[Editor’s note] Useful links:
- Original article by Sumaiya Shaikh, published July 18, 2017
- Rebuttal to the original by Shruti Muralidhar, published July 19, 2017
- Sumaiya Shaikh responds to the rebuttal, below
Shruti Muralidhar (writing in her rebuttal): This is in response to Sumaiya Shaikh’s article in The Wire titled ‘The Cognitive Neuroscience of a Lynching’. She has attempted to explain the human behaviour seen in acts of extreme violence, such as lynching. As a trained and practising neuroscientist who works in the field of learning and memory, I find that a lot of the neuroscience in her article is unsubstantiated, outdated or plainly incorrect. Following are some chosen paragraphs from her write-up, accompanied by my comments.
Sumaiya Shaikh: Since the ongoing global terror related incidents, there has been substantial focus diverted to the study of the neural underpinnings of areas such as violence, fear, learning and economics. The field of research in human behaviour, in particular of aggression, has been fairly new and has recently attracted interest from the field of neuroscience. The limitations of human models in the subjects of these experiments require them to be consciously awake while performing tasks. Hence, invasive methods are not used and inferences are made on the basis of analogies from animals, biological processes and brain imaging.
Perhaps the author of the rebuttal has completely missed the point of the article. It was not an article submitted to a mainstream physiology journal emerging from primary data. The article was written to comprehend the social tragedy in the form of a lynching using biological examples to give an insight into the brain and behaviour of everyone involved in the attack. How the science of the analogies have been dissected shows how wrongly this article has been interpreted by the author of the rebuttal. For the author to have taken the focus away from the purpose of a large part of my article suggests a bias that is associated with discrediting the experiences of the people suffering from this violence.
SM: In the absence of information exchange from the hand and the brain, a new altered communication pattern harbours reduced neuronal synaptic connections or ‘empty space’ in the brain corresponding to the injured part.
If I understand Shaikh’s analogy correctly, she is using the term ‘empty space’ to denote reduced or lack of normal synaptic connections. But the reference to ‘empty space’ is misleading.
Years of studies in anatomy, morphology and physiology have clearly shown that neurons, glia, epithelial cells, immune cells and blood vessels sit packed very tightly in the confined space of a mammalian skull. A recent study by Jeff William Lichtman, of Harvard University, in high-definition, high-throughput electron microscopy shows that, in fact, there is no ‘empty space’ in the brain.
SS: The ‘empty space’ is a figurative term used here. I have also not seen such vacuums from my dissection of human brains in healthy and diseased cadavers – nor in animal brains with labelled neurons. The reduced synaptic connections simply correspond to the reduced connectivity from the periphery of the injured motor or sensory neurons. It would be naive to think of a physical, empty patch in the brain devoid of glia, supporting cells and blood supply. A very important study of phantom pain in amputees has also shown that there was a high correlation between the magnitudes of the shift of the cortical representation of the mouth into the hand area, showing afferent reorganisation of that ‘empty’ space.
This event is called plasticity – a theory of restructuring the brain’s connectivity. However, in one study, there was indeed a space created and visualised through immunohistochemistry in much lower-order neurons, i.e. in the dorsal horn, where a chemical injury at the periphery produced a physical gap of a particular type of pain afferents. This study also used the term ‘gap’ in the connectivity map of the spinal cord but it doesn’t mean that there was a physical gap.
SM: An attempt to rationalise the racial attack by the victim and its incomprehension can lead to a long term memory consolidation that links previous experiences of the people in the mobs with the current situation.
In this excerpt, Shaikh appears to have misunderstood and misused the term ‘long term memory consolidation’.
Long term memory consolidation is a slow and multi-step process that occurs over hours, days or even weeks. It involves the strengthening of connections between neurons or groups of neurons in the brain, with the final goal of retaining a particular memory. It involves changes at many different levels: neurons start or stop making specific proteins; they grow or retract protrusions known as spines to contact neighbouring neurons; they change the profile of receptors on their surfaces and sometimes even increase or decrease the amount of neurotransmitters they release.
Using the term ‘long term memory consolidation’ simply in lieu of ‘memory’ or ‘remembering’ is inappropriate and wrong – especially in the context mentioned by the author.
SS: As you may know, short-term memories generally lasts between 30 and 60 minutes, and long term memory is in the context of hours to days. Mice studies rely on a 24-hour or longer cycle to study the effects of protein changes like cAMP-responsive element-binding protein (CREB), which have been implicated in the activation of protein synthesis required for long-term facilitation. I agree that there are structural or anatomical and biochemical changes but I never mentioned that it occurs on the spot.
The neurotransmitter norepinephrine is released in order to prepare the body or the brain for action, an enhanced activity which is also linked to memory consolidation, for emotionally arousing events that create long term memories in humans and subsequent biochemical changes occur following release.
I also agree these changes happen at many levels and the physical changes underlying the encoding and processing of the information, such as a trace, that can remain in a fragile state for some time. However, a traumatic event such as this leads to a retrieval and reactivation process that, over the years, consolidates and stabilises with the age of the memory.
Also, I do not agree that there isn’t any long term memory consolidation here. The memories created by fear or trauma are different than a memory of simply remembering an uneventful time. An article published in 1998 discusses how the traumatic memories differ from the ordinary memories.
I disagree that any event that renders this magnitude of trauma can fail to be retried in an unaffected system and subsequently fails to be reconsolidated over time.
SM: Neuroscientists have also shown that mirror neurons, using the same mechanism that activates empathetic response for others’ pain, mimic the goal-oriented movements by activating the premotor cortex. The amygdala, a part of the brain related to empathy, is thought to be involved with the premotor cortex in initiating a mob response that requires physical action.
