The Prefrontal Cortex Is Holistic

The question of whether the brain is "modular" - whether different parts do different things - has been a neuroscientific talking point since the days of the phrenologists.

They were the guys who believed that, not only were there modules, but that you could tell how big they were by measuring the shape of someone's skull, and so learn about their personality.

Phrenology made modules unfashionable for a while, but today they're back, and most of fMRI consists in trying to find areas of the brain that do different stuff, but in a new paper Wilson et al argue against taking modularism too far: Functional localization within the prefrontal cortex: missing the forest for the trees?

Their focus is the prefrontal cortex (PFC), a large chunk of the front of the brain which is bigger in humans than in any other species. The PFC is routinely subdivided into segments, each with (presumably) a different function. So we have the "emotional" vmPFC, the "memory" dlPFC, the "pleasure" OFC, etc.

Wilson et al don't dispute that there are some variations in function between different bits of the PFC, but they say that in all the excitement over localization, we may have overlooked the role of the PFC as a whole.

They discuss evidence from monkeys with PFC damage (or lesions which disconnect it from the rest of the brain). Damage to the entire PFC, they say, leaves monkeys completely unable to perform tasks which require storing concepts over time. For example, they can't learn that whenever they see, say, a red button, they ought to press it to get food. But if part of the PFC is intact, and it doesn't matter which part, monkeys can do this with only minor problems.

However, the PFC isn't required for all tasks. If the task only involves information which is all presented at once, the lesioned monkeys are OK. So they could learn, given a big panel covered in red buttons, to push the buttons to get food, because the buttons are all there simultaneously.

Hence the data from these tasks are congruent with the notion that [the PFC] is only crucial in memory during tasks requiring the processing of temporally complex events. This can be defined as an event to be learned about, in which information that is crucial to that learning is presented at more than one point in time, or that can only be interpreted with respect to a preceding event.

They say that evidence from human neuroimaging studies supports this view.

A meta-analysis has shown consistent recruitment of the same network of regions in the PFC across a range of cognitive demands. The authors argue that this supports specialization of function within the PFC, but of an unexpected nature, namely ‘a specific frontal-lobe network that is consistently recruited for solution of diverse cognitive problems’. The idea that large and different regions of the PFC are recruited by any task at hand supports our argument that the function of the PFC as a whole exceeds the sum of the functions of its subcomponents.

This all has echoes of Karl Lashley, an early neuroscientist (died 1958) who proposed the theory of "mass action" - that the whole cortex contributes to behaviour, rather than each part doing different things ("modularism").

Jerry Fodor, whose classic book The Modularity of Mind (1983) helped to rehabilitate modularism from its reputation as "phrenological", was also an advocate of this view - within limits.

Fodor argued that some brain systems, like vision, hearing and language, were cortical modules, but that above this, there was a non-modular system which was the basis for thought, intelligence and decision making. If I remember correctly, he didn't explicitly say that the prefrontal cortex was this system, but I'm sure he'd have no objections to Wilson et al's account.

Wilson CR, Gaffan D, Browning PG, & Baxter MG (2010). Functional localization within the prefrontal cortex: missing the forest for the trees? Trends in neurosciences PMID: 20864190

The Prefrontal Cortex Is Holistic

The question of whether the brain is "modular" - whether different parts do different things - has been a neuroscientific talking point since the days of the phrenologists.

They were the guys who believed that, not only were there modules, but that you could tell how big they were by measuring the shape of someone's skull, and so learn about their personality.

Phrenology made modules unfashionable for a while, but today they're back, and most of fMRI consists in trying to find areas of the brain that do different stuff, but in a new paper Wilson et al argue against taking modularism too far: Functional localization within the prefrontal cortex: missing the forest for the trees?

Their focus is the prefrontal cortex (PFC), a large chunk of the front of the brain which is bigger in humans than in any other species. The PFC is routinely subdivided into segments, each with (presumably) a different function. So we have the "emotional" vmPFC, the "memory" dlPFC, the "pleasure" OFC, etc.

