Wednesday, June 29, 2011
But the story behind it is rather spicy.
Back in 2009, a Cambridge group - different authors, but led by "SBC", published a report claiming that people with autism have exceptionally acute vision. Their average visual acuity was claimed to be 2.8
On this scale, 1.0 is defined as normal, and a sharp-eyed young adult with excellent eyesight would get about 1.5. 2.8 means nearly three times as good. Which is, literally, superhuman - a bird of prey would be happy with that. The paper was titled "Eagle-Eyed Visual Acuity In Autism".
However, what followed was straight out of the Book of Obadiah - "Though you soar like the eagle ... from there I will bring you down, sayeth the Lord". Or in this case, sayeth two experts in visual acuity research, Bach and Dakin, whose qualifications included the fact that they wrote the software used in the original study, which is online here.
They wrote a knock-down critique, arguing that the results were a result of using the wrong settings, which meant that the task was extremely easy. In fact, even perfect performance would only correspond to an acuity of less than 1.
You could never make a test so hard that it would require an acuity of 3.0 on a standard computer. Pixels are just too big. A single pixel is easy to spot, for someone of normal-ish vision. The only way to make it harder would be to use a special, extremely high-res monitor, or to get people to sit a long way from the screen.
So how did a result of nearly 3.0 come out? Because they also turned on data extrapolation, basically saying that if you really aced the easy task, you'd probably do quite well on a harder one. This might be sensible in some situations, but it breaks down when the task was so easy. The autistics seemed to have super vision because they got, say, 99% right, as opposed to 98%.
Yet the present paper represents a happy ending as it's written by a combined team of Cambridge people, and Bach and Dakin as well, although the lead authors of the original weren't on it. This time, they used appropriate methods - they got people to sit 4 meters from the screen. To be extra sure, they also gave everyone an eye exam before testing.
And they found no difference at all. The present paper is heartening - rather than grimly sticking to their guns, they admitted their error.
This story should however serve as a cautionary tale; I previously wrote about the fact that in science, a little mistake can cause a lot of problems. This is one of those cases, although arguably there were two seperate mistakes, but one, the extrapolation, was only a problem because of the main mistake, the big pixels.
Tavassoli T, Latham K, Bach M, Dakin SC, & Baron-Cohen S (2011). Psychophysical measures of visual acuity in autism spectrum conditions. Vision research PMID: 21704058
Tuesday, June 28, 2011
A new paper aims to trawl medical records to work out how well depressed patients responded to treatment. The authors used Natural Language Processing or NLP (not that NLP) to interpret electronic medical records from over 5,000 patients treated at hospitals in New England. Each record included notes taken at multiple visits.
A crack team of "three experienced board-certiﬁed clinical psychiatrists" reviewed the notes and provided a "Gold Standard" classification as to whether patients were Depressed, Recovered or Intermediate at each visit. The problem here is that they didn't actually see the patients, they just had the notes. If the notes were bad, the result will have been bad too. Garbage In, Garbage Out. Even if you then put a big gold medal on the garbage.
They then found that an NLP algorithm was able to learn how to duplicate the expert opinion, based on the words used in the notes. Using a machine learning approach they were able to teach the computer that if the text contained the word "depressed", it was a sign that the patient was depressed while "much better" was associated with being... guess.
In fairness, it's not a bad attempt to turn text into numbers, and in future it could allow you to do interesting things such as comparing two drugs in terms of which ones make people "much better".
I'm concerned about this though. The essence of the original, narrative notes, is that they contain individual information about that patient's story. You could go through them with a computer and calculate what happens to the average patient given a certain drug. That might be useful information. But if you did that as a replacement for reading about individual patients, you'd be missing the whole point of the narrative notes.
Worse, as this kind of thing becomes feaisble it will feed back on itself and encourage clinicians to write their notes -and therefore to think, inevitably - in machine-readable terms. The authors suggest as much:
As more health care systems move to electronic medical records, there is a unique opportunity to better quantify outcomes. For example, the 16-item patient-rated QIDS-SR [questionairre] has been shown to be highly correlated with clinician-rated measures and sensitive to treatment eﬀects.... At minimum, EMR systems that utilize templates could require clinicians to record a clinical status for example, using the 7-point Clinical Global Impression scale...Indeed, many say that this already is happening. Now quantification is generally a good thing I think, but only so long as it's an aid to understanding, not a replacement for it.
Yet quantification often does become a replacement for understanding because there's a trap that we face when trying to deal with a complicated set of information. The temptation is to focus on the easiest bit to measure, because that's easy, and then assume that this represents the state of the whole thing. The reason that something's easy to measure is often because it doesn't capture the whole phenomena.
Perlis RH, Iosifescu DV, Castro VM, Murphy SN, Gainer VS, Minnier J, Cai T, Goryachev S, Zeng Q, Gallagher PJ, Fava M, Weilburg JB, Churchill SE, Kohane IS, & Smoller JW (2011). Using electronic medical records to enable large-scale studies in psychiatry: treatment resistant depression as a model. Psychological medicine, 1-10 PMID: 21682950
Saturday, June 25, 2011
Here's an article summarizing the original piece. The author's the head of a British think tank, but not a specialist in mental health, so he's probably a good example of the ''intelligent layman":
Neither – in relation to the fastest rising [mental health] diagnoses – is there any evidence of chemical imbalances in the brains of patients. In other words, the problem the [psychiatric] drugs are supposed to solve is an illusion.
There's no evidence of fairies in my garden, either. The concept of a 'chemical imbalance' in the human brain is one of the most fantastic oversimplifications in science, and one of the worst legacies of the modern pharmaceutical industry.
A bowl of soup could have a chemical imbalance. If you're making a chicken broth and you accidentally put in an extra spoonful of coriander, it'll taste horrible. Not enough salt, and it'll be bland. A soup is simple: too much or too little of one thing, and it comes out wrong.
