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Reduced affect display

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Reduced affect display, sometimes referred to as emotional blunting or emotional numbing, is a condition of reduced emotional reactivity in an individual. It manifests as a failure to express feelings either verbally or nonverbally, especially when talking about issues that would normally be expected to engage emotions. In this condition, expressive gestures are rare and there is little animation in facial expression or vocal inflection.[1] Additionally, reduced affect can be symptomatic of autism, schizophrenia, depression, post-traumatic stress disorder, depersonalization-derealization disorder,[2][3][4] schizoid personality disorder or brain damage.[5] It may also be a side effect of certain medications (e.g., antipsychotics[6] and antidepressants[7]).

However, reduced affect should be distinguished from apathy and anhedonia, which explicitly refer to a lack of emotional sensation.

Types

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Constricted affect

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A restricted or constricted affect is a reduction in an individual's expressive range and the intensity of emotional responses.[8]

Blunted and flat affect

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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".[9]

Shallow affect

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Shallow affect has an equivalent meaning to blunted affect. In the Psychopathy Checklist, Factor 1 identifies shallow affect as a common attribute of psychopathy.[10]

Brain structures

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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. For instance, 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. Whereas, 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.[11]

Limbic structures

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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.[11] 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.[12] 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.[13] 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.[11]

Brainstem

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Parts of the brainstem are responsible for passive emotional coping strategies characterized 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.[14] 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 the 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.[11]

Prefrontal cortex

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The prefrontal cortex, similarly to the limbic system, plays a role in the induction of an emotion and the regulation of emotions in healthy individuals.[15] Individuals with schizophrenia show no changes in activation of the prefrontal cortex (PFC) when observing external sad stimuli, whereas healthy controls[16] and patients with schizophrenia who were treated with quetiapine for blunted affect show activation of the medial PFC on fMRI. Individuals with schizophrenia who were reconditioned with quetiapine showed activation in other areas of the PFC as well, including the right medial prefrontal gyrus and the right and left orbitofrontal gyrus.[14] This lack of PFC activity in people with schizophrenia with blunted affect has been postulated to be related to the impaired emotional processing observed in such individuals.

Anterior cingulate cortex

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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.[11]

Diagnoses

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Schizophrenia

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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 expressions as well as the use of gestures.[17] 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".[18]

The study also reported a "dissociation between reported experience of emotion and its display"[18] – supporting the suggestion made elsewhere that "blunted affect, including flattened facial expressiveness and lack of vocal inflection ... often disguises an individual's true feelings."[19] Thus, feelings may merely be unexpressed, rather than 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".[20] In the most extreme cases, there is a complete "dissociation from affective states".[21] 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 the behavioral expression of their emotions.[22]

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.[23] 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.[24]

Post-traumatic stress disorder

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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.[25] 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 behaviorally. Blunted affect is often seen in veterans as a consequence of the psychological stressful experiences that caused PTSD.[25] 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.[26] In PTSD, blunted affect can be considered a psychological response to PTSD as a way to combat overwhelming anxiety that the patients feel.[27] In blunted affect, there are abnormalities in circuits that also include the prefrontal cortex.[28][29]

Assessment

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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";[5] 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".[30]

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".[31]

Differential diagnosis

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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".[32] Alexithymic patients however can provide clues via assessment presentation which may be indicative of emotional arousal.[33]

"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'".[34] In some cases, blunted affect can fade, but there is no conclusive evidence of why this can occur.