Wilson et al don't dispute that there are some variations in function between different bits of the PFC, but they say that in all the excitement over localization, we may have overlooked the role of the PFC as a whole.

They discuss evidence from monkeys with PFC damage (or lesions which disconnect it from the rest of the brain). Damage to the entire PFC, they say, leaves monkeys completely unable to perform tasks which require storing concepts over time. For example, they can't learn that whenever they see, say, a red button, they ought to press it to get food. But if part of the PFC is intact, and it doesn't matter which part, monkeys can do this with only minor problems.

However, the PFC isn't required for all tasks. If the task only involves information which is all presented at once, the lesioned monkeys are OK. So they could learn, given a big panel covered in red buttons, to push the buttons to get food, because the buttons are all there simultaneously.

Hence the data from these tasks are congruent with the notion that [the PFC] is only crucial in memory during tasks requiring the processing of temporally complex events. This can be defined as an event to be learned about, in which information that is crucial to that learning is presented at more than one point in time, or that can only be interpreted with respect to a preceding event.

They say that evidence from human neuroimaging studies supports this view.

A meta-analysis has shown consistent recruitment of the same network of regions in the PFC across a range of cognitive demands. The authors argue that this supports specialization of function within the PFC, but of an unexpected nature, namely ‘a specific frontal-lobe network that is consistently recruited for solution of diverse cognitive problems’. The idea that large and different regions of the PFC are recruited by any task at hand supports our argument that the function of the PFC as a whole exceeds the sum of the functions of its subcomponents.

This all has echoes of Karl Lashley, an early neuroscientist (died 1958) who proposed the theory of "mass action" - that the whole cortex contributes to behaviour, rather than each part doing different things ("modularism").

Jerry Fodor, whose classic book The Modularity of Mind (1983) helped to rehabilitate modularism from its reputation as "phrenological", was also an advocate of this view - within limits.

Fodor argued that some brain systems, like vision, hearing and language, were cortical modules, but that above this, there was a non-modular system which was the basis for thought, intelligence and decision making. If I remember correctly, he didn't explicitly say that the prefrontal cortex was this system, but I'm sure he'd have no objections to Wilson et al's account.

Wilson CR, Gaffan D, Browning PG, & Baxter MG (2010). Functional localization within the prefrontal cortex: missing the forest for the trees? Trends in neurosciences PMID: 20864190

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Big Pharma Explain How To Pick Cherries

Here at Neuroskeptic, we see a lot of bad science. Maybe, over the years (all 2 of them) that I've been writing this blog, I've become a bit jaded. Maybe I'm less distressed by it than I used to be. Cynical, even.

But this one really takes the biscuit. And then it takes the tin. And relieves itself in it: A New Population-Enrichment Strategy to Improve Efficiency of Placebo-Controlled Clinical Trials of Antidepressant Drugs.

Don't worry - it's from a big pharmaceutical company (GlaxoSmithKline), so I don't have to worry about hurting feelings.

It's is full to bursting with colourful graphs and pictures, but the basic idea is very simple. As in "simpleton".

Suppose you're testing a new drug against placebo. You decide to do a multicentre trial, i.e. you enlist lots of doctors to give the drug, or placebo, to their patients. Each clinic or hospital which takes part is a "centre". Multicentre trials are popular because they're an easy way of quickly testing a drug on a large number of patients.

Anyway, suppose that the results come in, and it turns out that the drug didn't work any better than placebo, which unfortunately is what happens rather often in modern trials of antidepressants. Oh dear. The drug's crap. That's the end of that chapter.

...or is it?!? say GSK. Maybe not. They have a clever trick. Look at the results from each centre individually. Placebo response rates will probably vary between centres: in some of them, the placebo people don't get better, in others, they get lots better.

