Introduction
Acathexis is a psychoanalytic term for a lack of emotional response to significant memories or actual interactions, where such a response would normally be expected.
The term also refers more broadly to a general absence of normal or expected feelings.
Acathexis has been linked to anxiety, bipolar disorder and dementia, while the phenomenon also appears in posttraumatic stress disorder (PTSD).
Refer to Cathexis, Decathexis, Body Cathexis, Anticathexis, and Alexithymia.
Reduced affect display, sometimes referred to as emotional blunting, is a condition of reduced emotional reactivity in an individual.
It manifests as a failure to express feelings (affect display) either verbally or nonverbally, especially when talking about issues that would normally be expected to engage the emotions. Expressive gestures are rare and there is little animation in facial expression or vocal inflection. Reduced affect can be symptomatic of autism, schizophrenia, depression, posttraumatic stress disorder, depersonalisation disorder, schizoid personality disorder or brain damage. It may also be a side effect of certain medications (e.g. antipsychotics and antidepressants).
Reduced affect should be distinguished from apathy and anhedonia, which explicitly refer to a lack of emotion, whereas reduced affect is a lack of emotional expression (affect display) regardless of whether emotion (underlying affect) is actually reduced or not.
A restricted or constricted affect is a reduction in an individual’s expressive range and the intensity of emotional responses.
Blunted affect is a lack of affect more severe than restricted or constricted affect, but less severe than flat or flattened affect. “The difference between flat and blunted affect is in degree. A person with flat affect has no or nearly no emotional expression. They may not react at all to circumstances that usually evoke strong emotions in others. A person with blunted affect, on the other hand, has a significantly reduced intensity in emotional expression”.
Shallow affect has equivalent meaning to blunted affect. Factor 1 of the Psychopathy Checklist identifies shallow affect as a common attribute of psychopathy.
Individuals with schizophrenia with blunted affect show different regional brain activity in fMRI scans when presented with emotional stimuli compared to individuals with schizophrenia without blunted affect. Individuals with schizophrenia without blunted affect show activation in the following brain areas when shown emotionally negative pictures: midbrain, pons, anterior cingulate cortex, insula, ventrolateral orbitofrontal cortex, anterior temporal pole, amygdala, medial prefrontal cortex, and extrastriate visual cortex. Individuals with schizophrenia with blunted affect show activation in the following brain regions when shown emotionally negative pictures: midbrain, pons, anterior temporal pole, and extrastriate visual cortex.
Individuals with schizophrenia with flat affect show decreased activation in the limbic system when viewing emotional stimuli. In individuals with schizophrenia with blunted affect neural processes begin in the occipitotemporal region of the brain and go through the ventral visual pathway and the limbic structures until they reach the inferior frontal areas. Damage to the amygdala of adult rhesus macaques early in life can permanently alter affective processing. Lesioning the amygdala causes blunted affect responses to both positive and negative stimuli. This effect is irreversible in the rhesus macaques; neonatal damage produces the same effect as damage that occurs later in life. The macaques’ brain cannot compensate for early amygdala damage even though significant neuronal growth may occur. There is some evidence that blunted affect symptoms in schizophrenia patients are not a result of just amygdala responsiveness, but a result of the amygdala not being integrated with other areas of the brain associated with emotional processing, particularly in amygdala-prefrontal cortex coupling. Damage in the limbic region prevents the amygdala from correctly interpreting emotional stimuli in individuals with schizophrenia by compromising the link between the amygdala and other brain regions associated with emotion.
Parts of the brainstem are responsible for passive emotional coping strategies that are characterised by disengagement or withdrawal from the external environment (quiescence, immobility, hyporeactivity), similar to what is seen in blunted affect. Individuals with schizophrenia with blunted affect show activation of the brainstem during fMRI scans, particularly the right medulla and the left pons, when shown “sad” film excerpts. The bilateral midbrain is also activated in individuals with schizophrenia diagnosed with blunted affect. Activation of the midbrain is thought to be related to autonomic responses associated with perceptual processing of emotional stimuli. This region usually becomes activated in diverse emotional states. When the connectivity between the midbrain and the medial prefrontal cortex is compromised in individuals with schizophrenia with blunted affect an absence of emotional reaction to external stimuli results.
Individuals with schizophrenia, as well as patients being successfully reconditioned with quetiapine for blunted affect, show activation of the prefrontal cortex (PFC). Failure to activate the PFC is possibly involved in impaired emotional processing in individuals with schizophrenia with blunted affect. The mesial PFC is activated in aver individuals in response to external emotional stimuli. This structure possibly receives information from the limbic structures to regulate emotional experiences and behaviour. Individuals being reconditioned with quetiapine, who show reduced symptoms, show activation in other areas of the PFC as well, including the right medial prefrontal gyrus and the left orbitofrontal gyrus.
A positive correlation has been found between activation of the anterior cingulate cortex and the reported magnitude of sad feelings evoked by viewing sad film excerpts. The rostral subdivision of this region is possibly involved in detecting emotional signals. This region is different in individuals with schizophrenia with blunted affect.
Flat and blunted affect is a defining characteristic in the presentation of schizophrenia. To reiterate, these individuals have a decrease in observed vocal and facial expression as well as the use of gestures. One study of flat affect in schizophrenia found that “flat affect was more common in men, and was associated with worse current quality of life” as well as having “an adverse effect on course of illness”.
