I’ve previously addressed the surprising finding that people with extensive damage to the brain’s “fear center” are capable of experiencing fear and how this can be explained, in part, by recognizing that features of human psychology do not exclusively rely upon individual brain structures.
But, this leaves us with a dilemma: even if emotions like fear are encoded across many structures of the brain simultaneously, damage to some of these structures should still impair or eliminate these emotions. Indeed, if we consider the case of SM, she was capable of experiencing a state akin to fear or panic, but only in very specific circumstances: she couldn’t detect external threats, but internal threats (e.g. CO2-mediated suffocation) do appear to register. Perhaps then the amygdala is not a “fear center” so much as a threat or salience (“important stuff”) detector, which is commonly used to elicit fear responses to threatening stimuli.
Part of the confusion about the role of this brain structure comes from the words that we use. The earliest research on brain structures such as the amygdala suggested a key role in “fear conditioning”: animals with damage to the amygdala do not freeze when presented with known threats. Recently, Joseph LeDoux, who pioneered the term fear conditioning has re-labelled this term “threat-conditioning” to differentiate between the emotion or feeling of fear and the activation of innate “survival circuits” that produce the physiological and behavioral responses that tend to co-occur with this feeling. According to LeDoux this basic distinction implies that different neural circuitry correspond to these two aspects of fear, i) responding to threats and ii) experiencing fear:
“‘Threat-triggered defense responses’ and fearful feelings can be separated in the brain. For example, people can respond to learned threats without being conscious of the stimulus and without any particular feeling of fear and can freeze or jump back from danger before feeling afraid. The brain systems that generate responses to threats are not one and the same as the circuits that allow us to experience fear. To understand ‘fear’ we need to understand consciousness.”
To suppress any skepticism that such a distinction could be possible, keep in mind that theories of emotion explicitly assume that the experience of fear can be induced or influenced by the detection of threat-induced responses themselves (e.g. startle response, change in facial expression, heart rate increases, neurochemical release). Thus, while threat-responses alone are not equivalent to fear, they may be a precursor to or key causal factor in activating this experience. A simple example might be the experience of having a good friend jump out from behind a corner to yell: “Boo!”. The immediate “shock” probably corresponds to typical fear responses, which are quickly suppressed as the situation becomes clear. We might say “Wow, you scared me!”, but not, “I feared for my life!”. This rather simplistic example clearly illustrates how we might differentiate between rapid threat responses and potentially longer-lasting and qualitatively distinct feelings of “fear”.
If we can dissociate the state of fear from the physiological threat responses orchestrated by individual brain regions like the amygdala, then it immediately suggests a key difficulty in designing brain-based treatments for “fear disorders” like post-traumatic stress disorder. Pharmacological treatments under development are intended to target specific brain circuits with the intent to erase memories of fearful experiences, or at least the connections that promote threat hyper-responsiveness in the long term. Perhaps the source of this chronic illness is not in the simple threat or survival circuits that are so easily studied, but far more complex mental processes which tend to evoke and promote the behaviors and physiological responses which make such illnesses so disabling. Targeting these processes, so intrinsically linked to personal identity and belief may be far more difficult.