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Insights into the beginnings of microbiology

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Pasteur Institute
Over the holidays I rediscovered a book I picked up in an antique shop a year or so ago called “Milestones in Microbiology”. I had assumed it was going to be a standard history book with lots of dates and names and events, but it turned out to be a collection of groundbreaking microbiology papers from the 16th century to the early 20th century – quite a special find for a microbiology student. Many of the papers included were written by familiar names such as Pasteur, Leeuwenhoek, Lister, Koch, Fleming and more, and the collection was compiled and translated by Thomas Brock (a familiar name to anyone who’s been set Brock’s Biology of Microorganisms as a first year text book!).

I’ve not yet read the whole collection, but having read the first few papers I’m very much sold. The early texts on the field of microbiology are not just intriguing but fairly accessible too. The style of writing is far less technical than today’s academic papers, as well as being in full prose (in those days journals didn’t have strict word limits). My favourite example of this so far is when Leeuwenhoek describes one of his test subjects as “a good fellow” a comment that would be branded unneccessary and completely aside from the point in today’s academic world!

It’s not often you get the chance to view groundbreaking scientific advances through the eyes of the scientists you get taught about in the textbooks. Reading the paper in which Leeuwenhoek first describes bacteria (or “little animals” as he calls them) feels like something of a privelege, as well as a trip back in time, so definately worth a read for anyone with an interest in the field. A more up to date version of the book seems to be available on Amazon or for University of Sheffield students there’s a few copies in Western Bank Library – enjoy!

On another note, if you’re interested in this sort of thing I’d also definately recommend a trip to the Pasteur museum in Paris. I visited it a few years ago whilst in Paris and like the papers mentioned above it’s a fascinating insight into the work of pioneering microbiologists. It’s a fairly understated part of the modern Pasteur Institute, with the museum situated in the building of the original Pasteur Institute. The museum contains plenty of scientific curiosities, such as Pasteur’s original experimental equipment, and documents his work from his early background in chemistry and stereoisomers up to his more famous vaccine and microbiological work. Finally on a less biological theme, the museum also contains Pasteur’s living quarters and crypt, which were also part of the original institute building!

 

 

Want to lie convincingly? Get practicing!

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Lying, the deliberate attempt to mislead someone, is a processes that we all engage in at some time or another. Indeed research has found that the average person lies at least once a day, suggesting that lying is a standard part of social interaction (1). Despite its common occurrence lying is not an automatic process. Instead it represents an advanced cognitive function; a skill that requires more basic cognitive abilities to be present before it can emerge. To lie an individual first needs to be able to appreciate the benefits of lying (e.g. a desire to increase social status) so that they have the motivation to behave deceitfully. Successful lying also requires ‘theory of mind’ or the ability to understand what another person knows. This is necessary so that the would-be liar can spot firstly the opportunity to lie, and secondly what sort of deception might be required to produce a successful lie. Finally lying also requires the ability to generate a plausible and coherent, but nonetheless fabricated description of an event. Given these prerequisites it is unlikely that we are ‘born liars’. Instead the ability to lie is believed to develop sometime between the ages of 2 and 4 (2). The fact that the ability to lie develops over time suggests that the our performance of the ‘skill’ of lying should be sensitive to practice. Do people who lie more often become better at it?

Lying is tiring!
Lying is considered more cognitively demanding that telling the truth due to the extra cognitive functions that need to be utilised to produce a lie. The idea that lying is cognitively demanding is supported both by behavioural data showing that deliberately producing a  misleading response takes longer, and is more prone to error, than producing a truthful response (3) and by neurological data showing that lying requires additional activity in the prefrontal areas of the brain when compared to truth telling (4). These observable differences between truth telling and lying allow a measure of ‘lying success’ to be created. For example a successful, or skilled liar, should be able to perform lies more quickly and accurately than a less successful liar, perhaps to the extent that there is no noticeable difference in performance between truth telling and lying in such individuals. Likewise, if the ability to lie is affected by practice, then practice should make lies appear more like the truth in terms of behavioural performance.

Practice makes perfect (but is this a lie)?
Despite the intuitive appeal of the idea that lying becomes easier with practice, much past research has failed to find an effect of practice on lying, either when measuring behavioural (3) or neuroimaging (5) markers of lying. Such results have led to the conclusion that lying may always be significantly more effortful than truth telling, no matter how practiced an individual is at deception.

A recent study (6) has re-examined this issue. They used a version of the ‘Sheffield Lie Test’ where participants are presented with a list of questions that require a yes/no response (e.g. ‘Did you buy chocolate today?’). The experiment involved three main phases. In the first, baseline phase, participants were required to respond truthfully to half the statements and to lie in response to the other half of the statements. In the middle, training phase, the statements were split into two groups. For a control group of statements the proportion that required a truthful response remained at 50% for all participants. For an experimental group of statements the proportion that required a truthful response was varied between participants. Participants either had to lie in response to 25%, 50% or 75% of these statements, thus giving the participants differing levels of ‘practice’ at lying. The final, test phase, was a repeat of the baseline phase. This design allowed two research questions to be assessed. Firstly the researchers could identify whether practice at lying reduced the ‘lie effect’ on reaction time and error rate (e.g. the increased reaction time and error rate that occurs when a participant is required to lie, compared to when they are required to tell the truth). Secondly the researchers could identify whether any reduction in the lie effect applied just to the statements on which the groups had experienced differing practice levels, or whether it also generalised to those statements where all groups had the same level of practice.

The results revealed that practice did produce an improvement in the ability to lie during the period when the training was actually taking place, and that this improvement applied to both the control statements and the experimental statements. The participants who had to lie more demonstrated reduced error rates and reaction times compared to those who had to lie less during the training phase. However in the test phase this improvement was only maintained for the set of statements where the frequency of lying had been manipulated. The group who had practiced lying on 75% of the experimental statements were no faster or more accurate at lying on the control statements than the group who had to lie in response to just 25% of the experimental statements. These results suggest that practice can make you better at lying, but this improvement is only sustained over time for the specific lies that you have rehearsed.

Some lies may be better than others!
One important criticism of most studies on the effect of practice on lying is that they tend to use questions or tasks that require binary responses (i.e. yes/no questions). However in real life lying often involves the concoction of complex false narratives,a form of lying that is likely to be far more cognitively demanding than just saying ‘No’ in response to a question whose answer is ‘Yes’. Likewise the lies tested in laboratory studies tend to be rehearsed, or at least prepared lies. In contrast many real-life lies are concocted at short notice, with the deceptive narrative being constructed in ‘real-time’, whilst the person is in the process of lying. It is likely that the effect of training, and how that training generalises to other lies, will be different for these more advanced forms of lying than it is for the more simple types of lies that tend to be tested under laboratory conditions. Given this, if a psychologist tells you that we know for certain how practice impacts on the ability to deceive, you can be sure that they are lying!

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References

(1) DePaulo, B.M., Kashy, D.A., Kirkendol, S.E., Wyer, M.M. & Epstein, J.A. (1996) Lying in everyday life. Journal of Personality and Social Psychology, 70 (5) 979-995. http://smg.media.mit.edu/library/DePauloEtAl.LyingEverydayLife.pdf
(2) Ahern, E.C., Lyon, T.D. & Quas, J.A. (2011) Young Children’s Emerging Ability to Make False Statements. Developmental Psychology. 47 (1) 61-66. http://www.ncbi.nlm.nih.gov/pubmed/21244149
(3) Vendemia, J.M.C., Buzan,R.F., & Green,E.P. (2005) Practice effects, workload and reaction time in deception. American Journal of Psychology. 5, 413–429. http://www.jstor.org/discover/10.2307/30039073?uid=3738032&uid=2129&uid=2&uid=70&uid=4&sid=21101917386241
(4)Spence, S.A. (2008) Playing Devil’s Advocate: The case against MRI lie detection. Legal and Criminological Psychology 13, 11-25. http://psychsource.bps.org.uk/details/journalArticle/3154771/Playing-Devils-advocate-The-case-against-fMRI-lie-detection.html
(5) Johnson,R., Barnhardt,J., & Zhu, J.(2005) Differential effects of practice on the executive processes used for truthful and deceptive responses: an event-related brain potential study. Brain Research: Cognitive Brain Research 24, 386–404. http://www.ncbi.nlm.nih.gov/pubmed/16099352
(6) Van Bockstaele, B., Verschuere, B., Moens, T., Suchotzki, K., Debey, E. & Spruyt, A. (2012) Learning to lie: effects of practice on the cognitive cost of lying. Frontiers in Psychology, November (3) 1-8. http://www.ncbi.nlm.nih.gov/pubmed/23226137

How delusions occur, and why they may be widespread!

