Saturday, March 27, 2010

Paranormal Seizure Activity

Scene from Paranormal Activity

After a young, middle class couple moves into what seems like a typical suburban “starter” tract house, they become increasingly disturbed by a presence that may or may not be demonic but is certainly most active in the middle of the night.

Especially when they sleep. Or try to.
A new case study in Cortex by neurologist Dr. Fabienne Picard (2010) reports on a patient who experienced unusual phenomena during epileptic seizures. She had the convincing sense that several familiar people (family members) were standing before her. This experience of a "sensed presence" is a classic trope in movies with supernatural themes (e.g., Carnival of Souls [available at Internet Archive], The Haunting [trailer for the 1963 version], Poltergeist, Dark Water), but it's generally attributed to ghosts and not to seizure activity.

Here's the case report:
A 62-year-old right-handed woman of normal psychiatric history presented a simple focal epileptic seizure including a complex sensation characterized by feeling the presence of several members of her family in the immediate environment, associated with paresthesia of the right hemibody (excluding the face). The feeling of presences and the paresthesia (numbness) appeared concomitantly and lasted in total several minutes. The episode occurred while she was sitting alone on the sofa of her living room and immediately felt the presence of four persons in her frontal space. She did not see or hear these persons (no visual or auditory hallucinations), but felt vividly their presence in her peripersonal [within reach] and near extrapersonal space [just outside of reach]. She “recognized” them as close family members. Closest was her grand-daughter who was sitting on the floor immediately in front of her, without any left or right lateralization in relation to her body, whereas the three other persons, her daughter and two other grand-children, were experienced to be localized at a distance of several meters. ... This highly vivid and convincing feeling of presences was described by the patient as deeply pleasant, although she guessed that it was not possible that they were really there, as she was alone just before. ... She was treated with pregabalin (300 mg/day) and there was no recurrence of simple or complex partial seizures and no further feeling of presences.
MRIs revealed abnormal findings due to a right hemisphere subcortical stroke 10 months before the episode (Fig. 1A). The patient's stroke affected a portion of the basal ganglia (the putamen and the globus pallidus) and a large white matter tract within (the internal capsule). Left hemisphere findings in the insular cortex were also apparent, and this was the likely seizure focus. Strokes are known to increase the incidence of seizures: in one study 8.6% of those with ischemic stroke [occlusion of blood supply] and 10.6% of those with hemorrhagic stroke [bleed] had one or more seizures within a year (Bladin et al., 2000).


Fig. 1 (adapted from Picard, 2010). FLAIR coronal MR images of the patient. (A) two days after a right capsulo-lenticular haemorragic stroke. (B) ten months later, at the time of the episode of feeling of presence. In addition to the right capsulo-lenticular sequela extending to the insula, a hypersignal is visible in the white matter/grey matter border of the left insular region [already visible in (A)], as well as a diffuse corticosubcortical atrophy, predominating in the right hemisphere, and a leukoencephalopathy [white matter disease].

Picard (
2010) thinks this particular case is unique and not a more typical disorder of body perception:
Most authors consider the feeling of a presence (FP) as a disorder of own body perception, an illusory reduplicative phenomena involving the self. Thus FP would be akin to the three main forms of autoscopic phenomena (seeing a double of oneself) which include a) out-of-body experience. The subjects appear to see themselves and the world from a location above their physical body. The self is localized outside one's physical body (disembodiment); b) autoscopic hallucination, which consists of seeing one's body in extracorporeal space (as a double) without disembodiment; and c) heautoscopy, an intermediate form between out-of-body experience and autoscopic hallucination.
Instead, the felt presence was more akin to a "hallucination" for known people going about normal daily activities. Nonetheless, involvement of the insula, important for interoceptive awareness of bodily states (Craig, 2009), is still suggestive of a disruption in the sense of self and its interaction with the external world.

To end our story, the patient's experience of a sensed presence did not recur once her seizures were controlled with medication. A short neurological horror film resolved by prescription of an anticonvulsant drug might not be a strong sell in Hollywood.

References

Bladin CF, Alexandrov AV, Bellavance A, Bornstein N, Chambers B, Coté R, Lebrun L, Pirisi A, Norris JW. (2000). Seizures after stroke: a prospective multicenter study. Arch Neurol. 57:1617-22.

Craig AD. How do you feel--now? The anterior insula and human awareness. (2009). Nat Rev Neurosci. 10:59-70.

Picard, F. (2010). Epileptic feeling of multiple presences in the frontal space. Cortex DOI: 10.1016/j.cortex.2010.02.002

Read about Carnival of Souls and an fMRI study of horror films.

