Dissociative disorders unclear? Think ‘rainbows from pain blows’

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Dissociative disorders unclear? Think ‘rainbows from pain blows’

Mr. D, age 45, presents to his primary care physician with panic attacks, nausea, shortness of breath, nightmares, and dizziness 6 months after being assaulted and robbed at an ATM. Following a routine medical workup, the physician diagnoses posttraumatic stress disorder (PTSD) and refers Mr. D for exposure and response prevention therapy.

During graded exposure sessions, Mr. D’s eyes sometimes glaze over and he seems to “float away” from the discussion. When the therapist asks about these symptoms, Mr. D reports having had them as long as he can remember. In school, he says, teachers thought he was a slow learner, a daydreamer, or had attention-deficit/hyperactivity disorder. From what he can recall of his childhood, he describes a history of trauma and neglect with a violent, drug-abusing father and absent mother.

Patients with a history of early abuse or neglect are at risk for dissociative phenomena and other trauma-related psychiatric disorders.1 The heterogeneous dissociative disorders are often hidden and unrecognized2 —as in Mr. D’s case—or present with unfamiliar or atypical symptoms. Understanding and identifying dissociative symptoms is important because:

  • Dissociative symptoms worsen prognosis, whether patients have conversion disorders1 or psychogenic seizures3 or are in psychotherapy.4
  • Dissociative states may impair memory encoding5 and decrease patients’ ability to remember therapeutic information.
  • Symptoms (such as hearing voices in multiple personality disorder) can be confused with those of disorders with different treatment strategies (such as psychotic disorders).6
  • Peritraumatic dissociation may be a risk factor for PTSD.7

This article presents a practical model for understanding dissociation, reviews clinical characteristics of this family of symptoms, and offers suggestions for assessing and treating patients with dissociative disorders.

Coming together, falling apart

Since Pierre Janet’s first reports on dissociative disorders, a number of theories and models of dissociation have been proposed,8 including empirically based, taxonomic models that address DSM-IV-TR categories (Table 1). The model I propose—which attaches a visual metaphor to dissociative phenomena—answers the question, “What is ‘dissociated’ in dissociation disorders?”

Table 1

DSM-IV-TR classification of dissociative disorders

DisorderSymptoms
Dissociative amnesiaA reversible loss of memory, typically preceded by a stressor
Dissociative fugueLoss of memory and identity, along with travel away from home
Dissociative identity disorder (formerly multiple personality disorder)Presence of different identity states, often with lack of connection between them; current models highlight the presence of recurrent dissociative intrusions into many aspects of executive function and self
Depersonalization disorderDetachment from oneself as a present, feeling person (depersonalization) and the world (derealization)
Dissociative identity disorder NOSFunctionally disturbing dissociative symptoms that do not fit into any of the above
NOS: not otherwise specified
Source: Diagnostic and statistical manual of mental disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000
5 components of consciousness. Just as separable wavelengths compose a beam of white light, dissociable “colors” or components of subjective experience constitute a normal state of consciousness. Five implicit components of normal consciousness—present in various degrees, at different times—are seamlessly integrated and associated in real time.

One paired component is a detached “observer” and a more embodied, feeling “experiencer.” The observer is a perspective that begets metacognition (thinking about one’s inner world) and self-observation; it resides in the same body as soma-based “feelings” that unconsciously contribute to the sense of “being present” with oneself and the world in the moment.9

A second component is voluntary access to one’s autobiographical memories (memories about the self in time), which are constantly “updated” and integrated with current experiences. This component allows one to distinguish between remembered (past) experiences and “firsthand” (present) experience.

Three other components of normal consciousness are:

  • a sense of agency and voluntary control over one’s mental contents, mental activity, and bodily movements
  • an ongoing connection with one’s body and mind and an understanding of where sensations and images come from
  • a sense of sequential experience, with relatively smooth transitions (from self at work to self at home, self a week ago to self today, etc) that have a singular referent (an identity).

Pathologic dissociation occurs when a prism of distress disperses one of these component “wavelengths” from the main “beam” of consciousness. For example:

  • separation of the “observer” and “experiencer” occurs in depersonalization disorder
  • reversible loss of ability to access memories characterizes dissociative amnesia
  • disconnection between sequential experiences is a part of dissociative identity disorder.
This modular perspective of dissociative disorders parallels a neurophysiologic perspective of mental states as arising from the synchronized integration of the activity of separate, functionally specialized brain regions.
 

 

10 Functional neuroimaging of dissociation supports an understanding of these symptoms as “disconnection syndromes” (Box).

Box

Dissociation’s neurobiology: Evidence of brain ‘disconnections’

From a neurophysiologic perspective, mental states may be viewed as arising from synchronized integration of the activity of functionally specialized brain regions. Functional neuroimaging of dissociation supports an understanding of these symptoms as ‘disconnection syndromes.’

Functional neuroimaging. Different ‘identities’—sometimes called a traumatic personality state and neutral personality state—demonstrate different patterns of cerebral blood flow, subjective reports, and peripheral physiologic parameters (blood pressure, heart rate).a

Functional imaging of traumatic dissociation shows active suppression of limbic regions (amygdala) and increased activity in dorsolateral prefrontal areas.b Similarly, neuroimaging of depersonalization disorder show increased neural activity in prefrontal regions associated with affect regulation and decreased activity in emotion-related areas.c,d

Speed. Dissociative responses occur extremely rapidly. Using EEG, which allows finer temporal resolution than functional imaging studies, Kirino et ale showed reversible attenuation of a specific EEG signal within 300 msec during dissociative episodes. This ultra-rapid neural reflex was correlated with allocation of attentional and working memory resources, perhaps with the goal of minimizing memory activation and resurgence of affect-laden memories.e

Hormonal. Stress-related disorders cause perturbations in neurohormonal function. Simeon et alf found a distinct pattern of stress-induced HPA axis dysregulation in dissociative patients compared with PTSD patients and healthy controls. Similar results were seen in patients with borderline personality disorder and dissociative symptoms.g

Structural imaging. Stress-related neurohormonal perturbations are known to affect critical neural structures, including the hippocampus. Using MRI, Vermetten et alh found significantly decreased amygdala and hippocampal volumes in patients with dissociative identity disorder.

