Dr Neil Harrison: Webinar on neuroimaging (MRI, fMRI, SPECT and PET scans

[lansbergen]

The implication is that these temporary changes that accompany inflammation/sickness have somehow persisted in our brains after the inflammation has gone, and may still be visible in fMRI etc.

But how to prove the causing agent has gone when there is no test for it? And how to explain the fluctions if it is not from inflammation flares?

 

[Woolie]

But how to prove the causing agent has gone when there is no test for it? And how to explain the fluctions if it is not from inflammation flares?

Well exactly, @lansbergen. The same logical weakness as in the standard psychological explanation. Just cos we can't detect anything on standard tests doesn't mean there's "no illness in the body", nor does it mean that it must be all in our heads OR all in our brains. This assumes we have a complete understanding of all bodily illnesses/abnormalities and 100% accuracy at detecting them using standard tests. Who knows? I expect that in 100 years, our present understanding will look more like 25% than 100%.

 

[Sasha]

I read #77 the opposite way, @Woolie - that it's all about how ongoing inflammation in the brain is driving sickness behaviour. Maybe I'm reading it out of context.

 

[Scarecrow]

That's all the transcripts from 78 to 81 converted to the original English, starting here.

Thanks once again to @Effi for the Dutch translations. It made it so much easier than starting from nothing.

 

[Woolie]

I read #77 the opposite way, @Woolie - that it's all about how ongoing inflammation in the brain is driving sickness behaviour. Maybe I'm reading it out of context.

No, that's not correct. There is no mention of "inflammation in the brain". The suggestion is that there is continued brain activity of the kind we see when there's inflammation in the body. When there isn't.

In some of the interviews, I think Harrison is being very careful to phrase things in a certain way, to obscure some aspects of his theory that we might not like. In the other clips, he talks a lot about the Japanese study as showing "inflammation on the brain", but doesn't mention that he believes this occurs because we are misprocessing incoming information from the body.

[btw, in the Japanese "brain inflammation" study, the authors' favoured explanation was that the "inflammation" response in microglial cells was a consequence of our dysfunctional brain processes (perception of fatigue when there isn't any), not a cause. To their credit, though, they do say this is only one explanation]

Also, you're right that Harrison is interested in PEM, but not for the reasons you hope. In his model, PEM is created by a false expectation that certain events or activities will lead to malaise. The expectation is learned when a person is "actually ill". Later, that same pattern of events occurs (e.g., we go for a walk), the expectation remains and is not revised. So PEM occurs.

@Sasha, I don't see what else I can do to alert you to the potential dangers of this way of thinking. Yes, its not quite as pejorative as the standard psyc model - or at least doesn't appear to be to outsiders. Which is a plus. Yes, many of the mechanisms are outside of our awareness (although the standard BPS model is compatible with this idea too). Yes, it could lead to objective markers that may help validate our complaints.

But if those "markers" are themselves used to support a largely psychological model of our illness (phrased in neuroscience terms), then are we really any better off?

 

[Sasha]

@Sasha, I don't see what else I can do to alert you to the potential dangers of this way of thinking.

I'm sorry I'm not able to put the time in to do this discussion more justice! It would involve too much reading and ultimately, it doesn't matter what I think. If there's a problem with his model, it needs addressing with him directly in some sort of forum (in the broad sense) where there could be some back-and-forth that would allow his view to be challenged and force him to clarify it.

 

[Woolie]

If there's a problem with his model, it needs addressing with him directly in some sort of forum (in the broad sense) where there could be some back-and-forth that would allow his view to be challenged and force him to clarify it.

Unfortunately, I'm not as optimistic as you - I don't think we're likely to get straight answers. In these clips, he had a lot of opportunities to set out his claims, and he fudged and sidestepped. That's why you don't get the feeling you quite understand what he's saying.

Plus, this is not just about Harrison et al. In the near future, we're going to be seeing increasing numbers of neuroscience explanations of MECFS. I predict the BPSers will be using this terminology soon, and embedding their own ideas within a neuro framework. We need to be able to spot this when it happens.

On another thread, in a discussion with @duncan, we talked about how important it is to ignore the neuroscience language and focus on the suggested cause of the illness. If the cause is learning/experience, and the treatment is "unlearning", then its essentially a psychological model.

 

[Sidereal]

Neurobabble is the new psychobabble.

 

[Cheshire]

Neurobabble is the new psychobabble.

Yes, neuroscience is the new boat everybody wants to be in. Even French psychoanalysts invented a new field, neuropsychoanalysis.

The ideal playground for psychobabblers; something that looks scientific with not much know yet, so that you can just invent the missing bits.

 

[duncan]

It's like trying to work through all the Terms and Conditions clauses in a wireless carrier contract - first you have to find them as they are usually hidden, then struggle to interpret them so you know what you are actually getting yourself into..

It would be helpful if we could - straight off - reliably identify obsfucation and cut to the core and intent of their writings each time.

Perhaps we should ready a Rosetta Stone, or a legend as it were.

 

[Valentijn]

From his profile at https://www.bsms.ac.uk/about/contact-us/staff/dr-neil-harrison.aspx

His research investigates how changes in bodily physiology particularly, infection/inflammation interact with the brain to modulate emotion, motivation and cognition and contribute to common mental illnesses such as depression, chronic fatigue and Alzheimer’s disease.

Okay, maybe "mental illnesses" is just a weird use of terminology.

http://bjp.rcpsych.org/content/200/6/508.full is a piece he co-authored, exploring the relationship between hypermobility and psychiatric symptoms:

Hypermobility is also linked to stress-sensitive psychosomatic disorders including irritable bowel syndrome, fibromyalgia and chronic fatigue and is associated with hypersensitivity to nociceptive stimuli.