Or...does it? Actually, flavour isn't just the sum of the ingredients. You might put in some extra coriander, and also put in some chilli powder, and that would end up delicious whereas if you left the coriander the same, it would be overwhelmed by the chilli. But you'll need to rethink the paprika as well...
Soups are pretty complicated.
The brain is a restaurant with a hundred billion tables. At each table sits a food critic. An army of chefs prepares an infinity of soups - no two are the same, although some areas of the restaurant tend to get certain kinds - and a legion of waiters serves them up, collects the old bowls and takes them to the kitchen to be washed and refilled.
Each critic has his own preferences. If she gets the right soup, she'll be happy. One soup will be great for one critic, disgusting to another. Some critics demand an ever-changing series of courses, others want the same thing day in day out.
Whether the restaurant gets a good review will depend on the composition of the soups, of course, but on so much else as well: are they delivered on time? Do the waiters collect the empty bowls quickly enough - or do they do it too fast, snatching soup away before it's been eaten? Who are the critics, anyhow?
This is still far too simple. In fact, the waiters and the chefs and the dishwashers are the critics, and how they do their job depends on what soup they're getting. That depends on how they've done their jobs in the past... and everyone's also a musician, playing their part in a symphony that we can't hear and couldn't begin to understand if we did.
Our technology for investigating the chemistry of the brain is comically crude. We can't even take a sample of all of the soups in the whole restaurant, mix them all up and measure their average ingredients. You can do that in animals, but for ethical reasons, not in humans. No-one has ever measured the chemical composition of a living human brain.
We can approximately measure a few very common ingredients. After death we can measure a few more. We can also do a kind of straw poll of critics to see what they like, but we don't know which particular critics answer it, or what soups they are in fact being served. Every month, someone discovers a whole new ingredient.
We can sneak into the kitchen and chuck some spice into the pots, to see what kind of noise the critics make. We can't hear what they're saying, we can only measure the volume from different parts of the restaurant. Some of the most informative studies come from measuring the composition of the waste that gets thrown out in the bins every night.
So next time someone confidently tells you that mental illness either is, or isn't, a chemical imbalance, ask them - which one?
1. The addict did not get the right treatment
2. Treatment was not personalized
3. The addict did not get involved with a follow up program
4. The addict only underwent a thirty day rehabilitation process
5. The addict returned to old friends
6. The addict returned to old habits
7. The addict was not committed totally to treatment
8. The addict did not receive support from important family members, which could be a parent or a child
9. The addict did not take the treatment seriously
10. The addict did not learn and adapt to the tools and resources provided while in the treatment center.
There are other reasons that are too many to mention here, but substance abuse relapse is something that can be avoided if all of the above reasons are addressed properly.If the addict had to go through an outpatient treatment program, then it is likely that this could also cause relapse because the addict will have structure within the program, but outside of the program, there is no way that they can be supervised. This is difficult for all involved; the addict, the therapist and family members. Outpatient treatment allows the addict to go on with some type of normal life and keep their jobs and be with their families. However, it has its disadvantages because the addict who is recovering is able to still be around the same friends that influenced them. Of course, drug addiction treatment is a choice and the therapist can tell the addict not to hang around these people, but cannot force them to do so. In fact, the therapist is not aware of the addict's external activities unless it is mentioned during therapy.
Family members who are afraid of substance abuse relapse should lend a hand in ensuring that their loved one does not cling to those that are a bad influence to them during their treatment process. Those addicts who have gone through numerous treatment programs and returned to their old destructive habits will find that it is like a revolving door and family members get tired of the same old story and want to move on and forget about everything. However, family members cannot do this or they will be contributors of a destroyed life. They should probably think about an aggressive intervention that will either allow the individual to accept rehabilitation or reject it.
In the rehab center, the addict needs to stick close to other residents who are doing well. They can both support each other and motivate each other to keep focused so that they can experience full recovery. All it takes is encouragement to stay on the course that has been set by the therapist for the addict. It calls for willpower and the strength of God in order to make it to complete recovery.
Friday, June 24, 2011
The pair may come from the same publisher (Princeton), but they couldn't be more different.
Blind Spots is a good book. It tells a story in a clear and compelling fashion, which is what a book is for.
The story is that we often act unethically, not because we're faced with ethical questions and decide to pick the "bad" option, but because we fail to see that there is an ethical issue at all.
This is not the same as saying that 'the road to hell is paved with good intentions'. That old phrase warns against trying to be good and, as a result, causing evil, because your plans go wrong. Blind Spots is saying, even if all of your attempts to be good work out just fine, you might still cause evil despite that.
For example, you could be a good employee, who never calls in sick unnecessarily, kind to your friends and colleagues, and a generous charity donor.
Unfortunately, you're an accountant connected to Enron, and your work - ultimately - consists of defrauding innocent people. But of course, you don't think of it like that, because we don't tend to think about things "ultimately".
Which is hard to disagree with. At worst, you could say it's obvious, although I think it's still something we ought to be reminded of. That's not all there is to the book, though: it also discusses how this happens and suggests ways to avoid it within organizations.
For example, the authors give an example of how setting up rewards and punishments to "make people be ethical", can make them less so, by encouraging people to think of the issue as a personal trade-off between gain and loss, rather than an ethical dilemma - what the authors call "ethical fading".
A day-care centre was annoyed at the fact that some parents were picking up their children late. This was antisocial because it meant staff had to work late into the evening.
So they started charging parents a late fee. Not a big one, but enough to send people a message: this is wrong, don't do. But in fact what happened was that late pickups became more common.
Previously, many people were making an effort to be on time, as a matter of principle. Once the fees were in place, it stopped being an ethical issue and just became a financial trade-off: is it worth paying the fee to get an extra hour?
Of course, you could make the fees higher to get around this, but even then, you've caused ethical fading, and you'll be relying on the sanctions from that point on.
Braintrust, by contrast, is just not a good read. The bulk of the book consists of discussions of various neurotransmitters and brain areas and how they may be related to human social behaviour. Oxytocin, for example, may make us behave all trusting and kindly, as it's involved in maternal bonding. There's a long discussion of the neurochemistry of male sexual behaviour in voles.
