuaded but that they are wolves, or some such beasts. Aetius and Paulus call it a kind of melancholy; but I should rather refer it to madness, as most do. Some make a doubt of it whether there be any such disease. Donat ab Altomari saith, that he saw two of them in his time: Wierus tells a story of such a one at Padua 1541, that would not believe to the contrary, but that he was a wolf... And Nebuchadnezzar in Daniel, as some interpreters hold, was only troubled with this kind of madness. This disease perhaps gave occasion to that bold assertion of Pliny, some men were turned into wolves in his time, and from wolves to men again: and to that fable of Pausanias, of a man that was ten years a wolf, and afterwards turned to his former shape: to Ovid's tale of Lycaon, &c.

Not surprisingly, the modern-day diagnosis given to individuals afflicted with this delusion is usually a psychotic disorder in the context of schizophrenia (Fahy, 1989), severe depression (Coll et al., 1985; Rao et al., 1999; Younis & Moselhy, 2009), or bipolar disorder (Verdoux & Bourgeois, 1993).

Benicio del Toro stars in The Wolfman, to be released in Feb. 2010.

However, imaginary transmogrification isn't restricted to the lupine variety. A comprehensive review of the literature between 1966–2002 (Garlipp et al., 2004) identified 21 articles, primarily case studies:

In the current medical literature man–animal metamorphoses were described concerning the following animals: wolf/werewolf, dog, gerbil, rabbit, horse, tiger, cat, bird, unspecified animal species, frog and bee. In Asia, Africa and South America, metamorphoses in tiger, hyena, crocodile and shark were observed.

The authors mention that the specifics can be influenced by cultural factors. But then they deliver the psychodynamic perspective promised in the review's title (and a bit of condescension):

The symptomatology can be seen as a continuity spectrum of developmental and culture dependent normal behaviour via transitional – a fantasy of an artist – and partial forms to the whole picture of lycanthropy described by Keck et al. (1988). The length of transformation is usually short, symptomatology has mostly disappeared in a week's time. People who live in preindustrial societies and people living on isolated countrysides are predisposed. Other precipitating factors seem to be subconscious sexual conflicts.

Finally, they end with precipitating psychopathology:

Lycanthropic symptomatology can be seen in different mental diseases. Most of the patients suffer from an affective disorder or from schizophrenia. Furthermore, the man–animal metamorphosis can be seen after the intake of psychotropic substances including cannabinoids as well as alcohol abuse. Rarely, lycanthropy is reported in personality disorders. Case reports can be found concerning organic psychosyndromes, dementia and epilepsy.

We'll end with an article from the Canadian Journal of Psychiatry, on two unusual case reports (Gödecke-Koch et al., 2001):

Case Report 1
A 34-year old woman suffering from schizophrenia came to the emergency department. At first, she was mutistic; later she seemed agitated and tense. Suddenly, she started moving like a frog, jumping around, making frog-like noises, and showing her tongue as though in tend ing to catch a fly. We found out that she had taken part in a workshop about fairy tales prior to becoming symptomatic. An organic cause was excluded, and no drug intake was found.
Case report 2
A 24-year-old woman suffering from schizophrenia reported a strange feeling that could not be properly described, together with the feeling that she was becoming a bee and getting smaller and smaller. She also felt a burning sensation in her thighs. She attributed her metamorphosis to her being stung by bees as a child and the “splashes of bee” that had touched her. ... No organic causes could be found, and drug screening tested negative.
To date, the metamorphosis into a frog or a bee has not been described in the medical literature.

It's nearly a full moon, but somehow the idea of human/frog hybrids (and human bees, if not in swarms or of the killer variety) isn't all that scary.

References

Coll PG, O'Sullivan G, Browne PJ. (1985). Lycanthropy lives on. Br J Psychiatry 147:201-2. [PDF]

Fahy TA. (1989). Lycanthropy: a review. J R Soc Med. 82:37-9.

Garlipp, P., Gödecke-Koch, T., Dietrich, D., & Haltenhof, H. (2004). Lycanthropy - psychopathological and psychodynamical aspects. Acta Psychiatrica Scandinavica, 109 (1), 19-22. DOI: 10.1046/j.1600-0447.2003.00243.x

Gödecke-Koch T, Garlipp P, Haltenhof H, Dietrich DE. (2001). Lycanthropy: 2 case reports. Can J Psychiatry 46:659.

Rao K, Gangadhar BN, Janakiramiah N. (1999). Lycanthropy in depression: two case reports. Psychopathology 32:169-72.

Verdoux H, Bourgeois M. (1993). A partial form of lycanthropy with hair delusion in a manic-depressive patient. Br J Psychiatry 163:684-6.

Younis AA, Moselhy HF. (2009). Lycanthropy alive in Babylon: the existence of archetype. Acta Psychiatr Scand. 119:161-4

Psychopharmacology of Lycanthropy

2009-10-31T03:07:00.000-07:00

Fig. 5 (Davis et al., 1992): Drawing from an original photograph by Kirschbaum of one of his subjects undergoing transmogrification after experimental exposure to amplified illumination at lunar wavelengths.

VERY ORIGINAL RESEARCH * RECHERCHES EXTRAORDINAIRES

From the Orphan Drug Research Institute (an affiliate of Yoknapatawpha University), 666 Rowanoak Circle, Jefferson, Miss. This is the first report from the institute's Orphan Drug Development Program.

Objective: To develop pharmacotherapies for the orphan disease lycanthropy through the pursuit of the etiologic hypothesis of a genetically determined hypersecretion of endogenous lycanthropogens.
Design: Quadruple-blind, Rubik's Cube matrix analysis.
Setting: Community practice and malpractice.
Participants: Subjects selected from inbred Ruficolla populations in Mississippi, Georgia, North Carolina and Minnesota. All who entered the study finished it.
Interventions: Chemical screening of blood samples over a hypothesized secretory cycle of lycanthropogen peaking on the day of maximum lunar illumination. Administration of synthetic lycanthropogens for behavioural testing. Experimental lycosomatization through the illumination method of Kirschbaum.
Outcome measures: None were post hoc, but some are still in hock.
Main results: Two putative lycanthropogens were isolated from the blood samples. Structural elucidation and synthesis permitted animal and clinical trials; in each of these, behavioural dysfunction was observed. Antilycanthropogen strategies included application of the principle of caged compounds and generation of a therapeutic immunoglobulin. The effects of a newly developed antihirsutic agent seemed promising. An interaction of the lycanthropogen-secretion system and ethanol was noted, which may explain behavioural aspects of alcoholism.
Conclusions: The incidence of lycomania in North America is underestimated. Soon-to-be-available pharmacotherapies should promote its early detection and treatment. Full control may depend upon advances in gene therapy.

Fig. 1 (Davis et al., 1992): Structural formulas of endogenous lycanthropogens.

The full paper is available as an open access article, so don't delay in reading this RECHERCHES EXTRAORDINAIRES in its entirety. It's Halloween, and there's a Bad Moon Rising...

Reference

Davis WM, Wellwuff HG, Garew L, Kydd OU. (1992). Psychopharmacology of lycanthropy. CMAJ Apr 1;146(7):1191-7.

Teen Wolf, shown Car Surfin' USA (Kids! Don't try this at home)...

The Electroencephalographer's Couch

2009-10-30T02:29:00.000-07:00

BRAIN WAVE SOFA, by lucas maassen

The Brain Wave Sofa is a representation of a 3 second wave of Alpha brain activity captured with a 3d EEG.
It shows the 3 seconds when the eyes closed.

From the 3d-EEG the file got directly milled in faom by a 3d milling machine and then upholstred in felt by hand.

in cooperation with Dries Verbruggen (Unfold)

Close your eyes and relax...

However, information aesthetics was a bit wrong when they said the purpose of alpha waves (in the EEG frequency band of 8-12 Hz) is only "to prepare the brain for the large input of signals when one opens the eyes." According to Başar et al. (1997), their function is much more complex:

The old concept stating that EEG alpha (10-Hz) activity reflects passive or idling states of the brain is giving way to modern views of 10-Hz oscillations in relation to diverse brain functions comprising sensory, motor, and memory processes: (1) Spontaneous alpha activity is not pure noise as shown by methods of chaos analysis. (2) Evoked alpha oscillations patterns (precisely time-locked to a stimulus; duration approx. 200-300 ms) depend on the modality of stimulation and the recording site. (3) Induced alpha oscillations are initiated by, but not closely time-locked to a stimulus. (4) 10-Hz oscillations are recorded in nervous systems of different complexities, from the human brain to isolated ganglia of invertebrates. The neural origins of 10-Hz oscillations are demonstrated by recordings at the cellular level. (5) Rather than trying to locate a unique alpha generator, it is preferable to assume that a 'diffuse and distributed alpha system' exists. A particular support for this hypothesis is given by stimulus-dependent hippocampal alpha responses in the cat brain. (6) The major physiological meaning of 10-Hz oscillations may be comparable to the putative universal role of gamma responses in brain signaling.

From Fig. 1A (Hughes & Crunelli, 2007).

References

Başar E, Schürmann M, Başar-Eroglu C, Karakaş S. (1997). Alpha oscillations in brain functioning: an integrative theory. Int J Psychophysiol. 26:5-29.

Hughes SW, Crunelli V. (2007). Just a phase they're going through: the complex interaction of intrinsic high-threshold bursting and gap junctions in the generation of thalamic alpha and theta rhythms. Int J Psychophysiol. 64:3-17.

via @channelNvideo

Unusual Changes in Sexuality: Case Studies in Neurology

2009-10-26T03:07:00.000-07:00

Fig. 1 (Currier et al., 1971). Scalp EEG showing sharp wave activity from left anterior temporal region.

In the last post we learned a bit about hypergraphia, a compulsion to write that sometimes occurs in those with temporal lobe epilepsy (TLE). According to the late behavioral neurologist Norman Geschwind (reprinted in 2009; also see Devinsky & Schachter, 2009), hypergraphia is one in a cluster of interictal [between seizure] personality traits in some TLE patients¹ which can also include religiosity, hypermorality, aggressiveness, clinginess, increased emotionality, and sexual changes (mostly hyposexuality but also other alterations):

Hyposexuality is the most common, but other kinds of sexual changes do occur. ... In England, Davies and Morgenstern went out and found, among the temporal lobe epileptics, several other patients who were transvestites. ... I’m sure that the great majority of transvestites don’t have temporal lobe epilepsy, but it’s interesting that for whatever reason it can cause this. Although I’ve seen many women with temporal lobe epilepsy, someone called to my attention a phenomenon that I hadn’t observed before. The last four women I have seen have all been bisexual, which again is a rather striking finding.

Sexual behavior preceding (auras) or during (automatisms) seizures is another story. The EEG traces in Fig. 1 above are from an epilepsy patient who experienced "sexual seizures" during which she engaged in somewhat purposeless "pseudointercourse" behavior, with no memory for the event afterward. Although the general consensus is that sexual automatisms are usually associated with seizure foci in the temporal lobes (Mascia et al., 2005), an influential earlier paper insisted the origin of "sexual seizures" was in the frontal lobes (Spencer et al., 1983).

Changes in sexuality can also occur after strokes or due to brain tumors. Neurophilosopher Patricia Churchland drew attention to one of these case reports in a New Scientist article on free will and criminal responsibility:

In 2003, the Archives of Neurology carried a startling clinical report [Burns & Swerdlow, 2003]. A middle-aged Virginian man with no history of any misdemeanour began to stash child pornography and sexually molest his 8-year-old stepdaughter. Placed in the court system, his sexual behaviour became increasingly compulsive. Eventually, after repeatedly complaining of headaches and vertigo, he was sent for a brain scan. It showed a large but benign tumour in the frontal area of his brain, invading the septum and hypothalmus - regions known to regulate sexual behaviour.
After removal of the tumour, his sexual interests returned to normal. Months later, his sexual focus on young girls rekindled, and a new scan revealed that bits of tissue missed in the surgery had grown into a sizeable tumour. Surgery once again restored his behavioural profile to "normal".

Figure 1 (Burns & Swerdlow, 2003). MRI scans at the time of initial neurologic evaluation: T1 sagittal (A), contrast-enhanced coronal (B), and contrast-enhanced axial (C) views. In A and B, the tumor mass extends superiorly from the olfactory groove, displacing the right orbitofrontal cortex and distorting the dorsolateral prefrontal cortex.

This case raises the issues of diminished capacity and criminal responsibility. The man knew what he was doing was wrong -- intact capacity and moral knowledge -- but he could not inhibit his inappropriate sexual behavior. It's hard to argue against the finding of diminished responsibility when staring at a gigantic brain tumor. But many other examples of impulsive sexual offenses (Langevin, 2006) aren't nearly as obvious (e.g. after head injuries when the damage might not be visible on an MRI scan). How does society deal with them?

A key factor is a change in behavior...

Multidirectional disorders of sexual drive in a case of brain tumour

The next report is from Poland (Lesniak et al., 1972 -- before the days of MRI or even CT scans). This case history is even more disturbing and involves greater criminal offenses than the patient of Burns and Swerdlow (2003).

