Category: Inside the Brain

The New York Times has an excellent article on how the development of new and more focused brain surgery techniques for the treatment of mental illness are leading to a tight-rope situation where doctors are trying to balance enthusiasm for a potential new treatment while avoiding its inappropriate use and bad publicity.

The use of neurosurgery for treatment of psychiatric disorders has a bad name. It is associated with the frontal lobotomy and leucotomy procedures which were carried out in large numbers in the 1940s, 50s and 60s on the basis on poor evidence and with very little oversight.

The dreadful excesses of this era have thankfully passed, and, with an increased understanding of brain circuity, it has been possible to trial the effect of very focused surgical interventions on certain neurological and psychiatric disorders.

Deep brain stimulation (DBS) is the most popular procedure, which is partly because the implanted brain electrode can be very accurately targeted, and partly because, in principle, the effect is reversible as it relies on electrical current for its effect, although the dangers of brain surgery still remain.

Neurosurgical procedures are also being used to permanently alter the brain by making cuts or lesions to specific areas.

This has been used for many years in Parkinson’s disease to treat tremors (the distinctive ‘shaking’) because the circuits that control movement are quite well understand and easy to study because there are many objective and accurate ways of measuring movements.

Although the numbers are still tiny, the same strategy is being increasingly to treat severe mental illness. Searching PubMed for its common scientific name – ‘functional neurosurgery’ – brings up studies where it has been used on everything from addiction to chronic pain.

And this is where people get nervous, because the procedures are quite experimental still and the researchers are well aware of the dangers of being labelled as ‘modern day lobotomists’ if something goes wrong.

As the article nicely outlines, the challenge is not so much the control of symptoms, which is relatively easy, it’s doing this while avoiding of adverse effects, like cognitive impairments, brain damage or additional mental instability.

Link to NYT piece ‘Surgery for Mental Ills Offers Both Hope and Risk’.

Patient HM became famous for having a dense surgically-induced amnesia and taking part in numerous neuropsychology studies that told us a great deal about the structure of memory. He died last year but left his brain to science and Project HM has been set up to co-ordinate the scientific analysis of his brain.

According to a post on the Project blog, the process of dissecting and digitally recording the structure of HM’s brain will begin on Wednesday 2nd December and apparently you’ll be able to watch it live via video streamed from the site.

The best write up of the Project is over at Nature News who have unfortunately jailed their article behind a pay wall. However, here’s the punch line:

On 2 December, exactly one year after Molaison’s death, [Neuroanatomist Jacopo] Annese, of the University of California, San Diego, will begin dividing the brain into roughly 2,400 slices, each thinner than a human hair, and digitizing them. Annese hopes that Molaison’s brain will become the first of many in a digital human-brain library at the university.

Annese is one of the few people with the sophisticated equipment needed to slice whole human brains, which is how he came by Molaison’s brain. Most labs cut human brains into blocks before slicing them ‚Äî the fate that befell Albert Einstein’s brain.

Annese will mount and stain about every 30th slice for cell nuclei and projections, which will allow him to map the cellular architecture in three dimensions. The remaining slices will be available to the neuroscience community, with researchers able to view the particular slice they want to study before requesting it.

Link to Project HM website.

New Scientist reports on a new study on how a gene that gives protection against the deadly brain disease kuru became more common in people exposed to the condition through their cannibalistic tradition of eating the bodies of dead relatives.

Kuru is a prion disease, meaning the damage is caused by a poorly arranged or folded protein molecule which can trigger the same damaging changes in other proteins it comes into contact with.

The condition is related to what we know as ‘mad cow disease’ and causes a distinctive form of shaking, brain degeneration and eventually leads to death. It was restricted to the South Fore people of Papua New Guinea who seemed to pass on the condition by their tradition of to eating deceased relatives at mortuary feasts.

This new study shows that over time a new variant of the PRNP gene emerged in the population which gave protection against kuru.