Now, suppose that you just chucked out all of the data from centres where the people on placebo got much better, on the grounds that there must be something weird going on in those ones. They reanalyzed the data from 1,837 patients given paroxetine or placebo, across 124 centres. In the dataset as a whole, paroxetine barely outperformed placebo. However, in the centres where people on placebo only improved a little, the drug was much better than placebo!

Well, of course it was. Imagine that the drug has no effect. Some people just get better and others don't. Let's assume that each person randomly gets between 0 and 25 better, with an equal chance of any outcome. Half are on drug and half are on placebo, but it makes no difference.

Let's further assume that there are 50 centres, with 20 people per centre (1000 people total). I knocked up a "simulation" of this in Excel (it took 10 minutes). Here's what you get:

The blue dots show, for each imaginary centre, drug improvement vs. placebo improvement. There's no correlation (it's random), and, on average, there is no difference: both average out at 12 points. The drug doesn't work.

The red dots show the "Treatment Effect" i.e. [drug improvement - placebo improvement]. The average is 0 - because the drug doesn't work. But there's a strong negative correlation between Treatment Effect and the placebo improvement - in centres where people improved lots on placebo, the drug worked worse.

This is exactly what Glaxo show in Figure 1a (see above). They write:

The analysis of the surface response indicated the predominant role of center specific placebo response as compared with the dose strength in determining the Treatment Effect of paroxetine.

But of course they correlate. You're correlating placebo improvement with itself: the "Treatment Effect" is a function of the placebo improvement. It's classic regression to the mean.

Of course if you chuck out the centres where people on placebo do well (the grey box in my picture), the drug seems to work pretty nicely. But this is cheating. It is cherry-picking. It is completely unscientific. (To give the authors their due, they also eliminated the centres where the placebo response was very low. This could, under some assumptions, make the analysis unbiased, but they don't show that this was their intention, let alone that it would eliminate all of the bias.)

The authors note that this could be a source of bias, but say that it wouldn't be one if it was planned out in advance: "in order to overcome the bias risk, the enrichment strategy should be accounted for and pre-planned in the study protocol." This is like saying that if you announce, before playing chess, that you are going to cheat, it's not cheating.

To be fair to the authors, assuming the drug does work, this method would improve your chances of correctly detecting the effect. Centres with very high placebo responses quite possibly are junk. Assuming the drug works.

But if we're assuming the drug works, why are we bothering to do a trial? The whole point of a trial is to discover something we don't know. The authors justify their approach by suggesting that it would be useful for drug companies who want to do a "proof-of-concept" trial to find out whether an experimental drug might work under the most favourable conditions, i.e. whether they should bother continuing to research it.

They say that such trials "are inherently exploratory in their conception, aimed at signal detection, open to innovation..." - in other words, that they're not meant to be as rigorous as late-stage trials.

Fair enough. But this method is not even suitable for proof-of-concept, because it would (as I have shown above in my 10 minute simulation) increase your chance of finding an "effect" from a drug that doesn't work.

Whatever the truth is, this method will give the same result, so it's not useful evidence. It's like saying "Heads I win, tails you lose". You've set it up so that I lose - the coin toss doesn't tell us anything.

All of the author's results are based on trials in which the drug "should have worked": they do not appear to have simulated what would happen if they used this method on trials where it didn't work, as I just did. So I'm doing Pharma a big favour by writing this post, because if they adopt this approach, they're more likely to waste money on drugs that don't work.

They should be paying me for this stuff.

Merlo-Pich E, Alexander RC, Fava M, & Gomeni R (2010). A New Population-Enrichment Strategy to Improve Efficiency of Placebo-Controlled Clinical Trials of Antidepressant Drugs. Clinical Pharmacology and Therapeutics PMID: 20861834

Big Pharma Explain How To Pick Cherries

Here at Neuroskeptic, we see a lot of bad science. Maybe, over the years (all 2 of them) that I've been writing this blog, I've become a bit jaded. Maybe I'm less distressed by it than I used to be. Cynical, even.