The study also reported a “dissociation between reported experience of emotion and its display” – supporting the suggestion made elsewhere that “blunted affect, including flattened facial expressiveness and lack of vocal inflection … often disguises an individual’s true feelings.” Thus, feelings may merely be unexpressed, rather than totally lacking. On the other hand, “a lack of emotions which is due not to mere repression but to a real loss of contact with the objective world gives the observer a specific impression of ‘queerness’ … the remainders of emotions or the substitutes for emotions usually refer to rage and aggressiveness”. In the most extreme cases, there is a complete “dissociation from affective states”. To further support this idea, a study examining emotion dysregulation found that individuals with schizophrenia could not exaggerate their emotional expression as healthy controls could. Participants were asked to express whatever emotions they had during a clip of a film, and the participants with schizophrenia showed deficits in behavioural expression of their emotions.
There is still some debate regarding the source of flat affect in schizophrenia. However, some literature indicates abnormalities in the dorsal executive and ventral affective systems; it is argued that dorsal hypoactivation and ventral hyperactivation may be the source of flat affect. Further, the authors found deficits in the mirror neuron system may also contribute to flat affect in that the deficits may cause disruptions in the control of facial expression.
Another study found that when speaking, individuals with schizophrenia with flat affect demonstrate less inflection than normal controls and appear to be less fluent. Normal subjects appear to express themselves using more complex syntax, whereas flat affect subjects speak with fewer words, and fewer words per sentence. Flat affect individuals’ use of context-appropriate words in both sad and happy narratives are similar to that of controls. It is very likely that flat affect is a result of deficits in motor expression as opposed to emotional processing. The moods of display are compromised, but subjective, autonomic, and contextual aspects of emotion are left intact.
Post-traumatic stress disorder (PTSD) was previously known to cause negative feelings, such as depressed mood, re-experiencing and hyperarousal. However, recently, psychologists have started to focus their attention on the blunted affects and also the decrease in feeling and expressing positive emotions in PTSD patients. Blunted affect, or emotional numbness, is considered one of the consequences of PTSD because it causes a diminished interest in activities that produce pleasure (anhedonia) and produces feelings of detachment from others, restricted emotional expression and a reduced tendency to express emotions behaviourally. Blunted affect is often seen in veterans as a consequence of the psychological stressful experiences that caused PTSD. Blunted affect is a response to PTSD, it is considered one of the central symptoms in post-traumatic stress disorders and it is often seen in veterans who served in combat zones. In PTSD, blunted affect can be considered a psychological response to PTSD as a way to combat overwhelming anxiety that the patients feel. In blunted affect, there are abnormalities in circuits that also include the prefrontal cortex.
In making assessments of mood and affect the clinician is cautioned that “it is important to keep in mind that demonstrative expression can be influenced by cultural differences, medication, or situational factors”; while the layperson is warned to beware of applying the criterion lightly to “friends, otherwise [he or she] is likely to make false judgments, in view of the prevalence of schizoid and cyclothymic personalities in our ‘normal’ population, and our [US] tendency to psychological hypochondriasis”.
R.D. Laing in particular stressed that “such ‘clinical’ categories as schizoid, autistic, ‘impoverished’ affect … all presuppose that there are reliable, valid impersonal criteria for making attributions about the other person’s relation to [his or her] actions. There are no such reliable or valid criteria”.
Blunted affect is very similar to anhedonia, which is the decrease or cessation of all feelings of pleasure (which thus affects enjoyment, happiness, fun, interest, and satisfaction). In the case of anhedonia, emotions relating to pleasure will not be expressed as much or at all because they are literally not experienced or are decreased. Both blunted affect and anhedonia are considered negative symptoms of schizophrenia, meaning that they are indicative of a lack of something. There are some other negative symptoms of schizophrenia which include avolition, alogia and catatonic behaviour.
Closely related is alexithymia – a condition describing people who “lack words for their feelings. They seem to lack feelings altogether, although this may actually be because of their inability to express emotion rather than from an absence of emotion altogether”. Alexithymic patients however can provide clues via assessment presentation which may be indicative of emotional arousal.
“If the amygdala is severed from the rest of the brain, the result is a striking inability to gauge the emotional significance of events; this condition is sometimes called ‘affective blindness'”. In some cases, blunted affect can fade, but there is no conclusive evidence of why this can occur.
The Toronto Alexithymia Scale is a measure of deficiency in understanding, processing, or describing emotions.
It was developed in 1986 and later revised, removing some of the items.
The current version has twenty statements rated on a five-point Likert scale.
The reliability and validity of the TAS-20 was established by a series of articles by Bagby and colleagues (1994).
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(1), pp.23-32.
Alexithymia is a personality trait characterised by the subclinical inability to identify and describe emotions experienced by one’s self.
The core characteristic of alexithymia is marked dysfunction in emotional awareness, social attachment, and interpersonal relation. Furthermore, people with high levels of alexithymia can have difficulty distinguishing and appreciating the emotions of others, which is thought to lead to non-empathic and ineffective emotional responses.
High levels of alexithymia occur in approximately 10% of the population and can occur with a number of psychiatric conditions as well as any neurodevelopmental disorder. Difficulty with recognising and talking about their emotions appears at subclinical levels in men who conform to western cultural notions of masculinity (such as thinking that sadness is a feminine emotion). This is called normative male alexithymia by some researchers. However, both alexithymia itself and its association with traditionally masculine norms are consistent across genders.