A description and analysis of various disorders of sexual impulse are presented. They occurred gradually between the ages of 56 and 60 years in a man previously in good health. The disorders were as follows: harlotry, incestuous intercourse with his under-age daughter [used physical violence and threatened to kill her if she told], sodomy, hetero- and homosexual pedophilia, masochism [he demanded that his wife beat him with a club] with some symptoms of sadism, coprolalia and exhibitionism. [Also bestiality with cows and calves.] Pedophilia and exhibitionism [he fancied wearing a red ribbon around his exposed penis] were the counts of the man’s indictment. After twice-repeated forensic and psychiatric examination and observation, sexual psychopathy and male climacteric were also recognized; and the defendant was acknowledged to be responsible. In the course of further examination, the psychoorganic syndrome with symptoms of moria was recognized clinically. Further specialist examinations, especially by X-ray (pneumoencephalography) showed the presence of neoplasm (probably benign glioma or meningioma) situated at the basal paracentral part of the right forehead lobe [right orbitofrontal cortex again]. Its presence being acknowledged, the defendant was found irresponsible; due precautions and eventual neurosurgical treatment were proposed. It has been stressed that the appearance of the above disorders, especially in view of the age of the subject, must lead one to suspect an organic origin.

During the trial (reminiscent of the proceedings against serial child killer and cannibal Albert Fish), expert witnesses for the prosecution found nothing organically wrong, and declared the defendant “at the moment of committing the criminal acts he was charged with, had retained the ability to recognize the significance of these acts, whereas his ability to control his acts had been slightly restricted”. The defendant was found guilty, the defense appealed and a retrial was granted. He was placed under observation for 2 months at the Psychiatric Clinic in Cracow, when the authors became involved in his case:

The neurological examination revealed a considerable bilateral impairment of smell [a tell-tale sign of bilateral orbitofrontal damage] and a marked inequality of the reflexes of the lower extremities: the knee jerks and ankle jerks were weaker on the right. The EEG tracings showed a marked generalized flattening with scattered low-voltage theta waves. After stroboscopy the number of delta waves in the frontal and anterior temporal regions increased bilaterally.
...The pneumoencephalogram revealed ... a filling defect in the frontal horn of the right lateral ventricle which was, moreover, shifted dorsally... The radiological conclusion was that a tumour was present in the parabaso-central portions of the right frontal lobe.

The authors concluded their article with a fascinating discussion of sexual psychopathy, organic brain injury, and the question of legal responsibility. Thirty years before neuroethics and neurolaw emerged as recognized fields of study. And without the benefit of MRI.

A case of hair fetishism, transvestitism, and organic cerebral disorder

An unusual noncriminal case from Australia was reported by Dr. Ball (1968). The paper includes the author's regressive views of women and a Freudian explanation for hair fetishism:

Early in 1965 a forty six year old man suffering from severe anxiety was admitted to hospital. He had married after a short engagement, one month prior to admission, despite evasion and procrastination on his part. The marriage followed a brief courtship conducted with great ferocity by a childless widow in her early forties. Between the marriage and hospitalisation the patient became increasingly agitated, running away four times. The agitation had increased as his wife’s sexual demands stimulated his life-long hair fetishism and triggered fantasies of transvestitism which had been absent for some years.
When aged four, he became acutely upset on the day that his mother was about to have her long hair bobbed. As a result of his screaming and violent rage, the mother’s hair was not cut... Thereafter, the patient became increasingly preoccupied with long female hair. ... At about ten years of age he also began to transvest in his sister’s clothing. The transvestitism continued sporadically until his late thirties. ... He attempted intercourse very rarely and then with little success and less satisfaction.

Dr. Ball went on to state that "Hair fetishism can be the product of complex symbolisation." He also speculated that the boy's "aggressive outburst, associated with his mother’s hair, could have resulted in sexual stimulation." Yeah, OK, so where's the organic cerebral disorder? As a boy, the patient was delayed in walking and talking, was clumsy, and showed poor motor coordination. Doctors at the time (in the 1920s) could find nothing physically wrong with him. Back to the present day (1965), his demanding and ferocious wife had witnessed several nighttime grand mal seizures. And the guy's hair fetish was getting worse. When admitted to hospital the patient had abnormalities in his right hand and arm. He was diagnosed with:

invasive tumour affecting the left temporal region. [The tumor was causing the seizures.] It was felt that surgery was not indicated. He has since been maintained on an anticonvulsant, (Phenytoin Sodium), antiparkinsonian agents, (Benzhexol HCL [a muscarinic antagonist, not a dopamine drug]), and a phenothiazine, (Thioridazine [antipsychotic]). The phenothiazine was recently discontinued without ill effect. His epilepsy is less frequent, the abnormality of his right arm has not progressed and his fetishism is only occasionally troublesome. His sexual potency is much reduced, but his wife though despondent, copes well.

Or so the story goes.

Stroke turns Gay Man Straight!

A 57-year-old gay man, comfortable with his identity and aware of his sexual orientation since his early teens, came to the attention of Jawad et al. (2009) after suffering a stroke in the distribution of the left middle cerebral artery. He had experienced an earlier stroke 12 years before, a minor one in his right hemisphere but recovered completely. However...

The patient started complaining of his changed personality and heterosexual orientation 6 months after his second stroke. At the same time he complained of excessive mood swings and changed interests. He became preoccupied with photography and had a successful photographic exhibition a year after his second stroke. His sexual orientation remained heterosexual 4 years following the second stroke, and he preferred to describe himself as bisexual because of his previous homosexual orientation.

The authors did not present neuroimaging findings or results from neurological examination, which seems peculiar for a paper published in 2009. There was no mention of language or motor disturbances, but one is left to wonder. The middle cerebral artery is the blood supply for a rather large swath of cortex, so it's unclear exactly where the lesion was located. However, the authors do raise the obvious point that a change in sexual orientation is very unusual. Hyposexuality most often occurs after stroke (Tamam et al., 2008) and sometimes hypersexuality can be seen after brain injury (Miller et al., 1986). The Neurological Correlates blog describes two new cases of the latter in Manic Monday (late edition): Sudden hypersexuality.

Human sexuality is such a complex and multi-determined phenomenon that it's impossible to draw generalizations from the mix of case studies in the neurological literature. And it's important to avoid extrapolation from the few to the many. Very few people with temporal lobe epilepsy are transvestites or bisexuals, and the vast majority of transvestites and bisexuals do not have TLE. And all you fundamentalist reparative therapy advocates, take note: There is only one report in the literature of a "stroke turning a gay man straight." !! Nonetheless, it is informative to gather information about changes in sexuality and to relate them to lesions in specific brain areas, most often the frontal lobes (orbitofrontal cortex in particular) and the anterior and medial temporal lobes.

Footnote

¹ However, the specificity of the "TLE personality" classification is disputed by others (e.g. Mungus, 1982) who maintain that a substantial portion of the variance can be accounted for by psychiatric illness.

References

Ball, J. (1968). A CASE OF HAIR FETISHISM, TRANSVESTITISM, AND ORGANIC CEREBRAL DISORDER. Acta Psychiatrica Scandinavica, 44 (3), 249-254. DOI: 10.1111/j.1600-0447.1968.tb07511.x

Burns JM, Swerdlow RH. (2003). Right orbitofrontal tumor with pedophilia symptom and constructional apraxia sign. Arch Neurol. 60:437-40.

Currier RD, Little SC, Suess JF, Andy OJ. (1971). Sexual seizures. Arch Neurol. 25:260-4.

Jawad, S., Sidebothams, C., Sequira, R., & Jamil, N. (2009). Altered Sexual Orientation Following Dominant Hemisphere Infract [sic]. Journal of Neuropsychiatry, 21 (3), 353-354. DOI: 10.1176/appi.neuropsych.21.3.353

Langevin R. (2006). Sexual offenses and traumatic brain injury. Brain Cogn. 60:206-7.

Lesniak, R., Szymusik, A., & Chrzanowski, R. (1972). Multidirectional disorders of sexual drive in a case of brain tumour. Forensic Science, 1 (3), 333-338. DOI: 10.1016/0300-9432(72)90031-3

Mascia A, Di Gennaro G, Esposito V, Grammaldo LG, Meldolesi GN, Giampà T, Sebastiano F, Falco C, Onorati P, Manfredi M, Cantore G, Quarato PP. (2005). Genital and sexual manifestations in drug-resistant partial epilepsy. Seizure 14:133-8.

Miller BL, Cummings JL, McIntyre H, Ebers G, Grode M. (1986). Hypersexuality or altered sexual preference following brain injury. J Neurol Neurosurg Psychiatry 49:867-73.

Spencer SS, Spencer DD, Williamson PD, Mattson RH. (1983). Sexual automatisms in complex partial seizures. Neurology 33:527-33.

Tamam Y, Tamam L, Akil E, Yasan A, Tamam B. (2008). Post-stroke sexual functioning in first stroke patients. Eur J Neurol. 15:660-6.

Medellin's famous transvestite's debut on the silver screen

A group of Canadian filmmakers are releasing a movie on La Dany, the Medellin transvestite street artist that makes Andy Warhol look like a boring heterosexual. The film will see its first screening in Colombia's second largest city on Tuesday.

HYPERGRAPHIA, the movie

2009-10-23T16:37:00.000-07:00

A proto-Live Journal moment from The Inman diary: a public and private confession, Volume 2. By Arthur Crew Inman. Edited by Daniel Aaron.

"HYPERGRAPHIA", a film currently in production...

...is a narrative feature recounting the true story of the notorious Boston eccentric and recluse Arthur Crew Inman (1895-1963) and of "THE INMAN DIARY" he created. Published by Harvard University Press, Inman's gargantuan diary is one of the great literary curiosities of our age, a sprawling memory piece of more than 17 million words. A black comedy of epic proportions, the screenplay is a tightly wound biographical journey with documentary elements drawn from the extensive Inman Collection at Harvard. Historical scenes evoking world events of the first half of the 20th century (stock footage, news headlines, period movie montages) will be integrated with events from the entire 68 years of Inman's life and a good deal of human history in between, - a sort of March of Time with Arthur Inman as self-appointed narrator.

Hypergraphia, the behavior is defined as an overwhelming urge to write, often associated with the manic phase of bipolar disorder and with temporal lobe epilepsy (as one in a cluster of symptoms). Influential behavioral neurologist Norman Geschwind described the personality changes that can be observed in persons with temporal lobe epilepsy in a series of lectures¹ and papers from the 1970s and 80s (reviewed in Devinsky & Schachter, 2009). He viewed these changes as:

...resulting from a stimulating lesion in the limbic system. This neurobiology accounted for the overarching increased interictal [time between seizures] emotionality that underlay the increased religious interests, hypergraphia, increased aggression, increased moral and philosophical concerns, viscosity, and seriousness (lack of humor).

Russian novelist Fyodor Dostoevsky is the classic example (see Crime and Punishment, The Brothers Karamazov, etc.). According to Geschwind,

Dostoevsky typified many personality features of the temporal lobe epileptic—tremendous concern about moral details, many of them small details, extremely pedantic, he was angrily impulsive, an impossible person to live with in every way, and extremely aggressive, even toward people who had befriended him. Yet he was also deeply emotional and despite these negative personality traits, many of those close to him felt a strong emotional bond.

From Dostoevsky, by Richard Freeborn. Also see Dostoevsky's Doodles, an exhibit held at the Harriman Institute.

In 1974 Waxman and Geschwind (reprinted in 2005) described copious writing and temporal lobe seizures in a series of patients:

The phenomenon of hypergraphia, or the tendency toward extensive and, in some cases, compulsive writing, in temporal lobe epilepsy is described in seven patients, in each of whom there was electroencephalographic demonstration of a temporal lobe focus. Unusually detailed and strikingly copious writing was evidenced in each patient. Six patients provided documentation of their extensive writing, which often was concerned with religious or moral issues. A seventh patient claimed to have written extensively, but refused to exhibit his writings. Aggressiveness, religiosity, and changes in sexual behavior in temporal lobe disorders have been described previously. The hypergraphia of temporal lobe epilepsy appears to be part of a specific behavioral syndrome of special interest because of its association with dysfunction at specific anatomic loci.

Did Arthur Inman have temporal lobe epilepsy? It seems his hypergraphia might have been more psychiatric in nature, driven by a combination of obsessive-compulsive behavior, grandiosity, self-loathing, and paranoia.

From The Inman diary.

Inman was also an extreme hypochondriac. A series of "thirty-four eminent doctors" (plus his long-time osteopath) could find nothing physically wrong with him. However, a 1988 article in The Atlantic explored the possibility that Inman did indeed have temporal lobe epilepsy (TLE):

As for Inman, clearly he had many, if not all, of the traits of the behavior syndrome. On a questionnaire designed by [neuropsychiatrist David] Bear and the psychologist Paul Fedio to determine the extent to which the syndrome is present in patients [Bear & Fedio, 1977],² Inman scores well within the range of people with TLE and substantially above the control groups. The questionnaire was filled out for Inman separately by Bear and by Libby Smith, one of the editors of The Inman Diary. Smith, who spent seven years reviewing the unabridged diary and interviewing scores of people who knew its author, had never heard of TLE. Both she and Bear gave Inman high marks in nearly all of the eighteen traits listed on the questionnaire. ... "Compulsive attention to detail," for example, describes Inman's need to make lists and keep to rigid schedules. His childlike charm and tendency to fly into rages translate into high scores in several categories: "dependence," "deepening of all emotions," "humorlessness," and "paranoia." And his effort to chronicle his era demonstrates his "grandiosity" and "sense of personal destiny."

Read more at HYPERGRAPHIA INMAN DIARY blog.

Footnotes

¹ A 1974 lecture from Geschwind's course at Harvard Medical School (on The Neurology of Behavior) was reprinted in the journal Epilepsy & Behavior in 2009.

² The view of a distinctive TLE personality is not without controversy, however. Some clinicians maintain that a substantial portion of the variance can be accounted for by psychiatric illness, e.g. Mungus (1982) who reported that:

...none of the 18 traits (Bear & Fedio, 1977) discriminated among a group of temporal lobe epileptics with behavioral-psychiatric disorders, a group of patients with concomitant neurological and behavioral-psychiatric disorders, and a group of patients with psychiatric but not neurological illness.