Because kuru is deadly and was widespread, the emergence of the gene shows evolution in action:

The mutation first arose about 200 years ago by accident in a single individual, who then passed it down to his or her descendants. “When the kuru epidemic peaked about 100 years back, there were maybe a couple of families who found that they and their children survived while all their neighbours were dying, and so on to today’s generation, who still carry the gene,” says Mead. “So it was a very sudden genetic change under intense selection pressure from the disease,” he says.

If you want some background on kuru and how prion diseases affect the brain, you can’t go far wrong with a fantastic Neurophilosophy article from last year.

Link to NewSci on ‘Gene change in cannibals reveals evolution in action’.
Link to abstract of study.
Link to excellent Neurophilosophy article on kuru.

The New York Times has a fascinating article on how surgeons are attempting to treat aggressive and fatal brain tumours by injecting chemotherapy drugs directly into the brain.

One of the challenges for drug makers is that there are many substances that would otherwise have an effect in the brain, but it’s very hard to get them there from the bloodstream because the blood-brain barrier filters out all but the smallest molecules.

The NYT article discusses a technique borrowed from stroke treatment to deliver chemotherapy directly to the tumour or area from where the tumour has been removed.

In certain sorts of stroke a blood clot forms and blocks blood vessels, depriving the brain of oxygen. One important treatment is called thrombolysis where doctors can inject a clot dissolving enzyme through super fine flexible tubes called microcatheters.

They can insert these into a blood vessel in the lower body and then pass them through the the network of veins and arteries until they reach the affected blood vessel in the brain, delivering the ‘clot busting’ enzyme to exactly where it’s needed.

This new technique for brain cancer has apparently borrowed this technology to deliver chemotherapy to a specific area to treat one of the deadlist form of brain tumours – the glioblastoma.

The treatment is still in the research phase, so it’s not clear it has any benefits, but the article is an interesting take on a new approach to treating this condition with a life expectancy of little over a year:

The study, which began in August, is still in its earliest phase, meaning its main goal is to measure safety, not efficacy ‚Äî to find out if it is safe to spray Avastin directly into brain arteries and at what dose. Nonetheless, the doctors were pleased when M.R.I. scans of the first few patients showed that the treatment seemed to erase any sign of recurring glioblastomas. But how long the effect will last remains to be seen…

The complexity of a study like this goes beyond the science. Clinical trials are also a complicated pact, emotionally and ethically, between desperate patients and doctors who must balance their ambition as researchers against their duty as clinicians, and must walk a fine line between offering too much hope and not enough.

Link to NYT piece ‘Breaching a Barrier to Fight Brain Cancer’.

Wired UK has a fantastic investigative article concerning a recent case in India, where, for the first time, an ‘EEG lie detector’ was used to convict a 23-year-old woman of murder.

Aditi Sharma was described as being in a love triangle and her ex-boyfriend died through arsenic poisoning. She maintained it was suicide but the prosecution successfully argued that her and her new boyfriend murdered the ex. The judge apparently felt that the EEG was decisive and revealed ‘experiential knowledge’ which proved her to be guilty.

The general idea does have a scientific basis, but its not widely considered to be anything except a research tool because its never been tested thoroughly enough or proved to be reliable enough to form the basis of legal evidence.

The research version is called the guilty knowledge or concealed knowledge test and is based on the fact that, on average, recognising something you’ve seen before has a distinct EEG waveform when compared to seeing something completely new.

The idea is that the investigator can show you things from the crime scene and just ‘read off’ your brain’s electrical activity and infer whether you were there or not. The technology described in the Indian case apparently uses a technique where statements are read out to the accused, although this is not a common format.

It is currently not admissible as evidence in court, but as the Wired UK article reveals, a similar technology has now been turned into a minor industry in India and there is a shocking acceptance by the legal system that the technology is a genuine ‘lie detector’ – way beyond what anyone has shown reliably in the lab.

