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You’ll feel better in the morning: Sleep deprivation disconnects the emotional brain January 27, 2008

Posted by Johan in Emotion, Neuroscience, Sleep.
3 comments
Amygdala

Blogging on Peer-Reviewed ResearchDisturbed sleep patterns feature in a range of psychiatric disorders, many of which fall under the DSM’s mood disorder category. A recent paper by Yoo et al (2007) suggests that sleep deprivation itself can produce abnormal affective processing. In other words, sleep disturbances may be a cause as well as a symptom in conditions such as depression.

Yoo et al (2007) approached this issue with fMRI. Brain scans were taken of one participant group who had been sleep deprived for 35 hours, and one group who had slept normally. The participants viewed emotional pictures from a standardised set (the international affective picture system), which varied gradually in valence from neutral to aversive.

Yoo et al approached the imaging analysis with a few theoretical notions, which formed the basis of the brain areas that they investigated more closely. First, the amygdala is believed to mediate the emotional response to the aversive pictures, and secondly, it is argued that responding in the amygdala is mediated by an inhibitory projection from medial prefrontal cortex (a frequently invoked projection – see this related post).

To address the first issue, Yoo et al compared the amygdala response to the aversive pictures in the two groups. The amygdala was more activated bilaterally in the sleep-deprived group, and furthermore, a larger volume of amygdala was activated in this group as the figure at the top of this post shows. Note that the neutral pictures elicited no greater amygdala responses in the sleep-deprived group, so this is a case of greater amygdala re-activity, rather than an increase in baseline responding.

The role of medial prefrontal cortex in mediating the amygdala reactivity was investigated by measuring the regions that showed functional connectivity with the amygdala during the task. The method isn’t straightforward, but essentially it’s based on taking the activity in the amygdala voxels, and assessing which other brain regions show responses that covary. The results are given as a contrast between the two groups.

Amygdala Contrasts

As the yellow bits in the figure show, the sleep control group displayed stronger amygdala-prefrontal connectivity than the sleep-deprived group. Conversely, the amygdala had stronger connectivity with various regions of the brainstem in the sleep deprived group compared to the sleep control group.

So to re-cap: sleep-deprived participants showed larger amygdala responses, and their amygdalas showed weaker functional connectivity with medial prefrontal cortex. This finding does not prove that the greater amygdala response in the sleep-deprived group was caused by the weakened connectivity with medial prefrontal cortex, but it is certainly consistent with that notion. Yoo et al suggest that sleep acts as a kind of reset of brain reactivity, to ensure that emotional challenges can be met appropriately. But why is such a reset necessary in the first place? Why is the regulatory influence of medial prefrontal cortex weakened by sleep deprivation? The role of sleep in affect is only beginning to be understood.

References
Yoo, S-S., Gujar, N., Hu, P., Jolesz, F.A., & Walker, M.P. (2007). The human emotional brain without sleep – a prefrontal amygdala disconnect. Current Biology, 17, 877-878.

In Defense of Electroconvulsive Therapy October 30, 2007

Posted by Johan in Abnormal Psychology, Applied, Emotion.
2 comments

Blogging on Peer-Reviewed ResearchThe TED talks website contains material for a hundred posts, but a video posted earlier today hits particularly close to home. In this talk, Sherwin Nuland, a surgeon turned writer, gives an authoritative and unexpectedly personal account of the history of electroconvulsive therapy (ECT), sometimes known as electric shock therapy. The talk is only about 20 minutes, and gets very interesting around the 7 minute mark where Nuland describes how ECT once saved his life, as he puts it.

If the general public could be accused of placing too much trust in antidepressant medication, the reverse is certainly true of ECT. Ask anyone about electric shock therapy, and they’ll conjure up horror stories, and associations with frontal lobotomy. This is unfair, since there is some evidence that ECT actually works for depression.

The research on this issue has produced mixed results and plenty of controversy, as reviews by Challiner and Griffiths (2000) and by the UK ECT Review Group (2003) outline. However, there is no shortage of positive findings, and this in itself is rather remarkable, when you consider the patients that receive it. Since ECT is considered rather drastic, it is only really considered for patients who are severely depressed, and who have failed to respond to antidepressants. In other words, ECT is usually only considered in cases with the worst possible prognosis, so the fact that it does seem to help at times is quite powerful in itself, given the probability of spontaneous recovery from such conditions. That being said, a read of the ECT literature is unsatisfying. Because ECT is viewed as such a dramatic intervention (even in the absence of evidence that it causes long-term harm), it has rarely been tested on “normal” depressives in random control trials.

As Challiner and Griffiths (2000) outline, a lot of the popular conceptions of ECT are untrue. It doesn’t cause massive spasms – muscle relaxants are administered. It is not going to be a traumatic experience, because you will be put under a general anaesthetic. Although bilateral administration of ECT has been associated with memory loss, this does not appear to happen with unilateral administration, where both electrodes are kept on one side of the head (as shown in the picture at the top).

