Introduction
Alexithymia is a subclinical condition of difficulty in identifying, describing, and processing emotions. Alexithymic persons often experience difficulty distinguishing physical from emotional sensations, possess a poor vocabulary of affect terms (outward expressions of emotion), and are externally focused in their thought processes.
It is mostly assessed using the Toronto Alexithymia Scale (TAS-20), which tests factors such as difficulty in identifying feelings, difficulty in describing feelings, and externally oriented thinking. These traits affect around 10% of the general population, but in people with alexithymia, the rate is vastly increased.1 Between 50% of individuals with autism spectrum disorder, for instance, are also alexithymic, a connection that has been explained by common deficits in emotional self-awareness.2 Although not itself a disease, alexithymia has been shown to complicate emotional control, decrease empathy, and interfere with interpersonal relationships, typically appearing as other types of psychological problems.
Affected brain regions in alexithymia
Neuroimaging research has found links between alexithymia and abnormal structure and function in brain regions that are vital in the processing of emotions as well as self-awareness. The anterior cingulate cortex (ACC) plays a critical role in linking emotional cues to attention and decision-making. In subjects with high scores of alexithymia, activity within ACC has been decreased when performing emotional tasks, which is a sign of impaired emotion regulation.3 Additionally, the anterior insula, responsible for interoception (the ability to feel and understand internal signals in the body, such as feeling your heartbeat) and affective awareness, will also have diminished activity or grey matter volume in alexithymic patients.4 The amygdala, responsible for threat detection and emotional relevance, and the fusiform gyrus, responsible for face and emotion recognition, are similarly hypoactivated (under-activated). The posterior cingulate cortex and precuneus, which contribute to self-referential thinking and mentalising, are less active in tasks of emotional awareness and demonstrate an impaired emotional self-model in alexithymia.
Brain imaging
Functional imaging
Functional magnetic resonance imaging (fMRI) has shown that people with alexithymia have reduced activation of parts of the brain that are responsible for emotional awareness (including the ACC, insula, and amygdala) when exposed to emotional stimuli like facial expressions or emotional scenes.5 This hypoactivation is likely to account for the lack of emotional awareness in alexithymia.
Notably, some studies also report hyperactivation (over-activation) of frontal regions, such as the dorsolateral prefrontal cortex (dlPFC), which may suggest that the brain is trying to process emotions at a more analytical level to compensate for the under-activation of the aforementioned brain regions responsible for emotional awareness.6 This imbalance — low emotional reactivity combined with high cognitive load — may be the explanation for why emotional recognition feels mentally effortful in alexithymic individuals.
VBM studies on grey matter volume
Structural brain imaging through voxel-based morphometry (VBM) has shown that alexithymia is linked with reduced grey matter volume in several key brain regions involved in emotional awareness, interoception, and social cognition. Replicated findings indicate atrophy (reduced size) or thinning of the anterior cingulate cortex (ACC) and anterior insula, both of which are required for the integration of internal states of emotion with conscious awareness.7 In particular, the degree to which volume loss is associated with these regions typically is related to TAS-20 scores, especially on subscales assessing for difficulty in feeling and describing feelings.
Other areas, including the orbitofrontal cortex (which is concerned with the assessment of emotional salience), fusiform gyrus (crucial for the processing of facial and emotional expression), and parts of the temporal lobe, have also shown structural declines.8 These findings suggest a neuroanatomical aetiology (cause) of alexithymia, highlighting that emotional deficit could be the product either of developmental or pathological brain morphology alteration, as opposed to acquired behaviour.
EEG studies
Electroencephalogram (EEG) studies provide data about the patterns of the brain's electric activity in alexithymia, showing abnormal hemispheric asymmetries and altered connectivity. The research suggests a tendency toward hypoactivity of the right hemisphere, especially in the frontal regions, which may be responsible for decreased emotional awareness as the right hemisphere is primarily involved in emotion and social cue processing.9 Furthermore, alexithymic patients will also exhibit lower coherence between brain areas, indicative of impaired communication or coordination within and across emotional and cognitive networks.10 Aberrant EEG patterns also suggest that alexithymia involves not just regional brain dysfunction but also defective integration within the brain, which may disrupt the ability to link somatosensory experience and emotional experience.
Physical symptoms of alexithymia
Individuals with alexithymia tend to report increased sensitivity to bodily feelings, a process called somatosensory amplification. They become more attuned or more sensitive to body symptoms but cannot translate these body sensations into emotional cues, creating a level of confusion between physical pain and affective states.11 This confusion may enhance stress and anxiety levels, as body sensations that typically guide emotional processes are misinterpreted or overlooked. The tendency towards stressing somatic rather than emotional awareness can also be a causative factor in the prevalent co-morbidity of alexithymia with psychosomatic disorders.12
Causes of alexithymia
Alexithymia is believed to be caused by an interplay of developmental, genetic, and environmental factors:
- Early childhood trauma and adversity: Can disrupt the development of emotions, with alexithymic traits as a protective mechanism against being overwhelmed13
- Genetics: Some studies suggest an inherited aetiology, with certain genetic variants implicated in the impairment of emotional processing
- Neurobiological models: Highlight the role of interhemispheric disconnection, in which reduced communication between hemispheres of the brain deteriorates integration of affect and cognitive information14
All of these contribute to heterogeneity in perception and regulation of emotion.