EEG: electroencephalography; HPA: hypothalamic-pituitary-adrenal; PTSD: posttraumatic stress disorder

Reference Citations: click here

Causes of dissociative disorders

As with many psychiatric disorders, the etiology of dissociative phenomena is thought to include the individual patient’s temperamental or constitutional predispositions11 as well as a strong contribution of environmental trauma (early abuse, neglect).12

Constitutional predisposition for developing a dissociative disorder may include personality traits such as being easily hypnotized, mental absorption, suggestibility, and a tendency to fantasize.13 These characteristics fueled concerns in the 1990s that therapists may contribute to dissociative identity disorder by “digging” for repressed memories in susceptible patients and creating “pseudomemories” of events that did not happen.14

The issue of repressed traumatic memory and its role in therapy is extremely controversial and contributes to the complexity of psychotherapeutic treatment of dissociation.15

Early trauma. Factors that make it difficult to define the specific role of early trauma in dissociative disorders include:

  • shame and secrecy of early sexual or physical abuse and potential for victims to repress traumatic memories
  • lability of memory, potential for suggestibility, and difficulty with verification.14
Some experts—influenced by attachment theory—view dissociative phenomena as manifestations of an innate, reflexive relational pattern called disorganized attachment.16 Attachment theory notes that:

  • early relationships are one of the primary ways that humans learn to regulate distress
  • early trauma frequently includes pathology in caregiving relationships, including overt role reversal, abuse, and neglect.
Empathic treatment of dissociation, therefore, is based on appreciating the difficulties that arose from an individual’s experience of being alone with overwhelming distress. The relation of dissociation to attachment theory has specific therapeutic implications, including a focus on constructing a safe therapeutic relationship for patients.

Finally, remember that transient dissociative symptoms can be considered normal in high-stress situations. Intensive military training has been found to be associated with a very high incidence (96%) of dissociative symptoms in army recruits.17

Identifying ‘hidden’ phenomena

Dissociative disorders have been called “diseases of hiddenness”18 because:

  • Many of their clinical characteristics— sense of identity, memory, connectedness, somatosensory phenomena—are alterations in subjective phenomena that lack clearly observable symptoms.
  • Patients are often reluctant to seek help or divulge their symptoms to clinicians.
  • When dissociative symptoms are obvious—such as multiple personalities or sudden loss of memories—they may be dismissed or evoke skepticism because of their dramatic presentation.
Screening tools. To identify at-risk patients, consider screening with a validated questionnaire such as the Childhood Trauma Questionnaire (CTQ),19 particularly for patients with psychiatric comorbidity (Table 2). Using the CTQ—which assesses physical, emotional, and sexual abuse and neglect—is a high-yield procedure, given the role of early trauma in brain development and future mental health.20

For more targeted screening, the self-report Dissociative Experiences Scale (DES)21 is useful for clinical assessment in conjunction with the clinician-administered diagnostic Structured Clinical Interview for DSM-IV Dissociative Disorder (SCID-D).22

Table 2

With these findings, consider screening for dissociation

 

 

Posttraumatic stress disorder
Certain personality disorders (especially borderline personality disorder)
Somatoform disorders (conversion disorders and nonepileptic seizures)
Eating disorders
Substance use disorders
Extensive history of trauma or neglect
Self-harm behavior
Differential diagnosis. Diagnosing dissociative disorders includes ruling out psychopathologies that can present with “look-alike” symptoms (Table 3).

As in Mr. D’s case, dissociative phenomena may attenuate the benefit of post-trauma therapeutic interventions, especially those involving exposure. Therefore:

  • assess post-trauma patients for dissociation before you start treatment
  • make specific alterations in psychotherapy for such patients, as described below.
Educating trauma patients that detachment is a normal response to threat17 can reduce shame about not fighting back.

Table 3

Differential diagnosis: Dissociation ‘look-alikes’

Dissociation symptomCan be confused with:
Visual or auditory hallucinations, other ‘first-rank’ psychotic symptoms in dissociative identity disorderPsychotic disorder
‘Blanking out’ (cognitive disruption)ADHD, seizures
Somatoform (conversion) symptomsA variety of nonpsychiatric medical problems, including pelvic or abdominal pathology and headaches
Dissociative memory lapsesLearning disability, not paying attention
‘Switching’ between statesBipolar disorder, rapid cycling
Lack of emotional reaction to traumatic stimuli(numbing response)Healthy coping
ADHD: attention-deficit/hyperactivity disorder
Medical causes. Because complex partial seizures can cause dissociative symptoms,23 consider evaluating patients for seizures, head trauma, and structural lesions. Psychogenic nonepileptic seizures (PNES) often occur in conjunction with early trauma, dissociative symptoms, and PTSD.3

Recreational drugs such as ketamine, methylenedioxymethamphetamine (“Ecstasy”), hallucinogens, marijuana, and dextromethorphan also can induce dissociative states. Consider evaluating for use of these substances, some of which may not be detected on a routine drug screen.24

CASE CONTINUED: A tactical shift

Internal distress—such as when remembering painful events—clearly is linked with the appearance of Mr. D’s symptoms. The therapist—recognizing unacknowledged dissociative phenomena—changes Mr. D’s therapeutic strategy from exposure therapy to affect and anxiety regulation, with an explicit focus on attachment security (safety).

The therapist explains to Mr. D that dissociation symptoms are a response to distress, and he can learn more adaptive distress regulation in therapy. The in-session focus shifts to include more direct attention to components of the therapy relationship, including overt disclosure of the therapist’s positive regard and commitment to help the patient and frequent pauses to “check in” that the patient feels present, safe, and understood. With this new focus, Mr. D’s dissociative symptoms resolve and he feels more ready to face and overcome his fear and avoided memories.

Psychotherapy: Putting pieces together

Psychotherapy is the primary treatment, based on understanding dissociative disorders as manifestations of distress-related, traumatic fragmentation of the sense of self, interpersonal relatedness, and capacity for adaptive affect regulation (Table 4).

Depersonalization disorder. Cognitive-behavioral integration has been proposed, based on the idea that detachment from one’s self creates anxiety and reinforces efforts to avoid this internal state and events that trigger it. In an open study of 21 patients with depersonalization disorder, individual cognitive-behavioral therapy (CBT) reduced avoidance, safety behaviors, and symptom monitoring. Measures of dissociation, depression, anxiety, and general functioning also improved.25

Table 4

Tips for conceptualizing dissociative disorders

Ground your understanding of this class of disorders as distress-related breakdowns in functional connection and integration among components of normal consciousness
Consider the overlap among dissociation, certain somatoform disorders (conversion symptoms, pseudoseizures), and PTSD
Maintain a high index of suspicion for dissociative symptoms in patients with early trauma or neglect (consider screening for this); do further evaluation with dissociative-specific tools
Avoid the tendency to assume that reversible, unfamiliar, or peculiar symptoms imply volition or lack of an organic basis
PTSD: posttraumatic stress disorder
Dissociative identity disorder (DID)—the quintessential dissociative disorder—is usually treated by specialists. Treatment is complex, but some components are appropriate for less severe forms of dissociation, including dissociation as part of PTSD.26

Safety, stabilization, and symptom reduction. Providing a safe therapeutic relationship is a primary and necessary part of DID treatment. On that platform, a first step in reintegrating distressing material into the self involves building the patient’s capacity for conscious, flexible affect regulation. This keeps anxiety and distress within a therapeutic “window.”

