Deficits in emotional processes are often observed by clinicians in anorexia nervosa and may have an impact on social functioning. Recognition of emotion was mostly investigated using visual stimuli as faces of emotional scenes. Only one study (Kucharska-Pietura et al., 2004) demonstrated impairments in emotional prosody using positive and negative valenced stimuli. However, this study did not provide a highlight for the identification of emotional bias (for example, to recognize an intense fear in a friendly voice). The aim of this study is to better understand the recognition of emotional prosody in anorexia nervosa using a wide range of positive, negative and neutral stimuli (Belin et al., 2008). In order to test emotion recognition biases in emotional prosody, we exposed 15 patients with anorexia nervosa and 15 healthy controls (HCs) to emotional vocal tasks asking them to rate emotional intensity on visual analog scales. In addition, we assessed clinical symptomatology and cognitive functioning for all participants. We showed that patients with anorexia nervosa provided higher intensity ratings on the non-target scales (e.g., surprise scale for fear stimuli) than HCs for sadness, fear and neutral voices. Furthermore, with the exception of neutral vocal stimuli, they provided the same intensity ratings on the target scales as the HCs. These findings suggested a bias in the processing of emotional prosody and may impact the social functioning of patients with anorexia nervosa. The bias may result from a sensorial deficit or a high-order cognitive dysfunction and have to be investigated in future studies.

We discuss the importance of cognitive abnormalities in unipolar depression, drawing the distinction between “hot” (emotion-laden) and “cold” (emotion-independent) cognition. “Cold” cognitive impairments are present reliably in unipolar depression, underscored by their presence in the diagnostic criteria for major depressive episodes. There is good evidence that some “cold” cognitive abnormalities do not disappear completely upon remission, and that they predict poor response to antidepressant drug treatment. However, in many studies the degree of impairment is moderately related to symptoms. We suggest that “cold” cognitive deficits in unipolar depression may in part be explicable in terms of alterations in “hot” processing, particularly on tasks that utilize feedback, on which depressed patients have been reported to exhibit a “catastrophic response to perceived failure.” Other abnormalities in “hot” cognition are commonly observed on tasks utilizing emotionally valenced stimuli, with numerous studies reporting mood-congruent processing biases in depression across a range of cognitive domains. Additionally, an emerging literature indicates reliable reward and punishment processing abnormalities in depression, which are especially relevant for hard-to-treat symptoms such as anhedonia. Both emotional and reward biases are strongly influenced by manipulations of the neurochemical systems targeted by antidepressant drugs. Such a pattern of “hot” and “cold” cognitive abnormalities is consistent with our cognitive neuropsychological model of depression, which proposes central roles for cognitive abnormalities in the generation, maintenance, and treatment of depressive symptoms. Future work should examine in greater detail the role that “hot” and “cold” cognitive processes play in mediating symptomatic improvement following pharmacological, psychological, and novel brain circuit-level interventions.

Background: Divergences in cognitive disturbances in hypothyroidism reported in the literature are a result of a methodological bias. Methods: By using a precise methodology, we examined attention and executive functions in hypothyroidism, verified the presence of anxiety and depressive symptoms in hypothyroidism, and examined the possible link between these symptoms and the cognitive disturbances (searching for attentional bias for words with a negative emotional valence). We administered a battery of cognitive tests to 23 participants who had undergone thyroidectomy for thyroid carcinoma: for the first time in an euthyroid state, then 3 weeks later (still in the euthyroid state) to assess the test/retest effect, and finally 4 weeks later in an hypothyroid state. We compared their performance with that of a group of 26 control participants who were also administered the same cognitive tests, also 3 times. Results: In hypothyroidism, the thyroid participants were more anxious and depressed than the controls and presented attentional and executive disturbances that reflected general slowing and difficulties in using their capacities of inhibition. However, they did not exhibit an attentional bias for words with a negative emotional valence. Conclusions: Contrary to what was expected, symptoms of anxiety and not symptoms of depression interfered with the cognitive performance of participants in hypothyroidism. (JINS, 2005, 11, 535–544.)