Chapter 2 64 Due to the results of alexithymia research in the field of affective neuroscience during the last decades, alexithymia is nowadays conceptualized as a neurocognitive disturbance in the perception and representation of affective responses [5, 72, 76]. With this disturbance, the representation of emotions by the individual is hardly or not at all there, implying that no (differentiated) conceptual understanding of the experienced reaction occurs. There is no ‘feeling the feeling’ [10]. This conceptualization, due to its more in-depth description and biological underpinnings, goes beyond the original definition of ‘not having words’ for emotions and potentially offers possibilities for improving diagnostics and treatment. There still remains a good deal about alexithymia that is not well understood or known. For example, it is not clear whether psychological defense mechanisms play a role in alexithymia. It is assumed that the lack of emotional awareness in alexithymia arises from a disturbance in the cognitive processing (i.e., representation) of emotions, against a background of an intact initial (physiological) response to an emotional event. However, the theoretical framework of emotional awareness is a broader one than that of alexithymia [76, 122]; the absence of emotional awareness can result from processes other than a profound disturbance or deficit in cognitive-affective processing. In the case of the mechanism of ‘psychological defense’, the representation of the emotion is, in principle, intact, but no longer enters conscious experience. In daily clinical practice, it is very difficult to tell them apart. We put our hope on future research developments that will yield the necessary diagnostic instruments to distinguish one from the other, mainly because, in our view, defense mechanisms should not be considered part of the alexithymiaspectrum. Based on the neurocognitive model of emotional awareness, a psychological defense mechanism is part of the domain of (dysfunctional) emotion regulation; therefore, it is not a deficiency in the conception or representation of emotions. This is also true for emotional overload. Although emotional overload can lead to symptoms that mimic alexithymia, they have a different origin. In the newly proposed terminology by Lane [76], emotional overload would at best be a form of (temporary) anomia – as opposed to agnosia, or ‘true alexithymia’. Another outstanding point of debate is whether limited emotional arousability and/or (limited) emotional awareness are part of the concept(s) of alexithymia. Decades of research on low emotional arousability and alexithymia failed to yield clarity regarding the relationship between the two. Alexithymia (agnosia) could occupy the extreme pathological end of the broad spectrum of emotional awareness while impaired emotional – but not completely absent – arousability seems to find a place in the spectrum as well [59, 70, 106].
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