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Wednesday, March 24, 2010

Voodoo and Type II: Debate between Piotr Winkielman and Matt Lieberman


"Voodoo correlations in social neuroscience" was the original title of a paper that first caused a stir in late December 2008, when a manuscript accepted by Perspectives on Psychological Science was made available on the authors' websites. Vul, Harris, Winkielman, and Pashler produced a "bombshell of a paper" that questioned the implausibly high correlations observed in some fMRI studies in the field of Social Neuroscience. Ed Vul et al. surveyed the authors of 54 papers to determine the analytic methods used. All but three of the authors responded to the survey, and 54% admitted to using faulty methods to obtain their results:
More than half acknowledged using a strategy that computes separate correlations for individual voxels, and reports means of just the subset of voxels exceeding chosen thresholds. We show how this non-independent analysis grossly inflates correlations, while yielding reassuring-looking scattergrams. This analysis technique was used to obtain the vast majority of the implausibly high correlations in our survey sample. In addition, we argue that other analysis problems likely created entirely spurious correlations in some cases.
For background reading I suggest starting with Voodoo Correlations in Social Neuroscience. Given the paper's inflammatory title and its naming of names, the accused researchers did not take the criticism lying down (see Voodoo Schadenfreude).

Here we have a public debate between Dr. Piotr Winkielman, one of the authors of the Voodoo paper (Vul et al. 2009, PDF), and Dr. Matthew Lieberman, one of the accused (rebuttal: Lieberman et al. 2009, PDF) at the 2009 meeting of the Society of Experimental Social Psychologists. Dr. Lieberman has made these videos and papers available on his website, and I thank him for drawing my attention to them.

The Voodoo Debate Continues...


video

Piotr Winkielman, opening remarks (21:12)



video

Matt Lieberman, opening remarks (19:03) [better view of slides]



video

Piotr Winkielman, rebuttal (10:22)



video

Matt Lieberman, rebuttal (9:40) [better view of slides]


Lieberman did strike back (Lieberman et al., 2009), and attacked Vul et al. for cherry picking their data and for inappropriate use of statistics:
However, they imply that post hoc reporting of correlations constitutes an invalid inferential procedure, when in fact it is a descriptive procedure that is entirely valid. In addition, the quantitative claims that give their arguments the appearance of statistical rigor are based on problematic assumptions. Thus, it is ironic that Vul et al.’s article—which critiques social neuroscience as having achieved popularity in prominent journals and the press due to shaky statistical reasoning—itself achieved popularity based on problematic claims about the process of
statistical inference.

Additional Reading:

Voodoo correlations in social brain studies

Voodoo Gurus

"Voodoo Correlations" in fMRI - Whose voodoo?

The paper formerly known as "Voodoo Correlations in Social Neuroscience"


References

Lieberman, M., Berkman, E., & Wager, T. (2009). Correlations in Social Neuroscience Aren't Voodoo: Commentary on Vul et al. (2009) Perspectives on Psychological Science, 4 (3), 299-307 DOI: 10.1111/j.1745-6924.2009.01128.x

Vul E, Harris C, Winkielman P, Pashler H (2009). Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social Cognition.

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Sunday, March 21, 2010

A Bayesian Brain is a Freudian Brain

Anna O.'s Default Mode. Anna O. is the famous patient whose case was included in Studies on Hysteria by Josef Breuer and Sigmund Freud. Midsagittal brain image (PALS cortical surface atlas, Van Essen 2005) shows resting state functional connectivity in three cortical networks: (i) dorsal attention system (DAS, blue); (ii) the salience system (light green); and (iii) the default mode network (orange). [Taken from Fig. 2 of Carhart-Harris & Friston 2010. Justin Vincent and Randy Buckner are not to blame.]

"Given the nature of this synthesis, different readers will find merit in different aspects of it."

-R. L. Carhart-Harris and K. J. Friston, The default-mode, ego-functions and free-energy: a neurobiological account of Freudian ideas
Our previous post (Friston is Freudian) presented an overview of the new megawork [metawork?] of Carthart-Harris & Friston (2010), an ambitious project to map selected Freudian ideas (id and ego but not super-ego)1 onto the brain's large-scale intrinsic networks as revealed by modern neuroscientific methods (fMRI, resting state functional connectivity, intracranial EEG recordings, and computational models). As mentioned before, they marshalled the neuroscientific concepts of Bayesian Brain, Default Mode Network, Free Energy, Gamma Oscillations, Prediction, Prediction Error, Theta Oscillations, and Top-Down Control in support of their neuropsychoanalytic scheme. After reading the article, I was amazed at the boldness and creativity it took to develop this framework. The 70 pages of Supplementary Data included 493 quotes from Freud.