References

Devinsky, J., & Schachter, S. (2009). Norman Geschwind’s contribution to the understanding of behavioral changes in temporal lobe epilepsy: The February 1974 lecture. Epilepsy & Behavior, 15 (4), 417-424. DOI: 10.1016/j.yebeh.2009.06.006

Geschwind N. (2009). Personality changes in temporal lobe epilepsy. Epilepsy Behav. 15:425-33.

Waxman SG, Geschwind N. (2005). Hypergraphia in temporal lobe epilepsy. Epilepsy Behav. 6:282-91.

EEG Speed Dating

2009-10-19T18:43:00.000-07:00

Lust or Love?

The Science of Love

In Joyce Draganosky's The Science of Love, the battle between reason and emotion takes center stage. A professor, who believes she has found a way of determining scientifically whether someone is in love, clashes with her department chair, a woman who thinks love and attraction are far too complex to be mapped according to the certainties of science.

The director seems to have modeled her lead character after Helen Fisher, even down to the combination of evolutionary anthropology with brain imaging. Joy Hirsh at Columbia was a scientific consultant.

Further Reading (and viewing):

The Science of Love - Link to watch the entire short film (only if you live in the U.S.)

The EEG Mixer - Neurocritic classic

The Hyperscanning of 'Paranormal Activity': A Neurocinematic Study of Collective Fear

2009-10-12T05:15:00.000-07:00

Still from the promotional trailer for that viral movie phenomenon, Paranormal Activity.

Not since The Blair Witch Project (1999)¹ ten years ago (in the BT [Before Twitter] dark ages) has there been such a grassroots "underground" buzz surrounding a cult-like, deliberately amateur, mega-scary, "found" reality footage-type movie. Unlike its predecessor, Paranormal Activity does get to benefit from Twitter as a trending topic:

Paranormal Activity is a popular topic on Twitter right now.
A ultra low-budget horror film about a couple experiencing demonic forces at night. The US limited release was Sept. 29, 2009, and there will supposedly be a nationwide release if it gets a million votes on Eventful.

51 more tweets since you started searching.

Here's the trailer:

Beyond word-of-mouth from the original target demographic attending midnight shows in college towns, mainstream media outlets such as CNN have picked up on the buzz:

Surprise hit 'Paranormal Activity' scares money out of moviegoers
updated 8:01 p.m. EDT, Mon October 12, 2009
(CNN) -- The new horror movie "Paranormal Activity" could be filling movie studio marketing departments with fear.
Using a campaign of limited showings, social media and word-of-mouth fan buzz, the film has managed to become a breakout hit without the aid of a glitzy marketing campaign -- or even a traditional movie trailer.
According to Variety, the very low-budget film (it reportedly cost $11,000), which played in fewer than 200 theaters, raked in $7.1 million over the weekend -- a record for a limited-release film. The film had an impressive $44,163 per-screen average and placement in the top five of the box office ratings over the weekend.

Most relevant for the ongoing Neurocinema Collection™ is this observation:

"Watching it with 250 strangers in a movie theater and getting everybody to jump at the same time definitely has an effect," [Kevin Carr] said. "It's the event film right now of the year, which is something that needs to be experienced."

"Watching it with 250 strangers in a movie theater" is the key phrase. We'll return to that later.

In the last post we learned about the new interdisciplinary field of “neurocinematic” studies. The term first appeared² in the scholarly journal Projections: The Journal for Movies and Mind, in a 2008 paper written by Hasson and colleagues:

This article describes a new method for assessing the effect of a given film on viewers’ brain activity. Brain activity was measured using fMRI during free viewing of films, and inter-subject correlation analysis (ISC) was used to assess similarities in the spatiotemporal responses across viewers’ brains during movie watching. Our results demonstrate that some films can exert considerable control over brain activity and eye movements. However, this was not the case for all types of motion picture sequences, and the level of control over viewers’ brain activity differed as a function of movie content, editing, and directing style. We propose that ISC may be useful to film studies by providing a quantitative neuroscientific assessment of the impact of different styles of filmmaking on viewers’ brains, and a valuable method for the film industry to better assess its products.

The NYU researchers, led by Uri Hasson (now at Princeton), claim to study "to what extent are we all alike?"³ The research program originated in the laboratory of Prof. Rafael Malach and first hit the Science scene in 2004. In that study, five participants watched the first 30 min of The Good, The Bad, and The Ugly in an MRI scanner. The data were analyzed to determine commonalities in brain activation across subjects, revealing that 25% of the cortex showed significant intersubject correlation during the movie. The Projections article summarizes the results from subsequent experiments and develops the idea that different directors, and different filmmaking styles, exert varying levels of "control" over audio-visuo-higher-level cortical responses in the brains of the viewers.

This is all very interesting, you say, but it doesn't mimic the real life movie-going experience. How can you possibly evaluate the neural effects of watching a scary movie in a theater with 250 strangers?

The Hyperscanning of 'Paranormal Activity': A Neurocinematic Study of Collective Fear

In this imaginary experiment,⁴ the viewing experience is enhanced through several means. While in laying supine in the MRI scanner, individual research participants watch a specially-made DVD of Paranormal Activity shot from the perspective of the audience, as in the trailer. To encouraging bonding among the research subjects, the cool "hyperscanning" methodology is used. This technique was developed by Read Montague and his co-workers (Montague et al., 2002). Typically, hyperscanning involves two subjects who interact with each other while their brains are scanned simultaneously (in adjoining or distant magnets). Specially developed software (Networked Experiment Management Objects, or NEMO) coordinates the experiments across sites:

The scarcity of neuroimaging resources limits the ability to perform multi-subject experiments within the same facility, necessitating the ability to simultaneously scan across multiple institutions. Furthermore, in order to correlate behavior and brain activation among participants, sites participating in Hyperscan experiments must be synchronized so that the behavioral and imaging data gathered during the experiment can be reconciled to a common timeline.
Professional software developers at the Human Neuroimaging Laboratory (HNL) have created a distributed framework for executing Hyperscan experiments. The framework, called NEMO, consists of client and server components written in Java, a SQL database for storing experiment metadata and results, an experiment script execution environment based on the Jython scripting language, and pulse-sequence customizations to facilitate network-initiated scanning.

For our fright-filled neurocinematic study, five friends are scanned simultaneously. Each subject is informed that he/she will be watching the movie at the exact same time as the others, experiencing the exact same scanner environment (which can be claustrophobic, even under calm conditions). They're instructed that they must be still. They're asked to view the movie as a shared experience -- shared with the audience and with their friends. In an alternate scenario, ten strangers can meet each other beforehand through video conferencing and follow the same procedures. In either case, the data are analyzed for intersubject correlations not only in the cortex, but also in subcortical regions important for emotion (amygdala) and memory (hippocampus).

What percentage of brain activity will be correlated across subjects? Hasson et al. (2008) discussed the continuum of control employed by filmmakers: real life --> documentaries --> art films --> Hollywood --> propaganda. The filmmaking style of PA is not at all sophisticated in the vein of Alfred Hitchcock Presents, which

evoked similar responses across all viewers in over 65 percent of the cortex, indicating a high level of control of this particular episode on viewers’ minds.

Nevertheless, despite using shaky-cam real life amateurish filmmaking with little editing, the viewers' attention is directed to restricted locations: the bed, the door, the hallway, Katie Featherston's breasts [just out of frame, but there are a lot of deliberate close-ups], her face. These would activate category-specific regions in the visual processing stream: the parahippocampal place area, the fusiform face area, the extrastriate body area. Importantly, emotional reactions might be similar among like-minded friends, adding a new dimension to the ISC data.

But will the study provide a privileged (neural) measure of collective fright, beyond what can be revealed by eye movements and by peripheral autonomic responses such as heart rate and skin conductance? I don't know, but it'll sure make for great articles in Wired and CNN. And Science. Be sure to mention me in the Acknowledgments.

What is my opinion of Paranormal Activity? I went to the late show tonight, and I have to say...... the movie is WAY overrated.⁵ I didn't find it scary at all. You're waiting so long for something to happen, that a slight noise or movement of the door or a brief shadow are supposed to be scary. I kept waiting to jump out of my seat but never did, not even in the last 30 seconds. The trailer for Shutter Island was more frightening.

Footnotes

¹ I thought BWP was highly overrated and not scary at all.

² Correct me if I'm wrong.

³ From a neuroscientific standpoint, certain aspects of these findings can be considered trivial, as noted by an anonymous commenter. For this post, I have adopted a willing suspension of disbelief for artistic purposes.

⁴ For an earlier post about another fake experiment, see The Neurology of Twitter:

It was bound to happen. Some neuroimaging lab will conduct an actual fMRI experiment to examine the so-called "Neural Correlates of Twitter" -- so why not write a preemptive blog post to report on the predicted results from such a study, before anyone can publish the actual findings?

⁵ For like-minded reviews, see the Austin Chronicle and the New York Times.

References

Hasson U, Landesman O, Knappmeyer B, Vallines I, Rubin N, Heeger DJ. (2008). Neurocinematics: The Neuroscience of Film. Projections 2:1-26. [PDF]

Hasson U, Nir Y, Levy I, Fuhrmann G, Malach R. (2004). Intersubject Synchronization of Cortical Activity During Natural Vision. Science 303:1634-1640.

Montague PR, Berns GS, Cohen JD, McClure SM, Pagnoni G, Dhamala M, Wiest MC, Karpov I, King RD, Apple N, Fisher RE. (2002). Hyperscanning: simultaneous fMRI during linked social interactions. Neuroimage 16:1159-64.

Neurocinema, Neurocinematics

2009-10-12T00:22:00.000-07:00

Is there a difference?

In The Neurocinema Collection™, we established that the term "neurocinema" doesn't really refer to movies with "Neuro" in the title or films about neurology. Instead, neuromarketers have have used the word in the following fashion:

Neurocinema is a new filmmaking process that studies a viewer's sensorimotor, cognitive, and affective response to film stimuli. Researchers use technologies such as functional magnetic resonance imaging (fMRI) to measure changes in activity in parts of the brain,electroencephalography (EEG) to measure activity in specific regional spectra of the brain response, and/or sensors to measure changes in one's physiological state (heart rate, respiratory rate, galvanic skin response) to learn exactly what scenes excite or disinterest the viewer.

There have been no peer-review studies on this methodology, only articles in the popular press (e.g., Wired.com and CNN.com). And from what was available in those reports, there was plenty to be neurocritical about.

On the other hand, Uri Hasson and his NYU colleagues published an article entitled Neurocinematics: The Neuroscience of Film in Projections: The Journal for Movies and Mind. Granted, that article is lacking the methodological details one would see in NeuroImage or Human Brain Mapping, but in fact the authors have published their work in prestigious journals (like Science and Neuron) without the "Neurocinematics" title.

In their Projections article, Hasson et al. (2008) state:

We propose that ISC [inter-subject correlation analysis] may be useful to film studies by providing a quantitative neuroscientific assessment of the impact of different styles of filmmaking on viewers’ brains, and a valuable method for the film industry to better assess its products. Finally, we suggest that this method brings together two separate and largely unrelated disciplines, cognitive neuroscience and film studies, and may open the way for a new interdisciplinary field of “neurocinematic” studies.

Hasson and colleagues first described the ISC method in their 2004 paper. In that study five subjects watched 30 min of The Good, The Bad, and The Ugly while laying supine in an MRI scanner. Unlike a typical fMRI experiment involving controlled presentation of individual pictures and performance of a categorization task, free viewing of a dynamic film is a more naturalistic situation. It also presents a more challenging data analysis problem. To tackle this, the researchers eschewed standard hypothesis-testing and adopted a purely data-driven approach to determine commonalities in brain activation across subjects.¹

Figure 1B (Hasson et al., 2008). The ISC analysis measures similarity in brain activity across viewers by comparing the response time course in each brain region from one viewer with the response time courses obtained in the same brain region from other viewers during movie watching.

The results (Hasson et al., 2004) demonstrated that...

Despite the free viewing and complex nature of the movie, we found an extensive and highly significant correlation across individuals watching the same movie. Thus, on average over 29% ± 10 SD of the cortical surface showed a highly significant intersubject correlation during the movie.....
Close inspection of this across-subject correlation revealed that the synchronization was far more extensive than the boundaries of well-known audiovisual sensory cortex defined with conventional mapping approach. ...the across-subject correlation covered most of the visual system, including early retinotopic areas as well as high-order object areas within the occipitotemporal and intraparietal cortex. Moreover, the correlation extended far beyond the visual and auditory cortices to the entire superior temporal (STS) and lateral sulcus (LS), retrosplenial gyrus, even secondary somatosensory regions in the postcentral sulcus, as well as multimodal areas in the inferior frontal gyrus and parts of the limbic system in the cingulate gyrus.

When corrected for non-selective elements, the intersubject correlation remained at 24% ± 8.5. The other 75% of the brain not "in sync" across subjects included parietal lobe areas (supramarginal and angular gyri) and the bulk of prefrontal cortex. Subcortical areas important for emotion and memory (amygdala and hippocampus) were not examined.

A second analysis was also performed, which took a "reverse-correlation" approach to examine activity in two well-know category-specific areas: the fusiform face area (for faces) and the parahippocampal place area (for buildings). This type of functional specialization was demonstrated in an earlier paper as well (Bartels & Zeki, 2004). In that study, the participants watched a James Bond movie (Tomorrow Never Dies). Activity in category-specific regions (for color, faces, language, and human bodies) was correlated with the perceived intensity of these specific attributes (as rated by a separate group of subjects who watched the same movie).