The term alexithymia was coined by psychotherapists John Case Nemiah and Peter Sifneos in 1973. The word comes from Greek: ἀ- (a-, ‘not’, privative prefix, alpha privative) + λέξις (léxis, ‘words’) + θῡμός (thȳmós, ‘heart’ or ’emotions’ or ‘seat of speech’) (cf. dyslexia), literally meaning “no words for emotions”.
Another etymology: Greek: Αλεξιθυμία ἀλέξω (to ward off) + θῡμός. Means to push away emotions, feelings
Nonmedical terms describing similar conditions include emotionless and impassive. People with the condition are called alexithymics or alexithymiacs.
Alexithymia is considered to be a personality trait that places affected individuals at risk for other medical and psychiatric disorders while reducing the likelihood that these individuals will respond to conventional treatments for the other conditions. Alexithymia is not classified as a mental disorder in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders. It is a dimensional personality trait that varies in intensity from person to person. A person’s alexithymia score can be measured with questionnaires such as the Toronto Alexithymia Scale (TAS-20), the Perth Alexithymia Questionnaire (PAQ), the Bermond-Vorst Alexithymia Questionnaire (BVAQ), the Levels of Emotional Awareness Scale (LEAS), the Online Alexithymia Questionnaire (OAQ-G2), the Toronto Structured Interview for Alexithymia (TSIA), or the Observer Alexithymia Scale (OAS). It is distinct from the psychiatric personality disorders, such as antisocial personality disorder.
Traditionally, alexithymia has been conceptually defined by four components:
However, there is some ongoing disagreement in the field about the definition of alexithymia. When measured in empirical studies, constricted imaginal processes are often found not to statistically cohere with the other components of alexithymia. Such findings have led to debate in the field about whether IMP is indeed a component of alexithymia. For example, in 2017, Preece and colleagues introduced the attention-appraisal model of alexithymia, where they suggested that IMP be removed from the definition and that alexithymia be conceptually composed only of DIF, DDF, and EOT, as each of these three are specific to deficits in emotion processing. In practice, since the constricted imaginal processes items were removed from earlier versions of the TAS-20 in the 1990s, the most used alexithymia assessment tools (and consequently most alexithymia research studies) have only assessed the construct in terms of DIF, DDF, and EOT.
Studies (using measures of alexithymia assessing DIF, DDF, and EOT) have reported that the prevalence rate of high alexithymia is less than 10% of the population. A less common finding suggests that there may be a higher prevalence of alexithymia amongst males than females, which may be accounted for by difficulties some males have with “describing feelings”, but not by difficulties in “identifying feelings” in which males and females show similar abilities.
Psychologist R. Michael Bagby and psychiatrist Graeme J. Taylor have argued that the alexithymia construct is inversely related to the concepts of psychological mindedness and emotional intelligence and there is “strong empirical support for alexithymia being a stable personality trait rather than just a consequence of psychological distress”.
Typical deficiencies may include problems identifying, processing, describing, and working with one’s own feelings, often marked by a lack of understanding of the feelings of others; difficulty distinguishing between feelings and the bodily sensations of emotional arousal; confusion of physical sensations often associated with emotions; few dreams or fantasies due to restricted imagination; and concrete, realistic, logical thinking, often to the exclusion of emotional responses to problems. Those who have alexithymia also report very logical and realistic dreams, such as going to the store or eating a meal. Clinical experience suggests it is the structural features of dreams more than the ability to recall them that best characterises alexithymia.
Some alexithymic individuals may appear to contradict the above-mentioned characteristics because they can experience chronic dysphoria or manifest outbursts of crying or rage. However, questioning usually reveals that they are quite incapable of describing their feelings or appear confused by questions inquiring about specifics of feelings.
According to Henry Krystal, individuals exhibiting alexithymia think in an operative way and may appear to be super-adjusted to reality. In psychotherapy, however, a cognitive disturbance becomes apparent as patients tend to recount trivial, chronologically ordered actions, reactions, and events of daily life with monotonous detail. In general, these individuals can, but not always, seem oriented toward things and even treat themselves as robots. These problems seriously limit their responsiveness to psychoanalytic psychotherapy; psychosomatic illness or substance abuse is frequently exacerbated should these individuals enter psychotherapy.
A common misconception about alexithymia is that affected individuals are totally unable to express emotions verbally and that they may even fail to acknowledge that they experience emotions. Even before coining the term, Sifneos (1967) noted patients often mentioned things like anxiety or depression. The distinguishing factor was their inability to elaborate beyond a few limited adjectives such as “happy” or “unhappy” when describing these feelings. The core issue is that people with alexithymia have poorly differentiated emotions limiting their ability to distinguish and describe them to others. This contributes to the sense of emotional detachment from themselves and difficulty connecting with others, making alexithymia negatively associated with life satisfaction even when depression and other confounding factors are controlled for.
Alexithymia frequently co-occurs with other disorders. Research indicates that alexithymia overlaps with autism spectrum disorders (ASD). In a 2004 study using the TAS-20, 85% of the adults with ASD fell into the “impaired” category and almost half fell into the “severely impaired” category; in contrast, among the adult control population only 17% were “impaired”, none “severely impaired”. Fitzgerald & Bellgrove pointed out that, “Like alexithymia, Asperger’s syndrome is also characterised by core disturbances in speech and language and social relationships”. Hill & Berthoz agreed with Fitzgerald & Bellgrove (2006) and in response stated that “there is some form of overlap between alexithymia and ASDs”. They also pointed to studies that revealed impaired theory of mind skill in alexithymia, neuroanatomical evidence pointing to a shared aetiology and similar social skills deficits. The exact nature of the overlap is uncertain. Alexithymic traits in ASD may be linked to clinical depression or anxiety; the mediating factors are unknown and it is possible that alexithymia predisposes to anxiety. On the other hand, while the total alexithymia score as well as the difficulty in identifying feelings and externally oriented thinking factors are found to be significantly associated with ADHD, and while the total alexithymia score, the difficulty in identifying feelings, and the difficulty in describing feelings factors are also significantly associated with symptoms of hyperactivity/impulsivity, there is no significant relationship between alexithymia and inattentiveness symptom.
