Category: Integrating

I just found a some curious case reports on two people who had hallucinations in everyday life owing to unrecognised narcolepsy, but not realising it, they assumed their hallucinated episodes had genuinely occurred.

Unlike in psychosis, where affected people often believe that their hallucinations are real, people who have narcolepsy and have hallucinations are usually able to realise they were triggered by the condition.

In this case, the people were unaware that they had a tendency to hallucinate and so the boundaries between hallucination and reality began to blur.

The 45-year-old technical manager had a multi-year history of daytime sleepiness… He frequently had curious experiences during the day ‚Äì the neighbour throwing litter into the patient’s bin; his wife throwing precious objects away. Sometimes he saw himself trying to clean dirt on the side of a ditch. These memories and experiences were confusing. They gave rise to a surprised and suspicious state of mind.

Improbable and incomprehensible things happened, leaving him in doubt. Sometimes he gave sensitive-paranoid interpretations to the events, he also denounced the neighbour for filling his bin. His paranoidity drove his psychiatrist to the diagnostic conclusion of a delusional psychosis.

Recently he had a severe conflict with his chief on account of a vivid experience of having had sexual intercourse with the chief’s wife, which he mentioned to colleagues. Remembering every detail, he was convinced that his story was true, but the reactions of those around him gradually convinced him that this experience could be a hallucination.

The man was eventually referred to a sleep clinic, diagnosed with narcolepsy and successfully treated.

The other case is of a young woman who hallucinated that she had been sexually assaulted on a bus – an experience so vivid that she reported it to the police with numerous details of the offender.

She later realised that that she could have been wrong and as part of the court case for making a false police report she was medically assessed and also diagnosed with narcolepsy after a sleep lab assessment.

Link to PubMed entry for case reports.

Today’s Nature has an excellent piece about an increasing and currently not well-researched trend for fMRI brain scan ‘neurofeedback’ treatments, where the patient is shown a visual representation of the activity of a certain brain area in the hope of learning to control it.

In this case, the big idea is that a patient with chronic pain is shown real-time activity in their anterior cingulate cortex, an area in the frontal lobe associated with the ‘unpleasantness’ of pain (rather than just its physical sensation), and they can see when they doing something to successfully reduce the activity and can try and learn to do it reliably.

The article looks at the work of Sean Mackey who researches the area but is appropriately skeptical about a number of companies who have recently sprung up offering this as a treatment, despite the lack of firm evidence.

As you may recall, this premature commercialisation is a bit of a pattern with fMRI research, as you can also buy the services of companies offering ‘lie detection’ and ‘neuromarketing’ despite a similar lack of evidence for their usefulness.

However, the piece also looks more generally at the neuroscience of pain which is, if you’ll excuse the pun, becoming a hot area, both as the understanding of pain moves away from the idea that it happens ‘in the body’ to the idea that it is handled by numerous brain circuits, each which may be involved if different aspects of the experience and our behavioural reaction to it.

In some of his other work, Mackey’s laboratory has used fMRI to explore these connections between pain processing and cognitive processes. Fear of pain, for example, can increase the pain itself, and Mackey’s group studied some of the brain regions involved in this anticipation. In another study he showed that watching someone else in pain activates brain areas that are fairly distinct from those active during one’s own pain. And in unpublished work he has found that romantic love can lessen the experience of pain. Mackey says these connections demonstrate how strong an influence conscious thought may have over pain processing.

Link to Nature article ‘Shooting pain’.

New Scientist has an excellent article on how the brain makes sense of time and looks at why certain intense experiences seem to trigger the perception that time has slowed down.

It covers David Eagleman’s well-known study where he dropped people 30 metres into a safety net and while falling, asked them to read off numbers that were flashing by too fast for normal perception.

The idea was that if time really did ‘slow down’, or rather, if the brain became ‘over-clocked’ and the resolution of time perception genuinely became more fine-grained, the participants could read off some of the digits that they couldn’t normally make sense of. As it happened, they couldn’t, suggesting that time slowing effect is an illusion and not an effect of the brain going into overdrive.