There is another issue with ECT, which I think bothers practitioners than clients. In the case of antidepressants, we at least know how they work, although it is far from clear why boosting synaptic Serotonin levels should work, given the weak evidence for a lack of Serotonin in depression. With ECT, there are no convincing explanations for either the how or the why. Psychiatrists stumbled upon ECT in the happy days of wild experimentation that preceded Ethics Committees, without much of a theory. It is quite embarrassing that even to this day, we can say so little about what this treatment does, or indeed if it even does anything at all – a pertinent question given the claim on Wikipedia that 1 million people receive ECT each year worldwide.

If I ever developed a severe depression, I would try ECT before antidepressants. Unlike antidepressants, the effects of ECT can be instantaneous, and there are no long-term side-effects, nor any withdrawal symptoms when the treatment ends. Since the treatment is extremely safe when administered properly, there is really very little to lose.

References
Challiner, V., and Griffiths, L. (2000). Electroconvulsive therapy: a review of the literature. Journal of Psychiatric and Mental Health Nursing, 7, 191-198.

The UK ECT Review Group. (2003). Efficacy and safety of electroconvulsive therapy in depressive disorders: a systemic review and meta-analysis. Lancet, 361, 799-808.

Is is rational to Do No Harm? September 23, 2007

Posted by Johan in Abnormal Psychology, Behavioural Genetics, Emotion, Social Neuroscience.
1 comment so far

From the left: Josef Mengele, Rudolf Hoess, Josef Kramer, and unknown.

The picture above comes from a set recently added to the US Holocaust museum. The pictures have caused a stir since they depict staff at the Auschwitz concentration camp on what might in modern terms be described as corporate kick-offs and the like. I’m not sure why it’s surprising that the prison guards liked to relax and have fun now and then – clearly, they would not have taken up the position if they were not at least acceptant of the task at hand. There is little evidence that the third reich forced or ordered anyone to commit these atrocities, after all.

Mengele is an interesting character. As a leading physician in the camp, he (along with the other physicians) decided who would be sent to work and who would be sent to the gas chambers, as the captives disembarked their trains. He is also infamous for his cruel experiments on inmates. In particular, he collected twins, which were separated from the other inmates, and used to study the heredity of racial traits under much the same principles employed by modern-day twin studies in behavioural genetics, but without ethics committees or indeed basic human decency.

I came across an old NY Times article on Mengele, written by what I assume must be a psychoanalyst. Yes, the usual speculative attempts to explain the man’s behaviour as a function of repressed anxiety appear, but for the most part the article sticks to the story, re-telling the life and work of Mengele through witnesses.

Although this is probably not news to historians, I am struck by the contradictions and inexactness of the accounts, even though this is very recent history. Within the NY Times article, witness accounts frequently contradict eachother: Mengele is described as being an aloof person with no emotions, next he is playful, friendly (even in his role in deciding life and death on the ramp), and entertains his young twin subjects. When comparing the NY Times article to the Wikipedia entry or his entry at the Holocaust History Project, further discrepancies arise.

Yet, a clear picture emerges, and it is one of supreme rationalism and dedication to science (albeit science that turned out to be fundamentally flawed). These are terms that are usually considered positive in our society, so you may be excused if you think me a Nazi apologist for saying so. It’s quite the contrary, however. I think Mengele’s case highlights how the idealised image of the objective Academic, struggling only to further knowledge, can be a road straight to hell.

From a rationalist standpoint, it is relatively easy to understand Mengele’s decisions. As an anthropologist with an interest in heredity, he must have recognised that Auschwitz offered an unprecedented opportunity for all kinds of forbidden experiments. The NY Times article implies that this research opportunity may have been the very reason why he actively sought a position at the camp. From a moral standpoint, the prisoners at Auschwitz were going to suffer terrible suffering or immediate death regardless – one could then argue that Mengele only tries to make the best of the situation by adding to human knowledge, while killing and maiming. For Mengele, the suffering of the prisoners was likely a non-issue in any case, since the man was a rabid anti-semite, and considered his subjects less than human. In this sense, the work may have presented no more of a dilemma to Mengele than the dilemma a contemporary researcher faces in killing a macaque monkey after the conclusion of a single-cell recording study, in order to verify that the electrodes were placed in the right cortical location.

My point here is not to defend Mengele – he was clearly an appalling person who, apart from all other damage done, sullied the name of science. Still today, Mengele is the original template for the evil scientist, who seeks knowledge at any (human) cost. But it is unsatisfying to merely state that Mengele was “evil”, and thus did what he did. The NY Times article finally lets loose the full-on psychoanalysis towards the end, and this explanation proves no more satisfying:

His impulse toward omnipotence and total control of the world around him were means of fending off anxiety and doubt, fears of falling apart – ultimately, fear of death. That fear also activated his sadism and extreme psychic numbing.