The most fascinating result in my opinion was obtained in subsequent experiments (described in Hasson et al., 2008) that compared the ISC for The Good, The Bad, and The Ugly to those observed for an episode of the TV series Alfred Hitchcock Presents (which is on Hulu!!!), an episode of the semi-improvised comedy Curb Your Enthusiasm, and a real-life unedited video shot in Washington Square Park. Not surprisingly,

The extent of ISC differed for the four movies (Figure 7A). The percentage of cortex exhibiting high ISC provided a measure of the overall effectiveness, or collective engagement power, of each movie to induce similar responses across viewers (Figure 7B). The Hitchcock episode (green) evoked similar responses across all viewers in over 65 percent of the cortex, indicating a high level of control of this particular episode on viewers’ minds. The high ISC was also extensive (45%) for the Good, the Bad and the Ugly (blue), but much less so (18%) for Curb Your Enthusiasm (red). Finally... the unstructured segment of reality (orange) induced high ISC only in a small fraction of the cortex (less than 5%).

Figure 7 (Hasson et al., 2008).

Glossing over the technical details [I didn't read the 5 other cited papers] and discrepancies between the 2004 and 2008 studies [divergence in ISC values of 25% vs. 45% for the same film], the implication is that different directors, and different filmmaking styles, exert varying levels of "control" over audio-visuo-higher-level cortical responses in the brains of the viewers:

The fact that Hitchcock was able to orchestrate the responses of so many different brain regions (Figure 7, green), turning them on and off at the same time across all viewers, may provide neuroscientific evidence for his notoriously famous ability to master and manipulate viewers’ minds. Hitchcock often liked to tell interviewers that for him “creation is based on an exact science of audience reactions” (Douchet 1985).
Different filmmakers strive to achieve different levels of control over their viewers’ reactions. Our findings provide empirical evidence to support the long-lasting distinction in film theory between films that remain faithful as much as possible to reality and those that seek to control or distort it.

The amount of control employed by filmmakers exists on continuum that ranges from real life --> documentaries --> art films --> Hollywood --> propaganda. The authors conclude with a discussion of collective engagement in film and suggest that it can be measured in an "objective" fashion using ISC. Overall, the 2008 Projections paper was a BOLD proposal for a true merger of art and science in academia.

Neurocinema, Neurocinematics? A semantic distinction perhaps, but the terms first appeared in different contexts. The former was used to describe an unvalidated filmmaking "process" [and underdeveloped commercial application] aimed squarely at attracting Hollywood megabucks, whereas the latter was used in a scholarly publication to describe a new field of inquiry. Will a merger (of sorts) be far behind? Or more to the point, has the NYU group applied for a patent yet?

Footnote

¹ The methods for this were pretty brief and largely contained within Footnote 15 of the paper:

15. In order to search for correlation between two corresponding regions across subjects (intersubject correlation), we first aligned all brains into Talairach coordinate system and used a Gaussian filter of 12 mm full width at half maximum value (FWHM) to the data... To remove preprocessing artifacts, we excluded the first and last 10 time points of the experiment from the analysis. We then used the time course of each voxel of the source subject as a GLM predictor for modeling the activity in the corresponding voxel of the target subject. Only voxels whose P value was no more than 0.05 (corrected) were considered significant.

References

Bartels A, Zeki S. (2004). Functional brain mapping during free viewing of natural scenes. Hum Brain Mapp. 21:75-85.

Hasson U, Landesman O, Knappmeyer B, Vallines I, Rubin N, Heeger DJ. (2008). Neurocinematics: The Neuroscience of Film. Projections 2:1-26. [PDF]

Hasson, U. et al. (2004). Intersubject Synchronization of Cortical Activity During Natural Vision. Science, 303 (5664), 1634-1640. DOI: 10.1126/science.1089506

Further Reading

Neurocinematics - The Valve - A Literary Organ

Neurocinematics - Neurophilosophy blog

Neurocinematics! Where Neuroscience Meets Filmmaking - NYU panel discussion held May 4, 2009

The Neurocinema Collection™

2009-10-07T04:41:00.000-07:00

First poster for Joseph Kahn's adaptation of William Gibson's Neuromancer?

The term "neurocinema" has been in the news lately. What does it mean? Movies with the prefix "neuro" somewhere in the title?

Titles (20 Approx Matches)

		Neuro (2004)
		Neurosia - 50 Jahre pervers (1995) aka "Neurosia-Fifty Years of Perversion" - USA aka "Neurosia" - Germany (short title) aka "Neurosia - Who Shot Rosa von Praunheim" - USA (video box title)
		Labyrinth (1959) aka "Neurose" - Italy
		Revenge in the House of Usher (1982) aka "Neurosis"
		Neuromancer (2011)

Movies having to do with neurology, such as the NEURO CINEMA FESTIVAL sponsored by the San Francisco Neurological Society?

Awakenings (encephalitis, Parkinsons Disease)
Rainman (autistic disorder)
Away From Her (Alzheimers Disease)
M (psychotic disorder)
The Diving Bell and The Butterfly (stroke)

No, that's not right, either. "Neurocinema" has a short (and controversial) Wikipedia page:

Neurocinema is a new filmmaking process that studies a viewer's sensorimotor, cognitive, and affective response to film stimuli. Researchers use technologies such as functional magnetic resonance imaging (fMRI) to measure changes in activity in parts of the brain,electroencephalography (EEG) to measure activity in specific regional spectra of the brain response, and/or sensors to measure changes in one's physiological state (heart rate, respiratory rate, galvanic skin response) to learn exactly what scenes excite or disinterest the viewer.

The entry was originally marked for deletion on Sept. 25 (as a neologism with little coverage), but apparently it was reinstated after articles appeared in Wired.com and CNN.com. This minimalistic and poorly written entry is also a source of free publicity:

Peter Katz and MindSign Neuromarketing have done early studies into neurocinema that Wired.com and CNN has covered.

Dutifully following the links, here's what we learn from the CNN article:

Brain scans gauge horror flick fear factor
LONDON, England (CNN) -- Film producer Peter Katz doesn't just want his horror movies to scare you. He wants to pinpoint how frightened you are down to an exact moment in a scene.
To do that, he recently teamed up with researchers and used MRI scans of brain function to determine the degree of fright caused by certain scenes from his latest horror flick, "Pop Skull."
For the experiment, researchers at functional MRI research facility Mindsign Neuromarketing, based in San Diego, California, scanned the brain activity of a subject [NOTE: my emphasis] while she watched two scenes of his movie. Analyzing the data from the scan, they were able to pinpoint the exact moments when her brain was lit up with fear.
. . .
During Katz's experiment, researchers analyzed scans to identify the exact moment during each film scene that the viewer's amygdala -- the part of the brain linked to several emotions, including fear -- was activated, and to what degree.

Let's see where they went wrong scientifically: (1) Calling one subject "an experiment" -- was he making a movie just for her? (2) Saying fMRI can pinpoint the exact moment of anything -- there's a significant delay between initial neural firing and the peak of the hemodynamic response, which is estimated using a procedure that is not trivial for something as complex as an emotional response. (3) Using amygdala activity as a proxy for fear and thereby committing the cardinal sin of reverse inference (one cannot directly infer emotional state from the observed pattern of brain activity) -- didn't they learn from the op-ed neuroimaging fiasco in the New York Times ("This Is Your Brain on Politics")?

Then at Wired, Neurocinema Aims to Change the Way Movies are Made: [NOTE: or hyped]

Recently they finished their first full test with results that could change the way films are made. Yes, someone had to lie still in an MRI machine. The objective of the research, specifically, was to determine the brain response in the amygdala to watching scenes from the horror film Pop Skull. For those that don’t know, the amygdala is the emotional center of the brain. It’s involved in feelings of disgust, anger, lust and fear — all emotions especially elicited during a horror film. [NOTE: because it doesn't matter if your audience is feeling horny or disgusted instead of scared.]
. . .
For two sessions of 48 seconds and 68 seconds, a 24-year-old female watched two scenes from the movie while being scanned in a Siemens 3T MRI scanner. With a 20-second break in between three viewings of each scene (to refocus her eyes to center), the data was converted into a BrainMovie... and analyzed by the team at MindSign. What they saw (and what you can see in the movie) is that for most of the two movie scenes, the amygdala lit up like a Christmas tree out of fear. This activity was pinpointed to the frame, the exact scene and action that registered the response. For instance, “The scariest moment in Scene 1 came when the hand reaches further around the corner.” It is that precise.

Oh please spare me. I watched the BrainMovie and there were implausible jumps in activity from one frame to the next (compare "scary hand" at 2:42 to "scary hand again" at 2:48). Plus, don't you lose the element of surprise the second time you watch a specific scene? Who is going to see the infamous Alien chestburster scene the same way twice (i.e., 20 seconds after the first viewing)?

Then the Wired author interviewed film maker Katz and Dr. David Hubbard, "a board-certified neurologist who is the leading neurologist on the project." Although Dr. Hubbard has published respectable work on pain and headache using EMG, he has no papers at all using fMRI. Nonetheless, he is founder and chairman of The Hubbard Foundation for fMRI Research, "a charitable foundation supporting research and education in applied psychophysiology." He is also managing director of the Applied fMRI Institute, which presumably charges customers for "neuropsychological testing, neuromarketing and neurocinema, traditional academic research studies and explorations of meditation." No conflict of interest there. Oh wait, his education credits include STUDENT, Cognitive Science, University of California, San Diego, 2003-present. Good to know he's getting on the job fMRI training. This brain image doesn't instill a lot of confidence however given the extensive deactivation occurring outside the brain.

My final Google query was for MindSign Neuromarketing, whose motto is "Don’t rely on a focus group, or consumer’s ability to express their opinion about a product, let their minds speak for themselves." The organizational structure of MindSign was opaque at first, but I eventually discovered their scanning is done at "the cutting-edge Applied fMRI Institute, the only privately owned, market-friendly fMRI facility in the world."

In my view, the most successful aspect of this entire enterprise has been a boatload of uncritical coverage from the popular press.

For balanced blog coverage of the hype, see Neurovid: Neurocinema. And a neuromarketer presents a Scary Idea: Forget Focus Groups.

It Hurts Less When I Can See It

2009-10-03T13:52:00.000-07:00

Fig. 1 (Longo et al., 2009). The mirror box technique in which the subject has the experience of viewing their right hand, while in fact seeing their left hand reflected in a mirror.

Sight modifies somatosensation, by either enhancing or diminishing the subjective intensity of touch (Kennett et al., 2001) and pain (Ramachandran & Altschuler, 2009), respectively. These phenomena provide fascinating and lesser studied examples of crossmodal integration, or how signals from one sensory modality are combined with those of another to produce a unified percept. In an elegant series of experiments by Longo and colleagues, subjects who could see their own hand (either in a mirror or the real thing) reported less pain when exposed to the heat of a laser.

Laser ‘Pain Beam’ under development by the U.S. military. NOT used in the "elegant" laser evoked potential experiments.

Furthermore, an electrophysiological marker of pain was attenuated. This was measured from the EEG, time-locked to the application of the painful laser heat. These stimuli elicit a specific type of EEG response, called laser evoked potentials (LEPs). A sequence of three LEPs is generated in rapid succession, within the first 400 milliseconds after laser stimulation. These responses are called the N1, N2 and P2 potentials. As described in a review by Plaghki and Mouraux (2005),

Laser heat stimulators selectively activate Aδ and C-nociceptors ["pain receptors"] in the superficial layers of the skin. Their high power output produces steep heating ramps, which improve synchronization of afferent volleys and therefore allow the recording of time-locked events, such as laser-evoked brain potentials. Study of the electrical brain activity evoked by Aδ- and C-nociceptor afferent volleys revealed the existence of an extensive, sequentially activated, cortical network. These electrophysiological responses are modulated by stimulus-driven and, even more extensively, top-down processes.

These top-down processes include things like attention, expectation, and perhaps input from other sensory modalities. One advantage of LEPs is that you can determine exactly when in the pain processing stream these influences are active. Of greatest interest in this context is the N2-P2 complex, recorded at 195 milliseconds and 375 milliseconds after stimulation.

Fig. 5 (Longo et al., 2009). Grand mean LEPs recorded from electrode Cz in the three experiments and N2/P2 peak-to-peak amplitudes at Cz (bottom right). Error bars are 1 SEM.

The results demonstrated a cool new form of visually induced analgesia:

Looking at one's hand produced significant reductions of subjective intensity and unpleasantness of laser pain and in the amplitude of the N2/P2 complex.... These effects were observed both when the illusion of looking directly at the hand was induced with a mirror box (Exps. 1 and 3) and when participants viewed their hand directly during stimulation (Exp. 2). The reduction was specific to seeing one's own hand (Exp. 3).

What is the mechanism of action for these effects? First it's useful to know where in the brain the N2-P2 signals arise, because you can't tell from EEG alone. Plaghki and Mouraux review evidence from dipole models and invasive recordings, which have

consistently revealed the activation of an extensive bilateral cortical network, comprising the secondary somatosensory cortex (S2), the insular cortex and the anterior cingulate cortex.

It is noteworthy that the N1 response prior to the N2-P2 complex (not discussed here) is insensitive to the attentional and cognitive manipulations that affect the latter.

