J Autism Dev Disord (2006) 36:1143–1145 DOI 10.1007/s10803-006-0287-7

LETTER

Response to ‘‘Letter to the Editor: The Overlap Between Alexithymia and Asperger’s Syndrome’’, Fitzgerald and Bellgrove, Journal of Autism and Developmental Disorders, 36(4) Elisabeth L. Hill Æ Sylvie Berthoz

Published online: 1 November 2006 Ó Springer Science+Business Media, LLC 2006

Dear Editor We read with interest the letter of Fitzgerald and Bellgrove outlining their views on the possibility of an overlap between Alexithymia and Asperger syndrome (Fitzgerald & Bellgrove, 2006). It is refreshing to see that others are noting a similarity between certain aspects of these two conditions. However, a number of relevant studies were not mentioned. Consequently we feel that it is important to provide information concerning direct studies of this topic, as well as of recent neuroimaging studies of alexithymia, in order to provide a broader, and more direct base of evidence with which to inform these discussions. We have reported data from two studies investigating the presence of alexithymia-type symptoms in a group of high-functioning adults with ASD, many of whom had a specific diagnosis of Asperger syndrome. In the first of these studies, we assessed levels of alexithymia using the TAS-20 (Bagby, Parker, & Taylor, 1994; Bagby, Taylor, & Parker, 1994) in a group of high-functioning adults with ASD. We reported the responses of 27 ASD adults in comparison to 35 controls (matched for age and gender) and 49 relatives of people with ASD on this self-report measure (Hill, Berthoz, & Frith, 2004). As far as we E. L. Hill (&) Department of Psychology Goldsmiths College, University of London, New Cross, London SE14 6NW, UK e-mail: [email protected] S. Berthoz Department of Psychiatry for Adolescents and Young Adults, Institut Mutualiste Montsouris, University Paris V, Paris, France

are aware, this was the first study to address directly the issue of the existence of such aspects of emotion regulation difficulties in ASD. In addition to showing that adults with high-functioning forms of ASD are able to report their own emotional processes, we also showed that these individuals had significantly higher alexithymia scores than the control group (ASD mean 60.44, SD 10.84; control mean 42.51, SD 9.09). Furthermore, the individuals with ASD had significantly higher alexithymia scores than the group of relatives (who did not differ from the control group; relatives mean 42.4, SD 10.07). When placing participants into non-impaired, slightly impaired and severely impaired alexithymia categories using previously established cut-off scores (Bagby et al., 1994), adults with ASD fell overwhelmingly into the slightly and severely impaired categories, while few of the controls or relatives fell into the slightly impaired group, and none of these groups were categorised as severely impaired. The hypothesis that the results may be explained by between-group differences in depression scores was ruled out (Hill et al., 2004). In a second study we demonstrated that deficits in emotion regulation are stable over time in ASD, with TAS-20 test-retest reliability being high for both the total score on this test (r2 = 0.9, P < 0.001) and for each of the three subscales (difficulty identifying feelings, r2 = 0.81, P < 0.001; difficulty describing feelings, r2 = 0.79, P < 0.001; externally oriented feelings, r2 = 0.86, P < 0.001) (Berthoz & Hill, 2005). Furthermore, the deficits observed on the TAS-20 were replicated in another alexithymia scale, the BermondVorst Alexithymia Questionnaire-B (BVAQ-B) (Vorst & Bermond, 2001). More specifically, deficits in emotion regulation were found in ASD in the cognitive

123

1144

factors of the BVAQ-B (measuring: difficulties verbalizing emotional experiences, poor insight into one’s emotional experiences, difficulties analyzing one’s own emotional states and reactions), but not in its affective factors (measuring: poor daydreaming and fantasies, low emotional excitability to emotion-inducing events). This corresponds to the alexithymia Type II proposed by Bermond (1997). According to this account, Type I alexithymia is characterised by a low degree of conscious awareness of emotional arousal and a low degree of emotion accompanying cognitions. Type II alexithymia is characterised by a normal or high degree of conscious awareness of emotional arousal together with a low degree of accompanying cognitions. Finally, we have since replicated all of the findings described above in a larger study in which we assessed alexithymia using both the TAS-20 and BVAQ-B in a sample of 42 adults with high-functioning forms of ASD, 73 controls and 96 relatives of individuals with ASD. The consistency of our findings is striking and provides clear support for the view that those with ASD are likely to show symptoms of alexithymia. It is important to note, however, that in no study were all participants with ASD categorised as alexithymic according to their responses to the TAS-20. In their section on the ‘aetiology of alexithymia’, Fitzgerald & Bellgrove suggest a potential link between a cognitive processing style proposed to explain some of the assets observed in those with ASDs (weak central coherence) and alexithymia. There are, however, other potential explanations that should also be investigated. Following our first study, we speculated that a deficit in theory of mind (mentalising) might be the cause of the emotion processing difficulties observed in our sample of adults with ASD. The theory of mind deficit account is an influential theory explaining many of the difficulties seen in ASD and highlights how poor understanding of, and participation in, social interaction and communication might arise from a difficulty in understanding that one’s own beliefs, desires etc can be different from those of another person. A similar speculation has been offered by Gillberg and Ra˚stam (1992) in relation to individuals with anorexia nervosa, a psychiatric disorder in which a high prevalence of emotional processing deficit has been documented (Taylor, 1997). While many of the adults with ASD who participated in our studies showed a great deal of compensatory learning of social communication, our results suggested that even this degree of compensation was not enough to eliminate emotion processing difficulties. As a result, these may remain tell-tale signs of underlying theory of mind problems in ASDs. Since unaffected relatives do not