The piece also has an interesting discussion of how cognitive scientists are using the wagon wheel effect to study time perception in the brain. This is where after a certain speed, spokes on a wheel seem to starting moving backward.

This has been used to work out the brain’s ‘refresh rate’, but it turns out that this is unlikely to be a global process because when looking at two such objects moving at exactly the same rate, only one of them might be subject to the effect.

This suggests that the brain might have many clocks, perhaps each assigned to a different task:

The case for discrete perception is far from closed, however. When Eagleman showed subjects a pair of overlapping patterns, both moving at the same rate, they often saw one pattern reverse independently of the other. “If you were taking frames of the world, then everything would have to reverse at the same time,” says Eagleman.

VanRullen has an alternative explanation. The brain processes different objects within the visual field independently of one another, even if they overlap in space, he suggests. So the RPL [right inferior parietal lobe] may well be taking the “snapshots” of the two moving patterns at separate instances – and possibly at slightly different rates – making it plausible that the illusions could happen independently for each object.

This implies that there is not a single “film roll” in the brain, but many separate streams, each recording a separate piece of information. What’s more, this way of dealing with incoming information may not apply solely to motion perception. Other brain processes, such as object or sound recognition, might also be processed as discrete packets.

Link to NewSci piece ‘Timewarp’.

With uncanny echoes of the modern interest in ‘cognitive enhancers’, a 1958 edition of Popular Science hails a new drug that “tunes up the brain” allowing us “to perform at peak efficiency all the time”.

The drug is iproniazid, marketed then as Marsilid. It was the first ever antidepressant, but the concept of an ‘antidepressant’ had yet to be created by the pharmaceutical companies and instead it is described as ‘psychic energizer’.

It was originally used a treatment for tuberculosis, as it stops the bacterial infection, but it was noticed that patients treated with iproniazid seemed to have a lift in mood at low doses and risked becoming confused and psychotic at higher doses.

At the time, the only widely used psychiatric drugs were tranquilisers, and the idea that a drug might be an ‘anti-tranquiliser’ was quite puzzling. It was trialled on some patients with diagnoses of mental illness patients and then marketed as a ‘psychic energizer’.

According to David Healy’s book (p66) on the history of drug treatments for depression, The Antidepressant Era, this label came from the discoverers trying to interpret its effects in Freudian terms – in which ‘psychic’ is used broadly to mean ‘psychological’:

Kline and Ostow speculated that as psychic conflicts all involved the binding of psychic energy in various different ways and as a great deal of ego energy went into binding instinctual (or id) energy down to produce a range of inhibited states, it was conceivable that a drug that took energy away from the ego might lead to liberation of instinctual energy – it might be a psychic energizer.

However, the drug was rapidly taken off the market as it was found to damage the liver to the point where a number of patients died of hepatitis.

The Popular Science article is interesting because it is remarkably similar to modern day articles on cognitive enhancers – relating it’s effects to improving performance rather than treating an illness and musing over whether healthy people should take drugs to make them ‘better than well’.

Therefore, let’s imagine that a few years from now there is a psychic energizer known to be completely harmless. And suppose its effect on body chemistry is perfectly normal and natural. In that case, what about the healthy person who just want more vim and vigor to go dancing?

“Well”, Dr Kline answers, “why not?” After all, nobody sees anything wrong about a dentist working to give perfect teeth. Why shouldn’t a doctor try to give perfect metabolism?

Or perfect tits, as the comparison more commonly goes in the 21st century.

It’s an interesting insight into how the drug companies were trying to find a place in the market for their puzzling new compounds in the 1950s and another demonstration of how concerns about ‘cognitive enhancers’ are as old as drugs themselves.

Link to Popular Science article ‘New Drugs to Tune Up Our Brains’.