There are many more psychiatric disorders that overlap with alexithymia. One study found that 41% of US veterans of the Vietnam War with post-traumatic stress disorder (PTSD) were alexithymic. Another study found higher levels of alexithymia among Holocaust survivors with PTSD compared to those without. Higher levels of alexithymia among mothers with interpersonal violence-related PTSD were found in one study to have proportionally less caregiving sensitivity. This latter study suggested that when treating adult PTSD patients who are parents, alexithymia should be assessed and addressed also with attention to the parent-child relationship and the child’s social-emotional development.
Single study prevalence findings for other disorders include 63% in anorexia nervosa, 56% in bulimia, 45% to 50% in major depressive disorder, 34% in panic disorder, 28% in social phobia, and 50% in substance abusers. Alexithymia is also exhibited by a large proportion of individuals with acquired brain injuries such as stroke or traumatic brain injury.
Alexithymia is correlated with certain personality disorders, particularly schizoid, avoidant, dependent and schizotypal, substance use disorders, some anxiety disorders and sexual disorders as well as certain physical illnesses, such as hypertension, inflammatory bowel disease and functional dyspepsia. Alexithymia is further linked with disorders such as migraine headaches, lower back pain, irritable bowel syndrome, asthma, nausea, allergies and fibromyalgia.
An inability to modulate emotions is a possibility in explaining why some people with alexithymia are prone to discharge tension arising from unpleasant emotional states through impulsive acts or compulsive behaviours such as binge eating, substance abuse, perverse sexual behaviour or anorexia nervosa. The failure to regulate emotions cognitively might result in prolonged elevations of the autonomic nervous system (ANS) and neuroendocrine systems, which can lead to somatic diseases. People with alexithymia also show a limited ability to experience positive emotions leading Krystal (1988) and Sifneos (1987) to describe many of these individuals as anhedonic.
Alexisomia is a clinical concept that refers to the difficulty in the awareness and expression of somatic, or bodily, sensations. The concept was first proposed in 1979 by Dr. Yujiro Ikemi when he observed characteristics of both alexithymia and alexisomia in patients with psychosomatic diseases.
It is unclear what causes alexithymia, though several theories have been proposed.
Early studies showed evidence that there may be an interhemispheric transfer deficit among people with alexithymia; that is, the emotional information from the right hemisphere of the brain is not being properly transferred to the language regions in the left hemisphere, as can be caused by a decreased corpus callosum, often present in psychiatric patients who have suffered severe childhood abuse. A neuropsychological study in 1997 indicated that alexithymia may be due to a disturbance to the right hemisphere of the brain, which is largely responsible for processing emotions. In addition, another neuropsychological model suggests that alexithymia may be related to a dysfunction of the anterior cingulate cortex. These studies have some shortcomings, however, and the empirical evidence about the neural mechanisms behind alexithymia remains inconclusive.
French psychoanalyst Joyce McDougall objected to the strong focus by clinicians on neurophysiological explanations at the expense of psychological ones for the genesis and operation of alexithymia, and introduced the alternative term “disaffectation” to stand for psychogenic alexithymia. For McDougall, the disaffected individual had at some point “experienced overwhelming emotion that threatened to attack their sense of integrity and identity”, to which they applied psychological defences to pulverise and eject all emotional representations from consciousness. A similar line of interpretation has been taken up using the methods of phenomenology. McDougall has also noted that all infants are born unable to identify, organize, and speak about their emotional experiences (the word infans is from the Latin “not speaking”), and are “by reason of their immaturity inevitably alexithymic”. Based on this fact McDougall proposed in 1985 that the alexithymic part of an adult personality could be “an extremely arrested and infantile psychic structure”. The first language of an infant is nonverbal facial expressions. The parent’s emotional state is important for determining how any child might develop. Neglect or indifference to varying changes in a child’s facial expressions without proper feedback can promote an invalidation of the facial expressions manifested by the child. The parent’s ability to reflect self-awareness to the child is another important factor. If the adult is incapable of recognising and distinguishing emotional expressions in the child, it can influence the child’s capacity to understand emotional expressions.
Molecular genetic research into alexithymia remains minimal, but promising candidates have been identified from studies examining connections between certain genes and alexithymia among those with psychiatric conditions as well as the general population. A study recruiting a test population of Japanese males found higher scores on the Toronto Alexithymia Scale among those with the 5-HTTLPR homozygous long (L) allele. The 5-HTTLPR region on the serotonin transporter gene influences the transcription of the serotonin transporter that removes serotonin from the synaptic cleft, and is well studied for its association with numerous psychiatric disorders. Another study examining the 5-HT1A receptor, a receptor that binds serotonin, found higher levels of alexithymia among those with the G allele of the Rs6295 polymorphism within the HTR1A gene. Also, a study examining alexithymia in subjects with obsessive-compulsive disorder found higher alexithymia levels associated with the Val/Val allele of the Rs4680 polymorphism in the gene that encodes Catechol-O-methyltransferase (COMT), an enzyme which degrades catecholamine neurotransmitters such as dopamine. These links are tentative, and further research will be needed to clarify how these genes relate to the neurological anomalies found in the brains of people with alexithymia.