Freud's Model of the Mind: "The ego is not sharply separated from the id; its lower portion merges into it.... But the repressed merges into the id as well, and is merely a part of it. The repressed is only cut off sharply from the ego by the resistances of repression; it can communicate with the ego through the id." (From Freud's 1923 paper "The Ego and the Id")

However, not all 493 quotes were used in support of selected characteristics of the ego (Secondary Process - ‘normal waking consciousness of adult humans’) and the id (Primary Process - ‘altered’ or ‘non-ordinary’ states of consciousness). For instance, I don't see Q439 (on early childhood sexuality) anywhere in Table 1 or the text:
The sexual life of human beings exhibits an efflorescence which comes to an end at about the fifth year and it followed by what is known as the period of latency (till puberty)… [Q439, Freud, 1939, p. 75]
Likewise, the super-ego is neglected (see also Footnote 1):
If we consider once more the origin of the super-ego as we have described it, we shall recognise that it is the outcome of two highly important factors, once biological and the other of a historical nature: namely, the lengthy duration in man of his childhood helplessness and dependence, and the fact of his Oedipus complex, the repression of which we have shown to be connected with the interruption of libidinal development by the latency period and so with the diphasic onset of man’s sexual life... [Q344, Freud, 1923, p. 35]
But let's return to what they did include in their synthesis. C-H and F want to establish the construct validity of Freudian concepts (id and ego) to operationalize them and subject them to empirical scrutiny. In brief, the ego (normal adult human consciousness) is more or less equated with activity in the brain's "default mode" network (Raichle et al., 2001), measured as spontaneous fluctuations in the BOLD signal during unconstrained cognition. Activity in the default mode network (DMN)2 is anti-correlated with activity in "active task" networks, which are engaged by typical neuroimaging experiments. In contrast to the ego, the limbic id is equated with unusual and altered states of consciousness, as seen in psychosis, the aura of temporal lobe epilepsy, hallucinogenic states, and REM sleep.3

Added to this is a key concept in recent Fristonian thought. The "free-energy principle" is the idea that the brain is an inference engine (Helmhotz, 1860) that makes probabilistic predictions about the world (i.e., its external and internal input) based on past experience, then updates these predictions based on current events (Friston, 2010). The goal is to minimize "free-energy"4 or prediction error.



In The Prophetic Brain, Friston attempts to explain this for a lay audience:5
The emerging picture is that the brain makes its inferences by minimizing the free-energy of messages passing between hierarchical brain regions. ... Information from these exchanges passes on to “higher” levels (those responsible for cognitive functions) through “bottom up” connections. The higher levels respond with “top down” messages to the lower levels. This reciprocal exchange repeats itself hierarchically, back and forth, layer by layer, until the highest level ... becomes engaged. Only then will you consciously register a perception. In this scheme, the free-energy is essentially the collective prediction error over all levels of the hierarchy: Top-down cognitive messages provide predictions based on representations from above, and lower sensory levels reciprocate with bottom-up prediction errors. These “error messages” drive encoded representations (such as neuronal activity) to improve the predictions for lower levels (that is, to reduce free-energy).
This is a variant on the Bayesian Brain view that has been applied to spike coding in computational neuroscience. Friston and colleagues (Friston et al., 2006; Friston, 2009; Friston, 2010) have extended this approach to neuroimaging data.



To learn more, a good place to start is this New Scientist article, with a title that reflects the ambitions of some of the researchers quoted therein:
Is this a unified theory of the brain?

. . .

Friston’s ideas build on an existing theory known as the “Bayesian brain”, which conceptualises the brain as a probability machine that constantly makes predictions about the world and then updates them based on what it senses.

The idea was born in 1983, when Geoffrey Hinton ... and Terry Sejnowski ... suggested that the brain could be seen as a machine that makes decisions based on the uncertainties of the outside world. In the 1990s, other researchers proposed that the brain represents knowledge of the world in terms of probabilities. Instead of estimating the distance to an object as a number, for instance, the brain would treat it as a range of possible values, some more likely than others.

A crucial element of the approach is that the probabilities are based on experience, but they change when relevant new information, such as visual information about the object’s location, becomes available. “The brain is an inferential agent, optimising its models of what’s going on at this moment and in the future,” says Friston. In other words, the brain runs on Bayesian probability. Named after the 18th-century mathematician Thomas Bayes, this is a systematic way of calculating how the likelihood of an event changes as new information comes to light.
How are all of these biological and mathematical observations related to Freudian psychology? The helpful table below gives a summary.