Sensory deprivation lasting only 15 minutes is enough to trigger hallucinations in healthy members of the public, according to a new study published in the Journal of Nervous and Mental Disease.

The researchers were interested in resurrecting the somewhat uncontrolled research done in the 50s and 60s where participants were dunked into dark, silent, body temperature float tanks where they subsequently reported various unusual perceptions.

In this study the researchers screening a large number of healthy participants using a questionnaire that asks about hallucinatory experiences in everyday life. On the basis of this, they recruited two groups: one of ‘high’ hallucinators and another of ‘low’ hallucinators.

They then put the participants, one by one, in a dark anechoic chamber which shields all incoming sounds and deadens any noise made by the participant. The room had a ‘panic button’ to stop the experiment but apparently no-one needed to use it.

They asked participants to sit in the chamber for 15 minutes and then, immediately after, used a standard assessment to see whether they’d had an unusual experiences.

After a twenty minute break, they were asked again about perceptual distortions to see if there were any difference when normal sensation was restored.

Hallucinations, paranoid thoughts and low mood were reported more often after sensory deprivation for both groups but, interestingly, people already who had a tendency to have hallucinations in everyday life had a much greater level of perceptual distortion after leaving the chamber than the others.

This study complements research published in 2004 that found that visual hallucinations could be induced in healthy participants just by getting them to wear a blindfold for 96 hours.

However, my attention was grabbed by the researchers use of a ‘panic button’. The effect of having a panic button in sensory deprivation experiments was specifically studied in 1964 by psychologists Martin Orne and Karl Scheibe. They also asked about hallucinations and compared two groups of people.

One group was met by researchers in white coats, given a medical examination and told to press a ‘panic button’ if they wanted out. The other was met by researchers in causal clothes, weren’t given medical checks, and told to knock on the window if they wanted the experiment to stop.

The actual sensory deprivation part was the same, but the group with the panic button reported many more hallucinations, likely owing to ‘demand characteristics’, or, in other words, their expectations of what might happen.

We also know that an increase in anxiety also increases the likelihood of hallucinations, and having a ‘panic button’ during an experiment, I suspect, is likely put most people a little more on edge.

So we can’t be sure that the effect was purely due to sensory deprivation, but it does chime with various other studies showing that when we reduce our normal sensations, the brain has a tendency to ‘fill in’ with hallucinations.

Link to PubMed entry for sensory deprivation study.

An interesting case study from a 2002 edition of The Lancet of a man who suffered paralysis from drinking too much Earl Grey tea owing to the toxic effects of huge doses of bergamot oil – taken from orange rind and used as flavour:

A 44-year-old man presented in May, 2001, with muscle cramps. He had no medical history of note, but volunteered the fact that he had been drinking up to 4 L of black tea per day over the past 25 years. His preferred brand was GoldTeefix (Tekanne, Salzburg, Austria). Since this type of tea had given him occasional gastric pain, he changed to Earl Grey (Twinings & Company, London, UK), which he thought would be less harmful to his stomach. 1 week after the change, he noticed repeated muscle cramps for some seconds in his right foot. The longer he drank Earl Grey tea, the more intense the muscle cramps became. After 3 weeks, they also occurred in the left foot…

Earl Grey tea is composed of black tea and the essence of bergamot oil, an extract from the rind of bergamot orange (Citrus aurantium ssp bergamia), which has a pleasant, refreshing scent. Bergamot oil contains bergapten (5-methoxypsoralen), bergamottin (5-geranyloxypsoralen), and citropten (5,7-dimethoxycoumarin), which can be found in grapefruit juice, celery, parsnips, and Seville orange juice. Bergamot oil is a well-known UVA-induced photosensitiser with a strong phototoxic effect, and is used therapeutically in psoriasis, vitiligo, mycosis fungoides, and cutaneous lymphoma. Because of this side-effect, bergamot oil has been widely banned as an ingredient in cosmetics and tanning products. Bergamot oil also has a hepatotoxic effect and may cause contact-allergy. The adverse effects of bergamot oil in this patient are explained by the effect of bergapten as a largely selective axolemmal potassium channel blocker, reducing potassium permeability at the nodes of Ranvier in a time-dependent manner. This may lead to hyperexcitability of the axonal membrane and phasic alterations of potassium currents, causing fasciculations and muscle cramps.