Graded exposure. Exposure to feared mental contents—typically traumatic memories—is central to trauma-focused therapy. Dissociation is conceptualized as driven by distress greater than the system can bear, loss of adaptive integration, and subsequent fear-based, reflexive avoidance.27 Re-experiencing trauma-related memories in a safe relationship with a new regulatory capacity may work by anchoring patients in an autobiographical memory base.28

Integration of identity and person. Treatment ends when formerly unintegrated or dissociated experiences or parts of the self are integrated into a coherent whole, and the patient can deal adaptively with inter-personal relationships and distress without fragmentation.

 

 

Adjunctive medications

Few studies have addressed using psychopharmacologic interventions in the heterogeneous dissociative disorders. GABAA antagonism and 5-HT2a/2c agonism have induced psychotic and dissociative-like symptoms in healthy men,29 and alterations in enzymes such as catechol-O-methyltransferase (COMT) may explain individual vulnerability to trauma.30 Reports of dissociation related to ketamine31 and marijuana32 implicate other neurotransmitter systems in their etiology.

DID. Similar to guidelines for borderline personality disorder,33 guidelines for DID suggest using medications to treat the most prominent symptom clusters such as insomnia, affective instability, and posttraumatic intrusions.

Depersonalization disorder. Trials of fluoxetine and lamotrigine showed no benefit in depersonalization disorder.34,35 In an open trial of 14 patients, naloxone (mean 120 mg/d) reduced depersonalization symptoms by 30%, as measured by 3 validated scales.36

PTSD-related dissociation. If dissociative symptoms are associated with PTSD, selective serotonin reuptake inhibitors are considered first-line pharmacologic treatment.37 In a 10-week trial of 70 mostly minority adult outpatients with PTSD, paroxetine, ≤60 mg/d, was more effective than placebo in reducing dissociative symptoms, as shown by changes in DES scores.38

Related Resources

Drug Brand Names

  • Fluoxetine • Prozac
  • Lamotrigine • Lamictal
  • Naloxone • Narcan
  • Paroxetine • Paxil
Disclosure

Dr. MacDonald is a speaker for Eli Lilly and Company, Janssen, L.P., and Pfizer Inc.

References

1. Sar V, Akyuz G, Kundakci T, et al. Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. Am J Psychiatry 2004;161:2271-6.

2. Foote B, Smolin Y, Kaplan M, et al. Prevalence of dissociative disorders in psychiatric outpatients. Am J Psychiatry 2006;163:623-9.

3. Reuber M, Pukrop R, Bauer J, et al. Outcome in psychogenic nonepileptic seizures: 1 to 10-year follow-up in 164 patients. Ann Neurol 2003;53:305-11.

4. Spitzer C, Barnow S, Freyberger HJ, Grabe HJ. Dissociation predicts symptom-related treatment outcome in short-term inpatient psychotherapy. Aust N Z J Psychiatry 2007;41:682-7.

5. Allen JG, Console DA, Lewis L. Dissociative detachment and memory impairment: reversible amnesia or encoding failure? Compr Psychiatry 1999;40:160-71.

6. Dell PF. A new model of dissociative identity disorder. Psychiatr Clin North Am 2006;29:1-26.

7. Shalev AY, Freedman S. PTSD following terrorist attacks: a prospective evaluation. Am J Psychiatry 2005;162:1188-91.

8. Steinberg M, Rounsaville B, Cicchetti DV. The Structured Clinical Interview for DSM-III-R Dissociative Disorders: preliminary report on a new diagnostic instrument. Am J Psychiatry 1990;147:76-82.

9. Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York, NY: Harcourt, Inc; 1999.

10. Alkire MT, Miller J. General anesthesia and the neural correlates of consciousness. Prog Brain Res 2005;150:229-44.

11. Simeon D, Guralnik O, Knutelska M, Schmeidler J. Personality factors associated with dissociation: temperament, defenses, and cognitive schemata. Am J Psychiatry 2002;159(3):489-91.

12. Kihlstrom JF. Dissociative disorders. Annu Rev Clin Psychol 2005;1:227-53.

13. Isaac M, Chand PK. Dissociative and conversion disorders: defining boundaries. Curr Opin Psychiatry 2006;19(1):61-6.

14. Laney C, Loftus EF. Traumatic memories are not necessarily accurate memories. Can J Psychiatry 2005;50(13):823-8.

15. Loftus EF, Davis D. Recovered memories. Annu Rev Clin Psychol 2006;2:469-98.

16. Lyons-Ruth K, Dutra L, Schuder MR, Bianchi I. From infant attachment disorganization to adult dissociation: relational adaptations or traumatic experiences? Psychiatr Clin North Am 2006;29(1):63-86.

17. Morgan CA, 3rd, Hazlett G, Wang S, et al. Symptoms of dissociation in humans experiencing acute, uncontrollable stress: a prospective investigation. Am J Psychiatry 2001;158(8):1239-47.

18. Spiegel D. Recognizing traumatic dissociation. Am J Psychiatry 2006;163(4):566-8.

19. Scher CD, Stein MB, Asmundson GJ, et al. The childhood trauma questionnaire in a community sample: psychometric properties and normative data. J Trauma Stress 2001;14:843-57.

20. Teicher MH, Andersen SL, Polcari A, et al. The neurobiological consequences of early stress and childhood maltreatment. Neurosci Biobehav Rev 2003;27:33-44.

21. Bernstein EM, Putnam FW. Development, reliability, and validity of a dissociation scale. J Nerv Ment Dis 1986;174(12):727-35.

22. Steinberg M, Rounsaville B, Cicchetti D. Detection of dissociative disorders in psychiatric patients by a screening instrument and a structured diagnostic interview. Am J Psychiatry 1991;148(8):1050-4.