123

J Autism Dev Disord (2006) 36:1143–1145

suffer strikingly from an underlying theory of mind deficit, they would also not be expected to show the emotion processing difficulties that can be revealed by the emotion processing questionnaires Until recently there has been only indirect, but nonetheless supportive neuroanatomical evidence for a possible link between the alexithymia and autistic symptoms in social cognition. In the ‘normal’ brain a network of brain areas has been identified that is consistently active during mentalising over and above other task demands. This network involves the medial prefrontal cortex (especially anterior paracingulate cortex), the temporal-parietal junction, the insula and the temporal poles, and has been shown to be compromised in ASD (see Frith & Frith, 2006; Frith, 2001 for a review). Furthermore, anterior cingulate and its frontal connections have been implicated in affect perception and the regulation of emotion (Lane et al., 1998), leading Lane, Ahern, Schwartz, & Kaszniak (1997) to propose the ‘blindfeel’ hypothesis of alexithymia. In this account, anterior cingulate cortex dysfunction is implicated in alexithymia. Data from a functional MRI study of men with and without alexithymia provides partial support for this view, finding reduced cerebral activation in the left mediofrontal-paracingulate cortex in response to highly negative stimuli and increased activation in anterior cingulate, mediofrontal cortex and middle frontal gyrus in response to highly positive stimuli in men with versus men without alexithymia (Berthoz et al., 2002). In addition Kano et al. (2003) reported a number of interesting findings in a PET study including reduced activation in anterior cingulate and the insula in response to angry faces versus neutral faces in participants with and without alexithymia. A further neuroimaging study has provided similar evidence for atypical activation of areas known to be important in emotion processing in individuals with alexithymia, particularly posterior cingulate cortex (Mantani, Okamoto, Shirao, Okada, & Yamawaki, 2005; see Aleman, 2005 for review). Recently direct evidence of a link between alexithymia and theory of mind has been reported. Moriguchi et al. (2006) have shown an impairment in mentalising in individuals with alexithymia versus those without when describing what two triangles were doing in a silent, visual animation. While all participants showed activation in the neural network associated with mentalising, activation of the medial prefrontal cortices part of this network was lower in those with alexithymia. Activation in this area was correlated positively with mentalising score and with score on the interpersonal reactivity index (IRI), a

J Autism Dev Disord (2006) 36:1143–1145

measure of empathic ability. A positive correlation was also seen between activation of the right temporal pole and both mentalising and IRI personal distress score. Taken together, these findings suggest that individuals with alexithymia have an impairment in mentalising that is associated with an inability to take the perspective of another person. Finally, alexithymia has been reported to be inversely related to the capacity for empathy in those with disorders known to be associated with theory of mind deficits such as borderline personality disorders (Guttman & Laporte, 2002) and psychopathy (Haviland, Sonne, & Kowert, 2004). We agree with Fitzgerald & Bellgrove that there is some form of overlap between alexithymia and ASDs. Clearly this is an important area of investigation that assimilates a number of related areas (emotion processing per se, alexithymia, autism spectrum disorders, to name just three). In our opinion, there are two important aspects to future studies. One is to investigate directly the relationship between symptoms of alexithymia and autism spectrum disorders at the behavioural and cognitive levels. The second is to compare directly individuals with ASD who are/are not alexithymic on their behavioural performance on emotion processing tasks as well as in terms of their neural activity while performing these tasks (see Bird et al., 2006).

