What is Reduced Effect Display?


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.


Constricted Affect

A restricted or constricted affect is a reduction in an individual’s expressive range and the intensity of emotional responses.

Blunted and Flat Affect

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

Shallow affect has equivalent meaning to blunted affect. Factor 1 of the Psychopathy Checklist identifies shallow affect as a common attribute of psychopathy.

Brain structures

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.

Limbic Structures

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.

Prefrontal Cortex

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.

Anterior Cingulate Cortex

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

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”.

Differential Diagnosis

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.

What is Dissociative Disorder Not Otherwise Specified?


Dissociative disorder not otherwise specified (DDNOS) is a mental health diagnosis for pathological dissociation that matches the DSM-5 criteria for a dissociative disorder, but does not fit the full criteria for any of the specifically identified subtypes, which include dissociative identity disorder, dissociative amnesia, and depersonalisation/derealisation disorder, and the reasons why the previous diagnoses were not met are specified.

Refer to Depressive Disorder Not Otherwise Specified (DD-NOS).


“Unspecified dissociative disorder” is given when the clinician does not give a reason. The International Statistical Classification of Diseases and Related Health Problems (ICD-10) refers to the diagnosis as “Other dissociative and conversion disorders”.

Examples of DDNOS include chronic and recurrent syndromes of mixed dissociative symptoms, identity disturbance due to prolonged and intense coercive persuasion, disorders similar to dissociative identity disorder, acute dissociative reactions to stressful events, and dissociative trance.

DDNOS is the most common dissociative disorder and is diagnosed in 40% of dissociative disorder cases. It is often co-morbid with other mental illnesses such as complex posttraumatic stress disorder, major depressive disorder, generalised anxiety disorder, personality disorders, substance use disorders, and eating disorders.

What is Depersonalisation?


Depersonalisation can consist of a detachment within the self, regarding one’s mind or body, or being a detached observer of oneself.

Subjects feel they have changed and that the world has become vague, dreamlike, less real, lacking in significance or being outside reality while looking in. Chronic depersonalisation refers to depersonalisation/derealisation disorder, which is classified by the DSM-5 as a dissociative disorder, based on the findings that depersonalisation and derealisation are prevalent in other dissociative disorders including dissociative identity disorder.

Though degrees of depersonalisation and derealisation can happen to anyone who is subject to temporary anxiety or stress, chronic depersonalisation is more related to individuals who have experienced a severe trauma or prolonged stress/anxiety. Depersonalisation-derealisation is the single most important symptom in the spectrum of dissociative disorders, including dissociative identity disorder and “dissociative disorder not otherwise specified” (DD-NOS). It is also a prominent symptom in some other non-dissociative disorders, such as anxiety disorders, clinical depression, bipolar disorder, schizophrenia, schizoid personality disorder, hypothyroidism or endocrine disorders, schizotypal personality disorder, borderline personality disorder, obsessive compulsive disorder, migraines, and sleep deprivation; it can also be a symptom of some types of neurological seizure.

In social psychology, and in particular self-categorisation theory, the term depersonalisation has a different meaning and refers to “the stereotypical perception of the self as an example of some defining social category”.


Individuals who experience depersonalisation feel divorced from their own personal self by sensing their body sensations, feelings, emotions, behaviours etc. as not belonging to the same person or identity. Often a person who has experienced depersonalisation claims that things seem unreal or hazy. Also, a recognition of a self breaks down (hence the name). Depersonalisation can result in very high anxiety levels, which further increase these perceptions.

Depersonalisation is a subjective experience of unreality in one’s self, while derealisation is unreality of the outside world. Although most authors currently regard depersonalisation (self) and derealisation (surroundings) as independent constructs, many do not want to separate derealisation from depersonalisation.


Depersonalisation is a symptom of anxiety disorders, such as panic disorder. It can also accompany sleep deprivation (often occurring when suffering from jet lag), migraine, epilepsy (especially temporal lobe epilepsy, complex-partial seizure, both as part of the aura and during the seizure), obsessive compulsive disorder, severe stress or trauma, anxiety, the use of recreational drugs – especially cannabis, hallucinogens, ketamine, and MDMA, certain types of meditation, deep hypnosis, extended mirror or crystal gazing, sensory deprivation, and mild-to-moderate head injury with little or full loss of consciousness (less likely if unconscious for more than 30 mins). Interoceptive exposure is a non-pharmacological method that can be used to induce depersonalisation.

In the general population, transient depersonalisation/derealisation are common, having a lifetime prevalence between 26-74%. A random community-based survey of 1,000 adults in the US rural south found a 1-year depersonalisation prevalence rate at 19%. Several studies, but not all, found age to be a significant factor: adolescents and young adults in the normal population reported the highest rate. In a study, 46% of college students reported at least one significant episode in the previous year. In another study, 20% of patients with minor head injury experience significant depersonalisation and derealisation. Several studies found that up to 66% of individuals in life-threatening accidents report transient depersonalisation at minimum during or immediately after the accidents. Depersonalisation occurs 2-4 times more in women than in men.