See also

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References

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  1. ^ Liddle, Peter F. (2007). "Schizophrenia: the clinical picture". In Stein, George; Wilkinson, Greg (eds.). Seminars in General Adult Psychiatry. London: Royal College of Psychiatrists. pp. 167–86. ISBN 978-1-904671-44-2.
  2. ^ Ackner, B. (1954). "Depersonalisation: I. Aetiology and phenomenology". Journal of Mental Science. 100 (421): 838–853. doi:10.1192/bjp.100.421.838. PMID 13222014.
  3. ^ Saperstein, J.L. (1949). "Phenomena of depersonalization". The Journal of Nervous and Mental Disease. 110 (3): 236–251. doi:10.1097/00005053-194911030-00005. PMID 18147948.
  4. ^ Sierra, M.; Berrios, G.E. (2001). "The Phenomenological Stability of Depersonalization: Comparing the Old with the New". The Journal of Nervous and Mental Disease. 189 (9): 629–636. doi:10.1097/00005053-200109000-00010. PMID 11580008. S2CID 22920376.
  5. ^ a b Sue, David; Sue, Diane M. (2012). "Mental Status Exam". Foundations of Counseling and Psychotherapy: Evidence-Based Practices for a Diverse Society. Hoboken: John Wiley & Sons. pp. 64–6. ISBN 978-1-118-54210-1.
  6. ^ "Inkling".
  7. ^ Price, Jonathan; Cole, Victoria; Goodwin, Guy M. (August 2009). "Emotional side-effects of selective serotonin reuptake inhibitors: qualitative study". The British Journal of Psychiatry. 195 (3): 211–217. doi:10.1192/bjp.bp.108.051110. PMID 19721109.
  8. ^ Shives, Louise Rebraca (1 January 2008). Basic Concepts of Psychiatric-mental Health Nursing. Lippincott Williams & Wilkins. p. 110. ISBN 9780781797078.
  9. ^ A. Tasman/W. K. Mohn, Fundamentals of Psychiatry (2011) Section 25.2.3
  10. ^ Harpur, T. J., Hare, R. D., & Hakstian, A. R. (1989). "Two-factor conceptualization of psychopathy: Construct validity and assessment implications". Psychological Assessment. 1 (1): 6–17. doi:10.1037/1040-3590.1.1.6.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ a b c d e Fahim, Cherine; Stip, Emmanuel; Mancini-Marïe, Adham; Mensour, Boualem; Boulay, Luc J.; Leroux, Jean-Maxime; Beaudoin, Gilles; Bourgouin, Pierre; Beauregard, Mario (2005). "Brain activity during emotionally negative pictures in schizophrenia with and without flat affect: An fMRI study". Psychiatry Research: Neuroimaging. 140 (1): 1–15. doi:10.1016/j.pscychresns.2005.06.003. PMID 16143498. S2CID 23542860.
  12. ^ Bliss-Moreau, Eliza; Bauman, Melissa D.; Amaral, David G. (2011). "Neonatal amygdala lesions result in globally blunted affect in adult rhesus macaques". Behavioral Neuroscience. 125 (6): 848–58. doi:10.1037/a0025757. PMC 3313682. PMID 21988521.
  13. ^ Anticevic, A.; Repovs, G.; Barch, D. M. (2011). "Emotion Effects on Attention, Amygdala Activation, and Functional Connectivity in Schizophrenia". Schizophrenia Bulletin. 38 (5): 967–80. doi:10.1093/schbul/sbq168. PMC 3446234. PMID 21415225.
  14. ^ a b Stip, Emmanuel; Fahim, Cherine; Mancini-Marïe, Adham; Bentaleb, Lahcen Ait; Mensour, Boualem; Mendrek, Adrianna; Beauregard, Mario (2005). "Restoration of frontal activation during a treatment with quetiapine: An fMRI study of blunted affect in schizophrenia". Progress in Neuro-Psychopharmacology and Biological Psychiatry. 29 (1): 21–6. doi:10.1016/j.pnpbp.2004.08.015. PMID 15610941. S2CID 26614932.
  15. ^ Glotzbach, Evelyn; Mühlberger, Andreas; Gschwendtner, Kathrin; Fallgatter, Andreas J.; Pauli, Paul; Herrmann, Martin J. (11 May 2011). "Prefrontal Brain Activation During Emotional Processing: A Functional Near Infrared Spectroscopy Study (fNIRS)". The Open Neuroimaging Journal. 5 (1): 33–39. doi:10.2174/1874440001105010033. PMC 3109593. PMID 21673974.
  16. ^ Keedwell, Paul A.; Andrew, Chris; Williams, Steven C.R.; Brammer, Mick J.; Phillips, Mary L. (September 2005). "A Double Dissociation of Ventromedial Prefrontal Cortical Responses to Sad and Happy Stimuli in Depressed and Healthy Individuals". Biological Psychiatry. 58 (6): 495–503. doi:10.1016/j.biopsych.2005.04.035. ISSN 0006-3223. PMID 15993859.