Although there is evidence for the role of environmental and neurological factors, the role and influence of genetic factors for developing alexithymia is still unclear. A single large scale Danish study suggested that genetic factors contributed noticeably to the development of alexithymia. However, such twin studies are controversial, as they suffer from the “equal environments assumption” and the “heritability” estimates in no way correspond to actual DNA structures. Traumatic brain injury is also implicated in the development of alexithymia, and those with traumatic brain injury are six times more likely to exhibit alexithymia.
Alexithymia can create interpersonal problems because these individuals tend to avoid emotionally close relationships, or if they do form relationships with others they usually position themselves as either dependent, dominant, or impersonal, “such that the relationship remains superficial”. Inadequate “differentiation” between self and others by alexithymic individuals has also been observed. Their difficulty in processing interpersonal connections often develops where the person lacks a romantic partner.
In a study, a large group of alexithymic individuals completed the 64-item Inventory of Interpersonal Problems (IIP-64) which found that “two interpersonal problems are significantly and stably related to alexithymia: cold/distant and non-assertive social functioning. All other IIP-64 subscales were not significantly related to alexithymia.”
Chaotic interpersonal relations have also been observed by Sifneos. Due to the inherent difficulties identifying and describing emotional states in self and others, alexithymia also negatively affects relationship satisfaction between couples.
In a 2008 study alexithymia was found to be correlated with impaired understanding and demonstration of relational affection, and that this impairment contributes to poorer mental health, poorer relational well-being, and lowered relationship quality. Individuals high on the alexithymia spectrum also report less distress at seeing others in pain and behave less altruistically toward others.
Some individuals working for organisations in which control of emotions is the norm might show alexithymic-like behaviour but not be alexithymic. However, over time the lack of self-expressions can become routine and they may find it harder to identify with others.
Generally speaking, approaches to treating alexithymia are still in their infancy, with not many proven treatment options available.
In 2002, Kennedy and Franklin found that a skills-based intervention is an effective method for treating alexithymia. Kennedy and Franklin’s treatment plan involved giving the participants a series of questionnaires, psychodynamic therapies, cognitive-behavioural and skills-based therapies, and experiential therapies. After treatment, they found that participants were generally less ambivalent about expressing their emotion feelings and more attentive to their emotional states.
In 2017, based on their attention-appraisal model of alexithymia, Preece and colleagues recommended that alexithymia treatment should target trying to improve the developmental level of people’s emotion schemas and reduce people’s use of experiential avoidance of emotions as an emotion regulation strategy (i.e. the mechanisms hypothesized to underlie alexithymia difficulties in the attention-appraisal model of alexithymia).
In 2018, Löf, Clinton, Kaldo, and Rydén found that mentalisation-based treatment is also an effective method for treating alexithymia. Mentalisation is the ability to understand the mental state of oneself or others that underlies overt behaviour, and mentalisation-based treatment helps patients separate their own thoughts and feelings from those around them. This treatment is relational, and it focuses on gaining a better understanding and use of mentalising skills. The researchers found that all of the patients’ symptoms including alexithymia significantly improved, and the treatment promoted affect tolerance and the ability to think flexibly while expressing intense affect rather than impulsive behaviour.
A significant issue impacting alexithymia treatment is that alexithymia has comorbidity with other disorders. Mendelson’s 1982 study showed that alexithymia frequently presented in people with undiagnosed chronic pain. Participants in Kennedy and Franklin’s study all had anxiety disorders in conjunction with alexithymia, while those in Löf et al. were diagnosed with both alexithymia and borderline personality disorder. All these comorbidity issues complicate treatment because it is difficult to examine people who exclusively have alexithymia.
The term disaffectation was coined by noted French psychoanalyst Joyce McDougall as a strictly psychoanalytic term for alexithymia, a neurological condition characterised by severe lack of emotional awareness.
McDougall felt that alexithymia had become too strongly classified as a neuroanatomical defect and concretised as an intractable illness leaving little room for a purely psychoanalytic explanation for this phenomenon.
In coining the term McDougall hoped to indicate the behaviour of people who had experienced overwhelming emotion that threatened to attack their sense of integrity and identity. Such individuals, unable to repress the ideas linked to emotional pain and equally unable to project these feelings delusively onto representations of other people, simply ejected them from consciousness by “pulverizing all trace of feeling, so that an experience which has caused emotional flooding is not recognized as such and therefore cannot be contemplated”. They were not suffering from an inability to experience or express emotion, but from “an inability to contain and reflect over an excess of affective experience.”
‘Disaffectation’ conveys a deliberate double meaning. The Latin prefix dis-, indicates separation or loss and suggests, metaphorically, that certain people are psychologically separated from their emotions and may have “lost” the capacity to be in touch with interior psychic reality. Also included in this prefix is the secondary meaning from the Greek dys- with its implication of illness.