But this one really takes the biscuit. And then it takes the tin. And relieves itself in it: A New Population-Enrichment Strategy to Improve Efficiency of Placebo-Controlled Clinical Trials of Antidepressant Drugs.

Don't worry - it's from a big pharmaceutical company (GlaxoSmithKline), so I don't have to worry about hurting feelings.

It's is full to bursting with colourful graphs and pictures, but the basic idea is very simple. As in "simpleton".

Suppose you're testing a new drug against placebo. You decide to do a multicentre trial, i.e. you enlist lots of doctors to give the drug, or placebo, to their patients. Each clinic or hospital which takes part is a "centre". Multicentre trials are popular because they're an easy way of quickly testing a drug on a large number of patients.

Anyway, suppose that the results come in, and it turns out that the drug didn't work any better than placebo, which unfortunately is what happens rather often in modern trials of antidepressants. Oh dear. The drug's crap. That's the end of that chapter.

...or is it?!? say GSK. Maybe not. They have a clever trick. Look at the results from each centre individually. Placebo response rates will probably vary between centres: in some of them, the placebo people don't get better, in others, they get lots better.

Now, suppose that you just chucked out all of the data from centres where the people on placebo got much better, on the grounds that there must be something weird going on in those ones. They reanalyzed the data from 1,837 patients given paroxetine or placebo, across 124 centres. In the dataset as a whole, paroxetine barely outperformed placebo. However, in the centres where people on placebo only improved a little, the drug was much better than placebo!

Well, of course it was. Imagine that the drug has no effect. Some people just get better and others don't. Let's assume that each person randomly gets between 0 and 25 better, with an equal chance of any outcome. Half are on drug and half are on placebo, but it makes no difference.

Let's further assume that there are 50 centres, with 20 people per centre (1000 people total). I knocked up a "simulation" of this in Excel (it took 10 minutes). Here's what you get:

The blue dots show, for each imaginary centre, drug improvement vs. placebo improvement. There's no correlation (it's random), and, on average, there is no difference: both average out at 12 points. The drug doesn't work.

The red dots show the "Treatment Effect" i.e. [drug improvement - placebo improvement]. The average is 0 - because the drug doesn't work. But there's a strong negative correlation between Treatment Effect and the placebo improvement - in centres where people improved lots on placebo, the drug worked worse.

This is exactly what Glaxo show in Figure 1a (see above). They write:

The analysis of the surface response indicated the predominant role of center specific placebo response as compared with the dose strength in determining the Treatment Effect of paroxetine.

But of course they correlate. You're correlating placebo improvement with itself: the "Treatment Effect" is a function of the placebo improvement. It's classic regression to the mean.

Of course if you chuck out the centres where people on placebo do well (the grey box in my picture), the drug seems to work pretty nicely. But this is cheating. It is cherry-picking. It is completely unscientific. (To give the authors their due, they also eliminated the centres where the placebo response was very low. This could, under some assumptions, make the analysis unbiased, but they don't show that this was their intention, let alone that it would eliminate all of the bias.)

The authors note that this could be a source of bias, but say that it wouldn't be one if it was planned out in advance: "in order to overcome the bias risk, the enrichment strategy should be accounted for and pre-planned in the study protocol." This is like saying that if you announce, before playing chess, that you are going to cheat, it's not cheating.

To be fair to the authors, assuming the drug does work, this method would improve your chances of correctly detecting the effect. Centres with very high placebo responses quite possibly are junk. Assuming the drug works.

But if we're assuming the drug works, why are we bothering to do a trial? The whole point of a trial is to discover something we don't know. The authors justify their approach by suggesting that it would be useful for drug companies who want to do a "proof-of-concept" trial to find out whether an experimental drug might work under the most favourable conditions, i.e. whether they should bother continuing to research it.