I would prefer to invoke the behaviour of patients with damage to the ventromedial prefrontal cortex (VMPFC -the bit of brain just above and between the eyes). These patients display, among other symptoms, what can best be described as a lack of conscience. They are well aware of the conventions of society, but as the post linked above describes, their reasoning is defective. The defects do not appear in the expected, irrational direction, but rather in a rationality that is so extreme that is leads to horrendous decisions. These patients do advocate killing a crying baby in order to avoid the group’s capture and certain death at the hands of enemies. This is the most rational, utilitarian path to take – better the death of one than the death of all.

So did Mengele have an undetected lesion to the VMPFC? I don’t think so, and there is absolutely no way of finding out. Such an account would be as speculative as the psychoanalytic drivel cited above. I only wish to raise the possibility that sometimes, a behaviour as complex as immorality or a lack of conscience may arise from relatively simple lesions. Repressed traumas and anxiety may well cause such cruel behaviour too (who knows?), but a blow to the head strikes me as the more parsimonious explanation, if we’re going to speculate about it anyway

I don’t think Mengele was mad, evil, or suffered from repressed anxiety. He was a dedicated and supremely rational scientist. This is why he caused so much harm.

AI detection of facial expressions September 7, 2007

Posted by Johan in AI, Applied, Emotion, Face Perception.
1 comment so far

I’ve written previously about how algorithms that detect faces in images are appearing everywhere, including Google Images and many recent digital cameras, where they are used to ensure that focus is on the face (presumably, no one who buys a Cybershot is interested in the aesthetic effects of not having the face in focus).

This technology is being expanded into the realm of specific facial expressions by OMRON (among others), a company that just released software that promises to measure the smile factor of faces in a picture. The smile factor as OMRON conceives of it goes from 0 to 100 %, and will presumably serve to shift the blame nicely when you want people to smile more in a picture (“look, I think the picture is fine, but the camera thinks you should be smiling more”). It is only a matter of time before this makes it into digital cameras, soon followed by a spinach-on-the-teeth detector.

Other proposed applications for OMRON’s software include human-computer interactions, and as an objective measure of liking in food tasting studies. I imagine the software would also be useful for more theoretical investigations into emotional expressivity. As it stands, scoring the magnitude or kind of expression manually is quite tricky.

It never ceases to amaze me how object recognition software is steadily advancing along the ventral visual stream.

“Feel the heat… skips a beat” or the other way around? August 16, 2007

Posted by Johan in Emotion, Neuroscience, Social Neuroscience.
1 comment so far

Can’t go with my heart when I can’t feel what’s in it

Red House Painters – Katy Song

The common-sense understanding of emotions and their physical expressions is that the causal arrow goes one way only: if you feel upset, the feeling will cause your cheeks to flush and your heart to beat faster. However, the opposing notion is also possible: we experience physical arousal, and interpret this arousal as emotion. This is referred to as the James-Lange theory, or simply as feedback theory. This alternative idea is not much younger than the common-sense notion – William James was probably the first to propose it, in the 19th century. More recent simulationist accounts such as Damasio’s Somatic Marker Hypothesis could be said to build on this notion.

A story in the news (Washington Post via Gizmodo) seems to offer some anecdotal evidence for the role of physical arousal in the experience of emotion. Peter Houghton had a “ventricular assist device” installed, which is a developed version of the artificial heart. Unlike the more established Pacemaker, the Jarvik 2000 that Houghton had implanted not only paces the heart but moves blood for it, exchanging the familiar thuds with an even mechanical whir (as an aside, the Jarvik 2000 only helps the right ventricle, since the left ventricle is often left unharmed in cardiac illness – in other words, there is a bit of heartbeat left).

While this is impressive in itself as an example of the advances in medicine, the side-effect is what captures attention and perhaps imagination: Houghton claims to experience less emotion. For instance:

[…] he’s become more “coldhearted” — “less sympathetic in some ways.” He just doesn’t feel like he can connect with those close to him. He wishes he could bond with his twin grandsons, for example. “They’re 8, and I don’t want to be bothered to have a reasonable relationship with them and I don’t know why,” he says.

Judging by the Post story, the emotional flatness seems to occur mainly with regards to other people. This is a little surprising since heart rate is considered more of a marker for fear (which is associated with a raised pulse) or interest (which can lower the pulse) than for happiness or attachment. It is possible that these emotions are also affected, but this went unnoticed in a modern world where there are many opportunities to experience emotional attachment, but few to experience genuine fear.
As the Post article is quick to point out, it remains possible that the emotional symptoms are secondary to general depression, brought on by the ordeal of a life-threatening cardiac illness. However, one of the physicians hints at previous reports of these emotional symptoms occurring following implants. I haven’t been able to find any references – feel free to give me a shout if anyone should find some.

Generally speaking, I’m quite open to the idea that the removing one physical marker of emotion (ie, changes in heart rate) could produce a corresponding reduction in the experience of certain emotions. However, the complexity of the deficits in this particular case is perhaps more consistent with depression. The loss of a physical marker should – if the feedback has merit – result in more global deficits in the experience of basic emotions like fear or interest.

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