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Why do many people believe that Crop Circles are created by alien life forms?

It is a common occurrence to come across people who believe things that seem extraordinary, and who maintain that belief even in the face of huge amounts of contradictory evidence. For example despite vast amounts of evidence suggesting otherwise, there are people who believe that aliens create crop circles, that astrology can predict their future, and that the next Adam Sandler movie will be any good. A delusion can be defined as an extraordinary belief that is strongly held despite the presence of seemingly overwhelming evidence to the contrary. They are of particular interest to psychologists and neuroscientists because they occur in a number of neurological disorders, as well as in seemingly healthy individuals. For example a variety of paranoid or grandiose delusions frequently occur in psychotic disorders such as schizophrenia. Delusions relating to various bizarre forms of misidentification, such as the belief that a loved one is an imposter (the Capgras delusion) can also occur, often in forms of dementia such as Alzheimer’s Disease, and even in old age populations who do not exhibit any other noticeable cognitive impairment (1). Delusions of various types also occur in Parkinson’s disease, depression and as a result of other brain traumas such as those caused by strokes.

One error or two?
On a theoretical level there has traditionally been a distinction between 1-step and 2-step theories of delusions. 1-step theories (e.g. 2) suggest that a single perceptual deficit causes delusions. The delusion represents the most logical response to the bizarre perceptual information the brain is receiving as a result of the perceptual deficit. For example paranoid delusions may be caused by a perceptual bias towards threat signals which makes the sufferer conclude that some overbearing threat must be present to explain the constant warnings coming from the sensory environment. In contrast 2-step models (e.g. 3) argue that in addition to a perceptual deficit, there must also be a second, cognitive deficit. Such theories are motivated in part by the finding that there are some individuals who exhibit very similar perceptual deficits to those with delusions, but nevertheless do not hold delusional beliefs. For example there are individuals with bilateral damage to specific parts of the frontal lobe who, like patients with the Capgras delusion, experience a lack of familiarity when they come into contact with a particular close relative. However in contrast to the Capgras patients, the frontal lobe patients do not hold the belief that the relative is an imposter (4). Instead they are able to understand that it is their experience that has changed, rather than their relative. While 1-step theories suggest that delusions are caused by a single neuro-perceptual deficit, which varies in its nature depending on the nature of the delusion, 2-step theories require that an additional, separate deficit exists within the neural system involved in the formation and evaluation of beliefs. Variances in this second cognitive stage explain the likelihood of adopting a delusional belief in the context of disrupted perceptual experiences, and hence the difference between the Capgras and frontal lobe patients.

How are beliefs formed and updated?
If delusions are underpinned by a 2-step deficit, with the second, cognitive step being similar across delusional disorders, then the question arises as to what is the exact nature of this cognitive deficit? Recently an answer to this question has been proposed based off the insight that our ability to navigate the world is achieved through a process of inferential learning (e.g. 5). In short it is proposed that the brain creates representations as to how the external world is organized based off the information it receives. These models of the world by their nature encapsulate our belief system, as they contain representations of how different information is related, and what is likely to occur in any given situation. These models also allow the brain to predict both upcoming external stimulation, and internal experience. When actual experience differs from that which is expected, signals communicating this discrepancy (referred to as prediction-error signals) are sent back to the areas that generated the prediction, with the purpose of updating the model from which the original prediction arose. This process, when working optimally, allows us to adapt to new, unexpected information while at the same time enabling the majority of unexceptional information we encounter to be processed quickly and with minimum effort (because it has been predicted in advance).
Within this system the updating of beliefs can be framed using the principles of Bayesian inference, whereby the decision as to whether to adopt one of (say) two explanations to account for an unexpected stimulus is taken by balancing the inherent probability of each explanation (based off the current model of the world that the individual holds) with the likelihood of the unexpected stimulus having occurred if each explanation were true. When in the presence of a surprising or anomalous experience, such as those caused by the perceptual deficits believed to underpin the first step of delusion formation, an alteration in the belief pattern will only occur if the difference between the probability of the sensation occurring given that the new belief is true, compared to its probability of it occurring if the existing belief is true, is greater than the difference in the inherent probability of the two beliefs. In order to adopt an atypical or delusional belief, whose inherent probability would usually be very low, new evidence would have to appear that is almost inexplicable within the current belief system, while being fully explainable using the new belief. For example to believe that the moon is made of cheese would probably require you to actually travel to the moon, dig a bit of it up, put it in your mouth and taste cheese. Any lesser form of evidence would be discarded as a coincidence or trick, as the inherent probability of the moon being made of cheese given your existing belief system is (or at least should be) extremely low!

Delusions: A problem with prediction error?
In delusions it is proposed that this process of error-dependent updating of beliefs is disrupted. Most likely this occurs through a process whereby the weight (or importance) given to various prediction error signals is sub-optimal (e.g. 6, 7). If prediction error signals are given undue weight then potentially unimportant variances from expectation will become flagged as being highly salient. This in turn would mean that they are given unnecessary influence in updating our belief system. An anomalous experience that would normally not be treated as particularly relevant to understanding how the world works, either because of the unusual context in which it occurred, or its infrequency, would, if this deficit existed, be treated as important enough to warrant a change in the individual’s belief system. In terms of Bayesian inference, a system which gives undue weight to prediction errors would be one that had a bias towards accepting the influence of the new anomalous experiences without taking fully into account the relative inherent probabilities of the competing potential beliefs (which would usually strongly favour the non-delusional belief) (8). A less convincing anomalous experience would therefore be required in order to successfully challenge an existing non-delusional belief.
As an example, reconsider the aforementioned difference between patients with frontal lobe lesions and those with the Capgras delusion. In both types of patient the feeling of familiarity that is expected to appear on the physical recognition of a known person is absent. In the non-deluded individual, while this discrepancy is noted, it is not used to adopt the ‘imposter explanation’ because the correct weight is given to the prediction error and it is therefore not strong enough to overturn an otherwise functioning belief that the individual is who they claim to be (a belief that would be supported by several other pieces of information). In contrast the deluded individual gives far too much weight to the unexpected experience of non-familiarity, and the model is changed to accommodate it through the acquisition of the belief that the person is an imposter. As the prediction error deficit in such cases is restricted to the perceptual system dedicated to familiarity processing, other evidence that is contradictory to the imposter hypothesis, but which comes from a different source (e.g. people telling the deluded individual that they are wrong) is not treated with the same weight as the experience of absent familiarity. The delusion is therefore maintained even in light of strong contradictory evidence.

More widespread delusions
Whereas the Capgras delusion tends to be monothematic (i.e. it relates to just one known person having been replaced by an imposter, rather than people in general being imposters) faulty prediction error signalling can also be used to explain more widespread delusional thinking such as paranoia. For example one potentail consequence of the incorrect updating of belief systems is that the model of the world that the individual holds will itself become further divorced from reality, making it less able to accurately predict upcoming stimulation. This in turn will lead to a further increase in the frequency of prediction errors; to the extent that surprising or anomalous information would appear to occur with seemingly baffling frequency. If the deficit in prediction error exists across more than one perceptual domain, the inferential response to this might be to adopt a paranoid outlook to explain this constant uncertainty in the world. For example a delusion that MI5 are spying on the sufferer might be the best explanation for a world where objects and strangers seem to take on a sinister level of salience, and unexpected events seem to happen with alarming frequency (6).

Is healthy belief formation optimal, or are we all deluded?
The strength of a model of delusions based off deficits in the processes of inferential learning is that it can be used to explain the characteristics of general belief formation. For example deficits in prediction-error signaling may explain why some otherwise healthy individuals tend to adopt a wide variety of irrational beliefs. Such people may lack the perceptual deficit that causes the bizarre but specific anomalous experiences suffered by individuals with clinical delusions, but they may share with the clinical group a general deficit in inferential reasoning which results in a tendency to accept unusual beliefs that are poorly supported by available evidence. Along similar lines, variances from optimal processing (in terms of Bayesian inference) may explain more general cognitive biases that seem to be present in most people (including scientists!) and which are therefore presumably hard wired in the human brain because they have some adaptive evolutionary advantage. For example most people display a ‘belief bias’, the tendency to evaluate the validity of evidence based on their prior beliefs, rather than on the inherent validity of the evidence as could be assessed through logical reasoning (9). This bias could be said to be the result of our system of inferential learning being sub-optimal (in Bayesian terms) but in the opposite direction to that seen in delusion, such that we have a bias towards evaluating beliefs more in terms of their inherent probability (as we see it) without fully taking into account new evidence.
More generally the processes of inferential learning and belief formation may be able to explain why people who have had relatively similar types of upbringing and experience can often exhibit very different sets of beliefs. These differences are likely to be in part due to differences in the process of belief formation between individuals. It would seem very unlikely that anybody’s brain is able to process information in strict accordance with Bayesian inference, given that neural signals are coded through the transmission of neurotransmitters between groups of neurons, a process that is naturally susceptible to a significant amount of noise. Differences in beliefs between people are presumably therefore inevitable, as is the likelihood that we all, at some time, adopt irrational convictions. Of course these are just things that I believe, and I may be deluded in believing them!