23. Devinsky O, Putnam F, Grafman J, et al. Dissociative states and epilepsy. Neurology 1989;39:835-40.

24. Schonenberg M, Reichwald U, Domes G, et al. Effects of peritraumatic ketamine medication on early and sustained posttraumatic stress symptoms in moderately injured accident victims. Psychopharmacology (Berl) 2005;182(3):420-5.

25. Hunter EC, Phillips ML, Chalder T, et al. Depersonalisation disorder: a cognitive-behavioural conceptualisation. Behav Res Ther 2003;41:1451-67.

26. Guidelines for treating dissociative identity disorder in adults (2005). J Trauma Dissociation 2005;6(4):69-149.

27. van der Hart O, Nijenhuis E. Generalized dissociative amnesia: episodic, semantic and procedural memories lost and found. Aust N Z J Psychiatry 2001;35:589-600.

28. Holmes EA, Brown RJ, Mansell W, et al. Are there two qualitatively distinct forms of dissociation? A review and some clinical implications. Clin Psychol Rev 2005;25(1):1-23.

29. D’Souza DC, Gil RB, Zuzarte E, et al. gamma-Aminobutyric acid-serotonin interactions in healthy men: implications for network models of psychosis and dissociation. Biol Psychiatry 2006;59(2):128-37.

30. Savitz JB, van der Merwe L, Newman TK, et al. The relationship between childhood abuse and dissociation. Is it influenced by catechol-O-methyltransferase (COMT) activity? Int J Neuropsychopharmacol 2008;11:149-61.

31. Curran HV, Morgan C. Cognitive, dissociative and psychotogenic effects of ketamine in recreational users on the night of drug use and 3 days later. Addiction 2000;95:575-90.

32. Mathew RJ, Wilson WH, Humphreys D, et al. Depersonalization after marijuana smoking. Biol Psychiatry 1993;33:431-41.

33. American Psychiatric Association. Practice guideline for the treatment of patients with borderline personality disorder. Am J Psychiatry 2001;158(10 suppl):1-52.

34. Sierra M, Phillips ML, Ivin G, et al. A placebo-controlled, cross-over trial of lamotrigine in depersonalization disorder. J Psychopharmacol 2003;17:103-5.

35. Simeon D, Guralnik O, Schmeidler J, Knutelska M. Fluoxetine therapy in depersonalisation disorder: randomised controlled trial. Br J Psychiatry 2004;185:31-6.

36. Simeon D, Knutelska M. An open trial of naltrexone in the treatment of depersonalization disorder. J Clin Psychopharmacol 2005;25:267-70.

37. Stein DJ, Ipser JC, Seedat S. Pharmacotherapy for post traumatic stress disorder (PTSD). Cochrane Database Syst Rev 2006(1):CD002795.-

38. Marshall RD, Lewis-Fernandez R, Blanco C, et al. A controlled trial of paroxetine for chronic PTSD, dissociation, and interpersonal problems in mostly minority adults. Depress Anxiety 2007;24:77-84.

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Mr. D, age 45, presents to his primary care physician with panic attacks, nausea, shortness of breath, nightmares, and dizziness 6 months after being assaulted and robbed at an ATM. Following a routine medical workup, the physician diagnoses posttraumatic stress disorder (PTSD) and refers Mr. D for exposure and response prevention therapy.

During graded exposure sessions, Mr. D’s eyes sometimes glaze over and he seems to “float away” from the discussion. When the therapist asks about these symptoms, Mr. D reports having had them as long as he can remember. In school, he says, teachers thought he was a slow learner, a daydreamer, or had attention-deficit/hyperactivity disorder. From what he can recall of his childhood, he describes a history of trauma and neglect with a violent, drug-abusing father and absent mother.

Patients with a history of early abuse or neglect are at risk for dissociative phenomena and other trauma-related psychiatric disorders.1 The heterogeneous dissociative disorders are often hidden and unrecognized2 —as in Mr. D’s case—or present with unfamiliar or atypical symptoms. Understanding and identifying dissociative symptoms is important because:

  • Dissociative symptoms worsen prognosis, whether patients have conversion disorders1 or psychogenic seizures3 or are in psychotherapy.4
  • Dissociative states may impair memory encoding5 and decrease patients’ ability to remember therapeutic information.
  • Symptoms (such as hearing voices in multiple personality disorder) can be confused with those of disorders with different treatment strategies (such as psychotic disorders).6
  • Peritraumatic dissociation may be a risk factor for PTSD.7

This article presents a practical model for understanding dissociation, reviews clinical characteristics of this family of symptoms, and offers suggestions for assessing and treating patients with dissociative disorders.

Coming together, falling apart

Since Pierre Janet’s first reports on dissociative disorders, a number of theories and models of dissociation have been proposed,8 including empirically based, taxonomic models that address DSM-IV-TR categories (Table 1). The model I propose—which attaches a visual metaphor to dissociative phenomena—answers the question, “What is ‘dissociated’ in dissociation disorders?”

Table 1

DSM-IV-TR classification of dissociative disorders

DisorderSymptoms
Dissociative amnesiaA reversible loss of memory, typically preceded by a stressor
Dissociative fugueLoss of memory and identity, along with travel away from home
Dissociative identity disorder (formerly multiple personality disorder)Presence of different identity states, often with lack of connection between them; current models highlight the presence of recurrent dissociative intrusions into many aspects of executive function and self
Depersonalization disorderDetachment from oneself as a present, feeling person (depersonalization) and the world (derealization)
Dissociative identity disorder NOSFunctionally disturbing dissociative symptoms that do not fit into any of the above
NOS: not otherwise specified
Source: Diagnostic and statistical manual of mental disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000
5 components of consciousness. Just as separable wavelengths compose a beam of white light, dissociable “colors” or components of subjective experience constitute a normal state of consciousness. Five implicit components of normal consciousness—present in various degrees, at different times—are seamlessly integrated and associated in real time.

One paired component is a detached “observer” and a more embodied, feeling “experiencer.” The observer is a perspective that begets metacognition (thinking about one’s inner world) and self-observation; it resides in the same body as soma-based “feelings” that unconsciously contribute to the sense of “being present” with oneself and the world in the moment.9

A second component is voluntary access to one’s autobiographical memories (memories about the self in time), which are constantly “updated” and integrated with current experiences. This component allows one to distinguish between remembered (past) experiences and “firsthand” (present) experience.

Three other components of normal consciousness are:

  • a sense of agency and voluntary control over one’s mental contents, mental activity, and bodily movements
  • an ongoing connection with one’s body and mind and an understanding of where sensations and images come from
  • a sense of sequential experience, with relatively smooth transitions (from self at work to self at home, self a week ago to self today, etc) that have a singular referent (an identity).