According to Professor of Psychiatry of the University of Toronto, Graeme Taylor, this psychoanalytic conceptualisation departs from older, less applicable theories which emphasized the role of unconscious neurotic conflicts, and instead facilitates a psychoanalytic model of physical illness and disease based on the operation of primitive pre-neurotic pathology that has failed to achieve psychic representation. Henry Krystal Professor of Psychiatry at Michigan State University agreed, adding that it is useful to separate the consideration of psychotherapy for the “disaffected” individual from that of the classical psychosomatic neuroses. To Krystal this consideration is important because “since these patients may develop serious, even occasionally fatal exacerbations of illness during psychotherapy, treating them with psychotherapy for psychosomatic illness is not indicated”. This distinction has allowed the field of psychoanalysis to contribute constructively to the field of psychosomatic medicine.
Research Paper Title
Alexithymia Formation as an Adaptation to Everyday Stress is Determined by the Properties of the Nervous System.
Background
The aim of the study was to determine the psychological nature and mechanisms of alexithymia formation by way of the analysis of its relation to the properties of the nervous system, mental states, and characteristics of the emotional sphere of the personality.
Methods
In the process of the study, for the diagnostics of alexithymia, the researchers used the 26-item Toronto Alexithymia Scale (TAS-26) developed by G.J. Taylor and a block of psycho-diagnostic methods aimed at the diagnostics of properties of the nervous systems, the emotional sphere and mental states of respondents. The relationships were evaluated using Spearman’s rank correlation coefficient and Pearson’s correlation coefficient.
Results
The main factors related to alexithymia were weak nervous system, low stress resistance and such characteristics of the emotional sphere as marked extraversion, high level of trait anxiety, neuroticism, indirect verbal aggression, low levels of aggressiveness. The emotional exhaustion and reduction of personal achievements, the Resistance Phase, chronic fatigue and depression were the most pronounced within the alexithymia group. The alexithymic personality type demonstrated less developed spatial anticipation.
Conclusions
In accordance with the results, the weakness of the nervous system and high trait anxiety facilitate the adaption to stressful situations by avoiding and crowding out negative emotions, lead to the inability of verbal description and expression of emotions. A low level of stress resistance conduces to neurotisation, chronic fatigue, and emotional burnout. The predominance of refractory and dysphoric reactions causes a negative vision of the situation and can provoke the development of psychosomatic disorders.
Reference
Tukaiev, S.V., Vasheka, T.V., Dolgova, O.M., Fedorchuk, S.V. & Palamar, B.I. (2020) Alexithymia Formation as an Adaptation to Everyday Stress is Determined by the Properties of the Nervous System. Wiadomosci Lekarskie (Warsaw, Poland: 1960). 73(11), pp.2461-2467.
Introduction
Alexithymia is a personality trait characterised by the subclinical inability to identify and describe emotions experienced by one’s self or others. The core characteristic of alexithymia is marked dysfunction in emotional awareness, social attachment, and interpersonal relation. Furthermore, people with alexithymia have difficulty distinguishing and appreciating the emotions of others, which is thought to lead to nonempathic and ineffective emotional responses.
Alexithymia occurs in approximately 10% of the population and can occur with a number of psychiatric conditions as well as any neurodevelopmental disorder. When the difficulty with recognising and talking about their emotions appears at subclinical levels in men who conform to western cultural notions of masculinity (such as thinking that sadness is a feminine emotion), it may be called normative male alexithymia.
Refer to Dissaffection.
Classification
Alexithymia is considered to be a personality trait that places affected individuals at risk for other medical and psychiatric disorders while reducing the likelihood that these individuals will respond to conventional treatments for the other conditions. Alexithymia is not classified as a mental disorder in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). It is a dimensional personality trait that varies in intensity from person to person. A person’s alexithymia score can be measured with questionnaires such as the:
It is distinct from the psychiatric personality disorders, such as antisocial personality disorder.
Alexithymia is defined by:
Studies have reported that the prevalence rate of alexithymia is less than 10% of the population. A less common finding suggests that there may be a higher prevalence of alexithymia amongst males than females, which may be accounted for by difficulties some males have with “describing feelings”, but not by difficulties in “identifying feelings” in which males and females show similar abilities.
Psychologist R. Michael Bagby and psychiatrist Graeme J. Taylor have argued that the alexithymia construct is inversely related to the concepts of psychological mindedness and emotional intelligence and there is “strong empirical support for alexithymia being a stable personality trait rather than just a consequence of psychological distress”.
Signs and Symptoms
Typical deficiencies may include problems identifying, processing, describing, and working with one’s own feelings, often marked by a lack of understanding of the feelings of others; difficulty distinguishing between feelings and the bodily sensations of emotional arousal; confusion of physical sensations often associated with emotions; few dreams or fantasies due to restricted imagination; and concrete, realistic, logical thinking, often to the exclusion of emotional responses to problems. Those who have alexithymia also report very logical and realistic dreams, such as going to the store or eating a meal. Clinical experience suggests it is the structural features of dreams more than the ability to recall them that best characterises alexithymia.
Some alexithymic individuals may appear to contradict the above-mentioned characteristics because they can experience chronic dysphoria or manifest outbursts of crying or rage. However, questioning usually reveals that they are quite incapable of describing their feelings or appear confused by questions inquiring about specifics of feelings.
According to Henry Krystal, individuals suffering from alexithymia think in an operative way and may appear to be superadjusted to reality. In psychotherapy, however, a cognitive disturbance becomes apparent as patients tend to recount trivial, chronologically ordered actions, reactions, and events of daily life with monotonous detail. In general, these individuals can, but not always, seem oriented toward things and even treat themselves as robots. These problems seriously limit their responsiveness to psychoanalytic psychotherapy; psychosomatic illness or substance abuse is frequently exacerbated should these individuals enter psychotherapy.