In other words, it disrupts the way chemical flow through the membrane of the nerve fibre, causing the neurons that connect to the muscles to malfunction.

Link to DOI entry for the case study.

Not Exactly Rocket Science covers a fantastic study on how the structure of the brain changes as illiterate adults learn to read and write. The research was conducted on rather a novel group of participants. Most were ex-members of guerilla forces in Colombia that had recently put down their weapons to re-integrate in society.

Colombia has a sizeable program to rehabilitate ex-paramilitary ‘reinsertados’ that includes social support and education, as many have never attended school. As the researchers note, this sets up an interesting natural experiment:

After decades spent fighting, members of the guerrilla forces have begun re-integrating into mainstream Colombian society, introducing a sizeable population of illiterate adults who have no formal education. Upon putting down their weapons and returning to society, some had the opportunity to learn to read for the first time in their early twenties, providing the perfect natural situation for experiments investigating structural brain differences associated with the acquisition of literacy in the absence of other types of schooling or maturational development.

The researchers, led by neuroscientist Manuel Carreiras, recruited a group of ex-paramilitaries who could read less than five simple words on a Spanish reading and writing test, and compared them to a similar group who learnt to read and write from an early age.

The research team use MRI scans to compare differences in brain structure between the two groups to allow an insight into how brain anatomy changes to accommodate reading and writing.

While it is possible to do this with children, it is almost impossible to separate out which are the brain changes due specifically to acquiring literacy and which are just part of the massive changes that constantly take place as children develop.

The images above show the areas of the brain (in orange) where the structure was significantly different between literate and illiterate adults.

Rather neatly, these are also areas that have been identified in brain activation studies of reading and writing, and are known to be associated with visual perception, processing word sounds and dealing with the meaning of words.

Subsequent analyses showed that pathways the angular gyrus, a key language area, across each hemisphere were less developed in illiterate adults and were less active when the participants were asked to name objects.

A brilliantly innovative study, a good write-up from Not Exactly Rocket Science and perfectly timed for my arrival in Colombia.

Link to NERS on guerilla reading.
Link to summary of scientific paper.

There are a couple of excellent posts on Neurophilosophy covering recent studies that demonstrate the powerful effect of vision on the perception of physical sensations in our body.

The first covers an interesting study that found that looking directly at your hand reduces laser-induced pain compared to a condition where you are only looking at a visual substitute created with a mirror reflection of the other hand (akin to a mirror box set up).

The second post discusses the possibilities of taking advantage of the ‘rubber hand illusion‘ to allow us to feel like we’re physically inhabiting virtual bodies.

Numerous experiments have shown that we look at a rubber hand being touched simultaneously and in the same way as our real hand, the sensation seems to be located in the fake.

This new experiment attempted something similar but in virtual reality, demonstrating that a synchronised ‘touch’ could be perceived as arising from an avatar hand in a 3D computer generated environment.

While the same research team had demonstrated this effect before this new study showed how the effect could transfer, albeit more weakly, to a virtual arm controlled by a brain-computer interface driven solely from EEG readings.

Both of these studies demonstrate how vision is integrated with tactile information from the body to create our sense of body image, ownership and sensation and both get a great write-up from Neurophilosophy.

Link to Neurophilosophy post visual pain reduction.
Link to Neurophilosophy on the ‘virtual hand illusion’.

New Scientist has a fantastic issue on ‘strange journeys of the mind’ that has three great articles on the twilight zone of sleep, simulating psychopathology with hypnosis and laboratory-induced out-of-body experiences.