Table 2 (Carthart-Harris & Friston, 2010). Some points of contact between Freud’s account of the mind and empirical findings in neurobiology
  • The overlapping phenomenology of REM sleep, early and acute psychosis, the temporal lobe aura and the hallucinogenic drug state.
  • All these states have been independently compared with each other previously and described independently as conducive to primary process thinking.
  • The neurophysiology of these non-ordinary states is remarkably consistent both empirically and with Freud’s descriptions of the ‘free-flowing’ energy of the primary process.
  • LSD given immediately prior to or during sleep promotes REM sleep.
  • The overlap between Freud’s descriptions of the give-and-take relationship between ego–libido and object–libido and the give-and-take relationship between the DMN and its anti-correlated networks.
  • The concordance between Freud’s descriptions of the secondary process working to minimize free-energy and the free-energy account of the hierarchical organization of intrinsic networks working to minimize prediction errors.
  • The integrated, compound nature of the DMN and Freud’s descriptions of the integrated, compound nature of the ego.
  • The development of functional connectivity between the nodes of the DMN during ontogeny, a process that parallels the emergence of ego-functions.
  • Freud’s account of the ego as a recipient and product of regular endogenous activity concerned with drive, memory and affect and the functional and structural connectivity of the DMN’s cortical nodes with limbic structures concerned with drive, memory and affect.
  • Freud’s description of the ego as a tonic reservoir of activity and the high resting-state metabolism of the DMN.
  • Freud’s account of the ego as the seat of the sense-of-self and studies showing increased activity in the DMN during self-referential processing and a failure to deactivate the DMN in pathology characterized by withdrawal.
After reading the 10 page presentation of this formidable new framework for the mind we come to the Discussion, where Carthart-Harris and Friston make some concessions:
"For those opposed to Freud, who would rather see his constructs dissolved into pure phenomenology and neurobiology, we put up little resistance (e.g. Q176). Phenomenology and neurobiology can stand alone."

-Carthart-Harris & Friston (2010)
In essence what we've seen here is a surprising form of Reverse Reductionism, or Expansionism: a mapping of brain states onto the concepts of id and ego. Am I the only one who is unaware of this new trend in neurosciences/cognitive sciences? Although it is an impressive and scholarly treatment of Freud in light of the latest neurophysiological and computational principles, one can view the entire synthesis as a series of metaphors. The authors concede as much:
"Freud’s writings contain many useful heuristics for exploring global brain function, especially in non-ordinary states of consciousness."
Finally, we have an appeal to the long-lasting influence of Freud:
"If [Freud’s theories] were built on false inference and loose philosophy, it is unlikely they would have endured in the way that they have."
Just because the Freudian view has persisted doesn’t mean it’s correct. What about creationism? Or intelligent design? While we're on the topic of pseudoscience, are some of the less "scientific" interests of Freud (e.g., telepathy) irrelevant here? It seems to me that picking and choosing which Freudian ideas you want to implement in the brain and which you want to discard is akin to picking and choosing which biblical laws in Leviticus you do (or do not) want to follow.

Footnotes

1 They seem to have dispensed with the super-ego. Perhaps because that would entail discussion of the Oedipus complex?
Freud's theory implies that the super-ego is a symbolic internalization of the father figure and cultural regulations. ... The super-ego acts as the conscience, maintaining our sense of morality and proscription from taboos. Its formation takes place during the dissolution of the Oedipus complex and is formed by an identification with and internalization of the father figure after the little boy cannot successfully hold the mother as a love-object out of fear of castration.

...The concept of super-ego and the Oedipus complex is subject to criticism for its sexism. Women, who are considered to be already castrated, do not identify with the father, and therefore form a weak super-ego, leaving them susceptible to immorality and sexual identity complications.
2 For a critique of the DMN (also called the "resting state" network) see Morcom & Fletcher (2007) and RESISTING A RESTing State.

3 These altered states of consciousness were viewed in an interchangeable fashion and related to hippocampal theta activity. Does this mean that spatial navigation, learning, and memory are considered primary process modes of thought?

4 "An information theory measure that bounds or limits (by being greater than) the surprise on sampling some data, given a generative model" (Friston, 2010).

5 Friston's unhelpful onion metaphor was removed.

References

Carhart-Harris, R., & Friston, K. (2010). The default-mode, ego-functions and free-energy: a neurobiological account of Freudian ideas Brain DOI: 10.1093/brain/awq010

Friston K. (2009). The free-energy principle: a rough guide to the brain? Trends Cog Sci. 13:293-301.

Friston K. (2010). The free-energy principle: a unified brain theory? Nat Rev Neurosci. 11:127-38.

Friston K, Kilner J, Harrison L. (2006). A free energy principle for the brain. J Physiol Paris 100:70-87.

Helmholtz H. (1860/1962). Handbuch der Physiologischen Optik. English translation. In: Southall JPC, editor. Dover: New York. Vol. 3.

Morcom AM, Fletcher PC. (2007). Does the brain have a baseline? Why we should be resisting a rest. NeuroImage 37:1073-82.