  17. ^ Marder, Stephen R.; Galderisi, Silvana (February 2017). "The current conceptualization of negative symptoms in schizophrenia". World Psychiatry. 16 (1): 14–24. doi:10.1002/wps.20385. PMC 5269507. PMID 28127915.
  18. ^ a b Gur, R. E; Kohler, C. G; Ragland, J D.; Siegel, S. J; Lesko, K.; Bilker, W. B; Gur, R. C (2006). "Flat Affect in Schizophrenia: Relation to Emotion Processing and Neurocognitive Measures". Schizophrenia Bulletin. 32 (2): 279–87. doi:10.1093/schbul/sbj041. PMC 2632232. PMID 16452608.
  19. ^ Snyder, D. K.; Whisman, M. A. (2003). Treating Difficult Couples. p. 154.
  20. ^ Fenichel, Otto (1946). The Psychoanalytic Theory of Neurosis. London. pp. 445–6.{{cite book}}: CS1 maint: location missing publisher (link)
  21. ^ Symington, Neville (2003). Narcissism: A New Theory. London. p. 122.{{cite book}}: CS1 maint: location missing publisher (link)
  22. ^ Henry, Julie D.; Green, Melissa J.; de Lucia, Amber; Restuccia, Corinne; McDonald, Skye; O'Donnell, Maryanne (1 September 2007). "Emotion dysregulation in schizophrenia: Reduced amplification of emotional expression is associated with emotional blunting". Schizophrenia Research. 95 (1): 197–204. doi:10.1016/j.schres.2007.06.002. ISSN 0920-9964. PMID 17630254. S2CID 44415559.
  23. ^ Lee, Jung Suk; Chun, Ji Won; Yoon, Sang Young; Park, Hae-Jeong; Kim, Jae-Jin (1 January 2014). "Involvement of the mirror neuron system in blunted affect in schizophrenia". Schizophrenia Research. 152 (1): 268–274. doi:10.1016/j.schres.2013.10.043. ISSN 0920-9964. PMID 24268934. S2CID 34377252.
  24. ^ Alpert, Murray; Rosenberg, Stanley D.; Pouget, Enrique R.; Shaw, Richard J. (2000). "Prosody and lexical accuracy in flat affect schizophrenia". Psychiatry Research. 97 (2–3): 107–18. doi:10.1016/S0165-1781(00)00231-6. PMID 11166083. S2CID 22446103.
  25. ^ a b Kashdan, Todd B.; Elhai, Jon D.; Christopher Frueh, B. (2007). "Anhedonia, emotional numbing, and symptom overreporting in male veterans with PTSD". Personality and Individual Differences. 43 (4): 725–735. doi:10.1016/j.paid.2007.01.013. PMC 2084052. PMID 18769508.
  26. ^ Amdur, Richard L.; Larsen, Randy; Liberzon, Israel (2000). "Emotional Processing in Combat-Related Posttraumatic Stress Disorder". Journal of Anxiety Disorders. 14 (3): 219–38. doi:10.1016/S0887-6185(99)00035-3. PMID 10868981. S2CID 5824208.
  27. ^ Muenzenmaler, Kristina; Castille, Dorothy M.; Shelley, Anne-Marie; Jamison, Andrea; Battaglia, Joseph; Opler, Lewis A.; Alexander, Mary Jane (2005). "Comorbid Posttraumatic Stress Disorder and Schizophrenia-PTSD is particularly difficult to diagnose with schizophrenia, and the issues surrounding treatment of this comorbidity are addressed in". Psychiatric Annals. 35 (1): 50–6. ISSN 1938-2456. OCLC 27724748.
  28. ^ Panksepp, Jaak, ed. (2004). Textbook of Biological Psychiatry. New Jersey: John Wiley & Sons. ISBN 978-0-471-43478-8.[page needed]
  29. ^ Shin, L. M.; Rauch, SL; Pitman, RK (2006). "Amygdala, Medial Prefrontal Cortex, and Hippocampal Function in PTSD". Annals of the New York Academy of Sciences. 1071 (1): 67–79. Bibcode:2006NYASA1071...67S. CiteSeerX 10.1.1.523.5686. doi:10.1196/annals.1364.007. PMID 16891563. S2CID 14972288.
  30. ^ Berne, Eric (1976). A Layman's Guide to Psychiatry and Pscyhoanalysis. Penguin. p. 207.
  31. ^ Laing, R. D. (1969). Self and Others. Penguin. p. 128.
  32. ^ Goleman, p. 50[verification needed]
  33. ^ Troisi, Alfonso; Belsanti, Sergio; Bucci, Anna Rosaria; Mosco, Cristina; Sinti, Fabiola; Verucci, Monica (2000). "Affect Regulation in Alexithymia: An Ethological Study of Displacement Behavior during Psychiatric Interviews". The Journal of Nervous & Mental Disease. 188 (1): 13–8. doi:10.1097/00005053-200001000-00003. PMID 10665455.
  34. ^ Daniel Goleman, Emotional Intelligence, p. 15
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