They say that such trials "are inherently exploratory in their conception, aimed at signal detection, open to innovation..." - in other words, that they're not meant to be as rigorous as late-stage trials.

Fair enough. But this method is not even suitable for proof-of-concept, because it would (as I have shown above in my 10 minute simulation) increase your chance of finding an "effect" from a drug that doesn't work.

Whatever the truth is, this method will give the same result, so it's not useful evidence. It's like saying "Heads I win, tails you lose". You've set it up so that I lose - the coin toss doesn't tell us anything.

All of the author's results are based on trials in which the drug "should have worked": they do not appear to have simulated what would happen if they used this method on trials where it didn't work, as I just did. So I'm doing Pharma a big favour by writing this post, because if they adopt this approach, they're more likely to waste money on drugs that don't work.

They should be paying me for this stuff.

Merlo-Pich E, Alexander RC, Fava M, & Gomeni R (2010). A New Population-Enrichment Strategy to Improve Efficiency of Placebo-Controlled Clinical Trials of Antidepressant Drugs. Clinical Pharmacology and Therapeutics PMID: 20861834

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MAI UM LINDO MIMOSO PRESENTE RECEBIDO DA LUCIA.

Parabéns Sandra Feliz Aniversário!!!

Publicado em 22 de setembro de 2010 por Lúcia

Hoje é o dia da Sandra receber todo carinho do

mundo e muitos presentes fofinho ela está de

aniversário PARABÉNS SANDRA!!!

http://sandraandrade8.blogspot.com

MAIS PRESENTES DE ANIVER...OBRIGADA CRIS.
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Presente para Sandra - Blog Curiosa

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Parabéns amiga Sandra do blog Curiosa... mais um ano de vidaaa... festaaaaaaa!!! Este é o meu mimo para vc, é simples mas de coração, espero que gostes... fiz com mto carinho! E que Deus te abençoe e ilumine teus caminhos... Beijinhosssss

LINDO PRESENTE RECEBIDOS DO WILSON E DA SAN.

Presente para o blog "Curiosa."

Presentinho para minha amiga do blog "Curiosa" Parabéns, que seu blog permaneça por muito tempo nos trazendo alegrias. Com muito carinho Wilson.

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Muitos Parabéns!!!
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e que vc alcançe tudo aquilo que sempre quis:)

Muitas felicidades amiga!!
Este é o meu presente para vc!
Fiz com maior carinho! Espero que goste:)

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Sociopathic Dementia

Frontotemporal dementia (FTD) is a tragic, but scientifically fascinating, disease.


FTD only accounts for a small fraction of dementias in total (estimates range from 2% to 10%), but it typically strikes people aged in their 50s or 60s, i.e. much earlier than the average for Alzheimer's disease, the most common cause of dementia. As a result, FTD accounts for a large proportion of early-onset cases.

The symptoms are different to those of Alzheimer's, at least in the early stages. Memory problems and confusion are not prominent. Nor are hallucinations and delusions, which are seen in 20% of Alzheimer's, but only 2% of FTD.

Instead, patients often present with language problems - either forgetting what words mean, starting with uncommon words and progressing to easy ones ("semantic dementia"), or losing the ability to articulate speech ("nonfluent aphasia").

But the most disturbing effects are behavioural and personality changes. These are not seen in all cases, but in some people (the "behavioural variant"), they are the main symptom. Patients may begin to act entirely out of character, including criminal acts.

Aggressive behaviour is also sometimes seen in Alzheimer's, but it's usually associated with confusion or hallucinations: people "don't know what they're doing". In FTD, patients can commit serious crimes even though their cognitive function is pretty much intact: they do know what they're doing.

Mario F. Mendez discusses this in a new paper, The Unique Predisposition to Criminal Violations in Frontotemporal Dementia, and asks whether people who commit crimes while suffering from FTD should be considered legally responsible for their apparantly "sociopathic" actions. He presents 4 case histories.