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Friday, March 12, 2010

Friston is Freudian

Professor Karl Friston is one of the most prominent (and prolific) researchers in the field of neuroimaging. His contributions to methodological development in functional magnetic resonance imaging (fMRI) are immense:
He invented statistical parametric mapping; SPM is an international standard for analysing imaging data and rests on the general linear model and random field theory (developed with Keith Worsley). In 1994, his group developed voxel-based morphometry. VBM detects differences in neuroanatomy and is used clinically and as a surrogate in genetic studies... In 2003, he invented dynamic causal modelling (DCM), which is used to infer the architecture of distributed systems like the brain. Mathematical contributions include variational filtering and dynamic expectation maximization (DEM) for Bayesian model inversion and time-series analysis.
Dr Robin Carhart-Harris and Professor Friston have a new article in the Occasional Papers section of the journal Brain that might raise a few eyebrows. Its title? The default-mode, ego-functions and free-energy: a neurobiological account of Freudian ideas. What might cause the raising of eyebrows? Well, Freudian ideas have been largely rejected by mainstream neuroscience, although there have been some notable exceptions (Turnbull & Solms, 2007):
Psychoanalysis has had a turbulent and complex relationship with neuropsychology for the century in which the two fields have existed – largely side by side. Some within the neuroscientific community have found much of value in Freudian ideas – Paul Schilder springs to mind as an early example, with Eric Kandel as the most prominent recent advocate (Kandel, 1999). However, for most neuropsychologists, indeed for most scientists, the obvious response to the mention of psychoanalysis has been one of blanket rejection.
The renowned sleep and dreaming expert J. Allan Hobson (2007) has been a particularly harsh critic:
With respect to dreams, Sigmund Freud was not only not right. He was dead wrong. And so are Turnbull and Solms (2007) in their desperate effort to save Freudian psychoanalysis from the junk heap of speculative philosophy. Neuroscientists, psychologists, and psychiatrists beware: you are being led down the garden path by this pair of misguided neo-Freudians.
It is with this stormy background in mind that one should embark on reading the Brain paper. Mercifully, for those lacking the mathematical background to understand even the most rudimentary quantitative formulation of Friston's free-energy principle (2009, 2006), the paper is free of equations. No matter what you think of the final result, it's an intellectual tour de force with 493 quotes from Freud in 70 pages of Supplementary Data. Essentially, the approach is to take a collection of cutting-edge and trendy ideas in neuroscience and map them onto Freud's id and ego. For your convenience, here is a list of the main neuroscientific concepts:
  • Bayesian Brain
  • Default Mode Network
  • Free Energy
  • Gamma Oscillations
  • Prediction
  • Prediction Error
  • Theta Oscillations
  • Top-Down Control
You might be saddened by the lack of mirror neurons, social cognition, and empathy in the current conceptualization. But it should be all about sex, right? Well, actually, Carhart-Harris and Friston are much more chaste in their mapping of Freudian ideas onto neurobiology and default mode function. The words sex, sexual, sexuality (and any variants) appear zero times in the Brain article, but 18 times in the collection of Freud quotes. The word libido was mentioned 112 times in the Freud quotes but only 4 times by the present authors [excluding reproduction of Freud quotes in the main text].

For "accessibility" cathexis was interpreted in a generic (not specifically sexual) sense to mean activation or energy. But according to Freud, mental energy is the id, the psychic energy that powers the mind:
Freud defined Libido as the instinct energy or force. Freud later added the Death drive (also contained in the id) as a second source of mental energy.
Next time we'll take a closer look at this ambitious synthesis of psychoanalysis and neuroimaging.


Arrangement for psychotherapy fMRI studies using the couch of Sigmund Freud. See Psychodynamic Psychotherapy in the Scanner?

References

Carhart-Harris, R., & Friston, K. (2010). The default-mode, ego-functions and free-energy: a neurobiological account of Freudian ideas Brain DOI: 10.1093/brain/awq010

Friston K. (2009) The free-energy principle: a rough guide to the brain? Trends Cog Sci. 13:293-301. [PDF]

Friston K, Kilner J, Harrison L. (2006). A free energy principle for the brain. J Physiol Paris 100:70-87. [PDF]

Kandel ER. (1999). Biology and the future of psychoanalysis: A new intellectual framework for psychiatry revisited. Am J Psychiatry 156: 505-524.

Hobson JA. (2007). Wake up or dream on? Six questions for Turnbull and Solms. Cortex 43:1113-5; discussion 1116-21.

Turnbull OH, Solms M. (2007). Awareness, desire, and false beliefs: Freud in the light of modern neuropsychology. Cortex 43:1083-90.

