Both groups performed the same on the first order question about the conflicting belief. The same applied to the second order conflicting belief and the associated emotional state, but these latter questions were very difficult to interpret which may explain the lack of a difference. Both groups scored equally well on the control questions, which confirms that there was no difference in understanding of the story. Consistent with findings of Wastell and Taylor [44] who reported normal performance of alexithymic individuals in a false belief task, our findings confirm that the high alexithymic group was quite able to think about others in a different situation. Our results extend this by showing that the impairment is specific for emotions. Interestingly, in a study employing the same task, patients with early amygdala damage also made more errors in emotional attributions [36]. As both patients with amygdala damage and high alexithymic individuals fail to attribute the correct emotional state to another person, it would be interesting to specifically investigate the role of the amygdala in alexithymia. Subclinical amygdala damage could be the neural basis for certain forms of alexithymia. To some extent this has already been investigated but without confirming altered amygdala activation in alexithymia [17,45,46]. However, these studies did not specifically focus on the amygdala or used relatively small subject groups [45,46] or did not specifically look at emotion processing [17]. It therefore remains an interesting possibility that subclinical amygdala damage could be the neural basis for certain forms of alexithymia. Alexithymic individuals were not only impaired on higher order emotion processing but also on low level early processing of emotions. Lane et al. [8], already demonstrated that highly alexithymic participants have deficits in recognition of emotions. We observed that, after a training session, alexithymic individuals recognized micro-expressions less accurately than non-alexithymic participants. Thus, alexithymic individuals do not benefit from training in visual emotional features to such an extent that they can equal the performance of non-alexithymics’. To extend studies on visual emotional processing, we included an auditory emotional task: judging the emotional tone of spoken language i.e. prosody. This emotional prosody task previously indicated deficits in Klinefelter [47] and schizophrenia [48] patients. The current study is, as far as we know, the first to examine affective prosody in alexithymia. Sentences had an emotional semantic content and were spoken with an incongruent prosody. Alexithymic individuals did not demonstrate problems with recognizing emotional content nor prosody. It thus seems that alexithymia is not specifically an emotional language-related problem. Lane et al. [43] suggested that in alexithymia emotional experience is blunted or absent in contrast to aprosodic individuals who experience emotions fully. Thus, these two disorders rely on different mechanisms. On a more cognitive-emotional level high alexithymics were not impaired on associative emotional learning nor on identity References 1. Sifneos PE (1973) The prevalence of ‘alexithymic’ characteristics in psychoso- matic patients. Psychotherapy and Psychosomatics 22: 255–262. 2. Bagby RM, Taylor GJ (1997) Affect dysregulation and alexithymia. In: Taylor GJ, Bagby RM, Parker JDA, eds. Disorders of Affect regulation: alexithymia in medical and psychiatric illness. Cambridge: Cambridge University Press. 3. Taylor GJ, Bagby RM, Parker JDA (1997) Disorders of affect regulation alexithymia in medical and psychiatric illness. Cambridge: Cambridge University Press. 4. van ’t Wout M, Aleman A, Bermond B, Kahn RS (2007) No words for feelings: alexithymia in schizophrenia patients and first-degree relatives. Comprehensive Psychiatry 48: 27–33. Alexithymia and Emotion learning. This is in disagreement with the notion that they have difficulties coupling words to emotional states [19]. It thus appears that the task does not correlate well with the verbalizing scale of the BVAQ. Possibly, this is the case because verbalizing requires associating words with one’s own emotions whereas for this task words had to be associated with external images of facial expressions. Regarding any negative findings, it should be noted that neurophysiological differences may nevertheless be present. Specifically, Vermeulen et al. [49] found no effects of alexithymia on perception of emotional expressions, despite delayed neuro- physiologic responses. Furthermore, the generalizability of this study is limited by the fact that only healthy university students participated, who on average function at a high level. Studies on people with very high levels of alexithymia, e.g. patients with psychosomatic complaints, may present different results. A clinical implication of our findings might be that training or therapy focused on awareness, recognition and regulation of emotions might be beneficial for individuals with alexithymia. Greenberg [50] proposed one such approach, named ‘‘emotion- focused therapy’’. In this approach, patients are taught how to become aware of their emotions, to understand their bodily reactions, and to express emotion in a context appropriate way. Although not specifically designed for alexithymic individuals, it could be tailored to each individual [50]. In sum, questionnaires indicated that participants scoring high on the cognitive component of alexithymia are characterized by suppressive rather than reappraisal strategies. In addition, alexithymic individuals showed specific deficits in emotional processing. Alexithymic individuals were impaired on recognition of briefly presented emotional expressions and on emotional mentalizing. No deficits were seen in processing of emotional language nor in associating words to emotional faces. This implies that the interaction of language and emotions might not be at the core of alexithymia. Future studies are necessary to explore the specific emotion processing difficulties in alexithymia. The use of brain imaging may help unravel brain mechanisms underlying emotional processing deficits in alexithymia. For example, Aleman [19] suggested that compromised interactive processing in hippocampal–amygdala circuits during emotional relational mem- ory could underlie the verbalizing problems in alexithymia. Neuroimaging techniques and appropriate data analysis methods may enable us to shed more light on brain structures that are implicated in alexithymia. Author Contributions Conceived and designed the experiments: MS AA. Performed the experiments: MS. Analyzed the data: MS AA. Wrote the paper: MS AA. Interpreted the data: MS RK AA. Critically read the manuscript and gave helpful comments to improve the text: RK AA. 5. Mattila AK, Poutanen O, Koivisto AM, Salokangas RKR, Joukamaa M (2007) Alexithymia and life satisfaction in primary Healthcare patients. Psychosomatics 48: 523–529. 6. Salminen JK, Saarijarvi S, Aarela E, Toikka T, Kauhanen J (1999) Prevalence of alexithymia and its association with sociodemographic variables in the general population of Finland. Journal of Psychosomatic Research 46: 75–82. 7. Lane RD, Sechrest L, Reidel R, Weldon V, Kaszniak A, et al. (1996) Impaired verbal and nonverbal emotion recognition in alexithymia. Psychosomatic Medicine 58: 203–210. 8. Lane RD, Sechrest L, Reidel R, Weldon V, Kaszniak A, et al. (2000) Pervasive emotion recognition deficit common to alexithymia and the repressive coping style. Psychosomatic Medicine 62: 492–501. PLoS ONE | www.plosone.org 6 June 2009 | Volume 4 | Issue 6 | e5751