Mirror neurons were first discovered while recording from neurons in monkeys. Researchers found that certain groups of neurons in the cortex showed an increase in activity in two separate cases. One, when the monkey performed a certain action, and two, when the monkey observed the action being performed. This led to their moniker because these neurons ‘mirror’ activity, as if the primate itself was performing the action.
To begin with, mirror neuron research in neuroscience has been mired in controversy since 2009. A good part of this controversy relates to extending the idea of a ‘mirror neuron system’ to explain human behaviour. Direct observations of mirror-neuron activity have been performed in monkeys and higher primates – but not in humans. Non-invasive techniques such as positron emission tomography (PET) or functional magnetic resonance imaging (fMRI) applied to the human brain have only yielded information about changes in blood-flow in gross regions of the brain. However, there has been no direct evidence of changes in specific neuronal activity.
SS: The empathetic response ‘mirroring’ or replicating another’s pain has been conducted in humans. Here are some of the highly valued studies for mirror neurons behaviour in humans: Kohler et al 2002; Kaplan and Lacoboni 2007; and Chong et al 2008. The controversial mirror neuron has two sides to its story: the review you presented by Hickock can be countered by several studies that speak for the argument. My own study in pain mimicked mirrored-behaviour responses in pain after unilateral nerve injury.
Also, the noninvasive techniques such as imaging (fMRI) are the only way one can record brain activity in healthy conscious humans, and the study I am referring to is by a colleague of mine who specialises in human empathy and pain studied using fMRI.
Although, I am not sure which behaviour study in contemporary neuroscience allows one to ‘record’ perception in awake human subjects using invasive methods. This is ethically not acceptable and no legitimate university will approve of this study. Perception in humans can be only recorded using questionaries using psychophysical methods – unless there is an affective field maze study in mice for implied behaviour.
§ Methods to study perception and behaviour in humans
Specific neuronal activity studies, such as cortical electrophysiology, have not been conducted in humans in the brain, again due to the obvious ethical reasons. I have been a part of animal electrophysiology studies recording compound action potentials from the deep brain nuclei in pain modulation, but animals cannot be used to record perceptual responses such as empathy or emotion.
On the other hand, the only invasive neuronal activity recordings conducted in humans can be done in periphery, using micro-neurography developed by Swedish scientists, which is currently my work of interest in Sweden. This method can only be used in the context of peripheral afferents in conscious human subjects and not the brain itself.
Emotion and empathy are encoded in the brain and cannot be recorded unless you have ethic to conduct brain surgeries in healthy humans. Therefore, a PET, fMRI and other similar imaging studies, EMG, peripheral micro-neurography, electrical stimulation (transcutaneous or transcranial) and psychophysics may be the only methods to use to understand human behaviour. And none will incorporate an invasive electrode in the brain unless the human is not alive. What you are suggesting is inserting an electrode such as a gold or a tungsten needle in awake healthy human brains to ask how it feels (to study empathy).
SM: To use such an example to explain mob mentality – without explaining the caveats behind the research – is unfair to the readers and goes against good science communication practices.
Secondly, there are no known physical pathways that originate in the amygdala and terminate in the premotor cortex. This is factually incorrect.
The motor cortex is that part of the brain where physical actions – such as limb movement in response to stimuli – are planned and executed. There are many well-studied accessory areas such as the premotor cortex, the supplementary motor cortex and the secondary motor cortex. All of them play vital roles in integrating sensory information from across the brain to generate the movement response. To claim that part X of the brain ‘initiates’ a physical action, we first need to verify whether neurons from X send projections – physically – to any of the motor cortices.
There is no anatomical or morphological evidence that the amygdala sends such a physical projection to any of the brain areas involved in motor behaviour.
SS: Although brain connectomes are not as simple as connection X (affect or sensory) to Y (motor), a study from 1983 shows the connections of amygdala and premotor cortex. Your reference from the line above is just an undergraduate ‘notes’ link of the basic limbic system.
SM: The write-up under the sub-headline ‘Cognitive processes in the elimination of the self’ is terribly misleading. Shaikh does not explain anything related to cognitive processes in the elimination of the self. Instead, she abandons her original ‘autotomy’ analogy and starts using an ‘immune system’ analogy. Neither of these have anything to do with neuroscience, cognitive neuroscience nor any processes related to the self.
SS: The example of autoimmunity was to explain certain behaviour with a different biological analogy. My last sentence did indeed discuss the perils of nerve regrowth and the return of abnormal and painful sensations to the hand and the subsequent mutilated hands experiencing long term hypersensitivity and pain (in reference to the changing in social conditions for irreversible damage).
I believe the motive of this rebuttal was to discredit each of the original arguments and analogies I had made. As mentioned earlier, these were analogies or parallels drawn from what I observed through my own research and some of my peers and are true in scientific merit, especially where I had quoted references.
The author also needs to acknowledge the fallacy in the rebuttal where I am inferring references from animal work. Preclinical and invasive testing is based on animals, and there is no discomfort in acknowledging that we do not understand the whole picture, and that inferring human behaviour from animal studies is a legitimate work in mainstream science.
The original article is based on discussions of the current situation and my comprehension of the traumatic events, more than picking on the controversies of mirror neurons for example. Such controversies exist throughout the medical field. Perhaps the author of the rebuttal hasn’t acknowledged how young the field of neuroscience is. It is only from providing such hypotheses and inferred mechanisms that we can make sense of the system, biological or social.
Perhaps this reflects a bias in your thought process where an attempt such as this – to familiarise the readers with the victim’s and perpetrators’ cognition (mental action or process) – triggered you to focus instead on the controversial sides of the medical analogies that I have used to explain to a largely non-scientific readership.
Sumaiya Shaikh is a medical scientist with a PhD in neuroscience from Australia. She currently works as a postdoctoral fellow in Sweden and is the editor of AltNews’s science section.