But how does visual input influence pain processing in the insula and anterior cingulate? How does this crossmodal inhibition occur? This is tricky, because any coherent explanation would have to account for visual enhancement of touch perception. Longo and colleagues speculate that inhibitory GABA-containing neurons might be responsible:

Could a common mechanism produce such divergent effects on touch and pain? One possibility would be a visually induced crossmodal activation of GABAergic interneurons. Injection of GABA antagonists increases the size of SI tactile receptive fields, suggesting that GABAergic interneurons function to sharpen tactile receptive fields, increasing tactile acuity. Conversely, GABA agonists are effective treatments for chronic central pain, suggesting that reduced GABAergic inhibition may be a major cause of chronic pain...
Both the present results showing analgesic effects of seeing the body and previous findings showing tactile enhancement (Kennett et al., 2001) could therefore be explained by visual modulation of somatosensory GABAergic interneurons. This speculation is supported by multisensory influences on cortical inhibition in other physiological systems. For example, viewing a hand extends the TMS-evoked silent period compared with viewing a fixation cross.

A related phenomenon was described by Mo Costandi in Distorting the body image affects perception of pain. Here, chronic pain patients viewed either magnified or "minified" versions of their affected arm while carrying out standarized motions. Subjective pain ratings were reported to be magnified or minified accordingly.

Finally, looking at images other than of one's own body can affect the perception of pain as well. For instance, viewing aesthically pleasing art during the application of laser heat stimuli reduced pain ratings and LEP amplitudes (de Tommaso et al., 2008), as covered by The Neurocritic in Pain & Paintings: Beholding Beauty Reduces Pain Perception and Laser Evoked Potentials.

In conclusion, Longo et al. note their results have possible implications for non-pharmacological treatments for pain:

First, the present results show an analgesic effect of vision of the body for acute, rather than chronic, pain. Second, several authors have suggested that mirror therapy may operate by promoting plastic reorganization within somatosensory map or by correcting a distorted body image through visual recalibration of proprioception [e.g. Ramachandran & Altschuler, 2009], yet our results demonstrate analgesic effects of seeing the body in healthy participants without body image distortion. Third, previous studies have generally involved voluntary movement of the unaffected limb, inducing the illusion of control over the affected hand. Therapeutic effects are typically attributed to the mirror-induced match between visually perceived movement and efferent commands specifying movement. The present results, however, suggest that qualitatively similar analgesic effects may result from simply seeing the hand, independent of movement or match between efferent and afferent signals.

Another application might be for the increasingly popular laser tattoo removal industry. Would having the client view the tattooed body part during the procedure lessen the perception of pain? Anyone who has tried (or would like to try) this experiment, please leave a comment on this post.

For the full on laser pain experience, watch Tattoo removal, no numbing cream. It's a straight edge dude getting XPROVENX removed from his neck. Other than screaming, his harshest utterance is "oh my gosh!"

References

de Tommaso M, Sardaro M, Livrea P. (2008). Aesthetic value of paintings affects pain thresholds. Conscious Cogn. 17:1152-62.

Kennett S, Taylor-Clarke M, Haggard P (2001). Noninformative vision improves the spatial resolution of touch in humans. Curr Biol 11:1188–1191.

Longo, M., Betti, V., Aglioti, S., & Haggard, P. (2009). Visually Induced Analgesia: Seeing the Body Reduces Pain. Journal of Neuroscience, 29 (39), 12125-12130. DOI: 10.1523/JNEUROSCI.3072-09.2009

Plaghki L, Mouraux A. (2005). EEG and laser stimulation as tools for pain research. Curr Opin Investig Drugs 6:58-64. PDF

Ramachandran VS, Altschuler EL. (2009). The use of visual feedback, in particular mirror visual feedback, in restoring brain function. Brain 132:1693-710.

Fact or Fiction? There ten times more glia than neurons in the brain.

2009-09-27T22:29:00.000-07:00

"We only use 10% of our brains" is one of the most commonly held brain myths. But as the Neuroscience for Kids website tells us,

There is no scientific evidence to suggest that we use only 10% of our brains.

Neuroscientists, of course, already know that. But are there other false beliefs about the brain? Brain Mythology is a new column in the journal Brain Structure and Function, edited by Laszlo Zaborszky and Karl Zilles. In the first installment, Hilgetag and Barbas (2009) ask the question, Are there ten times more glia than neurons in the brain?

Neuroscience students take it for granted that there are many more glia than neurons in the brain. Neuroscience textbooks state with confidence: “Although there are many neurons in the human brain…, glia outnumber neurons by tenfold” (Bear et al. 2006) or, not to be outdone, even by “10–50 times”, as claimed in another text (Kandel et al. 2000). This fact is happily invoked by gliologists to promote the status of their field.

Damn those status-conscious gliologists! They've been leading us astray!

Given this well-accepted figure, we were surprised when our cell counts in the prefrontal cortex of the rhesus monkey turned up a glia-to-neuron ratio (GNR) of just about 1 (Dombrowski et al. 2001). There was some regional variation, but no prefrontal area had a GNR larger than 1.2. Maybe the proportion of glia is very different in other cortical regions or other parts of the brain, so that the overall ratio for the whole brain is much larger than 1? Classic studies, however, conducted by O’Kusky and Colonnier (1982) in the opposite pole of the brain, the visual cortex, had reported an even lower GNR of 0.5.

From Fig. 5A (Dombrowski et al., 2001). The ratio of glia/neurons in prefrontal areas or subdivisions of areas.

The origin of the glial dominance myth is not clear at all. Hilgetag and Barbas conclude by mentioning that...

Since the number of synapses increases faster than the number of neurons in larger brains, this affiliation of glia with the multitude of neural connection points may help explain... For example, in large brains such as the human brain... there may be as many as 1.4 astrocytes for each neuron, up from 0.33 in the rodent cortex (Nedergaard et al. 2003). Even that ratio, however, is still a long way from the myth of 10 times more glia than neurons, in any species.

Those species include humans of course, who are like monkeys with a nearly perfect 1:1 neuron:glia ratio [as noted by Jason Snyder].

References

Bear MF, Connors B, Paradiso M (2006). Neuroscience—exploring the brain, 3rd edn. Lippincott Williams & Wilkins, Philadelphia.

Dombrowski S, Hilgetag CC, Barbas H (2001). Quantitative architecture distinguishes prefrontal cortical systems in the rhesus monkey. Cereb Cortex 11:975–988.

Hilgetag, C., & Barbas, H. (2009). Are there ten times more glia than neurons in the brain? Brain Structure and Function, 213 (4-5), 365-366. DOI: 10.1007/s00429-009-0202-z

Kandel ER, Schwartz JH, Jessell TM (eds) (2000). Principles of neural science, nerve cells and behavior, 4th edn. McGraw-Hill, New York, p 22.

Nedergaard M, Ransom B, Goldman SA (2003). New roles for astrocytes: redefining the functional architecture of the brain. Trends Neurosci 26:523–530

O’Kusky J, Collonnier M (1982). A laminar analysis of the number of neurons, glia, and synapses in the adult cortex (area 17) of adult macaque monkeys. J Comp Neurol 210:278–290.

Image via EduSpaces.

A Highlighted Blog at Nature

2009-09-27T11:10:00.000-07:00

The Neurocritic has been mentioned as a highlighted blog at nature.com, along with Good Math, Bad Math. Check out some of the other blogs in the Nature Network and beyond. Of the major non-OA (open access) publishers, NPG has been ahead of the curve in its online presence.

Thanks for the honor!

Neuro Gasm Is Part Of The New Neuro Culture

2009-09-27T02:04:00.000-07:00

"Neuro is an innovative beverage company dedicated to developing the highest quality functional beverages available."

One gets PASSION IN EVERY BOTTLE with Neuro Gasm, which

utilizes L-arginine and L-citrulline to improve a healthy blood flow, improve performance and keep you at your best when you need it the most.

Neuro makes a total of 7 different drinks for adults and 7 for kids (junior, however, gets NeuroFun™ instead of Gasm). The company has great product placement, with many celebrity endorsements:

Paris Hilton Drinks Neuro, So Should You

Neuro Gaga

The products are unlikely to help your Neuro Anything, but the shapely packaging has drawn raves from marketers.

Now it's time for some Neuro Sleep...

...ZZzzzZz. If it actually worked.

Tortured Brains Tell Tall Tales

2009-09-22T02:55:00.000-07:00

OR: Neuroscience Shows Why Torture Doesn't Work

Former CIA Agent Speaks Out - The controversial interrogation technique known as waterboarding, which the CIA agent says was used on [Abu] Zubaydah [see this Justice Department memo, PDF], occurs when a suspect has water poured over his mouth and nose to stimulate a drowning reflex as demonstrated in the picture [above]. (ABC News)

With the Obama administration's recent release of the voluminous Bush-era memos authorizing torture, much has been written about whether or not "aggressive interrogation of captured terrorists" ¹ works, i.e. produces the desired result of extracting accurate and useful information.

Excerpt of Jay Bybee's memo (see Glen Greenwald's column in salon.com).

In a new Science and Society article in Trends in Cognitive Sciences, ² Shane O'Mara outlines the scientific reasons why a brain subjected to extreme stress will not yield accurate information:

The use of such techniques appears motivated by a folk psychology that is demonstrably incorrect. Solid scientific evidence on how repeated and extreme stress and pain affect memory and executive functions (such as planning or forming intentions) suggests these techniques are unlikely to do anything other than the opposite of that intended by coercive or ‘enhanced’ interrogation.

O'Mara didn't actually study the brains of individuals subjected to torture. Instead, he carefully read the memos and then made inferences from the literature on how memory is affected by physical and psychological stress, sleep deprivation, and anxiety.

Stress causes heightened excitability or arousal in the brain and body, a perception that present or future events will be very unpleasant combined with a lack of controllability over these events. Experiencing stress causes release of stress hormones (cortisol; catecholamines such as noradrenaline). Stress hormones provoke and control the ‘fight or flight’ response (the immediate and rapid preparation by body and brain for action in response to threat) which, if overly-prolonged, may result in compromised cognitive neurobiological function (and even tissue loss) in these brain regions. Both the hippocampus and the prefrontal cortex are particularly rich in receptors activated by stress hormones. Cortisol binds preferentially to glucocorticoid receptors in hippocampus and prefrontal cortex, increasing Ca++ access, and thus neuronal excitability which will compromise normal physiological functioning of neurons if it is sustained.

Importantly, O'Mara then reviews specific evidence that torture is likely to produce the exact opposite of the intended effect: false memories, confabulations, and less accurate information.

Extreme stress studies in Special Operations Soldiers (Morgan et al., 2006) have found impaired visuo-spatial capacity and impaired recall of previously-learned information in stressed soldiers (who undergo stress, including food and sleep deprivation, during training modelled on the experiences of American prisoners-of-war). Brain imaging in persons previously subjected to severe torture suggests that abnormal patterns of activation are present in the frontal and temporal lobes, leading to deficits in verbal memory for the recall of traumatic events (Ray et al., 2006; Catani et al. 2009).

A previous post by The Neurocritic covered The Guantánamo Testimonials Project and The Neurobiology of Psychological Torture. These research projects are being conducted at the Center for the Study of Human Rights in the Americas. CSHRA summarizes their work on The Neurobiology of Psychological Torture as follows:

... Psychological torture (henceforth PT) is a set of practices that are used worldwide to inflict pain or suffering without resorting to direct physical violence. PT includes the use of sleep deprivation, sensory disorientation, forced self-induced pain, solitary confinement, mock execution, severe humiliation, mind-altering drugs and threats of violence—as well as the exploitation of personal or cultural phobias. The psychiatric sequelae of PT are severe. They include delirium, psychosis, regression, self-mutilation, cognitive impairment, and anxiety disorders, including post-traumatic stress disorder. Neuroscience research on these and related mental disorders continues to establish their neurobiological underpinnings, thus challenging the popular view that PT is not physical, not serious, and perhaps not even torture at all.

Rendered brain showing abnormal brain activity in torture victims. This picture (white-gray matter border) shows regions in red with excess slow wave activity which is strongest in the left insula (see Kolassa et al. "Imaging the trauma: altered cortical dynamics after repeated traumatic stress") and the left frontal inferior region (see Ray, Elbert, et al. "Survivors of organized violence often left with traumatic memories." Psychological Science Volume 17, Issue 10, October 2006). Blue indicates less activity than normal. Photo: Courtesy of Dr. Thomas Elbert, Univerity of Konstanz, Germany.

The proceedings from a workshop conducted in 2006 were published as a book, The Trauma of Psychological Torture. Let's see Dick Cheney, John Yoo, Jay Bybee, and their ilk produce any scientific evidence to the contrary.

ADDENDUM: The paper is now available for download from Trends in Cognitive Sciences. DOI: 10.1016/j.tics.2009.09.001 [download PDF]

Footnotes

¹ "The Latest Euphemism From The Torture Party" according to Andrew Sullivan. I also recommend The Gestapo Precedent for "EITs" [Enhanced interrogation techniques]. For more on O'Mara's paper, read The Tortured Brain by Sharon Begley.

² Also covered by ScienceInsider, which made the paper available before it appeared on the TICS website. See Torture Can't Provide Good Information, Argues Neuroscientist (by John Bohannon).

References

Catani C, Adenauer H, Keil J, Aichinger H, Neuner F. (2009). Pattern of cortical activation during processing of aversive stimuli in traumatized survivors of war and torture. Eur Arch Psychiatry Clin Neurosci 259:340-51

Morgan CA 3rd, Doran A, Steffian G, Hazlett G, Southwick SM. (2006). Stress-induced deficits in working memory and visuo-constructive abilities in Special Operations soldiers. Biol Psychiatry 60:722-729.