Pathologic dissociation occurs when a prism of distress disperses one of these component “wavelengths” from the main “beam” of consciousness. For example:

  • separation of the “observer” and “experiencer” occurs in depersonalization disorder
  • reversible loss of ability to access memories characterizes dissociative amnesia
  • disconnection between sequential experiences is a part of dissociative identity disorder.
This modular perspective of dissociative disorders parallels a neurophysiologic perspective of mental states as arising from the synchronized integration of the activity of separate, functionally specialized brain regions.
 

 

10 Functional neuroimaging of dissociation supports an understanding of these symptoms as “disconnection syndromes” (Box).

Box

Dissociation’s neurobiology: Evidence of brain ‘disconnections’

From a neurophysiologic perspective, mental states may be viewed as arising from synchronized integration of the activity of functionally specialized brain regions. Functional neuroimaging of dissociation supports an understanding of these symptoms as ‘disconnection syndromes.’

Functional neuroimaging. Different ‘identities’—sometimes called a traumatic personality state and neutral personality state—demonstrate different patterns of cerebral blood flow, subjective reports, and peripheral physiologic parameters (blood pressure, heart rate).a

Functional imaging of traumatic dissociation shows active suppression of limbic regions (amygdala) and increased activity in dorsolateral prefrontal areas.b Similarly, neuroimaging of depersonalization disorder show increased neural activity in prefrontal regions associated with affect regulation and decreased activity in emotion-related areas.c,d

Speed. Dissociative responses occur extremely rapidly. Using EEG, which allows finer temporal resolution than functional imaging studies, Kirino et ale showed reversible attenuation of a specific EEG signal within 300 msec during dissociative episodes. This ultra-rapid neural reflex was correlated with allocation of attentional and working memory resources, perhaps with the goal of minimizing memory activation and resurgence of affect-laden memories.e

Hormonal. Stress-related disorders cause perturbations in neurohormonal function. Simeon et alf found a distinct pattern of stress-induced HPA axis dysregulation in dissociative patients compared with PTSD patients and healthy controls. Similar results were seen in patients with borderline personality disorder and dissociative symptoms.g

Structural imaging. Stress-related neurohormonal perturbations are known to affect critical neural structures, including the hippocampus. Using MRI, Vermetten et alh found significantly decreased amygdala and hippocampal volumes in patients with dissociative identity disorder.

EEG: electroencephalography; HPA: hypothalamic-pituitary-adrenal; PTSD: posttraumatic stress disorder

Reference Citations: click here

Causes of dissociative disorders

As with many psychiatric disorders, the etiology of dissociative phenomena is thought to include the individual patient’s temperamental or constitutional predispositions11 as well as a strong contribution of environmental trauma (early abuse, neglect).12

Constitutional predisposition for developing a dissociative disorder may include personality traits such as being easily hypnotized, mental absorption, suggestibility, and a tendency to fantasize.13 These characteristics fueled concerns in the 1990s that therapists may contribute to dissociative identity disorder by “digging” for repressed memories in susceptible patients and creating “pseudomemories” of events that did not happen.14

The issue of repressed traumatic memory and its role in therapy is extremely controversial and contributes to the complexity of psychotherapeutic treatment of dissociation.15

Early trauma. Factors that make it difficult to define the specific role of early trauma in dissociative disorders include:

  • shame and secrecy of early sexual or physical abuse and potential for victims to repress traumatic memories
  • lability of memory, potential for suggestibility, and difficulty with verification.14
Some experts—influenced by attachment theory—view dissociative phenomena as manifestations of an innate, reflexive relational pattern called disorganized attachment.16 Attachment theory notes that:

  • early relationships are one of the primary ways that humans learn to regulate distress
  • early trauma frequently includes pathology in caregiving relationships, including overt role reversal, abuse, and neglect.
Empathic treatment of dissociation, therefore, is based on appreciating the difficulties that arose from an individual’s experience of being alone with overwhelming distress. The relation of dissociation to attachment theory has specific therapeutic implications, including a focus on constructing a safe therapeutic relationship for patients.

Finally, remember that transient dissociative symptoms can be considered normal in high-stress situations. Intensive military training has been found to be associated with a very high incidence (96%) of dissociative symptoms in army recruits.17

Identifying ‘hidden’ phenomena

Dissociative disorders have been called “diseases of hiddenness”18 because:

  • Many of their clinical characteristics— sense of identity, memory, connectedness, somatosensory phenomena—are alterations in subjective phenomena that lack clearly observable symptoms.
  • Patients are often reluctant to seek help or divulge their symptoms to clinicians.
  • When dissociative symptoms are obvious—such as multiple personalities or sudden loss of memories—they may be dismissed or evoke skepticism because of their dramatic presentation.
Screening tools. To identify at-risk patients, consider screening with a validated questionnaire such as the Childhood Trauma Questionnaire (CTQ),19 particularly for patients with psychiatric comorbidity (Table 2). Using the CTQ—which assesses physical, emotional, and sexual abuse and neglect—is a high-yield procedure, given the role of early trauma in brain development and future mental health.20

For more targeted screening, the self-report Dissociative Experiences Scale (DES)21 is useful for clinical assessment in conjunction with the clinician-administered diagnostic Structured Clinical Interview for DSM-IV Dissociative Disorder (SCID-D).22

Table 2

With these findings, consider screening for dissociation

 

 

Posttraumatic stress disorder
Certain personality disorders (especially borderline personality disorder)
Somatoform disorders (conversion disorders and nonepileptic seizures)
Eating disorders
Substance use disorders
Extensive history of trauma or neglect
Self-harm behavior
Differential diagnosis. Diagnosing dissociative disorders includes ruling out psychopathologies that can present with “look-alike” symptoms (Table 3).

As in Mr. D’s case, dissociative phenomena may attenuate the benefit of post-trauma therapeutic interventions, especially those involving exposure. Therefore:

  • assess post-trauma patients for dissociation before you start treatment
  • make specific alterations in psychotherapy for such patients, as described below.
Educating trauma patients that detachment is a normal response to threat17 can reduce shame about not fighting back.

