The Ash Twins Blog

From O’Mara (2009):

On 16 April 2009, the US Department of Justice released legal memos detailing coercive interrogation techniques used with terrorism suspects during the Bush administration. . .

From reading the memos, the underlying neuropsychobiological model appears to be the following: a person possesses information (by definition, this information is in their long-term memory, that is, the enduring personal register of experience, events and facts that lasts at least for minutes and can extend to decades); they intentionally withhold this information under questioning; applying certain non-verbal techniques (Box 1) over prolonged periods of time (press and other reports indicate up to six months or more) will facilitate the release of this information from long-term memory by the captive. The memos do not fully articulate the mechanisms by which coercion makes captives reveal such information. Nevertheless, they appear to be based on the idea that repeatedly inducing shock, stress, anxiety, disorientation and lack of control is more effective than are standard interrogatory techniques in making suspects reveal information. Information retrieved from memory in this way is assumed to be reliable and veridical, as suspects will be motivated to end the interrogation by revealing this information from longterm memory. No supporting data for this model are provided; in fact, the model is unsupported by scientific evidence.

Contemporary neuroscientific models of human memory and executive function are very different. The structural and functional integrity of the hippocampus and the prefrontal cortices, as well as regular sleep, are essential for normal memory function. The hippocampus and the prefrontal cortices are extensively inter-linked and each co-regulates the other. Recalling previously learned information activates a variety of brain areas, especially the prefrontal cortex and the hippocampus. Moreover, activity in the prefrontal cortex is particularly associated with intentionally controlling access to, and retrieval of, memories. When these brain areas function improperly, both memory and executive functions (intention, planning and regulation of behaviour) can be impaired.

Stress causes heightened excitability or arousal in the brain and body, a perception that present or future events will be unpleasant combined with a lack of controllability over these events [1]. Experiencing stress causes release of stress hormones [2] (cortisol And catecholamines, such as noradrenaline. Stress hormones provoke and control the ‘fight or flight’ response (the immediate and rapid preparation by the body and brain for action in response to threat) that, if overly prolonged, can result in compromised cognitive neurobiological function (and even tissue loss) in these brain regions. Both the hippocampus and the prefrontal cortex are particularly rich in receptors activated by stress hormones. Cortisol binds preferentially to glucocorticoid receptors in hippocampus and prefrontal cortex, increasing Ca2+ access and, thus, neuronal excitability [2,3], which compromises normal physiological functioning of neurons if it is sustained over substantial time periods. Catecholamines modulate many sites in the brain (including the hippocampus and prefrontal cortex) and have many effects, including provoking glucose release, and increasing blood pressure and heart rate. These responses are beneficial over the short term, but cause long-term damage to the brain and body if this state of ‘hyperarousal’ is maintained over the long term. Furthermore, the amygdala [4] (involved in the processing of fear- and threat-related stimuli) can become enlarged, creating a negative feedback loop that amplifies the effects of subsequent stressful events. Finally, prolonged and sustained sleep deprivation, in part because it results in a substantial increase in cortisol levels, has a deleterious effect on memory.

There is a large literature on the effects of extreme stress on motivation, mood and memory, using both animals and humans. To summarise a complex literature briefly: chronic, prolonged and extreme stress: (i) inhibits long-term potentiation (LTP; the biological process believed to underlie memory formation in the brain) and facilitates long-term depression (the inverse of LTP) [1]; (ii) causes hippocampal atrophy and, hence, impairs learning in humans and animals [1–3,5,6]; and (iii) is implicated in many neuropsychiatric disorders (especially anxiety, depression and post- traumatic stress disorder) [5]. Notably, repeated chronic exposure to uncontrollable pain (e.g. electric shocks) causes many effects similar to those found under severe but non-painful stress.

A common argument in favour of torture is that it will reliably elicit veridical information from the captive’s long-term memory, as asserted by many media commentators in the context of the ‘ticking-time bomb’ scenario or in the case of a major imminent threat in which lives could be saved. A pragmatic anti-torture argument is that it will not; that torture is as likely to elicit false as it is true information and that separating the one from the other will be difficult. It is likely to be difficult or perhaps impossible to determine during interrogation whether the information that a suspect reveals is true: information presented by the captor to elicit responses during interrogation might inadvertently become part of the suspect’s memory, especially because suspects are under extreme stress and are required to tell and retell the same events that might have happened over a period of years. Other factors exacerbate this problem. Confabulation (the pathological production of false memories) is a common consequence of frontal lobe disorders [7] and, as already noted, prolonged and extreme stress has a deleterious effect on frontal lobe function [3]. Thus, distinguishing between confabulations and what is true in the verbal statements of tortured suspects will be difficult. . .

Brain imaging in people previously subjected to severe torture suggests that abnormal patterns of activation are present in the frontal and temporal lobes [9], leading to deficits in verbal memory for the recall of traumatic events [10,11]. A recent meta-analysis [12] of the relationship between pharmacologically induced cortisol elevations (in the upper physiological range) concluded that such elevations impair memory retrieval in humans, as do psychosocial stress-induced cortisol elevations. . .

[T]he fact that the captive is speaking also provides a safety signal to the captor; making the captive talk, rather than the truth of what the captive is revealing, might mark the end of the torture. As long as the captive is talking, the captor can avoid using torture. Waterboarding is cited in the legal memoranda as causing elevations in blood carbon dioxide levels (hypercapnia). Data on the effects of hypercapnia or hypoxia (decreased blood oxygen) on brain function are not cited; neither are data on carbon dioxide narcosis (deep stupor or unconsciousness), which might be expected as a result of acute and repeated waterboarding. Brain imaging data suggest that hypercapnia and associated feelings of breathlessness (dyspnoea) cause widespread increases in brain activity, including brain regions associated with stress and anxiety (the amygdala and prefrontal cortex) and pain (the periacquiductal gray) [15]. These data suggest that waterboarding in particular acts as a severe and extreme stressor, with the potential to cause widespread stress-induced changes in the brain, especially when this procedure is repeated frequently and intensively.

The proposed use of phobic stimuli (e.g. insects) underscores the unsophisticated folk psychological model underpinning coercive interrogation. Chronic controlled exposure to phobic stimuli is known as ‘flooding therapy’ and is among the most effective  methods applied under Cognitive-Behaviour Therapy (CBT) to treat phobias. Repeated and non-threatening exposure to a phobic stimulus usually results in individuals no longer being afraid of these stimuli.