Somatosensory amplification
Another well-reported characteristic of alexithymia is somatosensory amplification. Research has shown that patients with chronic pain have higher levels of alexithymia than control subjects, and alexithymia is associated with overreporting of physical symptoms [
13,
20,
53‐
55]. An association between alexithymia and increased pain intensity and sensitivity to experimentally induced pain has been demonstrated [
56‐
58]. The degree of alexithymia correlates with the score of somatosensory amplification [
59]. Therefore, alexithymics might perceive signals from the body in an aberrant manner such that low-intensity stimulation is perceived as high intensity. In particular, functional gastrointestinal disorders, such as irritable bowel syndrome, characterized by chronic gastrointestinal symptoms with no biochemical abnormalities, are associated with alexithymia [
14,
60,
61].
Therefore, in our second study, we investigated brain responses to visceral stimulation induced by colonic distension between alexithymics and nonalexithymics. During colonic distension, greater activation was observed in the pregenual ACC, right insula, and midbrain in subjects with alexithymia [
19]. The TAS-20 score correlated positively with both activity in the right insula and orbital gyrus and adrenaline levels in the blood in response to stimulation. Subjects with high scores for difficulty identifying feelings perceived strong pain, urgency for defecation, stress, and anxiety.
Visceral stimulation, especially by colonic distension, has been reported to elicit activation of various brain areas including the posterior insula, prefrontal cortex (PFC), ACC, and brainstem periaqueductal gray (PAG) [
62‐
64]. A detailed, dynamic representation of particular internal bodily states and the mapping of each interoceptive state occurs within the orbitofrontal and right insular cortices [
65,
66]. In the cingulate cortex, the pregenual ACC responds to visceral stimulation and is associated with the perception of secondary pain, which is characterized by greater unpleasantness [
67]. Electrical stimulation of the insula has been reported to elicit changes in blood pressure, heart rate, respiration, gastric motility, peristaltic activity, salivation, and adrenaline secretion [
68]. In addition, the orbitofrontal cortex has been shown to receive robust sensory input and to act as an internal environmental integrator that coordinates behavioral, autonomic, and endocrine responses [
69]. The brainstem is known to control ascending nociceptive input and nuclei such as the rostral ventromedial medulla and PAG, which are able to both inhibit and facilitate nociceptive responses. In particular, activation of the right PAG has been reported to correlate with anxiety during visceral stimulation but not somatic stimulation [
70]. Therefore, it may be assumed that activation of brain areas associated with alexithymia represents afferent representation of bodily states and efferent autonomic and endocrine responses that accompany it. Alexithymics may be more aroused by interoception of unpleasant feelings than nonalexithymics, thereby displaying more autonomic responses.
The evidence supports the somatosensory amplification hypothesis of alexithymia. There have been no other imaging studies investigating pain or interoception processing in alexithymia. However, a few, in which interoceptive or physiologic arousal was induced, have provided suggestive findings. Moriguchi et al. examined brain responses of alexithymics during visual perception of pictures depicting human hands and feet in painful situations [
26]. In this task assessing empathy to others’ pain, alexithymics showed greater brain activity in the posterior and anterior insula. The posterior insula is the primary endpoint of the interoceptive pathway, which represents sensory aspects from the body including pain, touch, and visceral sensation [
43,
65]. The information in the posterior insula is rerepresented in the right anterior insular cortex, which provides subjective awareness of the feelings from the body, that is, metarepresentation of interoception [
43,
65]. Other brain areas in the pain matrix, such as the dorsolateral PFC, dorsal pons, and left caudal ACC, which are associated with modulation of pain sensations, are less activated, and the pain rating is lower in alexithymics [
26]. Yet, the greater activity in the insula indicates a stronger response in the representation of the internal physiologic state in alexithymics [
26].
There are overlapping characteristics of deficits in emotional experience and expression between posttraumatic stress disorder (PTSD) and alexithymia [
7,
8]. Frewen et al. investigated functional neural responses to trauma script imagery associated with severity of alexithymia in a subsample of 26 individuals with PTSD [
71]. The TAS-20 score was correlated with increased activity in the right posterior insula and ventral posterior cingulate and decreased activity in the bilateral ventral ACC, ventromedial PFC (vmPFC), anterior insula, and right inferior frontal cortex [
71]. Correlation between alexithymic score and right insular activation might be associated with centrally represented body-state mapping of sympathetic arousal, coupled with reduced executive–regulatory cognitive–affective control via the ventral ACC, medial (mPFC), and right inferior frontal cortex [
43,
45,
65,
66].
Both Moriguchi’s [
22] and Frewen’s [
70] studies mentioned above provide further evidence that alexithymia is associated with greater activation in the insular cortex representing interoceptive arousal in response to the internal body-state condition. Interestingly, a recent study measured empathic brain responses in subjects with autism spectrum disorder and control subjects, in which participants anticipated their partner’s pain, which was indicated by an anticipatory cue (colored arrow) [
72]. Activity in the anterior insula during the task was negatively correlated with individual differences in TAS score in both subjects with autism spectrum disorder and control subjects [
72]. It is quite an interesting phenomenon that real pain and pictures of painful stimuli or a traumatic event induce hyperactivity in the posterior insula, whereas imagination of a partner’s pain provokes less activation in the anterior insula associated with alexithymia. This gradation of activity in the insular cortex accompanying the gradation of the real level of pain appears to explain alexithymic features remarkably. With regard to pain experience, alexithymics may experience pain more strongly at a primitive perceptual level and may not be able to experience pain at a more abstract, conceptual, formal, operational stage. This phenomenon matches the theory of deficient affect development in alexithymia [
7,
11].