O'Mara S (2009). Torturing the Brain: On the folk psychology and folk neurobiology motivating ‘enhanced and coercive interrogation techniques’. Trends in Cognitive Sciences. DOI: 10.1016/j.tics.2009.09.001

Ray WJ, Odenwald M, Neuner F, Schauer M, Ruf M, Wienbruch C, Rockstroh B, Elbert T. (2006). Decoupling neural networks from reality: dissociative experiences in torture victims are reflected in abnormal brain waves in left frontal cortex. Psychol Sci. 17:825-829.

Are Antidepressants UNDERprescribed in Primary Care Settings?

2009-09-18T02:22:00.000-07:00

Despite everything else you've heard and read (and watched on ABC) recently, the answer is yes. Or maybe. At least in Scotland. Antidepressants might be UNDERprescribed by General Practitioners, according to a new study published in the British Journal of General Practice (Cameron et al., 2009). The authors conducted a chart review of 898 adults screened for anxiety and depression in a general practice setting. They concluded:

Rather than prescribing indiscriminately (as has been widely assumed), it is likely that GPs are initiating antidepressant treatment conservatively.

However, another article in the same issue of the journal interviewed 63 GPs to determine their explanations for the dramatically increased rate of prescribing in Scotland (Macdonald et al., 2009). Many thought the present-day level of prescribing was too high and

believed that unhappiness, exacerbated by social deprivation and the breakdown of traditional social structures, was being 'medicalised' inappropriately.

In contrast to Cameron and colleagues, MacDonald et al. concluded that antidepressants are OVERprescribed by GPs in Scotland, and recommended a change in prescribing patterns (as have many others).

So which is it? Who are we to believe? Unfortunately, I don't have access to either paper, so we'll have to make do with the abstracts.

References

Cameron, I., Lawton, K., & Reid, I. (2009). Appropriateness of antidepressant prescribing: an observational study in a Scottish primary-care setting British Journal of General Practice, 59 (566), 644-649 DOI: 10.3399/bjgp09X454061

Background: Since the 1990s, Scottish community-based antidepressant prescribing has increased substantially. Aim: To assess whether GPs prescribe antidepressants appropriately. Design of study: Observational study of adults (aged ≥16 years) screened with the Hospital Anxiety and Depression Scale (HADS) attending a GP. Setting: Four practices in Grampian, Scotland. Method: Patients (n = 898) completed the HADS, and GPs independently estimated depression status. Notes were scrutinised for evidence of antidepressant use, and the appropriateness of prescribing was assessed. Results: A total of 237 (26%) participants had HADS scores indicating 'possible' (15%) or 'probable' (11%) depression. The proportion of participants rated as depressed by their GP differed significantly by HADS depression subscale scores. ... In 101 participants with 'probable' depression, GPs recognised 53 (52%) participants as having a clinically significant depression. Inappropriate initiation of antidepressant treatment occurred very infrequently. Prescribing to participants who were not symptomatic was accounted for by the treatment of pain, anxiety, or relapse prevention, and for ongoing treatment of previously identified depression. Conclusion: There was little evidence of prescribing without relevant indication. Around half of patients with significant symptoms were not identified by their GP as suffering from a depressive disorder: this varied inversely with severity ratings. Rather than prescribing indiscriminately (as has been widely assumed), it is likely that GPs are initiating antidepressant treatment conservatively.

Macdonald, S., Morrison, J., Maxwell, M., Munoz-Arroyo, R., Power, A., Smith, M., Sutton, M., & Wilson, P. (2009). ‘A coal face option’: GPs' perspectives on the rise in antidepressant prescribing British Journal of General Practice, 59 (566), 299-307 DOI: 10.3399/bjgp09X454106

Background: Levels of antidepressant prescribing have dramatically increased in Western countries in the last two decades. Aim: To explore GPs' views about, and explanations for, the increase in antidepressant prescribing in Scotland between 1995 and 2004. Design: Qualitative, interview study. Setting: General practices, Scotland. Participants: GPs in 30 practices (n = 63) purposively selected to reflect a range of practice characteristics and levels of antidepressant prescribing. Method: Interviews with GPs were taped and transcribed. Analysis followed a Framework Approach. Results: GPs offered a range of explanations for the rise in antidepressant prescribing in Scotland. Few doctors thought that the incidence of depression had increased, and many questioned the appropriateness of current levels of prescribing. A number of related factors were considered to have contributed to the increase. These included: the success of campaigns to raise awareness of depression; a willingness among patients to seek help; and the perceived safety of selective serotonin reuptake inhibitors, making it easier for GPs to manage depression in primary care. Many GPs believed that unhappiness, exacerbated by social deprivation and the breakdown of traditional social structures, was being 'medicalised' inappropriately. Conclusion: Most antidepressant prescriptions in Scotland are issued by GPs, and current policy aims to reduce levels of prescribing. To meet this aim, GPs' prescribing behaviour needs to change. ...

Chinese Dissidents Committed to Mental Hospitals

2009-09-17T15:50:00.000-07:00

The PBS Newshour reports on political dissidents and petitioners in China who are sentenced to psychiatric hospitals.

Special correspondent Shannon Van Sant reports:

SHANNON VAN SANT: ...I traveled to Wuhan to talk with another Chinese activist, Liu Feiyue, but he was under house arrest. Liu heads an NGO that is currently following 100 cases of wrongful psychiatric detention. Over the last three years, he says he knows of 500 more whistleblowers and protesters who have been detained in mental hospitals.
Robin Munro, who has extensively researched psychiatric detention in China and written two books on the topic, thinks the practice is widespread.
ROBIN MUNRO, human rights activist: China's experience in this area is far more serious and extensive than any other country.
SHANNON VAN SANT: Munro, who is based in Hong Kong, believes that since there are no national mental health laws protecting the rights of people who have been compulsorily hospitalized, but there are rules limiting arbitrary arrest, hospitals are becoming a convenient means of silencing protesters.
ROBIN MUNRO: Once diagnosed in this way, as dangerously mentally ill, citizens have no rights. They have no legal right to see a lawyer; they have no legal right to be brought before a judge so that a judicial determination can be made.

via China Digital Times.

Great and Desperate Cures for Addiction

2009-09-14T04:48:00.000-07:00

《Chinese Journal of Drug Dependence》1999-04

Does anyone know what aerosol bioelectricity is?? And why it might be used to treat heroin addiction? The entire literature seems to be in Chinese. I came across that particular paper while searching for others, specifically reports on ablative psychosurgery¹ for the treatment of opiate addiction in China (Gao et al., 2003 is the first in English). Hence, the title of the present post is a reference to the book by Elliot Valenstein, Great and Desperate Cures: The Rise and Decline of Psychosurgery and Other Radical Treatments for Mental Illness.

Are there other "unusual" Chinese treatments for addiction, beyond what might be expected (e.g., acupuncture and traditional medicine)? Tetrodotoxin (TTX), a neurotoxin found in puffer fish, is a worthy runner up to aerosol bioelectricity. TTX inhibits action potentials by blocking voltage-dependent sodium channels. It has been tested as a treatment for severe cancer pain, which motivated Shi and colleagues (2009) to compare low dose TTX to placebo in abstinent addicts. After watching a heroin-related video, the group receiving TTX reported lower levels of craving and anxiety, without alterations in heart rate or blood pressure. However, these acute results were from a single session with no long-term follow up.

Although Chinese treatments for internet addiction are getting all the headlines these days, drug addiction is actually a much more serious problem. In their review of the literature, Tang et al. (2006) inform us that:

Historically, China has had extraordinarily high rates of opiate dependence. These rates declined drastically following the 1949 revolution; however, opiate abuse has re-emerged in the late 1980's and has spread quickly since then. ... The number of registered addicts in 2004 was 1.14 million (more than 75% of them heroin addicts), but the actual number is probably far higher. Opiate abuse contributes substantially to the spread of HIV/AIDS in China, with intravenous drug use the most prevalent route of transmission (51.2%). Currently, the main treatments for opiate dependence in China include short-term detoxification with opiate agonists or non-opiate agents, such as clonidine or lofexidine [alpha-2 adrenergic drugs that inhibit norepinephrine release]; Chinese herbal medicine and traditional non-medication treatments are also used. Methadone maintenance treatment (MMT) has not been officially approved by the Chinese government for widespread implementation, but some pilot studies are currently underway.

Which brings us back to neurosurgery. But before discussing the results of Gao et al., a quick review. In the last post, we learned about a new and less desperate cure, the application of Deep Brain Stimulation for Severe Alcoholism. The target region in this small clinical trial (n=3) was the nucleus accumbens (NAcc), which has been called a "pleasure center" and "hedonic hot spot" that responds to food and pharmaceutical and financial and sexual rewards. The idea behind NAcc DBS was to reduce alcohol craving and "incentive sensitization" in severely impaired patients who had failed multiple treatments (Heinze et al., 2009). The researchers drew upon the experimental and theoretical work of Berridge and colleagues (2009) distinguishing between the "wanting" (incentive salience) and "liking" (hedonic impact) aspects of reward:

Usually a brain ‘likes’ the rewards that it ‘wants’. But sometimes it may just ‘want’ them. Research has established that ‘liking’ and ‘wanting’ rewards are dissociable both psychologically and neurobiologically. By ‘wanting’, we mean incentive salience, a type of incentive motivation that promotes approach toward and consumption of rewards, and which has distinct psychological and neurobiological features.

"Liking" has been strongly linked to endogenous opioid systems in the NAcc and ventral pallidum [part of the globus pallidus] as shown below.²

From Fig. 1 (Berridge et al., 2009). Forebrain hedonic hotspots in nucleus accumbens shell and in ventral pallidum where mu opioid agonist microinjections cause amplification of ‘liking’ reactions to sweetness. Red/yellow indicates greatest amplification of ‘liking’ for the sensory pleasure.

In contrast, "wanting" has been most strongly associated with dopamine in the NAcc, but in reality...

...brain substrates for ‘wanting’ are more widely distributed and more easily activated than substrates for ‘liking’. Neurochemical ‘wanting’ mechanisms are more numerous and diverse in both neurochemical and neuroanatomical domains... In addition to opioid systems, dopamine and dopamine interactions with corticolimbic glutamate and other neurochemical systems activate incentive salience ‘wanting’. Pharmacological manipulations of some of those systems can readily alter ‘wanting’ without changing ‘liking’. For example, suppression of endogenous dopamine neurotransmission reduces ‘wanting’ but not ‘liking’.

Addiction is conceived as a process by which drugs of abuse produce neural sensitization and compulsive "wanting" even in the absence of "liking". With this literature in mind, Gao et al. (2003) wished to:

...explore a new way of treating drug addiction by ablating the NAcc... using stereotactic surgery, blocking the mesocorticolimbic dopamine circuit, alleviating craving for drugs and lowering the relapse rate after detoxification. On the basis of animal experiments, stereotactic surgery was performed in 28 patients by making a lesion in the NAcc bilaterally to treat opiate drug dependence.

I'm not so sure the surgeons were able to isolate the "wanting" from the "liking" regions of the NAcc, since they seem to be anatomically adjacent as shown below.

Fig. 2 (Berridge et al., 2009). Expansion of mu opioid hotspot in nucleus accumbens with delineation of ‘liking’ versus ‘wanting’ zones. Green: the entire medial shell mediates opioid-stimulated increases in ‘wanting’ for food reward. Orange-red: circumscribed cubic-millimeter sized hedonic hotspot generates increases in ‘liking’ after the same opioid stimulation. Blue: a small hedonic ‘coldspot’ suppresses ‘liking’ reactions to sucrose, whereas a larger purple zone suppresses ‘disliking’ reactions to quinine.

Were the surgeries successful? Not so much:

The mean follow-up period was 15 months. Relapse has not occurred in 11 cases up till now. Drug-free time in these patients has been more than half a year in 4 cases (more than a year in 3 cases), and less than half a year in 7 cases. Relapse occurred in 15 cases after surgery. Drug-free time in these patients was more than half a year in 3 cases, between 1 month and half a year in 10 cases and less than 1 month in 2 cases.

Plus there were side effects in some patients: personality changes were seen in 2 and temporary memory loss in 4. Last but not least was the issue of informed consent, which wasn't discussed at all in the paper. Alarmingly, the psychological state of the patients before surgery seems to suggest they lacked capacity to give informed consent:

Analysis of the results showed that the patients’ psychohygienic situation was poor prior to the operation and their personalities were characterized by unstable emotion, being seriously distressed by tonicity and prone to following their own course, running risks and doing everything without considering the consequences, paranoid state, low intelligence level, mental aberration and weak-willedness.

In comparison, the careful screening procedures of Heinze et al. (2009) and the reversible nature of their intervention are vastly superior. Comments on my previous post have ranged from unbridled enthusiasm for DBS³ (also see Best Before Yesterday) to skepticism ("We still have no idea whether this will ~~this~~ actually work"), with caution and curiosity in between. I suspect the antipsychiatry trolls [the comment is priceless] might come out of the woodwork for this one. In this case, I would agree that criticism is warranted.

Footnotes

¹ Wikipedia warns us that "The medical procedure of psychosurgery should not be confused with psychic surgery — surgery purportedly performed by paranormal means."

² "Liking" has also been associated with endocannabinoid and GABA_A-benzodiazepine systems in the brain.

³ For more information on DBS for intractable depression, see The Neurocritic's archival posts:

The Sad Cingulate
Sad Cingulate on 60 Minutes and in Rats
NAcc Localization for DBS

...and two articles by science writer David Dobbs:

A Wiring Diagram in the Brain for Depression
A Depression Switch?

References

Berridge KC, Robinson TE, Aldridge JW. (2009). Dissecting components of reward: 'liking', 'wanting', and learning. Curr Opin Pharmacol. 9:65-73.