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Friday, March 05, 2010

Depression's Cognitive Downside



Author and blogger Jonah Lehrer has a lengthy (and controversial) essay in the Feb. 28 New York Times Magazine on Depression's Upside. The main idea, that depression has cognitive and evolutionary advantages, was largely based on a review paper by Andrews and Thomson (2009). In it, they put forth the analytical rumination hypothesis: depression is an evolved response to complex problems, and focusing on them to the exclusion of everything else is beneficial. Lehrer's piece generated an outpouring of comments (both pro and con), questions, and critiques. One notably critical rejoinder (The Myth of Depression’s Upside) was written by Dr. Ronald Pies, the Editor in Chief of Psychiatric Times:
Now, with all due respect to Dr. Thomson, I am inclined to ask, “[Insights gained during depression are] worth it to whom?” Perhaps the patients Dr. Thomson has treated emerge from their three-month bouts of depression saying, “Ya know what, Doc? It’s been a bad three months—lost my job, almost killed myself, and couldn’t get a damn thing done—but overall, it was worth it!” The depressed patients I evaluated over the past nearly 30 years almost never reported that their major depressive episodes had a “net mental benefit,” to quote Lehrer’s article. Most felt that their lives and souls had been stolen from them for the duration of their depressive episode.
In other words, Dr. Pies's patients don't feel like they've solved all their problems. Most of the studies cited in favor of improved problem-solving abilities involved a sad "mood induction" procedure such as watching a 10 min film showing a death from cancer or being given false negative feedback on cognitive test performance (Forgas, 2007). It should be obvious that a transient, slightly sad state is drastically different from a prolonged major depressive episode. Jonah does acknowledge this in his article, but the distinction appears to undermine Andrews and Thomson's entire basis for asserting analytical advantages for the depressed ruminator. It's another in a long line of evo psych just-so stories.

The literature is filled with papers describing the cognitive impairments associated with major depression. Jonah recognizes this as well, but then overstates how easy it is to dispense with the deficits:
The end result is poor performance on tests for memory and executive function, especially when the task involves lots of information. (These deficits disappear when test subjects are first distracted from their depression and thus better able to focus on the exercise.)
On the contrary, numerous papers have shown that impairments in cognitive processes such as executive control, attention, and memory persist after a depressed person has recovered (Andersson et al., 2010; Baune et al., 2010; Hammar et al., 2009). In actively depressed patients, Baune and colleagues (2010) found impairments in all domains tested: immediate memory, visuospatial construction, language, attention, and delayed memory. These deficits can contribute to lower social and occupational functioning and a diminished quality of life. In addition, depression can be associated with declines in problem solving abilities on neuropsychological tests such as the Wisconsin Card Sorting Test and the Tower of London test.

A recent review of the literature provided additional support for the existence of pervasive cognitive deficits (Hammar et al., 2009):
Research during the past decade has mainly focused on cognitive functioning in the severe phase of depression, and today it is widely accepted that the disease is characterized by cognitive impairment in the acute state. There are reports of findings in different cognitive domains, such as executive functions, attention, memory and psychomotor speed.
Well (you say), what about Social Dilemmas? Aren't these different from the Stroop task? The Psych Review manifesto on the Bright Side of Being Blue states that "Complex social problems may be the primary evolutionarily relevant trigger of depression in human beings." But support for the view that depression improves the ability to solve such problems is meager, apparently consisting of two old papers (Hokanson et al., 1980; Pietromonaco & Rook, 1987). The Hokanson paper turns out to be not-so-great for the analytical rumination hypothesis: (1) The "depressed" group had scores on the Beck Depression Inventory of 10 or greater, which includes those with only very mild depression. (2) Ironically, Hokanson et al. view their own results as evidence of social skills deficits, not enhanced social problem solving:
If, indeed, depressed individuals display different social responses, depending on situational or social role variables, one might expect that real-world relations are characterized by contradictory behaviors, mixed messages, emotional ambivalence, and so forth. Such stimulus arrays may indeed evoke several competing response tendencies in others, a situation that a simple reinforcement-punishment view would be hard pressed to handle.
The conclusion of the Pietromonaco and Rook (1987) paper is even more problematic:
This work suggests that depressives' cognitive analysis of common life situations leads them to make decisions that promote their social isolation and, thereby, perpetuate their depression.
The analytical rumination hypothesis even has the potential to be harmful. Belief in the glorious "upside" of their ailment could prevent some severely depressed individuals from getting proper treatment, placing them at greater risk of suicide and other adverse events. Needless to say, such an outcome would be of no evolutionary advantage.