It's not clear how this is relevant to ethics. Whether it's oxytocin that does it, or something else, and whether voles are a useful model of human behaviour or not, clearly sometimes we trust people and sometimes we don't. That's psychology. And biology can't yet explain it.
Churchland doesn't claim that the various biological concepts that she covers can fully explain anything, and she doesn't vouch that all of these findings are rock solid. Which is good, because they can't, and they're not. So why spend well over half of the book talking about them?
Churchland's big idea seems to be that human morality emerges out of our more general capacity for sociability. Hence all the stuff about oxytocin and "the social brain". OK. But I'd have said that's a given - there's obviously some relation between sociability and morality.
I think there is an interesting idea in here, albeit not very clearly expressed, namely that morality isn't a special function of the brain, but just one of the many forms in which our social cognition can take.
In other words, I think the claim is that ethics isn't just related to sociability, it is sociability. Even asocial animals care about their own welfare, in terms of pleasure and pain; social ones become social when they extend this caring to others; intelligent social animals including humans and maybe some primates also have a system for inferring the motivations and thoughts of others.
At the end of the book, Churchland stops reviewing neuroscience, and starts talking about the implications for philosophy. This is best section of the book, but it's too short.
Churchland makes the interesting point, for example, that when we are considering philosophical "ethical dilemmas", like the famous trolley problems, we may not be applying any kind of ethical "rules" as such. Rather, she thinks that our moral reasoning is pretty much a kind of pattern recognition based on previous experience - like all our other social reasoning.
Someone who'd just read a book about the horrors of Stalinism might tend to adopt an anti-consequentialist, every-life-is-sacred approach. Whereas if you'd just watched a movie in which the hero, reluctantly but rightly, decides to sacrifice one guy to save many other people, would do the opposite. Then the ethical "rules" might be confabulated to cover it.
This is a nice idea. It's open to criticism, but it's a serious suggestion, and one that deserves a decent discussion. Sadly, there isn't one. If only there were more room in the book for this kind of stuff - but oxytocin covers so many pages.
Basically, the good parts of this book are not about the brain at all.
Reading Braintrust is like going on date but then bumping into an annoying friend who insists on coming along for dinner. Jesus, The Brain, you want to say. I like you and all, but seriously, you are getting in the way right now.
Links: Other blog reviews.
Thursday, June 23, 2011
His defence is that he was drunk and/or high. Which from the video he fairly obviously was. But here's an interesting quote from his lawyer:
Some things may have come out of his mouth that didn’t come from his brain.So where did they come from, then... hmm. Don't answer that.
I doubt that the lawyer was actually trying to say that Galliano's mouth was moving of its own accord or under the control of some other organ. Rather she was expressing the idea that "my brain" in this context doesn't mean, literally, the whole of the grey blob of neurons in my skull.
Rather "my brain" means, roughly, "that part of my brain responsible for rational thought".
My grandmother once talked about a friend who'd had a stroke. She said, as far as I can remember, "Sometimes the stroke means you can't talk or walk, which is bad enough, but sometimes it gets into your brain and that can be really nasty."
Of course she knew that all strokes happen in the brain. What she was saying was that some strokes, but not all, affect the part of the brain responsible for "me" as a person - thoughts, emotions, and so forth.
So, this is all anecdotal evidence, but there seems to be a popular, common-sense temptation to believe in the "me part" of the brain, a tendency which neuroscientists are not immune to and which can lead to dubious conclusions.
I'd love to see someone do a proper study of what non-neuroscientists, ideally people with little exposure to neuroscience like children, think about the brain. A bit like this, but really in depth. I suspect that you'd find that many of the ideas underpinning today's neuroscience had their origins in pre-scientific, common sense intuitions.
We neuroscientists are human, and we have neuro-intuitions too. But if neuroscience has taught us anything, it's not to trust those.
Tuesday, June 21, 2011
A new study from Simon Baron-Cohen and colleagues asked pretty much this question, although rather than California, they looked at Eindhoven in Holland. Eindhoven is the tech hub of the Netherlands:
This region contains the Eindhoven University of Technology, as well as the High Tech Campus Eindhoven, where IT and technology companies such as Philips, ASML, IBM and ATOS Origin are based... 30% of jobs in Eindhoven are now in technology or ICT, in Haarlem and Utrecht this is, respectively, 16 and 17%The authors found that official rates of diagnosed autism amongst children enrolled in Eindhoven schools were more than twice as high as those in kids from the comparison cities of Haarlem and Utrecht. In Eindhoven, rates of any autism spectrum disorder were 2.3%, far higher than rates elsewhere (0.6-0.8%).
Narrowly defined "classical autism" was also higher. However, two control disorders, dyspraxia and ADHD, were no different.
A diagnosed autism prevalence of 2.3% is extremely high. Some recent studies have found similar figures when you actually go out and attempt to find undiagnosed cases and diagnose them. But for 2.3% of kids to already have a diagnosis, is remarkable.
Unfortunately, there's a big problem here, which is that this study has a sample size is 3. There were lots of data from each city: in total, 369 schools took part, with over 60,000 kids. But there were only three independent cities.
So while these data convincingly show that Eindhoven has higher rates of autism than the other two regions, this might just mean, say, that half of Dutch cities have local educational systems that promote diagnosis, and Eindhoven happens to be one of them.
To really answer the question of whether I.T. folk have more autism, you'd need to look at Silicon Valleys around the world, to increase your sample size.
I'd be surprised if there weren't a link. Autism is highly heritable and we know that the children of people with autism, or mild autistic traits, have a higher rate. I don't think it's too controversial to say that the average programmer has above-average autistic traits, and it's quite possible that a little autism is a positive advantage in IT professions.