The laboratory of the Directorate of Forensic Science in Mumbai has been running Brain Electrical Oscillations Signature (BEOS) tests on criminal suspects for two years. Business is good: when Wired visits, another room is being added to accommodate a second EEG machine, which sits covered in bubble wrap. ‚ÄúWe consider the brain as a computer, where information is stored and can be retrieved,‚Äù explains Sunny Joseph, the lab‚Äôs 33-year-old assistant chemical analyser. The psychology department has two other staff members ‚Äì both in their twenties, both rushed off their feet, with case after case being sent by the courts. ‚ÄúReferral rates have been really high,‚Äù Joseph adds. ‚ÄúWe do possibly 15 cases a month.‚Äù A growing heap of brown-foldered case reports sit in the corner…

A colleague of Joseph’s later points out that brain-imaging allows an overstretched police force to speed up the conviction process by eliminating innocent suspects from their enquiries and by corroborating evidence. That is why Mumbai is not the only Indian city to have invested in BEOS technology. The government’s forensic science directorate in Gandhinagar, in Gujarat, has been using it since 2003 and has now tested 163 subjects in 88 criminal cases. Support came directly from India’s chief forensic scientist, Dr MS Rao. “The technique has great potentiality to become an infallible tool in crime investigation,” he wrote in a paper presented to the All-India Forensic Science Conference in January. “It can become a revolutionary technique like DNA fingerprinting if its evidential strength and judicial acceptability are established.” A third such facility opens soon in the northern Indian city of Chandigarh.

The young lady accused of murder, Aditi Sharma, has apparently been sentenced to life imprisonment on the basis of the technology, although I’ve not been able to find out if there has been an appeal since her sentencing in June.

Link to article ‘The brain police: judging murder with an MRI’.

Full disclosure: I’m a contributing editor to Wired UK and have never been EEG lie-detected.

Discover Magazine has an article on an innovative project to create silicon chips which work like neurons. If you’re thinking these are standard digital chips that run neural network software you’d be wrong, they’re part-analogue devices that are specifically built to emulate the physical operation of brain cells.

The article riffs on the work of neuroscientist Kwabena Boahen who leads the ‘Brains in Silicon’ project.

If you’re not familiar with the difference between analogue and digital calculation it’s worth just briefly getting to grips with it so you can see how revolutionary this project is.

Most computer chips are digital. They encode numbers as lists of 0s and 1s because they are made up of millions of transistors which can switch on (a ‘1’) and off (a ‘0’). The chip can then do operations or maths on the numbers, by flipping the switches, depending on what functions are built-in and how software makes use of them.

So if you wanted to calculate, lets say, how fast a crowd of people walk through a door, you would need to enter numbers for the size of the door, how fast the people are walking, the amount of interference caused by jostling and crowding and your mathematical formulae which ties it all together. The chip would do the calculation, and you would get your answer.

An analogue calculation is more more like a simulation. For example, you might find that ball bearings and a funnel give you a good approximation of the answer. You just change the size of the funnel, the number of ball bearings and the pressure from behind and you just observe what is happening to get the answer. It might not be as pinpoint accurate, but its much easier to build and run.

The traditional approach to artificial neural networks is the first. Each virtual neuron is a mathematical simulation of the electrical and chemical processes and how it influences other virtual neurons. This needs huge amounts of calculations because each of the simulated neurons is mathematically complex and any change means every connected neuron needs also to be recalculated.

This is the approach taken by the Blue Brain Project and it is no accident that they use one of the world’s biggest supercomputers to run the simulation.

This is where Boahen’s project comes in. While the traditional digital approach is very accurate, its very time and energy intensive. While the Blue Brain project needs a warehouse of tech to support it, the actual noisy error-prone brain runs in the space of a bag of Doritos.

So instead of going for the pinpoint accuracy of digital simulation, Boahen has created chips that are an analogue simulation, or really, an analogue emulation of neurons.