Image courtesy of www.freedigitalphotos.net

References
(1) Holt, A.E., & Albert, M.L. (2007) Cognitive Neuroscience of delusions in aging. Neuropsychiatric disease and treatment, 2 (2) 181-189. Link
(2) Maher, B.A. (1974) Delusional thinking and perceptual disorder. Journal of Individual Psychology, 30:98-113. Link
(3) Coltheart, M, Langdon, R. & McKay, R. (2011) Delusional Belief. Annual Review of Psychology, 62, 271-298 Link
(4) Tranel, D., Damasio, H. & Damasio, A.R. (1995) Double dissociation between overt and covert face recognition. Journal of Cognitive Neuroscience, 7(4) 425-432. Link
(5) Friston, K. (2003). Learning and inference in the brain. Neural Networks, 16(9), 1325-1352. Link
(6) Fletcher, P. C., & Frith, C. D. (2009). Perceiving is believing: a Bayesian approach to explaining the positive symptoms of schizophrenia. Nature Reviews Neuroscience, 10(1), 48-58. Link
(7) Corlett, P. R., Taylor, J. R., Wang, X. J., Fletcher, P. C., & Krystal, J. H. (2010). Toward a neurobiology of delusions. Progress in Neurobiology, 92(3), 345-369. Link
(8) McKay, R. (2012). Delusional Inference. Mind & Language, 27(3), 330-355. Link
(9) Markovits, H. & Nantel, G. (1989). The belief bias effect in the production and evaluation of logical conclusions. Memory & Cognition, 17(1) 11-17. Link

Science in British Sign Language – Summer Lecture

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Science Brainwaves is proud to announce the details of our first summer lecture:

Science in British Sign Language

We are delighted to welcome Brainy and Brawny, aka Dr Audrey Cameron and Gary Quinn, and their fantastic science show! Gary and Audrey will be producing explosions, illusions, and a little bit of science…suitable for all ages and hearing abilities! The show will be performed in British Sign Language with audio interpretation.

The lecture is on Friday August 3rd from 6pm – 8pm at the Richard Roberts Building, University of Sheffield, Western Bank. Doors will open from 5.30

This event is FREE. To reserve your tickets, go to http://www.amiando.com/sciencebrainwaves0812

If you have any questions or special requirements, please contact Holly at h.rogers@sciencebrainwaves.com. We hope to see you at the lecture!

Consciousness In The Brain

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You see, but you do not observe…

A Scandal in Bohemia, The Adventures of Sherlock Holmes:  Arthur Conan Doyle

Can neuroscience provide an explanation as to how the brain enables us to consciously process information?

What is the distinction between seeing and observing? The term ‘seeing’ suggests a passive process, whereas observation clearly requires something additional; the attention to a particular detail or details within the visual scene, the extraction of salient information and perhaps the further evaluation of that information. Neuroscience has made great strides in understanding the functioning of our basic sensory mechanisms, such as those that allow seeing. This work has reached such a level that we are now coming close to being able to create ‘bionic eyes’; mechanical replicas which can mimic the workings of damaged parts of the visual system (1). However is it a much harder task to fully understand the myriad of different ‘higher order’ functions that serve to differentiate observation from merely seeing. These functions are the reason that human experience is much more than the sum of the output from our sensory systems. At the heart of this problem is the need to understand the phenomenon of consciousness. Consciousness can be difficult to define precisely, with different philosophers breaking consciousness down into different sets of features (2) producing concepts that, perhaps inevitably, tend to be somewhat vague and potentially overlapping. However the most fundamental aspect of consciousness would appear to be our ability to experience awareness of (certain) sensory information, and to impose our higher order abilities on that information. In short, given that the majority of sensory processing is performed outside of consciousness, how is it that certain information can be sectioned off and subject to processes such as attention, evaluation and reflection, and how is it that we are aware of both the selected data, and the cognitive processes we perform on it?

Brain waves and synchronisation
The simplest way of addressing the issue of consciousness is to compare the response of the brain during circumstances where the level of consciousness awareness is different. It has long been known that states of consciousness (such as wakefulness, sleep and coma) are marked by differences in the pattern of ‘brain waves’; the oscillating electrical signals that are produced by the brain. It would seem sensible therefore to assume that such changes in the pattern of brain waves reflect, at least in part, changes in the functioning of the mechanism that enables consciousness. Similar changes in brain oscillations are also seen in a wide variety of different brain areas during performance of cognitive tasks, which of course also require the conscious processing of information. In general cognitive processes appear not only to alter the power of such oscillations, but also to evoke an increase in synchronisation between these oscillations (such that the phase difference between the signals generated from the brain areas activated by the task remains constant over time). Such synchronisation is believed to allow communication between disparate brain areas; so-called ‘communication through coherence’ (3). If one takes the simple example of one neuronal population passing a signal to another, then to provide the greatest likelihood of that signal being received, the sending neurons must all fire at the same time (hence the oscillating nature of brain waves) thus maximising the signal sent to the receiving neurons. However the timing of this signal is also important. To maximise the chance of the signal being propagated, the firing of the sending neurons must be timed so that the signal arrives at a time when the receiving neurons are optimally receptive to the signal (or alternatively, if inhibition of signalling is required, at a time when the receiving neurons are optimally insensitive of the signal). Therefore when different brain areas need to communicate in order to facilitate cognitive processing their pattern of neuronal firing much achieve coherence, so they tend to synchronise with (for unidirectional, excitation signals at least) the conduction delay between the two areas being equal to the phase difference between the two oscillating signals.

Global Neuronal Workspace
As the cognitive tasks that produce neural synchrony all require conscious processing of some sort, we would expect that the experience of consciousness in general must rely on changes in synchrony between brain areas. Indeed studies that have directly compared conscious vs non conscious processing (e.g. comparing instances where the same stimulus is consciously perceived versus instances where it is not) have found an increase in synchronisation between distant cortical sites not directly related to the processing of the relevant sensory information (e.g. 4). Evidence from several MRI studies suggests that the location of these synchronising sites is consistent across different tasks, involving a specific set of areas in the frontal and parietal lobes as well as the thalamo-cortical circuits that control the flow of sensory information to and from the cortex (see 5 for a review). The relevance of this finding to consciousness is supported by evidence that the source of the altered brain response between different states of consciousness appears to be generated by a similar set of areas (6). This has led to the idea that these brain areas represent a ‘global neuronal workspace’ (GNW: 5,7) that supports consciousness. The GNW system is thought to be able to orchestrate synchronisation between different sensory processing areas in such a way as to allow certain sensory representations to be amplified and maintained, while inhibiting others. As synchronisation facilitates neuronal communication it may allow the specific information being held within different sensory areas to form a single, multi-sensory representation within the workspace, explaining how the conscious experience of perception is of a unified sensation, despite the fact that information from each sense is analysed separately (8 – the ‘perceptual binding’ problem). In addition the parietal and frontal areas of the GNW contain a large number of neurons with long axons which allow these areas to project information to a wide variety of disparate brain areas. This in turn is thought to allow them to make the representation held within the GNW available to the areas of the brain involved in higher processing functions. In effect the amplified representation that is maintained by the GNW is also broadcast to these other processing sites, thus allowing higher order processing of conscious information. It is this selection and amplification of a specific representation, and it’s subsequent global availability (to other brain areas) which we experience as consciousness. The concept of synchronous firing and a global neuronal workspace may also help explain other aspects of the conscious experience, such as metacognition (our ability to perform mental processing on the outputs of other mental processing e.g. to know what we know). Metacognition may simply be the conscious component of a much larger perceptual system that is continuously reflecting on our own activity and its likely consequences (9). The metacognition we experience consciously may therefore simply be the instances where this process reaches conscious access via the GNW and is therefore exposed to other higher order processing functions.