This is certainly Baron-Cohen's hypothesis, as he's long argued that people with autism have a tendency to be strong "systematizers":
This striking difference in the prevalence of ASC is in line with the hyper-systemizing theory, and will require the phase two study using diagnostic assessments and screening methods, to determine the exact nature of regional differences in population prevalence. Future research should test if this higher prevalence in a high tech region is found in other cultures (e.g., in Silicon Valley, California)...
Roelfsema MT, Hoekstra RA, Allison C, Wheelwright S, Brayne C, Matthews FE, & Baron-Cohen S (2011). Are Autism Spectrum Conditions More Prevalent in an Information-Technology Region? A School-Based Study of Three Regions in the Netherlands. Journal of autism and developmental disorders PMID: 21681590
Monday, June 20, 2011
Image of the week is this adorable, if anatomically not quite accurate, model of the brain which you can buy. It even has little eyes! This is not new, but what did come out this week was Google's image recognition search, which is how I found out about it.
You've probably heard of Bipolar 1 and 2, but 4 and 6? They're the next big thing, says a guy who's published no fewer than 155 papers in a journal he edits, as The Neurocritic reports.
What if autism Isn't a Neurodevelopmental Disorder? but rather a disorder caused by ongoing neurobiological processes in later life?
According to the BBC, children tend to be similar to their parents, presumably due to shared genes and/or environments. OK, they said that parents influence teenage drinking habits, but this is all the study showed. And maybe not even that. Not a great piece of journalism.
Two books about ethics are reviewed: Patricia Churchland's Braintrust is reviewed here while Blind Spots is covered here. I'm currently working on a joint review of both books so I won't comment further at this stage.
European neuroscientists including David Nutt warned this week that mental health research faces funding cuts, as pharmaceutical companies pull out of the psych market. It's certainly true that Pharma currently funds much of this research, however whether this has helped or hindered the progress of neuroscience and psychiatry is debatable.
"For the first time researchers have monitored the brain as it slips into unconsciousness", apparantly. Actually, people have been doing that for over 60 years, but this time around they did use an interesting new neuroimaging method.
Psych Your Mind blog has a list of psychology-based songs. Kind of. But it doesn't include any songs from the classic "The Mind's I", the only melodic death metal album named after a book about the nature of conciousness. Well, so far the only one. Rumours that In Flames are working on "Consciousness lost and found: A neuropsychological exploration" remain unconfirmed.
I can't read everything. So any tipoffs will be gratefully received. Either leave them in a comment or drop me an email.
Saturday, June 18, 2011
A walk through the narrow street of the Shah Wali Qataal area to see Shahrukh Khan’s ancestral home and hear some fascinating stories about the family from Munni, his first cousin
By Arshad Yusufzai
Bollywood superstar Shahrukh Khan is a household name in the subcontinent, but not many people are aware of his family’s origins.
It is none other than Peshawar, the oldest city in the region and home to other legendary actors and actresses like Prithviraj Kapoor, Raj Kapoor, Anil Kapoor, Dilip Kumar and Madhubala.
Shahrukh Khan’s father Taj Mohammad Mir belonged to Peshawar and lived in the old, walled part of the city before migrating to Delhi.
To reach the ancestral family home, one has to go through a narrow street of the Shah Wali Qataal locality on the back of the historic Qissa Khwani bazaar. This was once the bazaar of storytellers where travellers would be regaled with stories of chivalry and romance over cups of green tea. Now the place is congested with street shops selling pottery, shampoos, soaps and other cosmetics.
Shopkeepers in the street know about Shahrukh’s family house but are reluctant to tell its exact location. A labourer working in the nearby bamboo-ladder making workshops was kind enough to guide me and point to the dark and narrow lane on the left side of the entrance to the local mosque. “Come I will show you the house but don’t tell the family. The owners don’t like anyone showing visitors their house,” he politely requested.
The dilapidated four-story house where Shahrukh’s father, four uncles and aunt spent their childhood is situated at the dead end of the narrow street. A shirtless man in his mid-30s opened the big wooden doors painted in green on the second knock. He introduced himself as Javed Ahmad Mir, Shahrukh’s cousin. He led us through the narrow steps to the first floor where his sister Noor Jehan aka Munni and her three children lived. Javed Mir’s two brothers Mansoor Ahmad Mir and Farooq Ahmad Mir also lived in the house.
The top floor of the house has been damaged and its structure weakened due to repeated bomb blasts conducted by militants in the locality and was demolished a year ago. Still there is enough room to accommodate the four families.
Noor Jehan, commonly known as Munni, tells that her uncle Taj Muhammad Mir studied at the Edwardes College Peshawar before migrating to Delhi because he found harassment of his family at the hands of the police unbearable. “My father and uncles were staunch supporters of united India. My father was an active member of Khan Abdul Ghaffar Khan’s ‘Khudai Khidmatgar’ movement. Shahrukh’s father also actively participated in the ‘Quit India’ movement and was arrested on several occasions for delivering speeches against the British colonial rule,” she said.
Noor Jehan, who has served as an elected lady councillor in the city, said the police harassed the family so much that her uncle Taj Mohammad Mir one day decided to leave Peshawar and go to some faraway place in India. According to Noor Jehan, Taj Mohammad Mir ended up in Delhi and married Lateef Fatima, the daughter of Major General Shahnawaz Khan, a freedom fighter of the Indian National Army and an aide to the legendary Subhash Chandra Bose.
Noor has fond memories of her first meeting with the 13-year old Shahrukh, when he came to Peshawar with his father in 1978. “I was only 10 when I first met Shahrukh, he stayed in Peshawar for 22 days. I cannot forget the time we spent playing all day long,” she fondly recalls.
A year later, Shahrukh again visited Peshawar with his father and sister Shahnaz Lalarukh. “This time Shahrukh stayed at our home for a month and we thoroughly enjoyed his company, those were happy days,” she says.
Shahrukh’s two visits to Peshawar in 1978 and 1979 were before he started acting. The would-be King of Bollywood made his acting debut in a television series, ‘Fauji’ in 1988. After the death of his mother in 1991, Shahrukh moved to Mumbai where he made his film debut with the commercially successful ‘Deewana’ in 1992 — and there was no looking back!