Gao, G., Wang, X., He, S., Li, W., Wang, Q., Liang, Q., Zhao, Y., Hou, F., Chen, L., & Li, A. (2003). Clinical Study for Alleviating Opiate Drug Psychological Dependence by a Method of Ablating the Nucleus accumbens with Stereotactic Surgery. Stereotactic and Functional Neurosurgery, 81 (1-4), 96-104 DOI: 10.1159/000075111

Heinze, H. et al. (2009). Counteracting incentive sensitization in severe alcohol dependence using deep brain stimulation of the nucleus accumbens: clinical and basic science aspects. Frontiers in Human Neuroscience, 3.

Shi J, Liu TT, Wang X, Epstein DH, Zhao LY, Zhang XL, Lu L. (2009). Tetrodotoxin reduces cue-induced drug craving and anxiety in abstinent heroin addicts. Pharmacol Biochem Behav. 92:603-7.

Tang YL, Zhao D, Zhao C, Cubells JF. (2006). Opiate addiction in China: current situation and treatments. Addiction 101:657-65.

Deep Brain Stimulation for Severe Alcoholism

2009-09-09T10:38:00.000-07:00

Deep brain stimulation (DBS) for treatment-refractory psychiatric disorders has been gaining in popularity. The procedure involves neurosurgery to implant stimulating electrodes aimed at a target region inside the brain. It works using the same sort of pacemaker-like device used for DBS in Parkinson's disease, which has been remarkably successful at alleviating symptoms. DBS as a treatment for neurological disorders such as Parkinson's, primary generalised dystonia, atypical tremor syndromes, cluster headache, phantom limb pain, and epilepsy has been mostly unobjectionable.

However, the Neurological/Psychiatric Divide makes DBS for mental illnesses such as major depression and obsessive compulsive disorder more ethically problematic. A new paper in the Archives of General Psychiatry (Rabins et al., 2009)¹ summarizes a consensus conference held on this and related issues (such as human subjects protection and the design of clinical trials). A list of 16 guidelines was issued, which included the following:

2. Deep brain stimulation for disorders of MBT [Mood, Behavior, and Thought] is at an early proof-of-principle stage and must be considered investigational. Currently, no single target has been validated or demonstrated to be superior to others in any disorder of MBT. Therefore, it is premature to rule out the study of new implantation sites that have a good scientific rationale...
3. The comparative efficacy and safety of DBS vs other treatments, including ablative surgery, should be studied further. Such studies are ethical and scientifically necessary.
4. Given its history, neurosurgical intervention for disorders of MBT is a socially and culturally sensitive area of research and practice. Therefore, DBS for disorders of MBT should be studied in carefully designed trials and should be performed only at expert centers that are participating in such trials and that adhere to the highest scientific, clinical, and ethical standards.
. . .
12. The consent process should include discussion of what is and is not known about long-term consequences of DBS. Potential adverse outcomes include potentially limiting participation in future research, inability to use certain other treatments, and an inability to undergo certain tests. ... Additionally, the consent process should state explicitly that, even with positive outcomes, DBS for disorders of MBT is unlikely by itself to improve all aspects of the individual's mood, function, and interpersonal relationships: DBS is only one aspect of a comprehensive treatment program.

The specific indications mentioned by Rabins and his 18 co-authors were major depression, obsessive-compulsive disorder, and Tourette syndrome. Severe alcohol dependence was not included as one of the disorders. DBS for alcoholism sounds rather drastic, doesn't it? Nonetheless, a German research group led by Hans-Jochen Heinze (et al., 2009) was not deterred. They recently reported results from 3 male patients² with severe and refractory alcohol dependence as part of a small clinical trial that will ultimately include 10 patients.

Inclusion criteria are: male gender, age 25–60 years, finished detoxification and subsequent period of abstinence of at least 2 weeks. Moreover, the patients are required to have demonstrated treatment failures of at least two inpatient programs of at least 6 month duration, failure of anti-craving substances (e.g., acamprosate, naltrexone), failure of community and self-help programs. ... Patients are excluded, if they meet any of the following criteria: seizures during the detoxification phase, high score on neuroticism scales, antisocial personality disorder, clinically significant impairments on a neuropsychological test battery Further exclusion criteria were circumscribed brain damage or marked atrophy on MRI, alcohol-related personality change, and use of additional addictive substances.

The target region? The nucleus accumbens (NAcc), the “Universal Addiction Site” -- an oversimplification, they admit, but still, the NAcc is...

...a central place in orchestrating the events related to the “wanting” [Robinson & Berridge, 2008] of alcohol on the one hand and drug-induced neural sensitization on the other hand. Anatomically, the NAcc receives inputs from the prefrontal cortex on the one hand and limbic structures such as the hippocampus and amygdala on the other. This circuitry allows for the integration of contextual information arising from hippocampus and emotional information coming from the amygdala with cognitive information supplied by the PFC in the selection of goal-directed behaviors in general and behaviors related to drug “wanting” in particular, which is why the NAcc has been called a limbic-motor interface.

Since anatomical information was not illustrated in the current paper, a figure from the earlier work of Schlaepfer et al., (2007) is presented below.

The topographical location of the nucleus accumbens in relation to other brain structures on a horizontal plane 3 mm below the AC-PC plane (Schlaepfer et al., 2007).

That protocol was designed to relieve anhedonia (inability to experience pleasure from normally pleasurable life events) in major depression. Why not stimulate the "pleasure center" when you're feeling blue? Extensive research in animals and humans has demonstrated "hedonic hot spots" (Pecina et al., 2006) [or "liking" of pleasant sensory experiences] in the NAcc that respond to food and pharmaceutical and financial and sexual rewards.

But what are the procedures for targeting the same region to reduce reward and pleasure? Well, we don't know from reading Heinze et al. (2009): "Details regarding the stimulation protocols in the different patients can be found elsewhere" [insert citation of an in press paper that is not online yet]. Details on the "clinical aspects" are pretty sparse and the focus is on the "basic science aspects" (electrophysiological recording and cognitive task performance to assess action monitoring and the salience of drug-related cues).

Was the DBS treatment effective? All patients had failed multiple detox treatments, withdrawal therapies, and drug trials (acamprosate). Until the other paper is published, we have only anecdotal reports in the Methods.

Patient HM (age 36) had started to drink alcohol at age 12 and had a family history of alcoholism (father and two uncles). ... The patient was implanted on October 5, 2007 and has been abstinent since then. There were no psychological changes after the operation. The patient reported to have no craving symptoms and that he is thus able to derive pleasure from daily activities of life. He has found a job and has established new social contacts.

Patient GM (age 37) had started to drink alcohol at age 11 and had a positive family history (father, mother, several other relatives). ... Following the operation (January 13, 2008) this patient experienced a period of hypomania which stopped after stimulation parameters were changed. The patient has been abstinent since the operation and reports a complete reduction of his reaction to alcohol-related cues and craving.

Patient TM (age 40) had been alcohol-dependent since age 18 and had a positive family history (father). ... The patient was operated on September 13, 2007 and showed no psychological abnormalities in the postoperative period. He was fully abstinent until September 2008. Subsequently, he has experienced short periods of relapse of 1–2 weeks duration (10 weeks in the past 16 months). The patient remarked that he had never felt as good as currently and reported a considerable reduction in his reaction to alcohol-related cues.

To be continued....

Footnotes

1 Guidelines were also published by the German Deep Brain Stimulation Association (Voges et al., 2009).

² "A fourth had been implanted but electrodes had to be removed because of an infectious complication."

References

Heinze, H. et al. (2009). Counteracting incentive sensitization in severe alcohol dependence using deep brain stimulation of the nucleus accumbens: clinical and basic science aspects Frontiers in Human Neuroscience, 3. DOI: 10.3389/neuro.09.022.2009

Pecina S, Smith KS, Berridge KC. (2006). Hedonic hot spots in the brain. Neuroscientist 12:500-11.

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

Robinson TE, Berridge KC. (2008). Review. The incentive sensitization theory of addiction: some current issues. Philos Trans R. Soc Lond B Biol Sci. 363:3137-46.

Schlaepfer TE, Cohen MX, Frick C, Kosel M, Brodesser D, Axmacher N, Joe AY, Kreft M, Lenartz D, Sturm V. (2008). Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression. Neuropsychopharmacology 33:368–377.

090909090909

2009-09-09T09:09:00.000-07:00

In Chinese numerology the number 9 is a homophone of the word for "long-lasting". So today seems like a good day to do something that will last a long time, right? However, from AgarAgar we learn:

Today sounds like a nice date to remember.. 090909.. Lots of ple say it a good date for marriage.. 999 in Chinese means long-lasting. However, as it falls in the lunar 7th mth, aka ghost mth. Therefore no much weddings are held on this date. Maybe some ROMs or non-chinese are having weddings today bah.

In contrast, 080808 was such a lucky number that the Opening Ceremony of the 2008 Olympics in Beijing began at 8:08PM on 08/08/08.

The vagueness of Western Numerology is much like reading your horoscope or going to a fortune teller. Here's some information on the number nine:

In Numerology, the positive characteristics of nine (9) are selflessness, fulfillment, completion, universality, universal understanding, interrelatedness, compassion, idealism tolerance, forgiveness, generosity, benevolence, humanitarianism, emotionalism, and justice. Nine is also associated with accomplished artists and thinkers who are inspired by universal truths. Simultaneously, 9 can represent negative characteristics, from selfishness to extravagance to vulgarity -- essentially the opposites of the positive characteristics.

How very useful and specific!!

From nmnl’s posterous.

RULE 34: WHAT NETPORN TELLS US ABOUT THE BRAIN

2009-09-05T04:40:00.000-07:00

That is (or was) the title of a book by Ogi Ogas and Sai Gaddam,¹ to be published by Dutton in 2010. How on earth do I know this? Back in July, The Neurocritic noticed a number of visitors to the post Voodoo Correlations in Social Neuroscience (about the infamous paper by Vul et al.) who came from a link on the LiveJournal of shaggirl. Specifically, the traffic was from her entry A response from our friendly scientists... I took note of it, thought I might write about it but other topics took precedence. But this week, a larger surge of visitors arrived from various LiveJournal sites.² The reason? Let's start at the beginning.

Shaggirl was "contacted by a couple of guys researching and writing about online fanfic."

Hi, Shaggirl:

I'm a cognitive neuroscientist at Boston University writing a book for Dutton (an imprint of Penguin) about how the Internet reveals new insights into some of the oldest circuits in our brain which control romantic attraction and sexual behavior. I was very much hoping you might be willing to chat about Crack Van on LJ.
. . .
For our research, we're quite interested in learning about how people creatively use text and fiction to express and explore sexuality. If you're willing, we'd like to ask questions about Crack Van and about adult fanfic in general. If you'd like, we'd be happy to include a positive mention of you and/or Crack Van in the book (or respect your privacy, if you'd prefer).
If you have any questions about our research or book, please don't hesitate to ask! I look forward to hearing from you! :)
Dr. Ogi Ogas
Department of Cognitive and Neural Systems
Boston University

I do not want to begin a lengthy discourse on fan fiction, other than to quote Wikipedia:

Fan fiction (alternately referred to as fanfiction, fanfic, FF, or fic) is a broadly-defined term for fan labor regarding stories about characters or settings written by fans of the original work, rather than by the original creator. Works of fan fiction are rarely commissioned or authorized by the original work's owner, creator, or publisher; also, they are almost never professionally published. Fan fiction, therefore, is defined by being both related to its subject's canonical fictional universe and simultaneously existing outside the canon of that universe.

So who is Ogi Ogas? While a grad student at Boston University, he entered a well-known game show, won $500,000 and wrote about it in SEED magazine:

Who Wants to Be a Cognitive Neuroscientist Millionaire?
A researcher uses his understanding of the human brain to advance on a popular quiz show.

Even with all 4 choices available, it's obvious the answer is D ("Heroin: the sedative for coughs"). Prescription cough syrup contains codeine, which is a cough suppressant. [However, it is easy to say that when the stakes are nil. ANYWAY.]

In response to some questions about their book project, Gaddam replied:

Before putting any questions, let me give a brief overview of our scientific perspective and how it will inform the book. As cognitive neuroscientists, we are respectful of the fascinating diversity of the neural landscape. And this diversity, we believe, is reflected in the terrain of erotic fantasy.
The internet and e-publishing now allow for a revolutionary and unprecedented disclosure of all our fantasies, not just those decided as marketable and mainstream for print. Digital publishing seems to have lead to an explosion in the array of fantasies we can now experience and learn from; the loop of imagination, desire, and actuality is now tighter. We want to 'neuro-scientifically' explore what this blossoming of fantasy means for us as individuals, and as a society. How does this access to all manner of fantasies imaginable change our brains?
Given this broad overview, we have some specific questions, and more general ones about adult fanfic, that we are hoping you can help us with. I do apologize if some questions seem naive and/or I inadvertently mis-characterize something in my ignorance!

He then goes on to ask a number of questions about adult fanfic. Dana (shaggirl) replied in a lengthy, thoughtful post in which she explains fandom ("composed primarily of well educated women, most of whom self-identify as geeks"), objects to the word "netporn" in their book title, and answers all 7 questions. Then A response from our friendly scientists... where yours truly gets a mention:

. . .

One quick note about the subtitle of the book: the current title is largely driven by the pre-publication marketing needs of the publication industry, and was determined by our editor. The eventual subtitle will likely change; it may still contain the term netporn, though this is increasingly unlikely [NOTE: Unlike the screenshot above, the current book project list from Gail Ross shows the NETPORN subtitle has indeed been removed]. ...