Impact of alexithymia
Alexithymia causes impairment of empathy, which generally lowers the recognition and response to other individuals' emotions and has a burden on interpersonal relationships. Emotional detachment increases vulnerability to psychiatric illnesses such as depression, anxiety, and psychosomatic disorders by limiting effective regulation and coping with feelings.15
In addition, the absence of emotional awareness is responsible for social communication issues, such that it becomes hard to form and sustain personal relationships. These impacts highlight why alexithymia is also most closely associated with decreased quality of life and social functioning.16
Management
Whereas alexithymia is hard to treat due to reduced emotion awareness, a number of interventions hold potential:
- Emotion-focused therapy (EFT) helps clients engage in better emotional identification and expression through encouraging them to attend to body sensations and connect them with emotion17
- Mindfulness-based interventions promote awareness in the moment without criticism, which has been demonstrated to improve interoception and reduce emotional avoidance found in alexithymia.18 In addition, emotional literacy and labelling cognitive-behavioural skills assist the patients in acquiring a more sophisticated emotional vocabulary, thus improving their social functioning and mental health status
Summary
Alexithymia is characterised by difficulty in describing and naming emotions, which correlates with a decrease in size and function in discrete areas of the brain such as the anterior cingulate cortex, insula, and amygdala. Functional and structural neuroimaging studies demonstrate altered patterns of activation and reduced grey matter volume in these areas. EEG studies also indicate disrupted hemispheric asymmetry and connectivity. Somatosensory amplification tendency prioritises attention to bodily sensations over emotional significance.
Alexithymia has multifactorial aetiologies with developmental, genetic, and traumatic determinants. Alexithymia impacts empathy, mental health, and social functioning, but is manageable through emotional awareness, mindfulness, and emotion regulation treatments. Understanding these mechanisms in the brain and mind offers the prospect of improved intervention and quality of life.
FAQs
How can I tell if I have alexithymia?
Common signs include difficulty identifying or describing your feelings, feeling emotionally numb, or struggling to connect bodily sensations with emotions. Psychological assessments like the Toronto Alexithymia Scale (TAS-20) are used for diagnosis.
Does alexithymia affect relationships?
Yes, it often causes challenges in expressing emotions and understanding others’ feelings, which can lead to misunderstandings and emotional distance in personal relationships.
Can childhood experiences cause alexithymia?
Early trauma, neglect, or emotional unavailability in childhood can contribute to alexithymic traits by disrupting emotional development.
Are there any physical symptoms linked to alexithymia?
People with alexithymia may experience somatic symptoms such as unexplained pain or gastrointestinal issues due to a heightened focus on physical sensations instead of emotional cues.
What treatments help improve emotional awareness in alexithymia?
Therapies like emotion-focused therapy, mindfulness training, and cognitive-behavioural approaches focused on emotion recognition have shown benefits.
References
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- Kinnaird E, Stewart C, Tchanturia K. Investigating alexithymia in autism: A systematic review and meta-analysis. J Clin Med. 2019;8(3):314
- Moriguchi Y, Dziobek I, Heekeren HR, et al. Reduced activation in the anterior cingulate cortex during emotion processing in alexithymia. Neuroimage. 2006;32(3):1472–1482. PMID: 16875843
- Ernst J, Böker H, Hättenschwiler J, Schüpbach D, Northoff G. The association of alexithymia with altered insula activation in major depressive disorder. Psychiatry Res. 2014;214(2):132–140. PMID: 25107831
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- Mantani T, Okamoto Y, Shirao N, Okada G, Yamawaki S. Reduced activation of posterior cingulate cortex during imagery in subjects with high degrees of alexithymia. Neuropsychobiology. 2005;52(3):143–147. PMID: 16103688
- Grabe HJ, Spitzer C, Schwahn C, et al. Alexithymia, hypertension, and subclinical atherosclerosis in the general population. J Psychosom Res. 2010;68(2):139–147. PMID: 20105785
- Goerlich-Dobre KS, Bruce L, Martens S, Aleman A. Structural brain correlates of alexithymia in major depressive disorder: a voxel-based morphometry study. Psychol Med. 2015;45(14):3099–3107. PMID: 25990605
- Mohr C, Blanke O, Brugger P. Reduced hemispheric asymmetry in alexithymia: EEG evidence. Psychophysiology. 2005;42(6):790–797. PMID: 16262679
- Koven NS, Thomas CL. EEG coherence and alexithymia: disrupted neural integration in emotion processing. Clin Neurophysiol. 2010;121(2):345–353. PMID: 19897345
- Lumley MA, Stettner L, Wehmer F. Assessing alexithymia and its relationship to somatic symptoms. J Psychosom Res. 1996;41(6):541–552. PMID: 8955465
- Porcelli P, Taylor GJ, Bagby RM. Alexithymia and somatization: a quantitative review of the literature. Psychosomatics. 1995;36(6):535–546. PMID: 7490723
- Taylor GJ, Bagby RM. New trends in alexithymia research. Psychother Psychosom. 2004;73(2):68–77. PMID: 15085800
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- Berthoz S, Hill E. The validity of using self-report to assess emotion regulation abilities in alexithymia. Psychiatry Res. 2005;136(2-3):251–257. PMID: 16139873
- Grynberg D, Pollatos O. Alexithymia and social functioning: a systematic review. J Affect Disord. 2015;172:132–145. PMID: 25863214
- Elliott R, Greenberg LS, Lietaer G. Research on experiential psychotherapies. In: Lambert MJ, editor. Bergin and Garfield’s Handbook of Psychotherapy and Behavior Change. 5th ed. Wiley; 2004. p. 493–539.
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