The piece on the hypnotic simulation of brain disturbances is fantastic, not least because it features two researchers I work with, Peter Halligan and David Oakley, who have done some of the seminal work in the area.

Essentially, the approach views hypnosis as a tool that allows researchers, with the co-operation of the participant, to temporarily alter mental states in a completely safe and reversible way.

Importantly, these alterations, such as blindness or paralysis, seem like they’re happening ‘on their own’ – which helps us understand conditions like conversion disorder, where these sorts of symptoms appear without any neurological damage but without the patient seeming to have any control over them.

The other article which blew me away was on recent studies suggesting that sleep and alertness are not two distinct states of consciousness and in some people with a dementia-like brain disorder the boundaries between sleep and wakefulness completely break down.

That this can happen contradicts the way we usually think about sleep, but it came as no surprise to Mark Mahowald, medical director of the Minnesota Regional Sleep Disorders Center in Minneapolis, who has long contested the dogma that sleep and wakefulness are discrete and distinct states. “There is now overwhelming evidence that the primary states of being are not mutually exclusive,” he says. The blurring of sleep and wakefulness is very clear in status dissociatus, but he believes it can happen to us all. If he is right, we will have to rethink our understanding of what sleep is and what it is for. Maybe wakefulness is not the all-or-nothing phenomenon we thought it was either.

Finally, the piece on out of body experiences covers the work of Swiss researchers who have been studying these states in people with brain disorder, and managing to induce them in volunteers in a number of inventive ways.

Three awesome articles, all worth your time, all open-access. Three cheers New Scientist.

Link to article on sleep states.
Link to article on hypnotic simulations.
Link to article on out-of-body experiences.

In what sounds like a plot from an animated sci-fi film, I’ve just found a remarkable study where Japanese researchers put a Yoga Master in a brain scanner and fired lasers at him because he claimed not to be able to feel pain while meditating.

It turns out that he showed significantly less brain activity in areas typically activated by pain when meditating.

Intracerebral pain processing in a Yoga Master who claims not to feel pain during meditation.

Eur J Pain. 2005 Oct;9(5):581-9.

Kakigi R, Nakata H, Inui K, Hiroe N, Nagata O, Honda M, Tanaka S, Sadato N, Kawakami M.

We recorded magnetoencephalography (MEG) and functional magnetic resonance imaging (fMRI) following noxious laser stimulation in a Yoga Master who claims not to feel pain when meditating. As for background MEG activity, the power of alpha frequency bands peaking at around 10 Hz was much increased during meditation over occipital, parietal and temporal regions, when compared with the non-meditative state, which might mean the subject was very relaxed, though he did not fall asleep, during meditation.

Primary pain-related cortical activities recorded from primary (SI) and secondary somatosensory cortices (SII) by MEG were very weak or absent during meditation. As for fMRI recording, there were remarkable changes in levels of activity in the thalamus, SII-insula (mainly the insula) and cingulate cortex between meditation and non-meditation. Activities in all three regions were increased during non-meditation, similar to results in normal subjects. In contrast, activities in all three regions were weaker during meditation, and the level was lower than the baseline in the thalamus.

Recent neuroimaging and electrophysiological studies have clarified that the emotional aspect of pain perception mainly involves the insula and cingulate cortex. Though we cannot clearly explain this unusual condition in the Yoga Master, a change of multiple regions relating to pain perception could be responsible, since pain is a complex sensory and emotional experience.

I have an image of scientists shielding their eyes as lasers fail to penetrate the force field of the Yoga Master who serenely hovers a few inches above the ground, although I suspect that’s because I’ve read too many manga comics

Link to PubMed entry for study,

Earlier this year we covered a study on REM sleep behaviour disorder (RBD) where normal sleep paralysis breaks down and sleepers act out their dreams. The Journal of Forensic Science has just published a study on the dark side of the disorder, where affected sleepers experience nightmares and can unknowingly damage themselves or their partners in fits of dream world violence.