Table 3

Differential diagnosis: Dissociation ‘look-alikes’

Dissociation symptomCan be confused with:
Visual or auditory hallucinations, other ‘first-rank’ psychotic symptoms in dissociative identity disorderPsychotic disorder
‘Blanking out’ (cognitive disruption)ADHD, seizures
Somatoform (conversion) symptomsA variety of nonpsychiatric medical problems, including pelvic or abdominal pathology and headaches
Dissociative memory lapsesLearning disability, not paying attention
‘Switching’ between statesBipolar disorder, rapid cycling
Lack of emotional reaction to traumatic stimuli(numbing response)Healthy coping
ADHD: attention-deficit/hyperactivity disorder
Medical causes. Because complex partial seizures can cause dissociative symptoms,23 consider evaluating patients for seizures, head trauma, and structural lesions. Psychogenic nonepileptic seizures (PNES) often occur in conjunction with early trauma, dissociative symptoms, and PTSD.3

Recreational drugs such as ketamine, methylenedioxymethamphetamine (“Ecstasy”), hallucinogens, marijuana, and dextromethorphan also can induce dissociative states. Consider evaluating for use of these substances, some of which may not be detected on a routine drug screen.24

CASE CONTINUED: A tactical shift

Internal distress—such as when remembering painful events—clearly is linked with the appearance of Mr. D’s symptoms. The therapist—recognizing unacknowledged dissociative phenomena—changes Mr. D’s therapeutic strategy from exposure therapy to affect and anxiety regulation, with an explicit focus on attachment security (safety).

The therapist explains to Mr. D that dissociation symptoms are a response to distress, and he can learn more adaptive distress regulation in therapy. The in-session focus shifts to include more direct attention to components of the therapy relationship, including overt disclosure of the therapist’s positive regard and commitment to help the patient and frequent pauses to “check in” that the patient feels present, safe, and understood. With this new focus, Mr. D’s dissociative symptoms resolve and he feels more ready to face and overcome his fear and avoided memories.

Psychotherapy: Putting pieces together

Psychotherapy is the primary treatment, based on understanding dissociative disorders as manifestations of distress-related, traumatic fragmentation of the sense of self, interpersonal relatedness, and capacity for adaptive affect regulation (Table 4).

Depersonalization disorder. Cognitive-behavioral integration has been proposed, based on the idea that detachment from one’s self creates anxiety and reinforces efforts to avoid this internal state and events that trigger it. In an open study of 21 patients with depersonalization disorder, individual cognitive-behavioral therapy (CBT) reduced avoidance, safety behaviors, and symptom monitoring. Measures of dissociation, depression, anxiety, and general functioning also improved.25

Table 4

Tips for conceptualizing dissociative disorders

Ground your understanding of this class of disorders as distress-related breakdowns in functional connection and integration among components of normal consciousness
Consider the overlap among dissociation, certain somatoform disorders (conversion symptoms, pseudoseizures), and PTSD
Maintain a high index of suspicion for dissociative symptoms in patients with early trauma or neglect (consider screening for this); do further evaluation with dissociative-specific tools
Avoid the tendency to assume that reversible, unfamiliar, or peculiar symptoms imply volition or lack of an organic basis
PTSD: posttraumatic stress disorder
Dissociative identity disorder (DID)—the quintessential dissociative disorder—is usually treated by specialists. Treatment is complex, but some components are appropriate for less severe forms of dissociation, including dissociation as part of PTSD.26

Safety, stabilization, and symptom reduction. Providing a safe therapeutic relationship is a primary and necessary part of DID treatment. On that platform, a first step in reintegrating distressing material into the self involves building the patient’s capacity for conscious, flexible affect regulation. This keeps anxiety and distress within a therapeutic “window.”

Graded exposure. Exposure to feared mental contents—typically traumatic memories—is central to trauma-focused therapy. Dissociation is conceptualized as driven by distress greater than the system can bear, loss of adaptive integration, and subsequent fear-based, reflexive avoidance.27 Re-experiencing trauma-related memories in a safe relationship with a new regulatory capacity may work by anchoring patients in an autobiographical memory base.28

Integration of identity and person. Treatment ends when formerly unintegrated or dissociated experiences or parts of the self are integrated into a coherent whole, and the patient can deal adaptively with inter-personal relationships and distress without fragmentation.

 

 

Adjunctive medications

Few studies have addressed using psychopharmacologic interventions in the heterogeneous dissociative disorders. GABAA antagonism and 5-HT2a/2c agonism have induced psychotic and dissociative-like symptoms in healthy men,29 and alterations in enzymes such as catechol-O-methyltransferase (COMT) may explain individual vulnerability to trauma.30 Reports of dissociation related to ketamine31 and marijuana32 implicate other neurotransmitter systems in their etiology.

DID. Similar to guidelines for borderline personality disorder,33 guidelines for DID suggest using medications to treat the most prominent symptom clusters such as insomnia, affective instability, and posttraumatic intrusions.

Depersonalization disorder. Trials of fluoxetine and lamotrigine showed no benefit in depersonalization disorder.34,35 In an open trial of 14 patients, naloxone (mean 120 mg/d) reduced depersonalization symptoms by 30%, as measured by 3 validated scales.36

PTSD-related dissociation. If dissociative symptoms are associated with PTSD, selective serotonin reuptake inhibitors are considered first-line pharmacologic treatment.37 In a 10-week trial of 70 mostly minority adult outpatients with PTSD, paroxetine, ≤60 mg/d, was more effective than placebo in reducing dissociative symptoms, as shown by changes in DES scores.38

Related Resources

Drug Brand Names

  • Fluoxetine • Prozac
  • Lamotrigine • Lamictal
  • Naloxone • Narcan
  • Paroxetine • Paxil
Disclosure

Dr. MacDonald is a speaker for Eli Lilly and Company, Janssen, L.P., and Pfizer Inc.

Mr. D, age 45, presents to his primary care physician with panic attacks, nausea, shortness of breath, nightmares, and dizziness 6 months after being assaulted and robbed at an ATM. Following a routine medical workup, the physician diagnoses posttraumatic stress disorder (PTSD) and refers Mr. D for exposure and response prevention therapy.

During graded exposure sessions, Mr. D’s eyes sometimes glaze over and he seems to “float away” from the discussion. When the therapist asks about these symptoms, Mr. D reports having had them as long as he can remember. In school, he says, teachers thought he was a slow learner, a daydreamer, or had attention-deficit/hyperactivity disorder. From what he can recall of his childhood, he describes a history of trauma and neglect with a violent, drug-abusing father and absent mother.

