Flatworms Recall Familiar Environs, Even after Losing Their Heads: Scientific American.
Highly recommended reading. As it turns out, one does not have to go all the way down the evolutionary ladder to be reminded that even brain-impaired or brain-damaged individuals (whether through TBI, dementia, various levels of unconsciousness, or simply sleep) have not only memories, but continue to experience emotions, good and bad.
As an illustration that the brain is made of many different levels and parts, here is a recent paper by Feinstein et al. showing that individuals with a genetic absence of the amygdala, long highlighted as the brain’s influential “fear center”, can experience severe panic attacks.
They write:
“A substantial body of evidence has emphasized the importance of the amygdala in fear […]. In animals, amygdala-restricted manipulations interfere with the acquisition, expression and recall of conditioned fear and other forms of fear and anxiety-related behaviors. In humans, focal bilateral amygdala lesions are extraordinarily rare, and such cases have been crucial for understanding the role of the human amygdala in fear. […] The most intensively studied case is patient SM, whose amygdala damage stems from Urbach-Wiethe disease […] Previous studies have shown that patient SM does not condition to aversive stimuli […], fails to recognize fearful faces […] and demonstrates a marked absence of fear during exposure to a variety of fear-provoking stimuli, including life-threatening traumatic events […]. Patients with similar lesions have largely yielded similar results […].
One stimulus not previously tested in humans with amygdala damage is CO2 inhalation. Inhaling CO2 stimulates breathing and can provoke both air hunger and fear […] Furthermore, CO2 can trigger panic attacks, especially in patients with panic disorder […]. Recent work in mice found that the amygdala directly detects CO2 and acidosis to produce fear behaviors […]. Thus, we hypothesized that bilateral amygdala lesions would reduce CO2-evoked fear in humans.
In contrast with our prediction, patient SM reported fear in response to a 35% CO2 inhalation challenge. To the best of our knowledge, this was the first time patient SM experienced fear in any setting, laboratory or otherwise, since childhood […]. To further explore this issue, we tested two additional patients (AM and BG), monozygotic twin sisters with focal bilateral amygdala lesions resulting from Urbach-Wiethe disease […] As with patient SM, both patients also reported experiencing fear during the CO2 challenge.” (Feinstein et al., 2013)
These startling observations affirm that the reaction to carbon dioxide (and probably, hypoxia as well) must be due to an alternative alarm system, such as has been proposed for possible suffocation (Maurice Preter and Donald F. Klein. Lifelong opioidergic vulnerability through early life separation: A recent extension of the false suffocation alarm theory of panic disorder. Submitted for publication).