The researchers examined all the published cases on violence in REM sleep behaviour disorder with potential for a lethal outcome and found they fall into three groups: choking or headlock attacks, throwing someone or throwing yourself through a window, and diving from the bed.

Some of the descriptions are pretty intense:

A 63-year-old man with RBD and delayed-onset Shy-Drager Syndrome reported “a progressive 10-year history of abnormal behavior during sleep. He would at various times choke, kick, punch, and spit on his wife while he was asleep. In addition, complex behaviors such as getting out of bed and running into walls while asleep were reported by family members. This behavior occurred while the patient was dreaming, usually of being attacked.

A 67-year-old man had a 3-year history of progressive stiffness and slowing of his left side. Five years before the onset of these symptoms, he began having vivid dreams together with violent movements during sleep. Once he dreamed of being trapped in a house on fire, and he almost jumped out of the window, if not for his wife awakening and restraining him.

A 25-year-old woman with multiple sclerosis “presented with a 6-month history of sudden awakenings from fearful, often vivid‚Ķdreams and with terrified screams or violent behavior such as kicking, running to the door or to the window, crying and falling out of bed. If awakened, she always recalled a fighting dream. Once she repetitively banged her head against the floor, inducing a large facial hematoma. On that occasion, she was dreaming that a man was knocking her against the wall.

The idea that someone could be violent during sleep without any awareness was initially treated with suspicion but it has since been confirmed in sleep labs where patient are video-taped and wired up to an EEG to confirm they are in REM sleep.

There have now been numerous legal cases where ‘sleepwalking violence’ has been used as a defence for murders or attempted murders, and at least one case where it led to a successful acquittal.

Link to summary of RBD lethal violence study.

One of the most influential and controversial papers in psychiatry was from a 1976 study published in The Lancet that found that people with schizophrenia had larger fluid filled ventricles in the brain.

Yesterday, I looked up the original paper in London’s Institute of Psychiatry library and was amazed to see that the controversy seems ingrained into the paper copy, which has been ripped, repaired, damaged and defaced.

In the early days of scientific psychiatry, during the 1800s, many famous German psychiatrists expended a great deal of effort examining the post-mortem brains of patients with schizophrenia (also known at that time as dementia praecox) attempting to demonstrate Wilhelm Griesinger’s theory that “all mental illness is disease of the brain.”

Despite numerous studies, they were unable to replicate the success of studies on dementia, which they linked to specific changes in the brain. So for generations, schizophrenia came to be defined as a condition in which the brain was structurally normal.

This fact was often highlighted by the antipsychiatry movement to suggest that ‘mental illness’ was nothing more than a difference in human experience and there was no medical evidence supporting the work of psychiatrists.

But the fact was also cited by many psychiatrists resistant to the relatively new wave of medications that had appeared on the scene. The drugs were claimed to ‘fix’ the brain with the assumption that the discovery of clear evidence for brain differences would just be a matter of time.

Enter Eve Johnstone and her colleagues at Northwick Park Hospital in London, who, in the midst of this politically charged environment, completed a study that compared CAT brain scans of 18 patients with schizophrenia to a group of healthy control participants. Alongside the scans, the researchers also tested the participants’ mental abilities with psychological tests.

The results were striking. They found the size of the ventricles, the fluid filled spaces in the brain, was, on average, larger in patients with schizophrenia and that it was correlated with the degree of difficulty with tests of memory, concentration and problem solving.

This caused enormous interest and controversy at the time. The paper copy from London’s Institute of Psychiatry library clearly reflects this, as it has been read so many times (and possibly ripped out) that it is virtually in tatters and has been reattached with sticky tape in an otherwise pristine copy of the journal.

There are a few annotations on the page, including the word “Rubbish” written in the margin!

Although seminal, the study has been rightly criticised and one of the major difficulties with these sorts of studies is that because patients are normally taking antipsychotic medication, it’s hard to distinguish where the effect is linked to schizophrenia or the treatment.