The consequences a neural explanation of consciousness
The study of the neural basis of consciousness is an exciting, but complex subject. It also however raises significant philosophical questions. The idea that consciousness is merely a manifestation of the firing patterns of neurons and their arrangement vis-a-vis each other is not a particularly controversial conclusion from a neuroscience perspective, as one would expect every aspect of human cognition to manifest via changes in brain physiology. However the topic is controversial in general because it suggests that if something as core to our being, to our experience of being ‘human’, as consciousness is in fact solely reliant on biological mechanisms, then concepts such as the mind,  the soul and free are redundant. If there is no ‘ghost in the machine’ driving our conscious behaviour then are we really nothing more than just a collection of tissue; are we really just, in effect, extremely complex machines? The consequences of this discussion has important implications for philosophy and morality (for an interesting discussion on this topic see 10). More optimistically however, the ability to understand the biological underpinnings of consciousness can lead to greater understanding of the basis of neurological disorders that cause the loss of conscious abilities, and of psychiatric symptoms that relate to the disruption of consciousness. For example many people suffering from forms of psychosis can experience what could be termed failures of consciousness, such that patterns of conscious thought become disordered, or that they may feel that their thoughts are being read or even controlled by others. An understanding as to how the brain generates consciousness is surely an important step in identifying what has gone wrong in these situations, and potentially how they can be remedied.

                                                                                                                                                   

Image ‘Idea and Creative Concept’ by ‘Mr Lightman’, courtesy of freedigitalphotos.net http://www.freedigitalphotos.net/images/view_photog.php?photogid=3921

References
1. Mathieson et al (2012). Photovoltaic retinal prosthesis with high pixel density. Nature Photonics, 6, 391-397. http://www.nature.com/nphoton/journal/v6/n6/full/nphoton.2012.104.html
 2. Gok, S.E., and Sayan, E. (2012) A philosophical assessment of computational models of consciousness. Cognitive Systems Research 17–18 (2012) 49–62. http://www.sciencedirect.com/science/article/pii/S1389041711000635
3 Fries, P. (2005) A mechanisms for cognitive dynamics: neuronal communication through neuronal coherence. Trends in cognitive sciences. 9(10) 474-480. http://www.sciencedirect.com/science/article/pii/S1364661305002421
4. Doesburg, S.M., Green, J.J., McDonald, J.J., and Ward, L.M. (2009). Rhythms of consciousness: Binocular rivalry reveals large-scale oscillatory network dynamics mediating visual perception. PLoS ONE 4, e6142. http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0006142
 5. Dehaene, S. and Changeux, J.P., (2011). Experimental and Theoretical Approaches
to Conscious Processing. Neuron 70, 201-227. http://www.cell.com/neuron/abstract/S0896-6273%2811%2900258-3
6. Boly, M et al (2008) Intrinsic brain activity in altered states of consciousness – How conscious is the default mode of brain function? Annals of the New York Academy of Sciences. 1129, 119-129. http://www.ncbi.nlm.nih.gov/pubmed/18591474
7. Dehaene, S. & Naccache, L. (2001) Towards a cognitive neuroscience of consciousness: basic evidence and a workspace framework, Cognition 79 1–37. http://www.jsmf.org/meetings/2003/nov/Dehaene_Cognition_2001.pdf
8. Varela, F., Lachaux, J.P., Rodriguez, E., and Martinerie, J. (2001). The brainweb: Phase synchronization and large-scale integration. Nat. Rev. Neurosci. 2, 229–239. http://www.nature.com/nrn/journal/v2/n4/abs/nrn0401_229a.html
9. Timmermans, B., Schilbach, L., Pasquali, A., and Cleeremans, A. (2012) Higher order thoughts in action: consciousness as an unconscious re-description process. Phil. Trans. R. Soc. B (2012) 367, 1412–1423. http://rstb.royalsocietypublishing.org/content/367/1594/1412.abstract
10. http://www.time.com/time/magazine/article/0,9171,1580394-1,00.html

The addicted brain

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Addictive behaviours include, but are not limited to, the abuse of drugs

If you’ve got the money honey, we’ve got your disease — Guns n’ Roses: Welcome to the Jungle

One of the key challenges of cognitive neuroscience is to gain an understanding of the neural mechanisms behind the various psychiatric disorders that can blight mankind. Knowledge of the how various brain mechanisms work in health, and how, and in what way, they become defective is crucial for the development of neurological treatments for such conditions. Such an approach doesn’t imply tacit acceptance of the idea that all behaviour is guided by changes in the brain, or that psychiatric problems are solely of a biological origin. Indeed it is well established that social and psychological factors can drive changes in brain function (for example purely cognitive therapies can alter the patterns of neural firing [1]). What understanding the neural basis of disease does allow, is the development of better methods of tackling such conditions at a neurological level, which is important because in many patients the social and psychological factors that have triggered their condition may prove to be either impractical or impossible for clinicians to alter (e.g. changing the structure of society).

Addiction is an extremely prevalent problem in modern society. Alcohol and opiate addictions alone are estimated to affect 15million Europeans, costing around 65 million Euros a year in both health and non-health related costs (2). Addiction can be defined as the persistent, compulsive dependence on a behavior or substance (3) and therefore spans not just drug dependencies, but also ‘behavioural addictions’ such as gambling, overeating, sex addiction and compulsive shopping (oniomania).  Although the definition of addiction is reasonably straightforward, the process of addiction needs to be broken down into its constituent cognitive parts before it can be fully understood. Addiction, and indeed all psychiatric problems, are not unitary constructs; they reflect abnormalities in several different facets of human cognition. For example unipolar depression can involve not just low mood, but also failure to respond to pleasurable experiences (anhedonia), low energy, anxiety and loss of appetite. Breaking down such conditions into their components parts is crucial if we are to be able to understand how they develop and how they can be treated. From a clinical perspective, focusing on the array of symptoms rather than the overall condition can help identify sub-types of the condition, which in turn can allow treatments to be modified to address the particular set of symptoms presented by an individual patient.

So which cognitive processes may be at fault when an individual becomes addicted? While opinions vary on this subject, in general it can be said that addiction involves abnormalities in the following interconnected processes:

  • Reward processing
  • Motivation and learning
  • Decision Making
  • Cognitive control
  • Insight

By their nature addictive behaviours have, at least initially, a rewarding effect. Moreover these effects are felt both by those who later become addicted and those that do not. Clearly therefore something in the processing of rewarding events must either change during addiction, or be naturally defective in the addicted individual. Unfortunately, while there are a number of different theories concerning how reward processing is disrupted in addiction, the exact nature of the deficiency is as yet uncertain. For example do people become sensitized to a drug and thus gradually require more to be able to maintain a balanced physiological state, or are people at risk of addiction more naturally prone to negative emotions and therefore have a greater tendency to seek out rewarding stimuli despite the risk? Despite this uncertainty around the exact nature of the cognitive deficiencies in reward processing, neurological research has revealed that experience of reward (e.g. intoxication) is strongly associated with activity within circuits of the brain that make use of the neurotransmitter dopamine (neurotransmitters are the chemicals that facilitate communication between different neurons in the brain). This dopaminergic system encompasses subcortical areas directly related to processing of motivationally relevant stimuli, such as the striatum and amygdala, as well as cortical areas such as the prefrontal cortex which are involved in the prediction of future reward, the evaluation of existing rewards and decision making (4). Various addictive drugs appear to alter the balance of dopamine within this system, usually increasing it, presumably creating the feeling of high associated with drug taking. Over the long term an ‘exhaustion’ effect may occur, whereby the brain is unable to maintain its previous tonic (standard) level of dopamine because of the effect on dopamine levels of frequent performance of the  addictive behaviour. This may then lead to the withdrawal state and to a situation where the addicted user becomes trapped in a cycle of repeating the addictive behaviour, not to achieve the high that the behaviour was initially associated with, but merely to maintain a acceptable tonic level of dopamine, thus avoid the ‘low’ that occurs with withdrawal from the behaviour.  Other neurotransmitter systems which also innervate similar brain areas, such as the noradrenergic system, also play a part in addiction, although they have in general been less widely studied regarding their role in reward processing.

Stimuli that are not directly rewarding, but are predictive or otherwise associated with the positive effects of the addictive behaviour, act to induce cravings for the addictive behaviour. The processing of such ‘addictive cues’, in comparison to similar stimuli unassociated with the addiction, tend to provoke greater activity in a wide variety of brain areas including those involved in the actual processing of reward, alongside frontal-cortical circuits involved in the regulation of thoughts and actions,  and areas involved in memory, sensory processing and the engagement of motor actions (5). This suggests that contextual factors that induce cravings can not only evoke brain activity in the reward centers of the brain, but also engage greater perceptual processing and attention, and even trigger motor activity, presumably in preparation for seeking out or performing the addictive behavior. Dysfunctions within these circuits are likely to have a knock-on effect on the processes such as learning and memory. Persistent performance of the addictive behaviour after exposure to addictive cues will lead to a strengthening of the association between the cue and the behaviour, and between both the cue and behaviour and the subsequent hedonic effects of the reward. The strengthening of such associations can lead to a behaviour that was previously under conscious control becoming habitual. The more habitual or automatic a behaviour becomes, the more effort is required to control it, and ultimately the more likely the behaviour is to be performed regardless of its utility in a particular circumstance. In short, it becomes compulsive. Indeed the ease with which a behaviour can become habitual may distinguish addicts from those who remain ‘casual users’.