Patient 1: A left-handed male in his sixties began stalking and attempting to molest children for the first time in his life. He followed children home from school and tried to touch them... On another occasion, he stood at the foot of a pool and stared at the children for a prolonged time.

When he exposed himself to his neighbor’s children, he was arrested. The patient did not deny his actions, could describe them in detail, and endorsed them as wrong and harmful. Despite this, he stated that he did not feel that he was causing harm at the time of his acts.

The patient’s personality had deteriorated over the prior four years, with decreased concern for others, disinhibition, and compulsive hoarding. He had caused disturbances at work, such as intruding into others’ conversations and walking into others’ offices... constantly pilfering... hiding money.... In addition, he ate indiscriminately, even going through waste containers and eating garbage. He stopped showering and wore the same clothes every day.

Neuropsychological testing and brain scans suggested early FTD, and his mother had reportedly suffered unspecified dementia; FTD is often genetic. He was not prosecuted. This case has a lot in common with the man who became a pedophile after surgery for a brain tumour: not just the pedophilia, but other symptoms like compulsive hoarding, over-eating, etc.

Patient 4: A right-handed man in his early fifties had a hit-and-run accident and left the scene without concern. He had struck a van with passengers but kept driving. The police stopped him a short distance away from the scene, and he did not deny his action.

Leaving the scene of an accident was not characteristic of his premorbid personality, yet he had had several recent traffic violations... He could recall and describe the accident, knew that it was wrong to leave the scene, but did not feel the need to stop at the time.

Over the prior two years, the patient’s pervasive behavior had significantly changed. He had become disengaged and emotionally detached; for example, he did not react to the death of his mother...

He was no longer embarrassed over passing gas or belching in public or appearing partially clothed in front of others. The patient had a tendency toward hyperorality, especially for peanuts, and had a decline in personal hygiene. Other aspects of the history included dysarthria and a recent tendency to choke on liquids.

This patient showed clear signs of motor neuron disease, which occurs in up to 15% of FTD cases. He died, as a result of the progression of the motor neuron disease, one year later, after developing other symptoms of FTD. His death meant he could not be tried for the hit-and-run.

Mendez notes that legally, these patients would probably not qualify for the "insanity defence". Under the British M'Naghten Rules, also adopted by the USA, the defendant is only eligible if they were

labouring under such a defect of reason, from disease of the mind, as not to know the nature and quality of the act he was doing; or, if he did know it, that he did not know he was doing what was wrong.

These patients do not fit that bill.

Finally, why does FTD cause sociopathic behaviour? Mendez says that it is because it involves degeneration of the vmPFC, linking FTD patients to the classic case of Phineas Gage whose vmPFC was destroyed by a flying iron rod. But Gage, while he did show personality changes, actually managed to function fairly well in society.

So temporal lobe degeneration probably also contributes to the FTD behavioural syndrome, especially since many of the symptoms (like compulsive eating) are seen in monkeys with temporal lobe lesions.

Mendez MF (2010). The unique predisposition to criminal violations in frontotemporal dementia. The journal of the American Academy of Psychiatry and the Law, 38 (3), 318-23 PMID: 20852216

Sociopathic Dementia

Frontotemporal dementia (FTD) is a tragic, but scientifically fascinating, disease.


FTD only accounts for a small fraction of dementias in total (estimates range from 2% to 10%), but it typically strikes people aged in their 50s or 60s, i.e. much earlier than the average for Alzheimer's disease, the most common cause of dementia. As a result, FTD accounts for a large proportion of early-onset cases.

The symptoms are different to those of Alzheimer's, at least in the early stages. Memory problems and confusion are not prominent. Nor are hallucinations and delusions, which are seen in 20% of Alzheimer's, but only 2% of FTD.

Instead, patients often present with language problems - either forgetting what words mean, starting with uncommon words and progressing to easy ones ("semantic dementia"), or losing the ability to articulate speech ("nonfluent aphasia").