While some medication is thought to also thought to affect brain structure, a study on patients that have never taken medication seem to suggest some differences in ventricle size, on average, are still apparent.

The ‘on average’ bit is important though, as these differences are not present in everyone with the diagnosis. They’re just an average difference when you compare a group of people with and without schizophrenia. Furthermore, we’re still not quite sure of its significance.

So the topic is still as controversial as when Johnstone’s study first appeared in 1976, although the argument has shifted from whether differences in the structure of the brain are associated with schizophrenia, to whether they are telling us anything useful.

Link to scan of article from Institute of Psychiatry library.
Link to PubMed entry for same.

A fascinating study just published in the medical journal Pain examined the side-effects reported by patients taking placebos in clinical trials to test migraine drugs. It found that side-effects from placebo were almost as common as from the actual drug, but most interestingly, were specific to side-effects you would expected from the comparison medication.

In other words, the side-effects you get from a sugar pill in a study on anticonvulsant drugs closely resemble side-effects you get from anticonvulsants and are different from the side-effects you get from a sugar pill in a study on pain killers, which more closely resemble pain killer side-effects.

The researchers, led by neuroscientist Martina Amanzio, looked at trials for three type of migraine drugs: NSAIDs (like aspirin), triptans that work on the serotonin system, and anticonvulsant drugs more often used to treat epilepsy.

Side-effects from placebo are known as the nocebo effect and just the combined list of side-effects from the placebo groups in this study is surprising enough:

abdominal pain, anorexia or/and weight loss, attention difficulties, burning or/and flushing, chest discomfort, chills, diarrhea, dizziness, dry mouth, dyspepsia, fatigue, heaviness, injection side reaction, insomnia, language difficulties, memory difficulties, nasal signs and symptoms, nausea, numbness, paresthesia or/and tingling, pharyngitis, somnolence or/and drowsiness, stinging or/and pressure sensation, taste disturbance, tinnitus, upper respiratory tract infection, vomiting, weakness

It turns out that when placebo was being compared to an anticonvulsant, side-effects more common in these drugs – like fatigue, reduced appetite, sleepiness and tingling sensations – were more common in the placebo. In contrast, stomach upsets and dry mouth were more common in the placebo group when the comparison was with NSAID painkillers, which more often cause these symptoms themselves.

One explanation may be that before taking part in a clinical trial, patients are informed of the possible side-effects that the active drug may cause, regardless of whether they are going to be given placebo or the actual medication.

Information on the possible side-effects will be specific to the real medication, and, as we know that expectation plays a big part in the placebo effect, it is probably also shaping the nocebo effect and leading to the production of symptoms through expectancy.

Link to PubMed entry for study.

I’ve just found a curious historical article discussing the early debates over whether anaesthesia could trigger sexual dreams in patients. As this was Britain in the 1800s, much of the fuss was centred on whether the Victorian lady was actually capable of such things:

In January, 1849, a discussion of ‚ÄúChloroform in Midwifery‚Äù occurred during a meeting of the Westminster Medical Society in England. One of the physicians, Dr. G. T. Gream (Obstetrician, Queen Charlotte‚Äôs Lying-In Hospital, London, England) enumerated several reasons why he did not think that chloroform was appropriate for obstetric use, and in so doing, he ‚Äúalluded to several cases in which women had, under the influence of chloroform, made use of obscene and disgusting language. This latter fact alone he considered sufficient to prevent the use of chloroform in English women‚Äù…

In a subsequent issue of The Lancet, notes from the Medico-Chirurgical Society of Edinburgh of February 7, 1849, were published. Sir James Young Simpson (Obstetrician, Edinburgh, Scotland, developer of chloroform anesthesia, and President of the Royal College of Physicians in 1849; 1811–1870) stated that after 15 months of use in thousands of cases, “he had never seen, nor had he ever heard of any other person having seen, any manifestation of sexual excitement result from the exhibition of chloroform…. The excitement, he was inclined to think, existed not in the individuals anesthetized, but was the result of impressions harbored in the minds of the practitioners, not in the minds of the chloroformed.”