References

Andersson S, Lövdahl H, Malt UF. (2010). Neuropsychological function in unmedicated recurrent brief depression. J Affect Disord. Jan 18. [Epub ahead of print]

Andrews PW, Thomson JA Jr. (2009). The bright side of being blue: depression as an adaptation for analyzing complex problems. Psychol Rev. 116:620-54.

ResearchBlogging.org

Baune, B., Miller, R., McAfoose, J., Johnson, M., Quirk, F., & Mitchell, D. (2010). The role of cognitive impairment in general functioning in major depression. Psychiatry Research DOI: 10.1016/j.psychres.2008.12.001

Forgas JP (2007). When sad is better than happy : Negative affect can improve the quality and effectiveness of persuasive messages and social influence strategies. J Exp Social Psychol. 43:513-528.

Åsa Hammar, Guro Årdal (2009). Cognitive functioning in major depression – a summary Frontiers in Human Neuroscience. DOI: 10.3389/neuro.09.026.2009

Hammar A, Sørensen L, Ardal G, Oedegaard KJ, Kroken R, Roness A, Lund A. (2009). Enduring cognitive dysfunction in unipolar major depression: A test-retest study using the Stroop paradigm. Scand J Psychol. 2009 Dec 23.

Hokanson JE, Sacco WP, Blumberg SR, Landrum GC. (1980). Interpersonal behavior of depressive individuals in a mixed-motive game. J Abnorm Psychol. 89:320-32.

Pietromonaco PR, Rook KS. (1987). Decision style in depression: The contribution of perceived risks versus benefits. J Personality Social Psychology 52:399-408.


Supplementary Material

Below is a box/blob and arrow diagram of the analytic rumination model (click on image for a larger view). A critique of its ludicrous biological underpinnings is beyond the scope of this post.

Figure 1 (Andrews & Thomson, 2009). A diagram of the proposed causal relationships between the variables and the constructs that are prominent in the analytical rumination hypothesis. The diagram uses the terminology of structural equation modeling [NOTE: but none of its quantitative rigor], with the circles representing latent constructs, the rectangles representing manifest variables, and the arrows denoting the hypothesized direction of causation. The plus (+) sign denotes a positive or facilitative causal relationship between variables, and the minus (-) sign denotes a negative or inhibitory causal relationship. 5-HT = 5-hydroxytryptamine or serotonin; L-VLPFC = left ventrolateral prefrontal cortex; R-VLPFC = right ventrolateral prefrontal cortex; WM = working memory.

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Thursday, March 04, 2010

A Modest Appeal to Research Bloggers

Research Blogging Awards 2010
ResearchBlogging.org is having a contest to determine the Best Blogging on Peer Reviewed Research. The Neurocritic has been chosen as a finalist in the Best Blog -- Neuroscience category.* I kindly thank the judges for nominating my blog for this award.

Voting is limited to those who are registered with ResearchBlogging.org. If you do fall into that category, dear reader, your vote will be greatly appreciated. If I win, I will donate the entire $50 windfall to earthquake relief efforts in Haiti and Chile.

Good luck to all the nominees. Thank you for reading!

Research Blogging Awards 2010 Finalist

* I started this blog in January 2006 as an escape from the vicissitudes of peer review. So no matter what the outcome, I'll keep on doing what I'm doing...

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Tuesday, March 02, 2010

Unusual Headaches


Headache, by Robert Magginetti (Tranquility Base)

In the last post we learned about Alice in Wonderland syndrome, a rare phenomenon involving distortions of visual perception and body image, most often caused by migraines. Although a specialty practice in headache might seem dull [so to speak] at first glance to those interested in behavioral neurology, unusual and colorfully-named types of headaches can make things more interesting. In Case Studies of Uncommon Headaches (2006), Dr. Randolph Evans reviews a number of these unfortunate ailments, which include exploding head syndrome, neck-tongue syndrome, red ear syndrome, and burning mouth syndrome. So let's begin with a hot ear.

Case 6. My ear is red, hot, and burning

A 54-year-old white woman was seen who had a 10-year history of episodes of a burning sensation of the left ear. The episodes are preceded by nausea and a hot feeling for approximately 15 seconds and then the left ear becomes visibly red for an average of approximately 1 hour, with a range of approximately 30 minutes to 2 hours. Approximately once every 2 years, she had a flurry of episodes occurring over approximately a 1-month period during which she averaged approximately five episodes, with a range of 1 to 6.