In addition to the neural circuits involved in reward and learning, the frontal areas of the brain which are also activated by both the addictive behaviour itself and during craving are crucial in the process of addiction. Such areas are broadly believed to be involved in ‘cognitive control’; they act to regulate activity from the more primal, sub-cortical brain areas which are involved in motivation, emotional and learning. This effectively meaning that they provide control over thoughts and behavior. Perhaps unsurprisingly, the (partially separate) systems within the frontal cortex that are involved in decision making and in inhibiting pre-potent (i.e. habitual or natural) responses are both found to be deficient in addicted populations, thus explaining why addicts make decisions that are counter-productive to their health, even when they are fully aware of the likely consequences of their actions (8). Increasing sensitivity, or reactivity from the subcortical reward circuits, coupled with a weakening of the control exerted on them by the frontal control areas is likely to be behind the habituation of addictive behavior, and the subsequent failure to regulate that behavior. In some senses the addict (or more accurately, the frontal control areas of the addict’s brain) loses control over their instinctive behavior.

One of the most serious problems with addiction can be what is termed ‘insight’ or the ability to understand that you are ill. Lack of insight is a severe challenge for clinicians as it can be nearly impossible to effectively implement any treatment when the patient is unaware that the treatment is needed. Again frontal areas, most notably the Insula and anterior cingulate cortices, appear to be crucially involved in the lack of insight (6). The Insula is involved in monitoring internal body states (interoceptive awareness) and producing the ‘subjective experience’ relating to this. It also is involved in deriving salience from sensory information and, along with the anterior cingulate, influencing behavior accordingly (7) thus providing a crucial system for the expression of the effect of addictive cues on behaviour. Addiction-induced dysfunctions in this system may therefore lead to an inability to properly process and respond to changes in body state caused by the performance of (or withdrawal from) the addictive behavior, and may stop the individual from fully appreciating that addictive cues are provoking the cravings which are driving the addictive behaviour. Thus insight into the problematic nature of their condition is lost to the individual.

This article represents a very brief overview of the sorts of cognitive and neural structures involved in addiction. It isn’t unfortunately possible to do justice to the full scope of research into addictive behavior in a short article. What should be clear however is that drug abuse can induce changes in a multitude of different interconnected neural circuits, affecting a multitude of different cognitive functions. This effect can be somewhat different depending on the drug of abuse, but nevertheless also applies to a significant extent to non-drug addictions, implying that such neurological changes can occur without the direct influence of external chemical agents. It follows that these changes must therefore be at least partly the consequence of purely internal, cognitive shifts in the workings of the brain, which do, of course, also occur in drug based additions, thus exacerbating the natural neurochemical effects of the drug. Despite the complexity of the processes involved, increased understanding of the neurological and cognitive basis of addiction should enable, in time, more advanced and effective treatments to be designed. Future research into addiction will also hopefully enable ‘markers’ for the condition to be identified; biological or cognitive indices that predict those who are at potential risk of addiction. This in turn would improve our ability to take preventative measures to reduce the prevalence of this debilitating problem.

 

References

1) Porto, P. R., Oliveira, L., Mari, J., Volchan, E., Figueira, I., & Ventura, P. (2009). Does Cognitive Behavioral Therapy Change the Brain? A Systematic Review of Neuroimaging in Anxiety Disorders. Journal of Neuropsychiatry and Clinical Neurosciences, 21(2), 114-125. http://neuro.psychiatryonline.org/article.aspx?articleID=103678

2) Olesen, J., Gustavsson, A., Svensson, M., Wittchen, H. U., Jonsson, B., Grp, C. S., et al. (2012). The economic cost of brain disorders in Europe. European Journal of Neurology, 19(1), 155-162.  http://onlinelibrary.wiley.com/doi/10.1111/j.1468-1331.2011.03590.x/full

3) http://medical-dictionary.thefreedictionary.com/addiction

4) Parvaz, M. A., Alia-Klein, N., Woicik, P. A., Volkow, N. D., & Goldstein, R. Z. (2011). Neuroimaging for drug addiction and related behaviors. Reviews in the Neurosciences, 22(6), 609-624. http://www.bnl.gov/medical/Personnel/Rita-Goldstein/files/Parvaz_RNS2011.pdf

5) Yalachkov, Y., Kaiser, J., & Naumer, M. J. (2012). Functional neuroimaging studies in addiction: Multisensory drug stimuli and neural cue reactivity. Neuroscience and Biobehavioral Reviews, 36(2), 825-835. http://www.sciencedirect.com/science/article/pii/S0149763411002119

(6) Goldstein, R. Z., Craig, A. D., Bechara, A., Garavan, H., Childress, A. R., Paulus, M. P., et al. (2009). The Neurocircuitry of Impaired Insight in Drug Addiction. Trends in Cognitive Sciences, 13(9), 372-380. http://www.sciencedirect.com/science/article/pii/S1364661309001466

7) Menon, V., & Uddin, L. Q. (2010). Saliency, switching, attention and control: a network model of insula function. Brain Struct Funct, 214(5-6), 655-667. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2899886/

8 ) Duka, T., Crombag, H. S., & Stephens, D. N. (2011). Experimental medicine in drug addiction: towards behavioral, cognitive and neurobiological biomarkers. Journal of Psychopharmacology, 25(9), 1235-1255.  http://jop.sagepub.com/content/25/9/1235.short

Can a neuroscientist read your mind?

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Are the contents of your mind really 'confidential' or will your thoughts one day be accessible to others?

Media reports into recent research have claimed that neuroscientists are now effectively able to perform ‘mind reading’. Such reporting inevitable raises ethical questions about what applications such research might eventually be put to, and, judging by some of the comments that the on-line versions of these articles have provoked, have alarmed some people regarding the eventual path that such research might take. But how accurate is the claim that neuroscientific techniques can read minds?

Early this year an article in the Guardian  ( http://www.guardian.co.uk/science/2012/jan/31/mind-reading-program-brain-words ) reported that:

‘Scientists have picked up fragments of people’s thoughts by decoding the brain activity caused by words that they hear.’

Reporting on the same experiment the Daily Mail ( http://www.dailymail.co.uk/sciencetech/article-2095214/As-scientists-discover-translate-brainwaves-words–Could-machine-read-innermost-thoughts.html ) claimed:

 ’It’s a staggering development that could have tremendous implications….judges could use mind-reading machines to find out if murder suspects are telling the truth….mind reading devices might be used to eavesdrop covertly on the most private thoughts and dreams.’

The experiment in question, conducted by Dr Brian Pasley and colleagues (1) involved the recruitment of patients who were to undergo brain surgery. The researchers placed electrodes upon the auditory areas of the brain during the period when the patients’ skulls were open and their cerebral cortex exposed. They then played the patients a sequence of different words and recorded the electrical activity generated by the auditory cortex in response to this speech. Using complex modeling procedures they were able to reconstruct the spoken words solely from the neural signals recorded by the electrodes. Furthermore they were able to successfully apply this model to the electrical responses generated by a separate set of words that had not been used in creation of the model (e.g. which were in effect ‘novel’ to the model) suggesting that the model could theoretically be applied to reconstruct any speech heard by the patient.

While these results are undoubtedly impressive, has the media coverage of them been accurate? In terms of the Guardian’s report, their claim that this represents a decoding of ‘fragments of thoughts’ seems to depend on a rather broad definition of the term ‘thoughts’. What the research did was to reconstruct auditory stimuli that the auditory cortex was in the process of analysing. What has been achieved therefore is the decoding, at a detailed level, of the perceptual process, NOT the reading of internally generated thoughts. This is a significant step away from ‘decoding thoughts’ as the  process being decoded is entirely dependent on the presentation of an external stimulus. This doesn’t therefore represent ‘mind reading’ because the same result could theoretically be achieved without reference to the brain, e.g. by taking measurements from the relevant sensory organ or by just observing the sensory stimulus itself (2). Even if the research did represent mind reading, there seems little justification for the Daily Mail’s claim that the research could lead to ‘covert eavesdropping’. It should be obvious that the methodology required not only the opening up of the participant’s skull, but also the co-operation of the participant in allowing data to be taken for the construction of the model. Furthermore what is not mentioned by either article is that the reconstructed words were not actually intelligible to a human listener, but had to be ‘recognised’ via a speech recognition algorithm (an example of the reconstructed speech can be heard here:  http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001251#s5).