Of course, there are some cases of criminal clinicians who have used sedation to attack their patients, but we now know that some modern anaesthetics, particularly midazolam and propofol, really do seem to be involved in causing sexual hallucinations and imagery in patients.

As far as I know, the reason why certain anaesthetics spark sexual imagery is still a mystery.

As we discussed earlier this year, the introduction of anaesthesia was controversial, partly because of the belief that pain was useful in keeping people alive and partly because experiencing pain was considered morally virtuous.

Link to PubMed entry for paper.

I’ve just discovered that the classic James Dean movie Rebel Without a Cause was inspired by a true life account of a psychiatrist’s analysis of a young ‘psychopath’.

According to this 1944 article from Time magazine, the book, called Rebel Without A Cause: The Hypnoanalysis of a Criminal Psychopath, was written by psychiatrist Mitchell Lindner and gave the public “one of the few play-by-play accounts of a psychoanalytic treatment ever published”.

Lindner’s subject is Harold, 21, serving a long term for a serious, unnamed crime. Harold, the son of a bull-tempered Polish laborer who speaks no English, has been in trouble with the police, mostly for pilfering, since the age of twelve. His most conspicuous psychopathic symptom was a constant blinking of his eyes.

Lindner began in orthodox analytic fashion by having the boy lie on a couch and encouraging him to talk freely. (Lindner got his transcript via a microphone concealed in the couch. Told about this at the end of the analysis, Harold himself urged the analyst to publish the record.) Without much hesitation, Harold gave the details of a hair-raising career of gun-toting, stealing, vandalism, fornication. Like all psychopaths, Harold was “a rebel without a cause, a revolutionary without a program,” a grownup infant with no self-restraint and a craving for instant satisfactions.

If you’re puzzled by the term ‘hypnoanalysis’ in the title, it was a form of Freudian psychoanalysis but where the patient was put into a hypnotic trance supposedly to encourage free association and facilitate access to the unconscious.

The idea was that it was a type of cranked up psychoanalysis that could give quicker results but, as the article notes, it was considered rather suspect by the forever orthodox Freudians.

An alternative juiced up version was ‘narcoanalysis’ that typically used barbiturate drugs for the same reason. This was the origin of the truth drug as it was wrongly thought that people hiding the truth might let it slip through if their unconscious was ‘loosened’ somewhat.

The connection between the book and the film seems to be fairly cursory though, as while the movie shares the title and is also about an antisocial young man, it’s otherwise quite different.

Link to 1994 Time article on the book.

The Economist covers an interesting twist on the Turing test for artificial intelligence. Instead of software attempting to fool human judges into thinking they’re chatting to another person, it needs to fool gamers into thinking their playing against a human opponent.

In Turing’s original proposal, human judges would have a text-based conversation with a human and a machine, and the machine would be judged to be artificially intelligent if the judges couldn’t reliably determine who was human.

This is the same principal applied to first person shooter games like Doom, Quake and Call of Duty, where human players need to judge whether their opposite number is a fellow human or just a collection of cold hard data:

Computers can, of course, be programmed to shoot as quickly and accurately as you like. To err, however, is human, so too much accuracy does tend to give the game away. According to Chris Pelling, a student at the Australian National University in Canberra who was one of last year’s finalists and will compete again this year, a successeful bot must be smart enough to navigate the three-dimensional environment of the game, avoid obstacles, recognise the enemy, choose appropriate weapons and engage its quarry. But it must also have enough flaws to make it appear human. As Jeremy Cothran, a software developer from Columbia, South Carolina, who is another veteran of last year’s competition, puts it, “it is kind of like artificial stupidity”.

The competition is called the 2K BotPrize and is currently being held in Milan, Italy.

Link to The Economist on ‘Fighting it out’.
Link to 2K BotPrize website.