A common misconception about alexithymia is that affected individuals are totally unable to express emotions verbally and that they may even fail to acknowledge that they experience emotions. Even before coining the term, Sifneos (1967) noted patients often mentioned things like anxiety or depression. The distinguishing factor was their inability to elaborate beyond a few limited adjectives such as “happy” or “unhappy” when describing these feelings. The core issue is that people with alexithymia have poorly differentiated emotions limiting their ability to distinguish and describe them to others. This contributes to the sense of emotional detachment from themselves and difficulty connecting with others, making alexithymia negatively associated with life satisfaction even when depression and other confounding factors are controlled for.
Associated Conditions
Alexithymia frequently co-occurs with other disorders. Research indicates that alexithymia overlaps with autism spectrum disorders (ASD). In a 2004 study using the TAS-20, 85% of the adults with ASD fell into the impaired category; almost half of adults with ASD fell into the severely impaired category. Among the adult control, only 17% was impaired; none of them severely. Fitzgerald & Bellgrove pointed out that, “Like alexithymia, Asperger’s syndrome is also characterised by core disturbances in speech and language and social relationships”. Hill & Berthoz agreed with Fitzgerald & Bellgrove (2006) and in response stated that “there is some form of overlap between alexithymia and ASDs”. They also pointed to studies that revealed impaired theory of mind skill in alexithymia, neuroanatomical evidence pointing to a shared aetiology and similar social skills deficits. The exact nature of the overlap is uncertain. Alexithymic traits in AS may be linked to clinical depression or anxiety; the mediating factors are unknown and it is possible that alexithymia predisposes to anxiety. On the other hand, while the total alexithymia score as well as the difficulty in identifying feelings and externally oriented thinking factors are found to be significantly associated with ADHD, and while the total alexithymia score, the difficulty in identifying feelings, and the difficulty in describing feelings factors are also significantly associated with symptoms of hyperactivity/impulsivity, there’s no significant relationship between alexithymia and inattentiveness symptom.
There are many more psychiatric disorders that overlap with alexithymia. One study found that 41% of US veterans of the Vietnam War with post-traumatic stress disorder (PTSD) were alexithymic. Another study found higher levels of alexithymia among Holocaust survivors with PTSD compared to those without. Higher levels of alexithymia among mothers with interpersonal violence-related PTSD were found in one study to have proportionally less caregiving sensitivity. This latter study suggested that when treating adult PTSD patients who are parents, alexithymia should be assessed and addressed also with attention to the parent-child relationship and the child’s social-emotional development.
Single study prevalence findings for other disorders include 63% in anorexia nervosa, 56% in bulimia, 45% to 50% in major depressive disorder, 34% in panic disorder, 28% in social phobia, and 50% in substance abusers. Alexithymia is also exhibited by a large proportion of individuals with acquired brain injuries such as stroke or traumatic brain injury.
Alexithymia is correlated with certain personality disorders, particularly schizoid, avoidant, dependent and schizotypal, substance use disorders, some anxiety disorders and sexual disorders as well as certain physical illnesses, such as hypertension, inflammatory bowel disease and functional dyspepsia. Alexithymia is further linked with disorders such as migraine headaches, lower back pain, irritable bowel syndrome, asthma, nausea, allergies and fibromyalgia.
An inability to modulate emotions is a possibility in explaining why some people with alexithymia are prone to discharge tension arising from unpleasant emotional states through impulsive acts or compulsive behaviours such as binge eating, substance abuse, perverse sexual behaviour or anorexia nervosa. The failure to regulate emotions cognitively might result in prolonged elevations of the autonomic nervous system (ANS) and neuroendocrine systems, which can lead to somatic diseases. People with alexithymia also show a limited ability to experience positive emotions leading Krystal (1988) and Sifneos (1987) to describe many of these individuals as anhedonic.
Causes
It is unclear what causes alexithymia, though several theories have been proposed.
Early studies showed evidence that there may be an interhemispheric transfer deficit among people with alexithymia; that is, the emotional information from the right hemisphere of the brain is not being properly transferred to the language regions in the left hemisphere, as can be caused by a decreased corpus callosum, often present in psychiatric patients who have suffered severe childhood abuse. A neuropsychological study in 1997 indicated that alexithymia may be due to a disturbance to the right hemisphere of the brain, which is largely responsible for processing emotions. In addition, another neuropsychological model suggests that alexithymia may be related to a dysfunction of the anterior cingulate cortex. These studies have some shortcomings, however, and the empirical evidence about the neural mechanisms behind alexithymia remains inconclusive.
French psychoanalyst Joyce McDougall objected to the strong focus by clinicians on neurophysiological explanations at the expense of psychological ones for the genesis and operation of alexithymia, and introduced the alternative term “disaffectation” to stand for psychogenic alexithymia. For McDougall, the disaffected individual had at some point “experienced overwhelming emotion that threatened to attack their sense of integrity and identity”, to which they applied psychological defences to pulverise and eject all emotional representations from consciousness. A similar line of interpretation has been taken up using the methods of phenomenology. McDougall has also noted that all infants are born unable to identify, organize, and speak about their emotional experiences (the word infans is from the Latin “not speaking”), and are “by reason of their immaturity inevitably alexithymic”. Based on this fact McDougall proposed in 1985 that the alexithymic part of an adult personality could be “an extremely arrested and infantile psychic structure”. The first language of an infant is nonverbal facial expressions. The parent’s emotional state is important for determining how any child might develop. Neglect or indifference to varying changes in a child’s facial expressions without proper feedback can promote an invalidation of the facial expressions manifested by the child. The parent’s ability to reflect self-awareness to the child is another important factor. If the adult is incapable of recognizing and distinguishing emotional expressions in the child, it can influence the child’s capacity to understand emotional expressions.