Patients with a history of early abuse or neglect are at risk for dissociative phenomena and other trauma-related psychiatric disorders.1 The heterogeneous dissociative disorders are often hidden and unrecognized2 —as in Mr. D’s case—or present with unfamiliar or atypical symptoms. Understanding and identifying dissociative symptoms is important because:

  • Dissociative symptoms worsen prognosis, whether patients have conversion disorders1 or psychogenic seizures3 or are in psychotherapy.4
  • Dissociative states may impair memory encoding5 and decrease patients’ ability to remember therapeutic information.
  • Symptoms (such as hearing voices in multiple personality disorder) can be confused with those of disorders with different treatment strategies (such as psychotic disorders).6
  • Peritraumatic dissociation may be a risk factor for PTSD.7

This article presents a practical model for understanding dissociation, reviews clinical characteristics of this family of symptoms, and offers suggestions for assessing and treating patients with dissociative disorders.

Coming together, falling apart

Since Pierre Janet’s first reports on dissociative disorders, a number of theories and models of dissociation have been proposed,8 including empirically based, taxonomic models that address DSM-IV-TR categories (Table 1). The model I propose—which attaches a visual metaphor to dissociative phenomena—answers the question, “What is ‘dissociated’ in dissociation disorders?”

Table 1

DSM-IV-TR classification of dissociative disorders

DisorderSymptoms
Dissociative amnesiaA reversible loss of memory, typically preceded by a stressor
Dissociative fugueLoss of memory and identity, along with travel away from home
Dissociative identity disorder (formerly multiple personality disorder)Presence of different identity states, often with lack of connection between them; current models highlight the presence of recurrent dissociative intrusions into many aspects of executive function and self
Depersonalization disorderDetachment from oneself as a present, feeling person (depersonalization) and the world (derealization)
Dissociative identity disorder NOSFunctionally disturbing dissociative symptoms that do not fit into any of the above
NOS: not otherwise specified
Source: Diagnostic and statistical manual of mental disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000
5 components of consciousness. Just as separable wavelengths compose a beam of white light, dissociable “colors” or components of subjective experience constitute a normal state of consciousness. Five implicit components of normal consciousness—present in various degrees, at different times—are seamlessly integrated and associated in real time.

One paired component is a detached “observer” and a more embodied, feeling “experiencer.” The observer is a perspective that begets metacognition (thinking about one’s inner world) and self-observation; it resides in the same body as soma-based “feelings” that unconsciously contribute to the sense of “being present” with oneself and the world in the moment.9

A second component is voluntary access to one’s autobiographical memories (memories about the self in time), which are constantly “updated” and integrated with current experiences. This component allows one to distinguish between remembered (past) experiences and “firsthand” (present) experience.

Three other components of normal consciousness are:

  • a sense of agency and voluntary control over one’s mental contents, mental activity, and bodily movements
  • an ongoing connection with one’s body and mind and an understanding of where sensations and images come from
  • a sense of sequential experience, with relatively smooth transitions (from self at work to self at home, self a week ago to self today, etc) that have a singular referent (an identity).

Pathologic dissociation occurs when a prism of distress disperses one of these component “wavelengths” from the main “beam” of consciousness. For example:

  • separation of the “observer” and “experiencer” occurs in depersonalization disorder
  • reversible loss of ability to access memories characterizes dissociative amnesia
  • disconnection between sequential experiences is a part of dissociative identity disorder.
This modular perspective of dissociative disorders parallels a neurophysiologic perspective of mental states as arising from the synchronized integration of the activity of separate, functionally specialized brain regions.
 

 

10 Functional neuroimaging of dissociation supports an understanding of these symptoms as “disconnection syndromes” (Box).

Box

Dissociation’s neurobiology: Evidence of brain ‘disconnections’

From a neurophysiologic perspective, mental states may be viewed as arising from synchronized integration of the activity of functionally specialized brain regions. Functional neuroimaging of dissociation supports an understanding of these symptoms as ‘disconnection syndromes.’

Functional neuroimaging. Different ‘identities’—sometimes called a traumatic personality state and neutral personality state—demonstrate different patterns of cerebral blood flow, subjective reports, and peripheral physiologic parameters (blood pressure, heart rate).a

Functional imaging of traumatic dissociation shows active suppression of limbic regions (amygdala) and increased activity in dorsolateral prefrontal areas.b Similarly, neuroimaging of depersonalization disorder show increased neural activity in prefrontal regions associated with affect regulation and decreased activity in emotion-related areas.c,d

Speed. Dissociative responses occur extremely rapidly. Using EEG, which allows finer temporal resolution than functional imaging studies, Kirino et ale showed reversible attenuation of a specific EEG signal within 300 msec during dissociative episodes. This ultra-rapid neural reflex was correlated with allocation of attentional and working memory resources, perhaps with the goal of minimizing memory activation and resurgence of affect-laden memories.e

Hormonal. Stress-related disorders cause perturbations in neurohormonal function. Simeon et alf found a distinct pattern of stress-induced HPA axis dysregulation in dissociative patients compared with PTSD patients and healthy controls. Similar results were seen in patients with borderline personality disorder and dissociative symptoms.g

Structural imaging. Stress-related neurohormonal perturbations are known to affect critical neural structures, including the hippocampus. Using MRI, Vermetten et alh found significantly decreased amygdala and hippocampal volumes in patients with dissociative identity disorder.

EEG: electroencephalography; HPA: hypothalamic-pituitary-adrenal; PTSD: posttraumatic stress disorder

Reference Citations: click here

Causes of dissociative disorders

As with many psychiatric disorders, the etiology of dissociative phenomena is thought to include the individual patient’s temperamental or constitutional predispositions11 as well as a strong contribution of environmental trauma (early abuse, neglect).12

Constitutional predisposition for developing a dissociative disorder may include personality traits such as being easily hypnotized, mental absorption, suggestibility, and a tendency to fantasize.13 These characteristics fueled concerns in the 1990s that therapists may contribute to dissociative identity disorder by “digging” for repressed memories in susceptible patients and creating “pseudomemories” of events that did not happen.14

The issue of repressed traumatic memory and its role in therapy is extremely controversial and contributes to the complexity of psychotherapeutic treatment of dissociation.15

Early trauma. Factors that make it difficult to define the specific role of early trauma in dissociative disorders include:

  • shame and secrecy of early sexual or physical abuse and potential for victims to repress traumatic memories
  • lability of memory, potential for suggestibility, and difficulty with verification.14
Some experts—influenced by attachment theory—view dissociative phenomena as manifestations of an innate, reflexive relational pattern called disorganized attachment.16 Attachment theory notes that:

  • early relationships are one of the primary ways that humans learn to regulate distress
  • early trauma frequently includes pathology in caregiving relationships, including overt role reversal, abuse, and neglect.
Empathic treatment of dissociation, therefore, is based on appreciating the difficulties that arose from an individual’s experience of being alone with overwhelming distress. The relation of dissociation to attachment theory has specific therapeutic implications, including a focus on constructing a safe therapeutic relationship for patients.