Eighteen years after their last meeting with Shahrukh and his sister Shahnaz Lalarukh, Noor Jehan decided to visit her cousins in India. In 1997, she and her husband Asif Shahab arrived at the given address in Delhi only to find out that Shahrukh had moved to Mumbai.
“We had lost contact with Shahrukh after the death of our uncle in 1982 and did not know that he shifted to Mumbai. I called on the phone number that I got from the family living in Shahrukh’s old Delhi house and was relieved to hear Lalarukh’s voice on the other side,” said Noor.
And they hurried to Shahrukh’s Mannat (bungalow) in Mumbai. Shahrukh was on outdoor shooting for ‘Duplicate’ when they arrived at his Mumbai home. “I could not wait to see him but it was only at 2:15am that he came home. He was surprised to see me and shouted “Oye Munni tu kab aayi (O Munni when did you come!).” We talked for the next three hours till five in the morning,” she recalls with teary eyes.
Noor said that despite his busy schedule Shahrukh found time to be with her and her husband. “Shahrukh and Shahnaz took us to a number of places in Mumbai. He would also take us to his film shootings and introduce me to everyone as his sister from Peshawar. I met producer Yash Johar, his son Karan Johar, Juhi Chawla and Sonali Bandre during the shooting of ‘Duplicate’,” she revealed.
Interestingly, Noor tells us that the Peshawari chappal that Shahrukh wore in ‘Kal Ho Na Ho’ and the shalwar kameez he adorned in ‘Kuch Kuch Hota Hai’ were both presents that she gave to her superstar cousin. “Shahrukh told us he would love to wear Peshawari chappal so we sent him a pair along with a shalwar-kameez of the locally-famous China Boski fabric,” she said.
Meeting with his favourite actor was so exciting for Asif Shahab that he took his wife Noor Jehan again to Mumbai in 1998 and stayed there for over a month. The couple even named their first-born child as Shahrukh Khan after his superstar uncle.
The 10-year old Shahrukh Khan is a big fan of his Indian uncle. His desire to meet his hero SRK hasn’t been fulfilled yet because his four-year-old brother Shahreer Khan is too young to travel. Besides, as the couple argued, the relations between India and Pakistan for the past few years following the Mumbai attacks in 2008 have not been favourable for such visits. “I wish to visit my uncle but we are unable to go there as my little brother is very young. My mother says we have to wait for a few more years before we could visit India,” Shahrukh Khan junior said.
Asked if he wanted to become a movie star like SRK, he said that he loved his uncle and his movies but did not want to become an actor. “I love his movies, especially ‘Rab Ne Bana Di Jodi’ but I don’t wish to become an actor. I want to play cricket and become famous like Boom Boom Afridi,” he says with a sparkle in his eyes.
Both the families are in contact with each other via phone or the Internet. However, Noor said their communication with each other was limited due to their busy lives. “Shahrukh is a busy person. He cannot spare too much time to talk on the phone and Internet. I am also busy in too many things around here in Peshawar as a former councillor,” she said.
Friday, June 17, 2011
Back then, I said:
TDDD has been proposed in order to reduce the number of children being diagnosed with pediatric bipolar disorder... many people agree that pediatric bipolar is being over-diagnosed.Now, a bunch of psychiatrists have written to the Journal of Clinical Psychiatry to express their concerns over the proposed diagnosis. They make the same point that I did:
So we can all sympathize with the sentiment behind TDDD - but this is fighting fire with fire. Is the only way to stop kids getting one diagnosis, to give them another one? Should we really be creating diagnoses for more or less "strategic" purposes?
We believe that the creation of a new, unsubstantiated diagnosis in order to prevent misapplication of a different diagnosis is misguided and a step backward for the progression of psychiatry as a rational scientific discipline.Although they go into much more detail in critiquing the evidence held up in favor of the idea of TDDD. They also point out that it is rather optimistic to think, as some people apparantly do, that if we were to diagnose kids with TDDD, as opposed to childhood bipolar, we'd save them from getting nasty bipolar medications.
As they say, the risk is that drug companies would just get their drugs licensed to treat TDDD instead. Same drugs, different label. It would be fairly easy: just for starters, there are plenty of sedative drugs, such as atypical antipsychotics, which would certainly alter or mask the "symptoms" of TDDD, in the short term. Doing a clinical trial and showing that these drugs "work" would be easy. It wouldn't mean they actually worked, or that TDDD actually existed.
They also point out that the public perception of child psychiatry has already been harmed by the proposal of TDDD, and would suffer further if it were to become official.
Well, of course it would, and quite rightly so. That would be a sign that child psychiatry is so out of control that, literally, the only way it can stop diagnosing children, is to diagnose them with something else!
The same issue of the the same journal features another paper, claiming that "pediatric bipolar disorder" has a prevalence rate of 1.8%, and that rates of diagnosis of childhood bipolar are not higher in the USA than elsewhere, contrary to popular belief based on evidence.
Their data are a bunch of epidemiological studies on bipolar disorder. One of which included children up to the age of...21. The majority included kids of 17 or 18.
So, er, not children at all, then.
The older the "children" in the study, the more bipolar that study found. Everyone knows that bipolar disorder typically starts in late adolescence. That's the orthodoxy and it has been since Kraepelin. It's right there at the top of the Wikipedia page. That's not pediatric bipolar, that's just normal bipolar.
All the recent controversy is about bipolar in children. As in, like, 8 year olds. Yet this paper is still titled "Meta-analysis of epidemiologic studies of pediatric bipolar disorder". The senior author on this paper also signed the paper criticizing TDDD.
This, then, is the state of the debate over the future of our children.
P.S. I've just noticed that in the latest draft of DSM-V, TDDD has been renamed. It's now called "DMDD". What's next? DUDD? DEDD? P-DIDDY ?
