Transcallosal Inhibition in Patients with and without Alexithymia

Abstract

Objective: Previous results indicated a facilitated transcallosal inhibition via the corpus callosum (CC) in alexithymic male students. This study investigates transcallosal inhibition in alexithymic and nonalexithymic psychiatric inpatients. Method: Transcallosal inhibition was elicited by means of transcranial magnetic stimulation (TMS) of the primary motor cortex. Seven right-handed male and 12 female psychiatric patients with Toronto Alexithymia Scale (TAS-20) scores of ≧61 and 12 patients with TAS-20 scores of <51 were investigated. The transcallosal conduction time (TCT) reflects the TMS-induced inhibitory cortical activity that is mediated via the CC. Results: There was a significant effect of alexithymia on TCT (Wilks λ = 0.76; F = 4.1; d.f. = 2, 26; p = 0.027) indicating that alexithymic patients had shorter bidirectional TCTs than nonalexithymic patients. The in-between models showed a significant impact of alexithymia on both right to left TCT (F = 4.8; d.f. = 1; p = 0.038) and left to right TCT (F = 5.0; d.f. = 1; p = 0.033). Neither gender nor scores of depression (Montgomery-Asberg Depression Rating Scale) had any significant effects on TCT. Conclusion: Our results confirm and extend the previous findings of a facilitated, bidirectional transcallosal inhibition in alexithymia to male and female psychiatric inpatients. Facilitated transcallosal inhibition should be considered as a neurobiological correlate of alexithymia.

Brain potentials to emotional pictures are modulated by alexithymia during emotion regulation

“…In contrast, individuals scoring high in alexithymia are more frequent users of suppression and, therefore, more likely to have developed overtrained schemata of efficient suppression techniques, increasing thereby their chances of success when using suppression. This explanation is consistent with previous research indicating that alexithymia scores are linked to a more frequent utilization of suppression techniques (e.g., Dimsdale et al, 1986;Franz et al, 2004;Grabe et al, 2004;Kessler et al, 2010;Richter et al, 2006;Swart et al, 2009). This explanation is also consistent with research suggesting that long-term expertise in regulation techniques improves efficiency in controlling emotional responses (Dalgleish, Yiend, Schweizer, & Dunn, 2009;Wegner & Gold, 1995).…”

“…Alexithymia is a trait in which individuals have a reduced ability to regulate, identify, and communicate feelings or emotions (Franz, Schaefer, Schneider, Sitte, & Bachor, 2004;Sifneos, 1973). Importantly, alexithymia seems to be characterized by an emotion regulation style overreliant on suppression, rather than reappraisal, strategies (e.g., Dimsdale et al, 1986;Franz et al, 2004;Grabe et al, 2004;Kessler, Kammerer, Hoffmann, & Traue, 2010;Richter et al, 2006;Swart, Kortekaas, & Aleman, 2009). For instance, Kessler et al found a positive relationship between TAS scores and individual differences in expressive suppression.…”

Alexithymia, suicidal ideation, and serum lipid levels among drug-naïve outpatients with obsessive-compulsive disorder

“…Alexithymia probably results from an inhibitory mechanism that could contribute to a suppression of emotional processing within the right hemisphere and to poorer verbalization of emotional contents (within the left hemisphere). 38 Kano et al, 39 using positron emission tomography (PET), showed that alexithymic males had lower regional cerebral blood flow in the inferior and middle frontal cortex, OFC, inferior parietal cortex, and occipital cortex in the right hemisphere than nonalexithymics while viewing a range of emotional facial expressions. These findings were also largely confirmed by Berthoz et al 40 in a functional magnetic resonance imaging (fMRI) study.…”

Case report: Short-term psychotherapy for alexithymia in a patient with generalized anxiety disorder

“…Individuals with alexithymia exhibited heightened overall severity of disorder, a phenomenon particularly attributed to the increased severity of somatic symptoms associated with GAD ( 30 ). This correlation has been attributed to alexithymia originating from an inhibitory mechanism, which is believed to impede emotional processing within the right hemisphere, thereby diminishing the ability to verbalize emotional content within the left hemisphere ( 31 , 32 ). Moreover, it has been established that GAD is specifically marked by deficiencies in emotional intelligence and in the experiences and regulation of emotions.…”