In terms of turning this into hard science, our primary goal is to make a strong case for the study of fantasy as being accessible in this era of copious datastreams from humans. To give you one example of the kind of current study in neurosexual behavior that we feel is quite limited, there was an article in the Time magazine (http://www.time.com/time/health/article/0,8599,1911103,00.html) on how girls focus more on best friends while boys are more interested in group dynamics and 'packs'. The authors of the study tied this observation to the differential activation patterns in the brain based on how the subject group of boys and girls rated pictures of strangers. The article state that the "nucleus accumbens (which is associated with reward and motivation), hypothalamus (associated with hormone secretion), hippocampus (associated with social learning) and insula (associated with subjective feelings) all become more active."

The suspect and cavalier methodology of this study evoke some of the general problems that plague brain imaging experiments that purportedly examine social behavior [1]. We hope to make the case that such methodological contortions are not required when a vast pool of people provide behavioral data on the internet through quantifiable activity.

Polling feedback from groups would be immensely useful. We would definitely love your help in reaching other fans...

[1] Here's a paper criticizing such casual treatment of the brain-behavior linkage, which has received a lot of attention in the neuroscience community (http://cns.bu.edu/~gsc/Articles/Vul_09_Voodoo.pdf). The content requires an understanding of imaging methodology, but the abstract is definitely accessible. Here's a posting from a popular neuroscience blog describing the article (http://neurocritic.blogspot.com/2009/01/voodoo-correlations-in-social.html)

Two things:

(1) They said the content of their book will be "Using new digital sources of data to illuminate brain regions and neural pathways involved in romantic and sexual behavior." However, they did not actually propose to measure brain function at all. They might be skeptical of fMRI, but it's a lot better than no real neural data at all.

(2) A poll. That generated an enormous amount of controversy in the fanfic community. [They're a very prolific bunch.] Hundreds of posts. Thousands of comments.

SurveyFail - an entire wiki devoted to the controversy.

For Science!

The poll was taken down (although you can view the questions elsewhere: part 1, part 2) and the ogi_ogas LiveJournal deleted (but here's a remnant):

So what kind of scientists are you anyway?
We're brain modelers. We're aligned with the relatively new field of cognitive neuroscience...
. . .
Our current research project will result in a model that makes novel behavioral and physiological predictions.

From a poorly written survey? And just when you think their project is a wee bit grandiose, the pomposity reaches stunning proportions:

The greater one's mathematical ability, the greater the opportunity for designing a powerful and sophisticated model. Superior models, such as those of Stephen Grossberg and Gail Carpenter, may include unsolvable systems of differential equations. Still, useful and productive models can be constructed using relatively straightforward mathematics.

Oh, and here's a ridiculous question:

How is straight female interest in slash fiction like straight male interest in "shemale"* models? And why in the world does this matter?
* ...We are aware that the term "shemale" may be used as a pejorative, but we are here referring to the narrowly defined term used in the adult industry for certain models.

One does not need to be an expert in any of these fields to see the problems inherent in the Ogas and Gaddam approach of inferring brain function from data on netporn usage (broadly construed) and unscientific polls. But it gets worse...

The structure and activity of our subcortical circuits are shaped by neurohormones such as testosterone, estrogen, oxytocin, progesterone, and vasopressin; these circuits function differently in men and women. As cognitive neuroscientists, we draw upon a wide variety of empirical data sources to model these circuits, including brain imaging studies, primate research, cognitive science experiments, machine learning algorithms--and behavioral data. The Internet offers large, unprecedented sources of data on human activity: one of these data sets is fan fiction.
We're deeply interested in broad-based behavioral data that involves romantic or erotic cognition and evinces a clear distinction between men and women. Fan fiction matches this criteria perfectly. Let us make clear, however: fan fiction is not the subject of our research. Our subject is the human brain. For us, fan fiction is a wonderfully rich source of data--like single-neuron recordings in rhesus monkeys--albeit a unique and invaluable one.

...because fan fiction is just as precise as single-unit recording at revealing putative sex differences in subcortical circuits. In spite of a wink and a nod to "erotic cognition" Ogas & Gaddam reveal elsewhere in their manifesto that they're not at all interested in cortical function.

Furthermore, were the ethics of conducting research on human subjects taken into consideration? Did the pair have proper approval from Boston University's Institutional Review Board? Here's deadlychameleon's investigation:

I called the Boston University IRB office. The direct approach works.
They've gotten a lot of emails regarding Dr. Ogas. He is no longer in any way affiliated with Boston University, except as a recent graduate. They have asked him to stop using his official Boston University email address in connection with this project, or his website. He is officially on his own, and this project is NOT IRB APPROVED.
That is the official status as stated by the Boston University IRB office.

And in the end, from a neuroscientific viewpoint, the premise of their work was fatally flawed. Dutton, are you listening?

Footnotes

¹ You'll notice these links are from the Google cache, because they took down their websites after the resulting furor. Both are recent graduates from the Department of Cognitive and Neural Systems at Boston University. Gaddam had not yet updated his resume to reflect this.

² Other visitors were from dreamwidth.org, a LiveJournal knockoff that had escaped my awareness until now.

So You Think You Can Neuroblog?

2009-08-29T02:39:00.000-07:00

Real members of the Society for Neuroscience (as opposed to all those fake members with pseudonyms) can apply to be an Official SfN Neuroblogger at the 40th Annual Meeting in Chicago:

SfN Interactive: Blogging and Tweeting the Annual Meeting
SfN encourages members to blog and tweet about events specific to Neuroscience 2009 while it’s happening.
Interested in Serving as a Neuroblogger?
Is there a Special Lecture your colleagues should not miss? Is there an interesting Poster that catches your eye? Want to gather colleagues at an SfN-Sponsored Social? Consider being a Neuroblogger.

What are some of the benefits of being a Neuroblogger? Besides the possibility of greater exposure (for a limited time before, during, and after the meeting), you'll get......

An official “SfN Social Media” ribbon to wear at the annual meeting [!!]

NOTE: unOfficial SfN Social Media Ribbon designed by Sandra Kiume, who will not be liveblogging the meeting.

Yay!

But there's more! Your name will be entered into a drawing for a free iPod nano. And [better late than never] you'll have.....

The honor of taking part in SfN Interactive’s flagship year

The Neurocritic was rather skeptical when SfN first announced that attendees would need to apply in order to blog at the conference this year. Their media policy isn't exactly social media-friendly, in terms of who is eligible for press credentials:

Internet News Outlets
Bona fide Internet news organizations that distribute information directly to the general public are eligible. Personal Web site writers, writers from Web sites operated by non-media companies, or Web site creators are ineligible to register as media.

And their embargo policy actually prevents one from liveblogging or livetweeting:

Information from all other presentations, including lay language summaries, is embargoed until the conclusion of the relevant presentation.

Strictly speaking, this means that a poster is embargoed until the end of the 4 hour session. So you're not supposed to blog about a 1 PM poster until 5 PM (although I don't know how this will be enforced). The same is true for a 15 min talk, so no quick Twitter updates until after the speaker has finished.

There are other rules and requirements as well:

By applying to be a Neuroblogger, from October 17 to 21, you are expected to write one or more blog entries per day about activities, events, and experiences related to Neuroscience 2009 in Chicago.
SfN cannot provide blog hosting or online content management services...
You must be a current SfN member to submit an application.
On the application, provide a link to your current blog(s) or writing samples from entries you've composed in the past, preferably during a previous scientific meeting.
Selected bloggers will be categorized by theme but will not be limited to blogging about just that theme.
Selected blog links will be posted on this Web site two weeks before the meeting and will remain until two weeks after the meeting.

This all seems fairly regimented for the free-form blogging style that many of us know and love. On the other hand, this does mark the entry of a very large professional society into the world of social media. They face a difficult learning curve, however, as revealed by these exceptionally opaque hashtags that SfN recommends for use in the 140 character Twitter microblogging service:

If you plan to tweet with your colleagues about events occurring at Neuroscience 2009, use these theme-specific hash tags:

#sfnthemea
#sfnthemeb
#sfnthemec
#sfnthemed
#sfnthemee
#sfnthemef
#sfnthemeg
#sfnthemeh

...because (of course) everyone knows that #sfnthemef is Cognition and Behavior while #sfnthemec is Disorders of the Nervous System. These categories are just a wee bit difficult to parse. #sfn the meh, anyone??

She's smug, she's literate, she's Amber.

Studious Nerds Are Neurotic and Party Animals Are Antisocial

2009-08-23T14:52:00.000-07:00

From the authors who brought you "Religion is the Xanax of the people" (aka Neural Markers of Religious Conviction) comes the finding that college students with lower grades are similar to religious zealots on a specific neural response to making an error. Meanwhile, students with high GPAs resemble atheists on the same neural marker. However, the new paper by Hirsh and Inzlicht (2009) did not draw a parallel to their previous study (Inzlicht et al., 2009). In fact, the two findings were interpreted in very different terms. In the new article:

A greater ability to monitor performance and engage cognitive-control mechanisms when needed thus appears associated with improved real-world performance.

Meanwhile, in the prior paper:

...religious conviction is marked by reduced reactivity in the anterior cingulate cortex (ACC), a cortical system that is involved in the experience of anxiety and is important for self-regulation. ... These results suggest that religious conviction provides a framework for understanding and acting within one's environment, thereby acting as a buffer against anxiety and minimizing the experience of error.

So the religious people were not utter failures at engaging cognitive control mechanisms, instead they were less anxious. And the smart students were not neurotic, they were better able to monitor their task performance. Hmm.

Before going any further, let's look at the experimental design and the neural measures. Both experiments used EEG recordings, specifically event-related potentials. The ERP brain waves reflect electrophysiological activity recorded remotely from the scalp. While it's great for determining the temporal parameters of neural activity, it's not so great at determining where the activity is located in the brain.

The brain wave of interest is the error-related negativity (ERN), recorded at the time that people make mistakes in a task:

The ERN is evident as a large negative polarity peak in the event-related brain potential waveform that occurs when people make errors in reaction time tasks. It begins at the moment of the error and reaches a maximum about 100 milliseconds later (see Gehring et al., 1993, PDF). It is largest at fronto-central scalp locations and appears to come from an area of the brain called the anterior cingulate cortex...

The task used in both studies was the ever-popular Stroop task, in which color words are presented in font colors that either match or conflict with the printed word. Subjects are told to name the color and ignore the word. The Stroop interference effect (slower for BLUE than for RED) arises because reading is a more automatic process than color naming. Thus, subjects are prone to make errors on this task, and that's what the authors were interested in studying.

The participants were 31 undergraduates who consented to having their transcripts released. Their EEG was measured while they performed the Stroop task, and the ERN was calculated from the response-locked averages on all error trials. The results are illustrated below. Simply put, students with high GPA had a larger ERN response than those with low GPA.

Figure 2 (Hirsh & Inzlicht, 2009). The relation between academic success and the ERN. (A) Event-related potentials at Fz on error trials for individuals with high and low Grade Point Averages, as derived from a tertiary split of the sample. (B) Spatial distribution of the ERN, quantified as the peak minimum voltage deflection occurring between 50 and 150 ms after an error. (C) Headmap of correlations between GPA and ERN magnitude. (D) Source localization indicates an anterior cingulate generator for the ERN.

What might this mean? There is some disagreement about what the ERN wave represents: a direct response to the mismatch between the intended action and the actual one, a more generic response to conflict in general, or an emotional response to f***ing up. The authors opted to impose two different interpretations, so it's not surprising that the ERN can mean different things to different researchers. Or to the same researchers in different contexts. In the present context,

As predicted by models of self-regulation and cognitive control, academic performance was correlated with ERN magnitude, with better grades being associated with stronger (more negative) ERN responses, r= -.40.

"Cognitive control" (a sometimes murky concept) was evaluated by looking at post-error slowing, i.e. how much a person slows down on the trial immediately after making a mistake. If a subject has slowed down a lot, that means he's reined in the overly fast reaction time that led to the error in the first place (by responding more cautiously on the next trial). In the present study, a greater degree of post-error slowing was associated with larger ERN amplitudes and higher grades -- and viewed as an exemplar of greater cognitive control. This was taken to have sweeping implications for the rest of their lives:

Academic performance is a gateway to many important life outcomes, influencing the career options that are available to a student. At the broader societal level, achievement in academic domains plays a vital role in sustaining cultural and scientific innovation. The current study suggests that individuals who are better able to monitor their performance and engage cognitive control mechanisms when needed enjoy greater success in undergraduate programs.

How does this relate to smaller ERNs in highly religious persons? Do religious zealots have poor cognitive control? Or does it mean that lower grades are the Xanax of the people (Inzlicht et al., 2009)?

How is it that religion can bring about both peace of mind and zealous conviction? We suggest that religious conviction buffers against anxiety by providing relief from the experience of uncertainty and error, and in so doing, strengthening convictions and narrowing attention away from inconsistencies. We hypothesize that this muted response to uncertainty and error is evident neurophysiologically such that religious conviction is associated with reduced activity in the anterior cingulate cortex,¹ a cortical system involved in a form of attention that serves to regulate both cognitive and emotional processing.

Read more in Atheists Are Neurotic and Religious Zealots Are Antisocial.

Footnote

¹ However, one cannot say for certain that the anterior cingulate is the sole origin of the ERN, because EEG is recorded from the scalp and not inside the brain.

References

Hirsh, J., & Inzlicht, M. (2009). Error-related negativity predicts academic performance Psychophysiology. DOI: 10.1111/j.1469-8986.2009.00877.x

Inzlicht M, McGregor I, Hirsh JB, Nash K (2009). Neural Markers of Religious Conviction. Psychological Science 20:385-92.