Axelson DA, Birmaher B, Findling RL, Fristad MA, Kowatch RA, Youngstrom EA, Arnold EL, Goldstein BI, Goldstein TR, Chang KD, Delbello MP, Ryan ND, & Diler RS (2011). Concerns regarding the inclusion of temper dysregulation disorder with dysphoria in the DSM-V The Journal of clinical psychiatry PMID: 21672494
Van Meter AR, Moreira AL, & Youngstrom EA (2011). Meta-analysis of epidemiologic studies of pediatric bipolar disorder. The Journal of clinical psychiatry PMID: 21672501
Thursday, June 16, 2011
It is easy to spot drug addiction. Anyone that participates in using illegal drugs such as heroin, cocaine, methamphetamine, and marijuana has a problem. These drugs are not legal, and any use warrants a problem. Some addictions are worse than others, however, and at any stage of the addiction you need treatment. Catching it before the addiction gets out of control may make overcoming it that much easier.
Once it has been decided to seek treatment, there are many different styles of treatment. People can attend support groups like Narcotics Anonymous, go to individual counseling, attend outpatient treatment centers, or check into an inpatient treatment center. When deciding on what drug rehab program is the best, a professional can help diagnose the situation and provide a plan for a course of action.
Once the course has been plotted and the detoxification process has been completed, an addict will head to a rehab program to get better. These programs will help the addict overcome their issue and get ready to live a productive, functioning life once again. Following a treatment program at a rehab center will be easy with all the great support that is provided through professional, caring staff.
Don't let drug addiction ruin the lives of people you love. This disease is treatable, and untreated, you may be living your life without that person. There are various treatment programs that will work better for certain people, and a professional will help you assess the best choice for the situation.
With the available drug rehab program options, there is no reason why an addict can't get better.
The patient "M. S." was a previously healthy 29 year old Israeli graduate student who suffered injuries in a terrorist attack. As the MRI scans above show, she lost large parts of her orbitofrontal cortex and ventromedial prefrontal cortex, although the left side was only partially affected. She also lost her right eye.
These areas are known to be involved in emotion and decision making. Her lesions are somewhat similar to those suffered by the famous Phineas Gage, and as we'll see, her symptoms were too - but only temporarily.
One year after the injury...
M.S.’s complaints included a sense of general fatigue, loss of taste and smell, difﬁculty concentrating and emotional changes including irritability, lability, depression and social isolation. She reported failing to make new social contacts, having lost most of her old friends, and a diminished need for social relationships.These personality and mood changes are reminisicent of those Phineas Gage suffered. Strangely, she scored 33 on the self-report depression scale the BDI, which corresponds to "severe depression", but from the description she doesn't sound depressed in the normal sense. These scales were not designed for people with brain lesions. Her cognitive function and memory was mostly normal but with clear impairments on some tests.
M.S. reported that family and friends commented on her change from a quiet and pleasant person to a rude, annoying, uninhibited, and unstoppable talkative person following the injury... M.S. had become apathetic, without a sense of time, and with no plans for the future.
On examination, M.S. was fully cooperative. She had difﬁculty concentrating and required frequent breaks. She appeared euphoric, laughed frequently and inappropriately, talked too much,made inappropriate remarks and jokes, yawned loudly... M.S. found it difﬁcult to sit still and showed utilization behavior, continuously ﬁdgeting and touching objects on the table. She had a tendency to continue performing tasks after completion was stated.
Anyway, that was after 1 year, and if that were the end it would be a rather sad story, but there's a happy ending. After this she got psychotherapy and rehabilitation treatment. 7 years later she had a follow-up assessment and she was much improved.
Her mood, attention-span and so forth were reported as normal. She struggled with her graduate studies, finding them more difficult than before the injury, and had eventually quit them, but she'd got a new job. She had recently got married.
Her performance on neuropsychological tests designed to measure prefrontal cortex damage was mostly normal, and she did much better on the ones that she used to be impaired on. She still did poorly on the Iowa Gambling Task, which is very sensitive vmPFC damage.
Overall, though, she had made a "magnificent" recovery despite losing a large chunk of her brain. I've previously been skeptical of some of the stronger claims of neuroplasticity or "brain remodelling", but some parts of the brain are more plastic than others and the prefrontal cortex seems to be one of the most flexible.
Fisher T, Shamay-Tsoory SG, Eran A, & Aharon-Peretz J (2011). Characterization of recovery and neuropsychological consequences of orbitofrontal lesion: A case study. Neurocase, 17 (3), 285-93 PMID: 21667397
Tuesday, June 14, 2011
The authors propose that consciousness may be associated, not with activation in any given area of the brain, but with recurrent information processing between areas, a kind of neural ping-pong.
When presented with sensory information, say the sight of an object, signals travel up through the brain from "primary" sensory areas to "higher" areas associated with more complicated processing. They call this the Fast Feedforward Sweep, or "FFS". Maybe not the best acronym.
Anyway, depending on the nature of the stimulus, this can lead to activation in almost any part of the brain. However, they say that it's not enough to generate consciousness; only if the later areas feedback to the earlier areas, and start a recurrent processing loop, does this happen.
This stands in contrast to the popular view, which seems to fit with common sense, that primary areas are unconscious and that consciousness is directly associated with activity in the higher areas, in particular, the prefrontal cortex (PFC).
The authors refer to fMRI and EEG studies showing that even "high level" processes, such as selective attention to stimuli, and inhibition of an action, can be triggered by subconscious cues, and that this is associated with activation in the prefrontal cortex - unconscious activation.
The details of these studies are fairly arcane but the point is that the prefrontal cortex is generally agreed to be the most developed, "highest level" part of the brain. If anywhere in the brain was going to be the seat of the soul, it's the PFC.
This shouldn't come as a surprise, though. While it's tempting to look for a part of the brain which "does" conscious experience - the "me module" - Daniel Dennet pointed out a while ago that this temptation is motivated by a fundamental confusion.