A similar and overlapping concept called ipseity disturbance (ipse is Latin for “self” or “itself”) may be part of the core process of schizophrenia spectrum disorders. However, specific to the schizophrenia spectrum seems to be “a dislocation of first-person perspective such that self and other or self and world may seem to be non-distinguishable, or in which the individual self or field of consciousness takes on an inordinate significance in relation to the objective or intersubjective world” (emphasis in original).

For the purposes of evaluation and measurement depersonalisation can be conceived of as a construct and scales are now available to map its dimensions in time and space. A study of undergraduate students found that individuals high on the depersonalisation/derealisation subscale of the Dissociative Experiences Scale exhibited a more pronounced cortisol response in stress. Individuals high on the absorption subscale, which measures a subject’s experiences of concentration to the exclusion of awareness of other events, showed weaker cortisol responses.

In general infantry and special forces soldiers, measures of depersonalisation and derealisation increased significantly after training that includes experiences of uncontrollable stress, semi-starvation, sleep deprivation, as well as lack of control over hygiene, movement, communications, and social interactions.

Pharmacological and Situational Causes

Depersonalisation has been described by some as a desirable state, particularly by those that have experienced it under the influence of mood-altering recreational drugs. It is an effect of dissociatives and psychedelics, as well as a possible side effect of caffeine, alcohol, amphetamine, cannabis, and antidepressants. It is a classic withdrawal symptom from many drugs.

Benzodiazepine dependence, which can occur with long-term use of benzodiazepines, can induce chronic depersonalisation symptomatology and perceptual disturbances in some people, even in those who are taking a stable daily dosage, and it can also become a protracted feature of the benzodiazepine withdrawal syndrome.

Lieutenant Colonel Dave Grossman, in his book On Killing, suggests that military training artificially creates depersonalisation in soldiers, suppressing empathy and making it easier for them to kill other human beings.

Graham Reed (1974) claimed that depersonalisation occurs in relation to the experience of falling in love.

Depersonalisation as a Psychobiological Mechanism

Depersonalisation is a classic response to acute trauma, and may be highly prevalent in individuals involved in different traumatic situations including motor vehicle accident, and imprisonment.

Psychologically depersonalisation can, just like dissociation in general, be considered a type of coping mechanism. Depersonalisation is in that case unconsciously used to decrease the intensity of unpleasant experience, whether that is something as mild as stress or something as severe as chronically high anxiety and post-traumatic stress disorder. The decrease in anxiety and psychobiological hyperarousal helps preserving adaptive behaviours and resources under threat or danger. Depersonalisation is an overgeneralised reaction in that it does not diminish just the unpleasant experience, but more or less all experience – leading to a feeling of being detached from the world and experiencing it in a more bland way. An important distinction must be made between depersonalisation as a mild, short term reaction to unpleasant experience and depersonalisation as a chronic symptom stemming from a severe mental disorder such as PTSD or Dissociative Identity Disorder. Chronic symptoms may represent persistence of depersonalization beyond the situations under threat.


Treatment is dependent on the underlying cause, whether it is organic or psychological in origin. If depersonalisation is a symptom of neurological disease, then diagnosis and treatment of the specific disease is the first approach. Depersonalisation can be a cognitive symptom of such diseases as amyotrophic lateral sclerosis, Alzheimer’s, multiple sclerosis (MS), or any other neurological disease affecting the brain. For those suffering from depersonalisation with migraine, tricyclic antidepressants are often prescribed.

If depersonalization is a symptom of psychological causes such as developmental trauma, treatment depends on the diagnosis. In case of dissociative identity disorder or DD-NOS as a developmental disorder, in which extreme developmental trauma interferes with formation of a single cohesive identity, treatment requires proper psychotherapy, and – in the case of additional (co-morbid) disorders such as eating disorders – a team of specialists treating such an individual. It can also be a symptom of borderline personality disorder, which can be treated in the long term with proper psychotherapy and psychopharmacology.

The treatment of chronic depersonalisation is considered in depersonalisation disorder.

A recently completed study at Columbia University in New York City has shown positive effects from transcranial magnetic stimulation (TMS) to treat depersonalisation disorder. Currently, however, the FDA has not approved TMS to treat DP.

A 2001 Russian study showed that naloxone, a drug used to reverse the intoxicating effects of opioid drugs, can successfully treat depersonalization disorder. According to the study: “In three of 14 patients, depersonalization symptoms disappeared entirely and seven patients showed a marked improvement. The therapeutic effect of naloxone provides evidence for the role of the endogenous opioid system in the pathogenesis of depersonalization.” The anti convulsion drug Lamotrigine has shown some success in treating symptoms of depersonalisation, often in combination with a Selective serotonin reuptake inhibitor and is the first drug of choice at the depersonalisation research unit at King’s College London.


The Depersonalisation Research Unit at the Institute of Psychiatry in London conducts research into depersonalization disorder. Researchers there use the acronym DPAFU (Depersonalisation and Feelings of Unreality) as a shortened label for the disorder. In a 2020 article in the journal Nature, Vesuna, et al. describe experimental findings which show that layer 5 of the retrosplenial cortex is likely responsible for dissociative states of consciousness in mammals.