Actual Mind Reading?

While the results of Dr Pasley’s study required the participant’s brains to be exposed, other neuroimaging methods are not so intrusive, and could therefore be considered closer to the covert mind-reading reported by the Mail. Magnetic Resonance Imaging (MRI) allows brain activity to be measured in a non-invasive way, so that no surgery of any kind is required (although lying down in a scanner which costs millions of pounds and is the size of a small boat, is still required, making it far from ‘covert’!). MRI studies have produced some equivalent results to that of Pasley’s study, but using visual stimuli; with images (3) and short movies (4) having been reconstructed purely from data obtained from MRI scans. Of course such results don’t represent mind reading any more than Dr Pasley’s study, since they reflect a reconstruction of external sensory information. However other MRI studies have produced results that have allowed scientists to predict processes occurring within a participant’s brain that are not directly tied to the characteristic of external stimuli. A couple of studies by Yukiyasu Kamitani and Frank Tong (5,6) have shown that models can be created that allow an observer to identify to which stimulus a participant is (covertly) attending to. In effect these studies, and others like them, use the output from the perceptual processing mechanisms of the brain to identify how ‘top-down’ influences (such as expectation and attention) are driving perception. Strictly speaking they represent mindreading as although the mental processes in question are still involved in analysing external stimuli, it is not necessarily possible to garner the information provided by the MRI data in any other way (short of asking the person themselves). This is because the ‘top-down influences’ in question arise internally from the brain, rather than being a function of the external stimulus. Neuroimaging has enabled the concept of mind reading to be taken further however, into the realms of decoding mental events that don’t rely on any external stimulation at all. Recent studies have found that it is possible to decode what broad categories of objects someone is imagining, in the absence of any coincident external stimulation (7) although the performance level of the model is reasonably modest (~ 50%). Similarly, it also appears that the results of basic decision making processes can be identified from brain activity, with decisions relating to which button to press and when to press it (8) and whether a participant in lying (9) being decipherable using models constructed in a similar way to those already described. Interestingly the neural information that allows these decisions to be decoded occurs many seconds BEFORE the decision has actually been made, highlighting how conscious actions are likely driven by brain processes that are outside conscious awareness, rather than being the result of conscious ‘free will’. Most recently such work has been extended to more complex scenarios, with MRI data being used to predict at what point in solving an algebraic problem a child is at, and whether they are performing the calculation correctly (10).

The possibility of covert mind reading?

Clearly the aforementioned examples reflect mind reading, but do they represent the top of a ‘slippery slope’ that will lead to technology that will allow the sort of covert eavesdropping envisioned by the Daily Mail? The first impediment to such technology is the process of neuroimaging itself. MRI scanners are far from being portable enough to allow forced or covert application of brain scanning. Furthermore MRI scanning involves the production of a large magnetic field and the firing of electromagnetic pulses towards the object being imaged, both functions that would be totally impractical outside a controlled, isolated environment. Other neuroimaging methods, such as EEG, function by recording the electrical remnants of brain activity from outside the skull, and are therefore cheaper and more portable than MRI. However they lack the spatial resolution that would be required for any sophisticated mind reading application, and in any case they are extremely sensitive to external noise, again making them unsuitable for use outside of controlled environments.

Even if we assume that future technological advances would allow systems to be developed that would enable covert collection brain activity data, would such technology enable your innermost thoughts to be deciphered? There are a number of reasons to doubt that this would be possible. Current mind reading models are only able to distinguish between very broad categories of thoughts, or between very coarse categories of decisions (e.g. lie/truth, attending to one or other stimulus). To be able to read the specific details of an individual’s thoughts you would need models that distinguished between the literally billions of different things that someone could be thinking about, and the multitude of different decisions that they could make. To even create such models would involve the co-operation of individuals in a data collection process that would take an incalculable length of time. Even if such data were collected, and the subsequent required level of computation to create accurate models were possible, the ability to generalize such models to the brain activity of other individuals would rely on an assumption that every person’s brain being identical in terms of where different individual thoughts and memories are stored. This seems extremely unlikely, and is in fact counter to what we know about individual differences in brain anatomy and function. Thus while it is possible to aggregate data across participant to produce mind-reading for coarse decisions, it would be impossible to replicate such a method to distinguish between more subtle categories of thought. Even in situations where co-operation of the participant is attained, and only a coarse distinction between different psychological states is required, such mind reading techniques are problematic. Taking the example of the mooted ‘MRI Lie detector’ such a system will always be somewhat unreliable because, just like the current physiological lie detectors, they could be easily deceived if the participant can train themselves to act as if the truth is a lie (or vice versa). This is because the brain activity which is associated with lying most likely relates to the emotional and cognitive processes involved in creating a false story, rather than to lying per se. It follows that simply engaging in these same emotional and cognitive processes while telling the truth should produce neural activity which mimics that produced by a lie. If even the decoding of simple decisions can be subverted easily, it would seem impossible that attempts at more subtle discriminations of different thoughts would not be subject to even greater uncertainty. Finally it is important to note that all the forms of mind reading reviewed here are the result of probabilistic calculations. The parts of the brain that are deemed active at a certain point in time are the result of statistical computations as to whether a small signal is reflective of task-related neural activity or noise. Likewise the classification of such activity as belonging to one category of thought/decision over another is also based off probabilistic inference. There is no certainty in such a process; in fact it is fraught with uncertainty.

To conclude it seems very unlikely that neuroimaging methods will ever be able to perform the sort of mind reading predicted by scare stories in the press. In some cases such methods may not even represent a particular improvement on the sort of mind reading applications that already exist. What the mind reading research discussed in this article does allow is a greater understanding of how the brain works, which in turn provides insight into how the brain achieves the myriad feats it performs so frequently with apparent ease. The most fruitful practical application of such knowledge is likely to be in the treatment of patients with brain damage. For example the limited mind reading functions possible from existing neuroimaging methods may allow technology to be developed that would allow patients who suffer from brain damage to the extent that they cannot communicate using their peripheral nervous system, some primitive form of communication through their brain activity. In contrast your private thought and memories are likely to remain safe from the prying eyes of neuroscientists!

Image (top right) courtesy of Idea Go:  http://www.freedigitalphotos.net/images/view_photog.php?photogid=809

References

(1) Pasley BN, David SV, Mesgarani N, Flinker A, Shamma SA, et al. (2012) Reconstructing Speech from Human Auditory Cortex. PLoS Biol 10(1): e1001251. doi:10.1371/journal.pbio.1001251 http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001251

(2) Tong, F. & Pratte, M.S. (2012) Decoding Patterns of Human Brain Activity. Annual Review of Psychology, 63: 483-509.  http://www.ncbi.nlm.nih.gov/pubmed/21943172

(3)  Miyawaki, Y. Uchida, H. et al (2008) Visual Image Reconstruction from Human Brain Activity using a Combination of Multi-scale Local Image Decoders.. Neuron 60, 915–929, http://iopscience.iop.org/1742-6596/197/1/012021

(4)  Nishimoto, S., Vu, A.T., et al (2011) Reconstructing Visual Experiences from Brain Activity Evoked by Natural Movies. Current Biology 21, 1641–1646 http://www.sciencedirect.com/science/article/pii/S0960982211009377

(5) Kamitani Y, Tong F. 2005. Decoding the visual and subjective contents of the human brain. Nat. Neurosci. 8:679–85  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808230/

(6) Kamitani Y, Tong F. 2006. Decoding seen and attended motion directions from activity in the human visual cortex. Curr. Biol. 16:1096–102 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1635016/

(7) Reddy, L., Tsuchiya, N. & Serre, T. (2010). Reading the mind’s eye: Decoding category information during mental imagery. Neuroimage. 50(2) 818-825  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823980/

(8) Soon CS, Brass M, Heinze HJ, Haynes JD. 2008. Unconscious determinants of free decisions in the human brain. Nat. Neurosci. 11:543–45  http://www.nature.com/neuro/journal/v11/n5/full/nn.2112.html

(9) Davatzikos C, Ruparel K, Fan Y, Shen DG, Acharyya M, et al. 2005. Classifying spatial patterns of brain activity with machine learning methods: application to lie detection. NeuroImage 28:663–68  http://www.sciencedirect.com/science/article/pii/S1053811905005914