There also was an 18-year history of migraine without aura occurring approximately once a year. ... A cerebral arteriogram revealed a proximal left internal carotid artery occlusion of uncertain cause after extensive testing. MRI scan at age 45 was normal. Neurologic examination was normal. A carotid ultrasound study demonstrated complete occlusion of the left internal carotid artery and a normal right.
The diagnosis? Red Ear Syndrome, first described by Lance (1994) in the aptly-titled article, The mystery of one red ear. Following a plea to colleagues to "lend me your ear," Lance (1996) subsequently reported on 12 cases. He concluded that RES:
may be associated with irritation of the third cervical root [nerve in the neck], temporomandibular joint [jaw] dysfunction, or thalamic [pain] syndrome. It may also occur without obvious structural cause in response to touch or heat. The condition may be an example of the ABC (Angry Back-firing C-nociceptor) syndrome with the increase in ear temperature being caused by the antidromic ["backwards"] release of vasodilator peptides [calcitonin gene-related peptide and substance P].
It can also occur in association with migraines, glossopharyngeal and trigeminal neuralgia, upper cervical spine pathology, and herpes zoster [shingles]. The GABA analogue and anti-seizure medication gabapentin can be helpful in preventing RES.

By the way, the girl in the picture above [who is not Case 6] says her red ear doesn't hurt, and that she doesn't get headaches.

Case 7. My mouth is burning

A 49-year-old woman was referred by her primary care physician with a 1.5-year history of daily constant burning or numbness of the entirety of her tongue and the back of her throat. She also complains that the inside of her mouth is sensitive. She has had a dry mouth for the past year. ... Artificial saliva has not been helpful. She has tried a variety of pain pills without any help....
Burning Mouth Syndrome1 most often afflicts middle-aged and older women. Causes include dry mouth (e.g., from medications or diabetes), nutritional deficiency, food allergies, fungal infection (candidiasis aka thrush), trigeminal small fiber neuropathy (nerve damage), and hormonal changes. Treatments range from estrogen-progesterone replacement therapy to nutritional supplements to switching prescription medications to addressing an underlying medical condition. I don't know if this syndrome can be considered a "headache" in the standard usage of the word, but then again I'm not a neurologist.

Case 1. Noises in the night

A 43-year-old woman was seen with a 5-month history of a noise in her head. On an almost nightly basis, as she was falling asleep, she would hear a loud noise like "electrical current running" lasting a second. Sometimes her whole body would shake for a second afterwards. Very occasionally, she would have an associated flash of light. Frequently, a second episode of the loud noise occurred shortly after the first. She then could fall asleep without any problem.
Exploding Head Syndrome (Pearce, 1988) is a bang-up way to be aroused from your nightly slumber. A small percentage (~10%) of sufferers see a flash of light, even fewer feel as if they've stopped breathing for a short time. It's more frightening than it is painful. Interestingly, Evans (2006) suggests that EHS might be caused by delay in the reduction of activity in the brainstem reticular formation as the patient transitions from wakefulness to sleep. In 1949, Moruzzi and Magoun were the first to recognize that stimulation of the brainstem reticular formation produces low-voltage fast activity in the EEG, characteristic of an alert and attentive behavioral state. So something might be neurologically amiss with the EHS patient's sleep-wake cycle, although Evans gave no direct evidence of this. And the explosion phenomenology is largely unexplained, as noted by Pearce (1988):
The cause of the bomb-like noise remains a mystery: no known vascular or hydrodynamic changes in the brain, labyrinths, or cerebrospinal fluid would cause such a symptom, although a momentary (almost ictal) disinhibition of the cochlea or its central connections in the temporal lobes, or a sudden involuntary movement of the tympanum or tensor tympani, might be the explanation...
Evans' other case studies recounted complaints of numb tongue (neck-tongue syndrome), painful scalp (nummular headache), and moderately severe bifrontal pressing headaches between 1:00 AM and 2:30 AM (hypnic headache). Cough, exertional, and sex headaches (Cutrer & Boes, 2004) will have to wait for another time...

Footnote

1 On the NIH website, the photo illustrating this painful condition is that of a smiling older woman (rather comical, I thought). Synonyms for burning mouth syndrome include glossodynia, glossopyrosis, glossalgia, stomatodynia, stomatopyrosis, sore tongue and mouth, burning tongue, oral or lingual paresthesia, and oral dysesthesia.

References

Cutrer FM, Boes CJ. (2004). Cough, exertional, and sex headaches. Neurol Clin. 22:133-49.

ResearchBlogging.org

EVANS, R. (2006). Case Studies of Uncommon Headaches Neurologic Clinics, 24 (2), 347-362 DOI: 10.1016/j.ncl.2006.01.006

Lance JW. (1994). The mystery of one red ear. Clin Exp Neurol. 1994;31:13-8.

Lance JW. (1996). The red ear syndrome. Neurology 47:617-20.

Moruzzi G, Magoun HW. (1949). Brain stem reticular formation and activation of the EEG. Electroencephalogr Clin Neurophysiol. 1:455-73.

Pearce JM. (1988). Exploding head syndrome. Lancet 332:270-1.

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