As neurons use electrical impulses, much of their function can be described as electrical circuits. In fact, the Hodgkin-Huxley model of the neuron can be drawn as an electrical circuit.

So instead of writing mathematical equations to simulate the circuit and then getting a chip to do the digital calculations, you could just build the circuit. Using the circuit would tell you exactly how the neuron would behave.

Complete neurons are more complex than the simple Hodgkin–Huxley circuit (which just aims to describe the electrical action potential signal) but the same approach applies. Instead of building a chip to run digital simulations of circuits, just build the circuits. The result is noisy, dirty but fast, very low power and good enough Рjust like the human brain.

We covered Boahen’s work back in 2007 and there’s a great talk he did which introduces the project, but the Discover article is a great update on the research which has the potential to turn neurally inspired computing on its head.

It also has loads of background information and is a great introduction to how the brain deals with its noisy and surprisingly unreliable neurons.

Link to Discover article on brain chips.

The Neurocritic has compiled a collection of interesting neurological studies where a number of patients seems to have experienced a profound change in their sexual preferences as a result of brain disturbance.

One of the most well-known of these studies is a recent case of a man who was convicted of paedophilia late in life, but was later found to have a brain tumour, and on removal of the tumour his sudden interest in children disappeared. It reappeared again when the tumour once more began to grow.

The case has raised questions about free will and self-determination in light of the fact that such morally reprehensible acts seemed only to occur when a tumour was affecting brain function.

It’s importantly to mention that brain damage rarely causes such tragic events, although sexual difficulties, in general, are not uncommon. Problems can range from difficulties with arousal and enjoyment, to behavioural disturbances and inappropriate behaviour.

In some rare cases, preferences themselves seem to be affected, although it’s never clear whether it’s actually that the person has different desires, or whether they always had them but now are, perhaps, less able to stop themselves acting on them.

It’s easier to think that damage has changed people’s desires when the behaviour markedly unusual, such as this case of a man who was, to put it bluntly, screwing the coin return tray of a public telephone after brain deterioration.

But one thing we know from the forensic literature and cases of healthy people who accidentally die during sexual practices (for example, these two), is that no matter how strange the attraction seems to you, someone is out there expressing it.

Not all of the cases of changes sexuality after brain damage are where people act outside of the norm, of course. In one, admittedly, not brilliantly detailed case, an apparently exclusively homosexual man found he developed heterosexual attraction after a stroke.

Sadly, this area is massively under-researched so we really know relatively little about how different aspects of desire, emotional attachment and sexual behaviour are handled by the brain, but these case studies give us a window into the possibilities.

Link to The Neurocritic on ‘Unusual Changes in Sexuality’.

I’ve just discovered a curious medical finding that can be detected on MRI brain scans called the ‘face of the giant panda sign’ where, quite literally, it looks like there’s a panda face in the middle of the brain, indicating a specific pattern of neural damage.

The image you can see on the left is the ‘face of the giant panda sign’ that appeared in a brain scan of a patient with multiple sclerosis who started showing unusual sexual behaviour and is taken from a 2002 study. Click the image if you want to see the whole scan.

The pattern is apparently caused by “high signal in the tegmentum, normal signals in the red nuclei and lateral portion of the pars reticulata of the substantia nigra, and hypointensity of the superior colliculus”.

It is most associated with Wilson’s disease, a genetic condition which causes a toxic build-up of copper in the body, but obviously can appear in other disorders as well.

Thanks to Twitter user @sarcastic_f for alerting me to this.

It’s not just pandas that appear in brain scans of course, the Virgin Mary has also been known to make an appearance.

Link to PubMed entry for MS study.
Link to brief description from Neurology.

Technology Review has a fantastic photo essay that tracks how we’ve visualised the brain from times past and includes some of the most stunning images from the last century of neuroscience.

It’s been put together by Mo Costandi, the writer you may know from the Neurophilosophy blog, with each image concisely described so you can get an insight into exactly what you’re seeing.