(10) Anderson, J.R. (2012) Tracking Problem Solving by Multivariate Pattern Analysis and Hidden Markov Model algorithms. Neuropsychologia, 50(4) 487-498. http://www.sciencedirect.com/science/article/pii/S0028393211003605

 

The dangers of self-report

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A common methodology in behavioural science is to use self-report questionnaires to gather data. Data from these questionnaire can be used to identify relationships between scores on the variable(s) that the questionnaire is assumed to measure and either performance on behavioural tasks, physiological measures taken during an experiment, or even scores obtained from other questionnaires (some studies just report on the correlations between batches of self-report measures!). Self-report measures are popular for a number of reasons. Firstly they represent a ‘cheap’ way (in terms of both time and cost) of obtaining data. Secondly they can be easily implemented to large samples, especially with the advent of on-line questionnaire distribution sites such as Survey Monkey. Finally they can be used to measure constructs that would be difficult to obtain with behavioural or physiological measures (for example facets of personality such as introversion). This issue of self-report methodology is important because studies that use this method are regularly reported in the media (see http://www.bbc.co.uk/news/health-17209448 for a recent example) and therefore have a significant impact on how the general public perceive scientific research. I therefore think it is important to discuss potential problems with self-report measures.

Most (but certainly not all) questionnaires that are used in behavioural research undergo  testing for reliability, to check that they produce consistent results when applied to the same population over time. More importantly they are normally also tested for validity, to check that the questionnaire measures what it claims to measure. Such tests are done following the logic that the questionnaire should be able to discriminate participants in a similar way to relevant non-self report measures. For example scores on a questionnaire measuring depression should be able to discriminate between depressed patients and controls, while scores on a questionnaire measuring diet should be able to predict the ‘Body Fat Percentage’ of respondents with reasonable accuracy. While such tests can act to increase confidence that a questionnaire is measuring what it claims to measure they are not foolproof. For example just because a depression questionnaire can discriminate between patients and controls does not mean that it measures depression well, as the two groups will likely vary in several different ways. Likewise a questionnaire that distinguishes between patients and controls may not be able to identify the (presumably) more subtle differences between depressed and non-depressed healthy individuals, or the range of depressive tendencies within the healthy population. In fact that are a large number of reasons why questionnaire may not be entirely valid, including the following:

Honesty/Image management – researchers who use self-report questionnaires are relying on the honesty of their participants. The degree to which this is a problem will undoubtedly vary with the topic of the questionnaire, for example participants are less likely to be honest about measures relating to sexual behaviour, or drug use, than they are about caffeine consumption, although it is unwise to assume, even when you are measuring something relatively benign, that participants will always be truthful. Worse, the level at which participants will want to manage how they appear will no doubt vary depending on personality, which means that the level of dishonesty may vary significantly between different groups that a study is trying to compare.

Introspective ability – Even if a participant is trying to be honest, they may lack the introspective ability to provide an accurate response to a question. We are probably all aware of people who appear to view themselves in a completely different light to how others see them. Undoubtedly we are all to some extent unable to introspectively assess ourselves completely accurately. Therefore any self-report information we provide may be incorrect despite our best efforts to be honest and accurate.

Understanding – Participants may also varying regarding their understanding or interpretation of particular questions. This is less a problem with questionnaires measuring concrete things like alcohol consumption, but is a very big problem when measuring more abstract concepts such as personality. From personal experience I have participated in an experiment where I was asked at regular intervals to report how ‘dominant’ I felt. As I can honestly say I don’t monitor my feelings of ‘dominance’ and how they change over time, I know that my responses to the question were pretty random. Even if I could conjure an understanding of what the question was getting at, it would be impossible to ensure that everyone who completed the questionnaire interpreted that question in the same way that I did.

Rating scales – Many questionnaires use rating scales to allow respondents to provide more nuanced responses than just yes/no. While yes/no questions do often appear restrictive in terms of how you can respond, using rating scales can bring their own problems. People interpret and use scales differently, what I might rate as ’8′ on a 10 point scale, someone with the same opinion might only rate as a ’6′ because they interpret the meanings of the scale points differently. There is research which suggests that people have different ways of filling out ratings scales (1). Some people are ‘extreme responders’ who like to use the edges of the scales, whereas other like to hug around the midpoints and rarely use the most outer points. This naturally produces differences in scores between participants that reflects something other than what the questionnaire was designed to measure. A related problem is that of producing nonsense distinctions. For example studies sometimes appear where participants are given a huge rating scale to choose from, for example a scale of 1-100 to rate the confidence of a decision as to whether two lines are the same length (2).  Is anyone really capable of segmenting their certainty over such a decision into 100 different units? Is there really any meaningful difference, even within the same individual, between a certainty of 86 and a certainty of 72 in such a paradigm? Any differences found in such experiments therefore run the risk of being spurious.

Response bias – This refers to individual’s tendency to respond a certain way, regardless of the actual evidence they are assessing. For example on a yes/no questionnaire asking about personal experiences, some participants might be biased towards responding yes (i.e. they may only require minimal evidence to decide on a yes response, so if an experience has happened only once they may still respond ‘yes’ to a question relating to whether they have had that experience). Alternatively other participants may have a conservative response bias and only respond positively to such questions if the experience being inquired about has happened regularly. This is a particular problem when the relationship between different questionnaires is assessed, as a correlation between two different questionnaires may simply reflect the response bias of the participants being consistent across questionnaires, rather than any genuine relationship between the variables the questionnaire is measuring.

Ordinal Measures – Almost all self-report measures produce ordinal data. Ordinal data is that which only tells you the order that units can be ranked in, not the distances between them. It is contrasted with interval data which tells you the exact distances between different units. This distinction is easiest to define by thinking of a race. The position in which each runner finishes in is an ordinal measure. It tells you who is fastest and slowest, but not the relative differences between the different runners. In contrast the finishing time is an interval measure, as it provides information relating to the relative differences between the runners. Even when the questionnaire measures something that could be measured in SI units, and is therefore theoretically an interval scale (i.e. alcohol consumption) it is doubtful whether the responses can really be treated as interval because of the problems relating to response accuracy raised above. More pertinently most self-report measures in behavioural science relate to constructs, such a personality measures, that can’t be measured in interval units and are therefore always ordinal. The problem with ordinal data is not the data itself, but the common practice of using parametric statistical techniques with such data, because these tests make assumptions about the distribution of the data that cannot be met when said data is ordinal. Deviations from such assumptions can lead to incorrect inferences being made (3) bringing the conclusions of such studies into question.

Control of sample – this has become more of an issue with the advent of online questionnaire distribution sites like Survey Monkey. Previously a researcher had to be present when a participant completed a questionnaire, now with these tools the researcher need never meet any of their participants. While this allows much bigger samples to be collected much more quickly, it does cause several concerns over the sample make up. For example there are few controls to stop the same person filling in the same questionnaire multiple times. There is also little disincentive for participants to respond with spurious responses, and there is little control over how much attention the participant pays to various parts of the questionnaire. Conversely, from personal experience, I know that sometimes it is hard to complete these questionnaires because there is no way of asking the researcher for clarification as to the meaning of various questions. Finally as the researcher has lost control over the make up of their sample, they may end up with a sample which is vastly skewed towards a certain type of person, as only certain types of people are likely to fill in such questionnaires. These issues existed even before the advent of online data collection (e.g. (4)), but collecting data ‘in absentia’ exacerbates the size of such problems.

Although there are many problems with using self-report questionnaires they will continue to be a popular methodology in behavioural science because of their utility. While it might be preferable for every variable a researcher wants to investigate to be manipulated systematically using behavioural techniques, this is in practice impossible as it would severely restrict what each individual research design could achieve, and would make certain topics effectively impossible to research. Self-report measures are therefore a necessary tool for behavioural research. Furthermore some of the problems listed above can be countered through the careful design and application of self-report measures. For example response bias can be removed by ‘reversing’ half the questions on a questionnaire so that the variable is scored by positive responses on half the questions and negative responses on the other half, thus cancelling out any response bias. Likewise statistical techniques are being devised to attempt to pick out dishonest reporting, a problem that can also be attenuated by ensuring anonymity and confidentiality of responses (e.g. the researcher leaving the room when the participant is completing the questionnaire). Given this it would be wrong to dismiss any findings that are reliant on self-report measures. However whenever you read about research where self-report measures have been used to draw conclusions about human behaviour, it is always worth bearing in mind the multitude of problems associated with such measures, and how they might impact on the validity of the conclusions that have been drawn.