Likewise, while it seems common sense that conciousness is the "highest mental function" and therefore must be located in the highest brain area, this is a presumption: consciousness is a mystery, and we don't know if it's a high level function or not, or whether that question even makes sense.
Nor should the fact that consciousness isn't an inevitable consequence of high-level cognition come as a shock: in fact, that would be impossible. As Ryle pointed out in The Concept of Mind, this would create an infinite regression. Any conscious experience has to come from somewhere.
Right now I'm concious of choosing certain words rather than others in typing this post, in a conscious attempt to make it read better. But I'm not aware of all of the rules and experiences that guide my choices. I just feel that some words work. This feeling seems to come out of nowhere, or rather, out of the words themselves.
It isn't, of course, it's a product of calculations taking place in my brain, but I've no idea what they are. I wouldn't want to be, either: I'm too busy typing.
van Gaal S, & Lamme VA (2011). Unconscious High-Level Information Processing: Implication for Neurobiological Theories of Consciousness. The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry PMID: 21628675
Monday, June 13, 2011
After holding out for years, on the grounds that I "don't have time to spend on Twitter", I have given in and joined Twitter: http://twitter.com/#!/Neuro_Skeptic.
I still don't think I have time for it, but I guess we'll find out.
Please note that I'm Neuro_Skeptic, not "neuroskeptic", who is someone else entirely.
Sunday, June 12, 2011
Image of the week is this rather striking picture showing that slime moulds love to digest herbal sleeping tablets. This makes sense, because slime moulds are well known to experience severe insomnia. Because they're moulds, and moulds don't sleep.
Story of the week is that evolutionary biologist and writer Steven J. Gould relied on dodgy statistics in his classic book about race, science and intelligence, The Mismeasure of Man. That's according to a new paper, and there are excellent blog discussions here and here. Gould's to my mind the greatest science writer of all time. But you can write well without always being right.
Many neuroscience and psychology studies could be flawed because the "healthy controls" are just too healthy. This is a serious issue which doesn't get discussed enough.
Did dinosaurs sleep during the day, or the night? Until we get a working time machine, we'll never know for sure, but by examining the shapes of the eyes of different species, a new study has shed light on this question.
Studying psychology at university is not a good idea if you want to get a high salary, according to an upcoming paper.
An interesting legal case from the U.S: judge overturns federal law to impose less than the minimum sentence in a child pornography case. According to Forensic Psychologist blog, the ruling contains discussions of everything from neuroimaging to the arguments over DSM-V.
Psych Your Mind blogger posts his 'favourite' anonymous peer review judgements, along with the suggestion that psychology reviewers seem to be especially vicious compared to those in other fields.
British doctors, charities, and politicians all agreed that antipsychotic drugs are being over-used in dementia this week. Which is something, because they don't agree about anything else right now. I previously blogged about how an earthquake in Italy caused a spike in local elderly people getting these drugs.
The LA Times has an excellent piece on the attempts to build prosthetic limbs with a sense of touch. We've already got artificial retinas, but an artificial sense of touch is even harder, because it requires implanting electrodes directly into the brain.
Mind Hacks discusses a major study into Alzheimer's disease, conducted with the help of a Columbian family with a hereditary form of the disorder.
I can't read everything. So any tipoffs will be gratefully received. Either leave them in a comment or drop me an email.
Saturday, June 11, 2011
The authors trawled the French records of drug side effects from 1985 to 2008. By law, doctors in France must report any adverse event which is either serious, or unexpected, to the authorities.
They found a total of 540 reports mentioning "violence", but only 56 of these were clear-cut incidents of physical aggression towards others. Suicide and self-harm were not included, unless they also involved violence to other people.
There were 76 suspect drugs (because some reports included one or more). Here's the Hall of Shame:
16 reports involved benzodiazepines (Valium) or similar drugs.
13 implicated dopamine-boosting drugs used to treat Parkinson's disease.
4 were caused by serotonin-based antidepressants like Prozac. Older antidepressants were not associated.
Antipsychotics and anti-epileptics were also high on the list.
There were also reports involving and the antiviral drugs interferon (3), ribavarin(2), and efavirenz (3); the stop-smoking aid varenicline (4); anti-acne drug isotretinoin (4); and the banned weight-loss drug rimonabant (2). All of these can also cause depression, and I've blogged about some of them before for that reason.
Of the perpetrators, 86% were men. Nearly half had a prior psychiatric history, but that's not surprising because many of these drugs are prescribed to people with mental illness.
In terms of the number of reports of violence relative to the total number of adverse events for each drug, Parkinson's drugs were "worst". However, this doesn't mean much, because it might just mean that these drugs are generally mild in terms of side effects.
So it's an interesting dataset, but it's impossible to come to any firm conclusions as to how common these effects really are. Cases might go unreported if they're thought to be "normal" violence; and regular violence could also get wrongly blamed on a drug - criminals get sick too.
Finally, we ought to remember while these effects are inherently attention-grabbing (and Parkinson's drugs in particular have given rise to some tabloid-friendly stories), the overall rate was tiny - less than 3 cases per year, for all prescribed drugs, in a nation of over 60 million people.
Rouve N, Bagheri H, Telmon N, Pathak A, Franchitto N, Schmitt L, Rougé D, Lapeyre-Mestre M, Montastruc JL, & the French Association of Regional PharmacoVigilance Centres (2011). Prescribed drugs and violence: a case/noncase study in the French PharmacoVigilance Database. European journal of clinical pharmacology PMID: 21655992
Friday, June 10, 2011
There has been lots of research on mice who carry the same genes associated with autism in humans. Rats and recently monkeys have been studied as well. But the possibility of autistic pigs has been strangely neglected by science.
A new paper might just change that: Characterization of porcine autism susceptibility candidate 2 as a candidate gene for the number of corpora lutea in pigs. The authors found that, in female pigs, variation in a certain gene affects the function of the ovaries.