Link to ‘Time Travel Through the Brain’ photo essay.

BBC News has a fascinating short video report of a robotic hand that is connected to the nerve fibres of an amputated arm and which allows the patient to actually feel touches with the robot fingers.

Although it doesn’t mention it in the report, the technology is from the SmartHand research group who are attempting to use knowledge about the cognitive neuroscience of action and body sensation to make fully integrated naturally controlled prosthetics.

There’s an interesting part of the video where the patient says “When I grab something tightly I can feel it in the finger tips, which is strange because I don’t have them anymore”.

In other words, despite the fact that the robot hand feeds touch information into the nerve fibres into the arm stump, the patient feels the sensations ‘in’ the robot fingers.

This is essentially the ‘rubber hand illusion‘ and the same research group demonstrated exactly this in a recent experiment where they induced touch sensations in a robot hand by stroking it and the stump simultaneously.

This is interesting because a recent study found that sensations in people with intact arms only transferred to a realistic looking rubber hand and not a wooden one, whereas this research team uses a obviously false robot limb.

The fact that touches transfer to an obviously false hand for someone with an amputation but not for people with intact limbs is interesting, because it suggests that brain’s remaining body-image ‘maps’ for the amputated hand may be being recruited to enhance the illusion.

Link to BBC News video report “New robotic hand ‘can feel'”.
Link to SmartHand project.

The latest edition of the Journal of Neuroscience has a fantastic collection of articles by leading neuroscientists who look back on the last 40 years of discoveries in brain research.

The collection is to celebrate the 40th anniversary of the Society for Neuroscience. As the articles make clear, the last four decades have seen a huge expansion in our knowledge of how the brain works and the Society asked leading lights in the field to reflect on this scientific revolution.

Memory and Brain Systems: 1969–2009 by Larry R. Squire [link]

Neurotransmitters, Receptors, and Second Messengers Galore in 40 Years by Solomon H. Snyder [link]

Four Decades of Neurodegenerative Disease Research: How Far We Have Come! by Anne B. Young [link]

A Paradigm Shift in Functional Brain Imaging by Marcus E. Raichle [link]

The Development of Developmental Neuroscience by Carol Mason [link]

The Biology of Memory: A Forty-Year Perspective by Eric R. Kandel [link]

Strictly speaking, they’re not all retrospectives. For example, while Larry Squire gives a whistle-stop tour through the last 40 years of the cognitive neuroscience of memory (and you’ll probably not read a better brief article in this area), Marcus Raichle takes the opportunity to look forward and is clearly enthusiastic about the ‘default network‘ which he is co-credited with discovering.

They’re all academic articles, so are not the most accessible if you’re not familiar with the scientific literature, but as brief guides to some of the major areas of neuroscience they’re fantastic and freely available online.

Science News has a brilliant special issue on the ‘science of slumber’ that tackles sleep disorders, the mental impact of sleep deprivation, how sleep differs across species and the still mysterious question of why we need to sleep.

I found the article on two seemingly straightforward sleep disorders, insomnia and narcolepsy, the most interesting. They seem straightforward because they appear as a lack and an excess of sleep, but as the piece makes clear, they are still quite mysterious.

Insomnia is particularly interesting because having trouble sleeping happens to everyone at some point, so in itself, it’s not abnormal – meaning that research into what triggers it is unlikely to find anything striking.

Instead research has shifted to try and understand what prevents insomnia from resolving naturally so it becomes a chronic condition:

Sleeplessness may be brought on by traumatic events such as a death in the family, an illness such as cancer or anything else distressing, causing a person to lie awake at night with a racing mind. For a subset of people, though, insomnia has no prompting signal — a condition called primary insomnia.

Regardless of the trigger (or lack thereof), temporary insomnia has a nasty way of becoming a habit. Poor sleep habits can become ingrained. When trouble sleeping persists for three or four nights a week over several months, insomnia is considered chronic.