And @Woolie seems to be right about this framework leading in to certain psychological treatments, even when the dysfunction is attributed to a fault in the brain:

The observed differences in the structural integrity of specific emotional brain regions provide a starting point for future research into constitutional vulnerabilities to common psychiatric symptoms that have the potential to inform more individually tailored therapeutic approaches.

He is also a co-author of http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4362313/ which seems to be saying that chronic fatigue is a psychiatric symptom:

PoTS has also been associated with symptoms of chronic fatigue and high levels of a number of other psychiatric symptoms particularly panic, anxiety and depression.

There's also a lot of stuff regarding volitional control of heart rate, such as http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4373272/ . The conclusion seems to be that people can avoid anxiety by learning to control their heart rate. The implication of that and the other papers, is that POTS is controlled by the patient's emotions, and that emotional therapy might reduce POTS symptoms.

My general impression is that he does a lot work on acute neurological changes (such as sickness behavior) triggered by acute inflammation, and sees it in a very biological framework. But his view of chronic conditions seems to be starting from the paradigm of acute sickness behavior and applying it to the symptoms, instead of starting with an understanding of the illnesses themselves. And applying that acute model to a chronic condition is happening via psychosomatic explanations.

This is why he wants to focus on fatigue and portray it as being roughly approximate to PEM, and why chronic peripheral symptoms are being ignored. Basically he has his favored model to explain certain acute conditions, and is finding a way to make certain chronic conditions fit into his model. ME symptoms don't fit very well into his model, so some are being generalized and others are not being considered.

 

[Woolie]

Thanks, @Valentijn. I did look at a while ago, but good to be reminded. Nice analysis here:

This is why he wants to focus on fatigue and portray it as being roughly approximate to PEM, and why chronic peripheral symptoms are being ignored. Basically he has his favored model to explain certain acute conditions, and is finding a way to make certain chronic conditions fit into his model. ME symptoms don't fit very well into his model, so some are being generalized and others are not being considered.

Neuroscience explanations of psychiatric conditions are a thing right now. I personally think its quite interesting work (better than the DSM anyway), and it has got to be good in the long run for those who suffer from depression, anxiety, OCD, and other forms of psychological distress with no known cause. There might even be some treatments coming from this work (e.g., TMS stimulation of the anterior cingulate to treat anxiety). But why bother wasting time on illnesses that are not mental?

The answer might be that its not these researchers' fault. They just think its an established fact that ME is psychosomatic, they take that evidence at face value. They trust the behavioural researchers that have claimed that.

No excuse, I suppose. If you're studying a condition, you need to know about it inside and out.

 

[Cheshire]

I wrote my comment before reading yours @Woolie and @Valentijn and I think it's the same idea underlying it: these searchers thoughts are framed by their preconceived ideas. They equate fatigue with emotional destress and lack of motivation and other mental states that are not part of ME symptoms.

I'm very fed up particularly of this "motivational" problem we're supposed to have.
Like the vast majority of us, my main issue is to stop doing things in due time, not a lack of will, or desire.

One can explain motivational problems with brain dysfunction, emotional problem, moral weakness or witchcraft, that won't change the fact that they do not listen to the patients that keep saying "I have no motivational problem".

 

[Valentijn]

An article by Dr Neil Harrison on Conversion Disorder, with Dr Mark Hallett (functional movement disorder researcher from the upcoming NIH ME study) as one of the co-authors is at http://onlinelibrary.wiley.com.sci-hub.cc/doi/10.1002/mds.25435/full

This one is about patients who have uncontrolled movements. They find brain stuff in the images as usual, but ...

Although our results suggest a mechanism by which motor CD patients might be less able to inhibit unwanted movements during movement selection, this does not explain how such movements become repetitive and debilitating for these patients. Investigators have posited the role of “top-down” processes in these patients as inappropriately interpreting random movement as meaningful. In this way, a system of beliefs regarding volition is created and constantly updated, both misinterpreting movements as involuntary and bringing about further movement via greater attention.

If you get the Conversion Disorder, it's probably just because you have a mood disorder and/or personality disorder:

Although we controlled for depressive and anxiety differences, these findings may also represent premorbid differences in the patient population in characteristics such as underlying impulsivity, personality differences, and precipitants such as stressors.

Non-epileptic seizures are discussed for comparison, and of course are also presumed to be a conversion disorder.

 

[Woolie]

@Valentijn, Interesting that he's worked with Mark Hallet. That's a name I've heard in the FND literature (functional movement disorders, seizures). He is fully committed to a psychological explanation for these disorders.

FNDs (functional neurological disorders) are a great example of how fMRI can be used to support psychological explanations. There have been dozens of fMRI/PET studies of functional movement disorders. All have detected abnormalities. And ALL have interpreted these abnormalities as the neural signature of a psychological problem.

Let that be a lesson to us: Just cos it shows in a brain scan don't mean you're safe from the psychobabblers.

 

[Valentijn]

Interesting that he's worked with Mark Hallet. That's a name I've heard in the FND literature (functional movement disorders, seizures). He is fully committed to a psychological explanation for these disorders.

Yes, and it's especially scary that Dr Mark Hallett is one of the investigators in the upcoming study of ME/CFS at the NIH, along with two people who work under him in the same department. He's almost certainly to blame for the attempt to add an FND control group to the study, and they only interpret brain images one way when it comes to "unexplained" symptoms: psychosomatically.