Molecular genetic research into alexithymia remains minimal, but promising candidates have been identified from studies examining connections between certain genes and alexithymia among those with psychiatric conditions as well as the general population. A study recruiting a test population of Japanese males found higher scores on the Toronto Alexithymia Scale among those with the 5-HTTLPR homozygous long (L) allele. The 5-HTTLPR region on the serotonin transporter gene influences the transcription of the serotonin transporter that removes serotonin from the synaptic cleft, and is well studied for its association with numerous psychiatric disorders. Another study examining the 5-HT1A receptor, a receptor that binds serotonin, found higher levels of alexithymia among those with the G allele of the Rs6295 polymorphism within the HTR1A gene. Also, a study examining alexithymia in subjects with obsessive-compulsive disorder found higher alexithymia levels associated with the Val/Val allele of the Rs4680 polymorphism in the gene that encodes Catechol-O-methyltransferase (COMT), an enzyme which degrades catecholamine neurotransmitters such as dopamine. These links are tentative, and further research will be needed to clarify how these genes relate to the neurological anomalies found in the brains of people with alexithymia.
Although there is evidence for the role of environmental and neurological factors, the role and influence of genetic factors for developing alexithymia is still unclear. A single large scale Danish study suggested that genetic factors contributed noticeably to the development of alexithymia. However, such twin studies are controversial, as they suffer from the “equal environments assumption” and the “heritability” estimates in no way correspond to actual DNA structures. Traumatic brain injury is also implicated in the development of alexithymia, and those with traumatic brain injury are six times more likely to exhibit alexithymia.
In Relationships
Alexithymia can create interpersonal problems because these individuals tend to avoid emotionally close relationships, or if they do form relationships with others they usually position themselves as either dependent, dominant, or impersonal, “such that the relationship remains superficial”. Inadequate “differentiation” between self and others by alexithymic individuals has also been observed. Their difficulty in processing interpersonal connections often develops where the person lacks a romantic partner.
In a study, a large group of alexithymic individuals completed the 64-item Inventory of Interpersonal Problems (IIP-64) which found that “two interpersonal problems are significantly and stably related to alexithymia: cold/distant and non-assertive social functioning. All other IIP-64 subscales were not significantly related to alexithymia.”
Chaotic interpersonal relations have also been observed by Sifneos. Due to the inherent difficulties identifying and describing emotional states in self and others, alexithymia also negatively affects relationship satisfaction between couples.
In a 2008 study alexithymia was found to be correlated with impaired understanding and demonstration of relational affection, and that this impairment contributes to poorer mental health, poorer relational well-being, and lowered relationship quality. Individuals high on the alexithymia spectrum also report less distress at seeing others in pain and behave less altruistically toward others.
Some individuals working for organisations in which control of emotions is the norm might show alexithymic-like behaviour but not be alexithymic. However, over time the lack of self-expressions can become routine and they may find it harder to identify with others.
Treatment
Because alexithymia is still a fairly newly classified disorder without much research as of 2020, there are not many proven treatment options available.
In 2002, Kennedy and Franklin found that a skills-based intervention is an effective method for treating alexithymia. Kennedy and Franklin’s treatment plan involved giving the participants a series of questionnaires, psychodynamic therapies, cognitive behavioural and skills-based therapies, and experiential therapies. After treatment, they found that participants were generally less ambivalent about expressing their emotion feelings and more attentive to their emotional states.
In 2018, Löf, Clinton, Kaldo, and Rydén found that mentalisation-based treatment is also an effective method for treating alexithymia. Mentalisation is the ability to understand the mental state of oneself or others that underlies overt behaviour, and mentalisation-based treatment helps patients separate their own thoughts and feelings from those around them. This treatment is relational, and it focuses on gaining a better understanding and use of mentalising skills. The researchers found that all of the patients’ symptoms including alexithymia significantly improved, and the treatment promoted affect tolerance and the ability to think flexibly while expressing intense affect rather than impulsive behaviour.
A significant issue impacting alexithymia treatment is that alexithymia has comorbidity with other disorders. Mendelson’s 1982 study showed that alexithymia frequently presented in people with undiagnosed chronic pain. Participants in Kennedy and Franklin’s study all had anxiety disorders in conjunction with alexithymia, while those in Löf et al. were diagnosed with both alexithymia and borderline personality disorder. All these comorbidity issues complicate treatment because it is difficult to examine people who exclusively have alexithymia.
Lexicology
The term alexithymia was coined by psychotherapists John Case Nemiah and Peter Sifneos in 1973. The word comes from Greek: ἀ- (a-, ‘not’) + λέξις (léxis, ‘words’) + θῡμός (thȳmós, ‘heart’ or ’emotions’ or ‘seat of speech’) (cf. dyslexia), literally meaning “no words for emotions”.
Another etymology: Greek: Αλεξ(ι)θυμία άλεξ (διώχνω, απομακρίνω) to push away + θυμός emotion, feelings. Means to push away emotions, feelings
Nonmedical terms describing similar conditions include emotionless and impassive. People with the condition are called alexithymics or alexithymiacs.
Mental Health Matters 