It may turn out that untangling the prompting signals of insomnia, as many sleep researchers attempt, is a fool’s errand, says Michael Perlis, director of the University of Pennsylvania’s Behavioral Sleep Medicine Program in Philadelphia. “The whole zeitgeist has changed,” he says. Most sleep researchers now agree that “once insomnia goes chronic, it stays that way,” regardless of the prompting signal, Perlis says. So rather than focusing on the immediate trigger for insomnia, many scientists are trying to figure out why it becomes chronic and how to prevent that from happening.

I also liked the short piece that briefly compares the amount of type of sleep between lots of different animals. It seems dolphins don’t have REM sleep. I wonder if that means that they lack or have very limited dreams?

Anyway, a great collection of articles and all freely available online.

Link to SciNews ‘Science of Slumber’ collection.

There’s a curious case published in the medical journal Epilepsy and Behavior of a young man who had his epilepsy triggered by the sight of stairs. This would cause seizures that would trigger “repetitive hugging and affectionate kissing of one of the people around him”.

Our patient is currently 24 years old. He is a right-handed male with a history of right temporal lobe epilepsy. He had his first seizure when he was 10 years old. His seizures usually started with an aura of a “feeling” inside his body or abdomen. This feeling, described at times as pain or nausea, lasted a few seconds or a few minutes. His eyes would then widen, he would become confused, and he would look around right and left as if wondering. The seizure would last 1 to 2 minutes with altered consciousness, spitting, and often repetitive hugging and affectionate kissing of one of the people around him.

At times this was followed by head and eye deviation to the left and, sometimes, rotation of the whole body to the left side. Occasionally, he would walk around for a few seconds. These seizures were often precipitated by looking at stairs, whether or not he was walking up the stairs. He learned to avoid looking at stairs to avoid having seizures. He also noted that looking down a flight of stairs did not precipitate his seizures.

I am constantly amazed by both how seizures can be triggered by very specific experiences (such as seeing a certain thing, or hearing a specific sound) and how they can lead to very selective actions.

This is by no means a typical effect of epilepsy but it does raise the interesting question of how these very narrow experiences lead to destabilising brain states which trigger a seizure.

I have heard anecdotal reports from several clinicians that they’ve met patients who can ‘think their way out’ of a seizure by deliberately focusing their thoughts on a specific topic, presumably which reduces the destabilising effect of their original ‘trigger experience’.

I’ve not seen this discussed in the medical literature though, so if you know of any articles that do tackle it, I’d love to hear about them.

Link to PubMed entry for stair triggered epilepsy case.

Electrical readings from seven patients who died in hospital suggest that the brain undergoes a surge of activity at the moment of death, according to a study just published in the Journal of Palliative Medicine.

Palliative care is a medical approach that aims to make dying patients as comfortable as possible. As part of this, doctors from George Washington University Medical Centre’s intensive care unit were using standard alertness monitors for seven patients that include EEG measurements of the frontal lobes.

The monitors are commercial devices designed to help anaesthetists monitor how ‘awake’ patients are, and they combine the electrical readings from the brain into a single signal that reflects alertness.

For each of the seven patients, the researchers noticed that at the point where blood pressure dropped to zero there was a surge in brain activity. The graph on the right is from one of the patients and shows a typical activity burst.

This is not the first time these have been noticed, but previous reports were single cases and the electrical surges were explained away as due to electrical interference from other sources. In these new cases, the doctors could be pretty confident that previously suggested sources of interference weren’t present.

Instead, they suggest that the surge was due to ‘anoxic depolarisation’ – a process where the lack of oxygen destabilises the electrical balance of the neurons leading to one last cascade of activity.

Now, this is just a case series and the neuroelectrical measures aren’t the best. The researchers encourage more systematic research with appropriate tools, but they do suggest an intriguing hypothesis with regard to ‘near death experiences’:

We speculate that in those patients who suffer cardiac arrest who are successfully revived, they may recall the images and memories triggered by this cascade. We offer this as a potential explanation for the clarity in which many patients have “out of body experiences” when successfully revived from a near death event.