But the most disturbing effects are behavioural and personality changes. These are not seen in all cases, but in some people (the "behavioural variant"), they are the main symptom. Patients may begin to act entirely out of character, including criminal acts.

Aggressive behaviour is also sometimes seen in Alzheimer's, but it's usually associated with confusion or hallucinations: people "don't know what they're doing". In FTD, patients can commit serious crimes even though their cognitive function is pretty much intact: they do know what they're doing.

Mario F. Mendez discusses this in a new paper, The Unique Predisposition to Criminal Violations in Frontotemporal Dementia, and asks whether people who commit crimes while suffering from FTD should be considered legally responsible for their apparantly "sociopathic" actions. He presents 4 case histories.

Patient 1: A left-handed male in his sixties began stalking and attempting to molest children for the first time in his life. He followed children home from school and tried to touch them... On another occasion, he stood at the foot of a pool and stared at the children for a prolonged time.

When he exposed himself to his neighbor’s children, he was arrested. The patient did not deny his actions, could describe them in detail, and endorsed them as wrong and harmful. Despite this, he stated that he did not feel that he was causing harm at the time of his acts.

The patient’s personality had deteriorated over the prior four years, with decreased concern for others, disinhibition, and compulsive hoarding. He had caused disturbances at work, such as intruding into others’ conversations and walking into others’ offices... constantly pilfering... hiding money.... In addition, he ate indiscriminately, even going through waste containers and eating garbage. He stopped showering and wore the same clothes every day.

Neuropsychological testing and brain scans suggested early FTD, and his mother had reportedly suffered unspecified dementia; FTD is often genetic. He was not prosecuted. This case has a lot in common with the man who became a pedophile after surgery for a brain tumour: not just the pedophilia, but other symptoms like compulsive hoarding, over-eating, etc.

Patient 4: A right-handed man in his early fifties had a hit-and-run accident and left the scene without concern. He had struck a van with passengers but kept driving. The police stopped him a short distance away from the scene, and he did not deny his action.

Leaving the scene of an accident was not characteristic of his premorbid personality, yet he had had several recent traffic violations... He could recall and describe the accident, knew that it was wrong to leave the scene, but did not feel the need to stop at the time.

Over the prior two years, the patient’s pervasive behavior had significantly changed. He had become disengaged and emotionally detached; for example, he did not react to the death of his mother...

He was no longer embarrassed over passing gas or belching in public or appearing partially clothed in front of others. The patient had a tendency toward hyperorality, especially for peanuts, and had a decline in personal hygiene. Other aspects of the history included dysarthria and a recent tendency to choke on liquids.

This patient showed clear signs of motor neuron disease, which occurs in up to 15% of FTD cases. He died, as a result of the progression of the motor neuron disease, one year later, after developing other symptoms of FTD. His death meant he could not be tried for the hit-and-run.

Mendez notes that legally, these patients would probably not qualify for the "insanity defence". Under the British M'Naghten Rules, also adopted by the USA, the defendant is only eligible if they were

labouring under such a defect of reason, from disease of the mind, as not to know the nature and quality of the act he was doing; or, if he did know it, that he did not know he was doing what was wrong.

These patients do not fit that bill.

Finally, why does FTD cause sociopathic behaviour? Mendez says that it is because it involves degeneration of the vmPFC, linking FTD patients to the classic case of Phineas Gage whose vmPFC was destroyed by a flying iron rod. But Gage, while he did show personality changes, actually managed to function fairly well in society.

So temporal lobe degeneration probably also contributes to the FTD behavioural syndrome, especially since many of the symptoms (like compulsive eating) are seen in monkeys with temporal lobe lesions.

Mendez MF (2010). The unique predisposition to criminal violations in frontotemporal dementia. The journal of the American Academy of Psychiatry and the Law, 38 (3), 318-23 PMID: 20852216

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