References Aleman, A. (2005). Feelings you can’t imagine: towards a cognitive neuroscience of alexithymia. Trends in Cognitive Sciences, 9(12), 553–555. Bagby, R. M., Parker, J. D. A., & Taylor, G. J. (1994). The twenty item Toronto Alexithymia Scale-I. Item selection and cross-validation of the factor structure. Journal of Psychosomatic Research, 38, 23–32. Bagby, R. M., Taylor, G. J., & Parker, J. D. A. (1994). The twenty item Toronto Alexithymia Scale-II Convergent, discriminant, and concurrent validity. Journal of Psychosomatic Research, 38, 33–40. Bermond, B. (1997). Brain and Alexithymia. In A. Vingerhoets, F. Bussel, J., & Boelhouwer (Eds) The (non)Expression of emotions in health and disease (pp. 115–130). Tilburg University Press: Tilburg, The Netherlands. Berthoz, S., Artiges, E., Van de Moortele, P. F., Poline, J.-B., Rouquette, S., & Consoli, S. M., et al. (2002). Effect of impaired recognition and expression of emotions on frontocingulate cortices: an fMRI study of men with alexithymia. American Journal of Psychiatry, 159, 961–967.

1145 Berthoz, S., Hill, E. L. (2005). Reliability of the Bermond-Vorst Alexithymia Questionnaire. Data from adults with autism spectrum disorder, their relatives and normal controls. European Psychiatry, 20, 291–298. Bird, G., Silani, G., Brindley, R., Singer, T., Frith, C., & Frith, U. (2006). Alexithymia in autism spectrum disorders. Paper presented at the Human Brain Mapping, 11th–15th June, Florence, Italy. Fitzgerald, M., Bellgrove, M. A. (2006). Letter to the editor: The overlap between alexithymia and Asperger’s syndrome. Journal of Autism and Developmental Disorders, 36(4), 573– 576. Frith, C. D., Frith U. (2006). The neural basis of mentalizing. Neuron, 50, 531–534. Frith, U. (2001). Mindblindness and the brain in autism. Neuron, 32, 969–979. Gillberg, C., Ra˚stam, M. (1992). Do some cases of anorexia nervosa reflect autistic-like conditions? Behavioural Neurology, 5, 27–32. Guttman, H., Laporte, L. (2002). Alexithymia, empathy, and psychological symptoms in a family context. Comprehensive Psychiatry, 43(6), 448–455. Haviland, M. G., Sonne, J. L., Kowert, P. A. (2004). Alexithymia and psychopathy: comparison and application of California Q-set prototypes. Journal of Personality Assessment, 82(3), 306–316. Hill, E. L., Berthoz, S., Frith, U. (2004). Cognitive processing of own emotions in individuals with autistic spectrum disorder and their relatives. Journal of Autism and Developmental Disorders, 34, 229–235. Kano, M., Fukudo, S., Gyoba, J., Kamachi, M., Tagawa, M., Mochizuki, H., et al. (2003). Specific brain processing of facial expressions in people with alexithymia: an H15 2 O-PET study. Brain, 126, 1474–1484. Lane, R.D., Ahern, G.L., Schwartz, G. E., Kaszniak, A. W. (1997). Is alexithymia the emotional equivalent of blindsight? Biological Psychiatry, 42, 834–844. Lane, R. D., Reiman, E., Axelrod, B., Lang-Sheng, Y., Holmes, A., Schwartz, G. E. (1998). Neural correlates of levels of emotional awareness. Evidence of an interaction between emotion and attention in the anterior cingulate cortex. Journal of Cognitive Neuroscience, 10, 525–535. Mantani, T., Okamoto, Y., Shirao, N., Okada, G., Yamawaki, S. (2005). Reduced activation of posterior cingulate cortex during imagery in subjects with high degrees of alexithymia: a functional magnetic resonance study. Biological Psychiatry, 57, 982–990. Moriguchi, Y., Ohnishi, T., Lane, R. D., Maeda, M., Mori, T., Nemoto, K., et al. (2006). Impaired self-awareness and theory of mind: an fMRI study of mentalizing in alexithymia. NeuroImage, 32(3), 1472–1482. Taylor, G. J. (1997). Eating disorders. In G. J. Taylor, R. M. Bagby, & J. D. A. Parker (Eds) Disorders of affect regulation: Alexithymia in medical and psychiatric illness (pp. 190–215). Cambridge: Cambridge University Press. Vorst, H. C. M., Bermond, B. (2001). Validity and reliability of the Bermond-Vorst Alexithymia Questionnaire. Personality & Individual Differences, 30, 413–434.

123