One of the difficulties, of course, is that although ‘near death experiences’ are a well-known phenomenon, we only know about them from people who weren’t really dying (or even from people who were never actually ‘near death’ as one of my favourite studies attests).

Nevertheless, neuroscience studies on the dying are likely to be of increasing interest especially as the debate about what counts as death become more prominent.

Link to DOI entry and summary of study.

I just found a curious case study of a man who developed ‘robotic speech’ after being hit by lightning. Rather than the “I am a Dalek!” style mechanical sound it seems to be more like the very. deliberate. and. exact. speech synthesis style, somewhat like Data from Star Trek the Next Generation

Lightning-induced robotic speech

Neurology. 1994 May;44(5):991-2.

To the Editor

Because of a recently observed case, I was intrigued by the communication of Cherington et al[1] concerning lightning encephalopathy. The authors referred to evidence by Critchley[2] that the cerebellum can be selectively injured in lightning-struck patients, Two of their there patients had signs of cerebellar dysfunction. MRI in one of their patients evidenced superior cerebellar atrophy.

The force of a lightning strike threw a 20-year-old roofer to the ground from the truck in which he was standing. Panicked, he immediately began to run. A numbness and weakness of his arms and back cleared after several days, but the more striking abnormality was a profound alteration of his speech, which he described as having become robotic. Each syllable was clearly enunciated with a slight pause between syllables, so that while the flow of his speech was slowed, he was able to communicate well. His speech was actually easier to comprehend than that of some normal persons. His brother had indeed complained that the patient’s premorbid speech had been too rapid and word-jumbled; that speech was transformed to robotic speech, with fine diction and super-clear enunciation. Each morning, his speech was “normal” until shortly after he began to talk, when it reverted to the robotic pattern for the remainder of the day. The neurologic examination was normal except for right upper extremity hypalgesia. Brain MRI was normal.

I considered his robotic-speech problem to be most like the “scanning speech” of cerebellar disease. I have found no references to similar cases, but the reports of selective cerebellar injury by lightning strike[1-3] lead-me to suspect that robotic speech maybe a more common sequel than has been recognized.

Gordan J. Gilbeft, MD
St. Petersbutg, FL

1. Cherington M, Yarnell P, Hallmark D. MRI in lightning encephalopathy. Neurology 1993; 43(7):1437-8
2. Critchley M. Neurological effects of lightning and electricity. Lancet 1934;1:68–72
3. Morocutti C, Spadaro M, Amabile G. TRH treatment in cerebellar ataxia following a lighting stroke. Ital J Neurol Sci 1989;10:531.

The original authors reply and seemed somewhat baffled, saying that it could equally arise from the shock of the experience rather than damage to the brain.

Link to PubMed entry for case study.

The New York Times has an absolutely fantastic article on the psychology and neuroscience of anxiety and how an anxious temperament at birth can ebb and flow during our lifetime.

It’s an in-depth article that really does justice to the topic, looking at extensive research into our anxious states, but also carefully questioning some of the sloppy assumptions of many article where brain activity is described as directly representing mental states.

But having all the earmarks of anxiety in the brain does not always translate into a subjective experience of anxiety. “The brain state does not make it a disorder,” Kagan told me. “The brain state exists, and the statement ‘I’m anxious,’ exists, and the correlation is imperfect.” Two people can experience the same level of anxiety, he said, but one who has interesting work to distract her from the jittery feelings might do fine, while another who has just lost his job spends all day at home fretting and might be quicker to reach a point where the thrum becomes overwhelming. It’s all in the context, the interpretation, the ability to divert your attention from the knot in your gut.

The article is incredibly well written and it tackles a huge range of topics in the understanding of fear and anxiety. Highly recommended.

Link to NYT article ‘Understanding the Anxious Mind’ (via @mocost)