(1) Austin, E. J., Gibson, G. J., Deary, I. J., McGregor, M. J., & Dent, J. B. (1998). Individual response spread in self-report scales: personality correlations and consequences. Personality and Individual Differences, 24, 421–438. http://www.sciencedirect.com/science/article/pii/S019188699700175X

(2) Balakrishnan, J. D. (1999). Decision processes in discrimination: Fundamental misrepresentations of signal detection theory. Journal of Experimental Psychology: Human Perception & Performance, 25, 1189-1206. http://psycnet.apa.org/psycinfo/1999-11444-002

(3) Wilcox, R. R. (2005). Introduction to robust estimation and hypothesis testing. Academic Press. ISBN: 0127515429

(4) Fan, X., Miller, B. C., Park, K., Winward, B. W., Christensen, M., Grotevant, H. D., et al. (2006). An exploratory study about inaccuracy and invalidity in adolescent self-report surveys. Field Methods,18, 223–244. http://fmx.sagepub.com/content/18/3/223.short

The Immune Cell, the Neutrophil – the Good, the Bad, or the Ugly?

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By Kathryn Higgins

Throughout our lifetime our bodies sustain infections and injuries, and the body deals with them by mediating an inflammatory response. This happens by cells within our blood entering the site of infection or injury and carrying out multiple biological reactions. These reactions can kill the microorganism that has caused the infection, but also heal at the site of injury, and hence resolve inflammation. These blood cells are collectively called white blood cells or leukocytes, and there is one in particular, named the neutrophil, which not only helps to resolve inflammation but can also exacerbate the condition further. This has resulted in the neutrophil having a reputation for being both ‘good’ and ‘bad’ in inflammatory conditions.

The reputation of the neutrophil is influenced by many molecules that are released from other cell types during inflammation. These molecules influence the activity of the neutrophil in various ways, either stimulating the cell so inflammation can be resolved or inhibiting a particular function the cell has. The influence of these molecules determines whether the neutrophil is able to carry out its functions efficiently or whether the inflammatory condition will be aggravated further. The biological activities of neutrophils therefore need to be understood to comprehend how they function and how these roles can be modulated to determine what effect this has during an inflammatory response.

Neutrophils form part of the body’s innate immunity which involves a series of defence mechanisms that protect the host from infection and form the early barriers to infectious diseases without relying on the production and expansion of antibodies that form the adaptive immune response. When an infection occurs, the innate immune response is triggered to rapidly detect and destroy the infection. Neutrophils are one of the first blood cells to respond to infection and are recruited from the circulating blood into the tissue by molecules called chemoattractants1. These molecules, released from cells at the site of infection and also from the microorganism, also known as a pathogen, provide a chemical gradient for neutrophils to migrate along, with the highest concentration of these chemoattractants situated at the site of infection, so the cells are led directly to the infected site. Once in the tissue the lifespan of the cell is increased to approximately 1-2 days as opposed to 6-10 hours in the circulation. This is to lengthen the amount of time neutrophils have to carry out their functions and resolve inflammation.

A vital part of the innate immune response is the ability of the neutrophils to engulf pathogens and aid the resolution of infection. This process is called phagocytosis and classifies the neutrophil as a phagocyte, so called after the Greek for ‘devouring cells’. When the neutrophil has entered the infected site and detected the pathogen, the outer membrane of the neutrophil surrounds the pathogen to engulf it and so the pathogen becomes taken up into the cell. Neutrophils contain many granules and these are packed with lots of toxic reagents. Upon engulfment these granules fuse with the pathogen and release their toxic contents, by a process called degranulation, and these contents assist in the killing of the pathogen2.

In addition to degranulation, neutrophils can also kill pathogens by oxidative mechanisms, so called because molecular oxygen is required. This involves a process named the respiratory burst and it is the major mechanism by which neutrophils kill and digest pathogens. During the engulfment of a pathogen into the neutrophil, molecular oxygen is also rapidly taken up. The oxygen is then converted, by a series of chemical reactions, into several toxic compounds such as hydrogen peroxide. Further chemical reactions may occur producing even more potent substances3 and when the pathogen becomes exposed to these various toxic oxygen metabolites the pathogen is digested and destroyed within the cell.

Neutrophils have also been shown to kill pathogens outside of the cell, i.e. extracellularly, rather than engulfing them. This occurs by neutrophils releasing web-like structures of genetic material, called neutrophil extracellular traps (NETs)4. These NETs are composed of fibres that trap pathogens, and have been proposed to contain high concentrations of anti-microbial compounds, such as those contained within their granules, to kill pathogens and prevent the spread of infection. Some bacteria, however, have evolved to counteract being killed by NETs by producing substances that degrade the genetic material that make up NETs, such as Streptococcus pneumoniae5, which is known to be the common cause of pneumonia.

Once the pathogens have been dealt with, and to completely resolve inflammation, neutrophils need to be cleared from the tissue. If the cells do not become removed then all their toxic contents, such as the granule contents and oxygen metabolites that kill pathogens, may leak out of the cell and damage surrounding cells and tissues, which will only make the inflammatory condition worse. For removal, neutrophils firstly need to die. This is by a programmed type of cell death termed apoptosis6 which ensures that the cellular membrane remains intact so these toxic contents are retained within the cell and cannot be released. During this cell death a fatty (lipid) molecule called phosphatidylserine is flipped to the outer surface7. This lipid acts as a signal for tissue macrophages to target the dead neutrophil. Tissue macrophages are another class of white blood cell with a vital role of recognising apoptotic cells. Once the signal has been recognised, the neutrophil itself is then engulfed by the macrophage and cleared from the tissue. It is essential that these apoptotic cells are removed efficiently from the tissue because a delay in their clearance can also increase the chance of their intact membranes becoming leaky.

Apoptosis is therefore a process which needs to be tightly regulated to ensure inflammation is resolved efficiently. If cell death is stimulated too early then the number of functional neutrophils in the tissue is reduced. This would limit the hosts’ ability to fight infection and resolve inflammation. For example, some infections induce neutrophil apoptosis, such as the influenza A virus8 and the Pseudomonas aeruginosa bacterium9 to favour their own survival. In contrast to this, if apoptosis is delayed, as seen with the inflammatory joint disorder rheumatoid arthritis10, the number of circulating cells in the tissue increases, toxic contents may then be released from the cells, and surrounding tissue would be damaged potentiating inflammation further. This contrasting effect of the neutrophil is often referred to as the ‘double-edged sword’ effect, i.e. can be both ‘good’ and ‘bad’ during the inflammatory process, with the damaging effects of the neutrophil quickly out-weighing the benefits. Although neutrophils may often appear to be the ‘bad’ guy in certain inflammatory conditions this is typically due to the influence of other molecules released from surrounding cells. Without this influence the primary aim of the neutrophil is to resolve inflammation, making them overall the ‘good’ guys of the inflammatory process.

References:

  1. Yoshimura, T., Matsushima, K., Tanaka, S., Robinson, E.A., Appella, E., Oppenheim, J.J. and Leonard, E.J. (1987) Proc. Natl. Acad. Sci. USA 84, 9233-9237
  2. Campanelli, D., Detmers, P.A., Nathan, C.F. and Gabay (1990) J. Clin. Invest. 85, 904-915
  3. Albrich, J.M. and Hurst, J.K (1982) FEBS Lett. 144, 157-161
  4. Brinkmann, V., Reichard, U., Goosmann, C., Fauler, B., Uhlemann, Y., Weiss, D.S., Weinrauch, Y. and Zychlinsky, A. (2004) Science 303, 1532-1535
  5. Beiter, K., Wartha, F., Albiger, B., Normark, S., Zychlinsky, A. and Henriques-Normark, B. (2006) Curr. Biol. 16, 401-407
  6. Kerr, J.F., Wyllie, A.H. and Currie, A.R. (1972) Br. J. Cancer 26, 239-257
  7. Fadok, V.A., Voelker, D.R., Campbell, P.A., Cohen, J.J., Bratton, D.L. and Henson, P.M. (1992) J. Immunol. 148, 2207-2216
  8. Colamussi, M.L., White, M.R., Crouch, E. and Hartshorn, K.L. (1999) Blood 93, 2395-2403
  9. Usher, L.R., Lawson, R.A., Geary, I., Taylor, C.J., Bingle, C.D., Taylor, G.W. and Whyte, M.K.B. (2002) J. Immunol. 168, 1861-1868
  10. Ottonelo, L., Cutolo, M., Frumento, G., Arduino, N., Bertolotto, M., Mancini, M., Sottofattori, E. and Dallegri, F. (2002) Rheumatol. 41, 1249-1260