The corpus luteum is a little yellow blob (technically speaking) in the ovary. Its job is to secrete progesterone. Women's ovaries grow a new one during every menstrual cycle, and it normally breaks down and disappears before the period. However, if you get pregnant, the corpus luteum sticks around and continues producing that hormone.
Pigs, like many animals, can have more than one of these per ovary and it turns out that one of the genes controlling the number is a homolog of the human gene AUTS2. AUTS2 mutations are linked to autism (hence the name), smoking and mental retardation. The authors of this paper found several variants in this gene in domestic pig populations, and they show that it's expressed in the pig ovary.
It's quite a long leap from porcine lady bits to autism, I would say, but this actually does make sense, if you accept the Extreme Male Brain theory of autism. Boys are at least four times more likely to have autism than girls, and some say that masculinizing hormone testosterone may be the reason. This study fits with that, given that progesterone is a female hormone. Maybe mutations in AUTS2 gene alter sex hormone production?
On the other hand, it might be a coincidence. AUTS2 is strongly expressed in the brain, as well as the ovaries. Maybe it's just required for cell function, and if it's mutated, cells stop working normally: whether they be in the brain, or the corpus luteum.
Either way, it would be interesting to see whether AUTS2 affects pig behaviour... but I'm not sure what an autistic pig would look like.
Sato S, Hayashi T, & Kobayashi E (2011). Characterization of porcine autism susceptibility candidate 2 as a candidate gene for the number of corpora lutea in pigs. Animal reproduction science PMID: 21641132
Thursday, June 9, 2011
The first thing that leaps out is that "mental" is redundant. What other kind of distress is there? Distress is mental, by default.
This awkward wording seems to be a result of the fact that it's an attempt to fuse some of the features of "mental illness" with some of the implications of "distress", a kind of verbal alchemy. What is mental distress? It's not mental illness, but it's not exactly not mental illness.
Fair enough. Mental illness is a problematic concept, so I'm all in favor of rethinking it. But I'm worried. My worry is that "mental distress" takes the worst features of mental illness and perpetuates them in the guise of being a new and radical idea.
Were I to go around making sweeping statements about "the mentally ill" or "people with mental illness", someone would call me out on it, like this - Mental illness is an umbrella term, for all kinds of different experiences! You can't talk about all those people as if they're the same. They're individuals!
Which is quite right.
But it's equally bad to talk about "mental distress" in the same way, and this happens as well. I don't know if mental distress is more often used as a blanket statement, but it's certainly not immune and it's no better. See for example the top Google hit for mental distress:
The first signs of mental distress will be different for the onlooker than it is for the person in distress...Perfectly true, of some people. Not all. In this paragraph "mental distress" seems to mean "bipolar disorder", but in the course of the article it morphs into several other forms. All mental distress.
Changes in sleep patterns are a common sign, and appetite may also be affected. Lethargy, low energy levels, feeling antisocial and spending too much time in bed may indicate the onset of depression. Wanting to go out more, needing very little sleep, and feeling highly energetic, creative and sociable, may signal that a person is becoming 'high'.
The first time it happens, the effects of hearing or seeing things that other people don't are likely to be especially dramatic...
It's not good enough to make sweeping statements and say "...Of course, everyone is different, but..." That's a cop-out, not a serious attempt to be helpful. It's like being really offensive, and then quickly adding "No offence". If you think everyone's different, talk about them all differently.
I think there's a good case to be made that we shouldn't talk about "mental illness" at all. Take, say, bipolar disorder, social anxiety, and antisocial personality. I'm really not sure that these have anything in common.
They've only been considered to belong to the single category of "psychiatric disorders" for about 50 years. 100 years ago, bipolar was insanity, social anxiety was a character trait, or a 'nervous' problem, and antisocial behaviour was just evil. Different professionals dealt with each one, and few thought of them as being linked.
I'm not saying that we should go back to that. But categories are up for debate. "Mental distress" is a new label, but it's a 50 year old category.
My second problem is that "mental distress" implies that everyone who has it, is distressed. But they're just not - at least not if you're using that term as a replacement for "mental illness".
If you're bipolar, and in a manic or hypomanic episode, you might well be the opposite of distressed. More subtly, if you're severely depressed, you might be too low to be distressed. "Distress" implies an acute emotional response. Severe depression paralyses the emotions.
Maybe "mental distress" isn't like normal everyday distress. Maybe mania or depression are mental distress, but not distress. But that's rather confusing. If mental distress isn't distress, what on earth is it? You can't redefine words like that, unless you're Humpty Dumpty.
"Are you mentally distressed?"
"No, I'm fine. I'm just distressed."
It would also lead to even more people being treated in the mental health system. Already we're told that 1 in 4 people experience mental illness, but almost everyone gets distressed now and again.
You might say that you don't consider mental distress to be a form of pathology. I'm against medicalization! Mental distress isn't an illness! If so, fine, but to be consistent, you're going to have to stop talking about treatments. And causes. And symptoms. Those are all medical words. Discussions of mental distress are chock full of them.
Indeed, if you want to demedicalize "mental distress", you should probably just call it... distress. The "mental" part is a hangover from "mental illness", after all. If you're serious, you ought to junk that and stick with distress.
This would be perfectly clear, it doesn't require us to redefine words or use awkward phrases. Let's give it a go: "Mental illness" is distress. Easy. Unfortunately, when you put it like that, it looks a bit like a sweeping oversimplification, doesn't it? Hmm.
On the other hand, if you're not looking to demedicalize mental illness, why throw out the word illness?
The problem is that many people like the sound of demedicalization, but they're not sure how far they want to go. And in large organizations, some people will want to go much further than others.
Mental health charities seem to be particularly prone to this, so you often see them assuring people that "mental illness is an illness like any other", while simultaneously saying that seeing it just as a medical illness is far too narrow and unhelpful!
This is a serious debate, and it deserves a careful discussion. The compromise term "mental distress" seems to bridge this gap, and allows people with very different views to sound like they're agreeing with each other. This is not the best way to resolve debates like this. People still disagree with each other. They just lack the words to talk about it.