Finally, remember that transient dissociative symptoms can be considered normal in high-stress situations. Intensive military training has been found to be associated with a very high incidence (96%) of dissociative symptoms in army recruits.17

Identifying ‘hidden’ phenomena

Dissociative disorders have been called “diseases of hiddenness”18 because:

  • Many of their clinical characteristics— sense of identity, memory, connectedness, somatosensory phenomena—are alterations in subjective phenomena that lack clearly observable symptoms.
  • Patients are often reluctant to seek help or divulge their symptoms to clinicians.
  • When dissociative symptoms are obvious—such as multiple personalities or sudden loss of memories—they may be dismissed or evoke skepticism because of their dramatic presentation.
Screening tools. To identify at-risk patients, consider screening with a validated questionnaire such as the Childhood Trauma Questionnaire (CTQ),19 particularly for patients with psychiatric comorbidity (Table 2). Using the CTQ—which assesses physical, emotional, and sexual abuse and neglect—is a high-yield procedure, given the role of early trauma in brain development and future mental health.20

For more targeted screening, the self-report Dissociative Experiences Scale (DES)21 is useful for clinical assessment in conjunction with the clinician-administered diagnostic Structured Clinical Interview for DSM-IV Dissociative Disorder (SCID-D).22

Table 2

With these findings, consider screening for dissociation

 

 

Posttraumatic stress disorder
Certain personality disorders (especially borderline personality disorder)
Somatoform disorders (conversion disorders and nonepileptic seizures)
Eating disorders
Substance use disorders
Extensive history of trauma or neglect
Self-harm behavior
Differential diagnosis. Diagnosing dissociative disorders includes ruling out psychopathologies that can present with “look-alike” symptoms (Table 3).

As in Mr. D’s case, dissociative phenomena may attenuate the benefit of post-trauma therapeutic interventions, especially those involving exposure. Therefore:

  • assess post-trauma patients for dissociation before you start treatment
  • make specific alterations in psychotherapy for such patients, as described below.
Educating trauma patients that detachment is a normal response to threat17 can reduce shame about not fighting back.

Table 3

Differential diagnosis: Dissociation ‘look-alikes’

Dissociation symptomCan be confused with:
Visual or auditory hallucinations, other ‘first-rank’ psychotic symptoms in dissociative identity disorderPsychotic disorder
‘Blanking out’ (cognitive disruption)ADHD, seizures
Somatoform (conversion) symptomsA variety of nonpsychiatric medical problems, including pelvic or abdominal pathology and headaches
Dissociative memory lapsesLearning disability, not paying attention
‘Switching’ between statesBipolar disorder, rapid cycling
Lack of emotional reaction to traumatic stimuli(numbing response)Healthy coping
ADHD: attention-deficit/hyperactivity disorder
Medical causes. Because complex partial seizures can cause dissociative symptoms,23 consider evaluating patients for seizures, head trauma, and structural lesions. Psychogenic nonepileptic seizures (PNES) often occur in conjunction with early trauma, dissociative symptoms, and PTSD.3

Recreational drugs such as ketamine, methylenedioxymethamphetamine (“Ecstasy”), hallucinogens, marijuana, and dextromethorphan also can induce dissociative states. Consider evaluating for use of these substances, some of which may not be detected on a routine drug screen.24

CASE CONTINUED: A tactical shift

Internal distress—such as when remembering painful events—clearly is linked with the appearance of Mr. D’s symptoms. The therapist—recognizing unacknowledged dissociative phenomena—changes Mr. D’s therapeutic strategy from exposure therapy to affect and anxiety regulation, with an explicit focus on attachment security (safety).

The therapist explains to Mr. D that dissociation symptoms are a response to distress, and he can learn more adaptive distress regulation in therapy. The in-session focus shifts to include more direct attention to components of the therapy relationship, including overt disclosure of the therapist’s positive regard and commitment to help the patient and frequent pauses to “check in” that the patient feels present, safe, and understood. With this new focus, Mr. D’s dissociative symptoms resolve and he feels more ready to face and overcome his fear and avoided memories.

Psychotherapy: Putting pieces together

Psychotherapy is the primary treatment, based on understanding dissociative disorders as manifestations of distress-related, traumatic fragmentation of the sense of self, interpersonal relatedness, and capacity for adaptive affect regulation (Table 4).

Depersonalization disorder. Cognitive-behavioral integration has been proposed, based on the idea that detachment from one’s self creates anxiety and reinforces efforts to avoid this internal state and events that trigger it. In an open study of 21 patients with depersonalization disorder, individual cognitive-behavioral therapy (CBT) reduced avoidance, safety behaviors, and symptom monitoring. Measures of dissociation, depression, anxiety, and general functioning also improved.25

Table 4

Tips for conceptualizing dissociative disorders

Ground your understanding of this class of disorders as distress-related breakdowns in functional connection and integration among components of normal consciousness
Consider the overlap among dissociation, certain somatoform disorders (conversion symptoms, pseudoseizures), and PTSD
Maintain a high index of suspicion for dissociative symptoms in patients with early trauma or neglect (consider screening for this); do further evaluation with dissociative-specific tools
Avoid the tendency to assume that reversible, unfamiliar, or peculiar symptoms imply volition or lack of an organic basis
PTSD: posttraumatic stress disorder
Dissociative identity disorder (DID)—the quintessential dissociative disorder—is usually treated by specialists. Treatment is complex, but some components are appropriate for less severe forms of dissociation, including dissociation as part of PTSD.26

Safety, stabilization, and symptom reduction. Providing a safe therapeutic relationship is a primary and necessary part of DID treatment. On that platform, a first step in reintegrating distressing material into the self involves building the patient’s capacity for conscious, flexible affect regulation. This keeps anxiety and distress within a therapeutic “window.”

Graded exposure. Exposure to feared mental contents—typically traumatic memories—is central to trauma-focused therapy. Dissociation is conceptualized as driven by distress greater than the system can bear, loss of adaptive integration, and subsequent fear-based, reflexive avoidance.27 Re-experiencing trauma-related memories in a safe relationship with a new regulatory capacity may work by anchoring patients in an autobiographical memory base.28

Integration of identity and person. Treatment ends when formerly unintegrated or dissociated experiences or parts of the self are integrated into a coherent whole, and the patient can deal adaptively with inter-personal relationships and distress without fragmentation.

 

 

Adjunctive medications

Few studies have addressed using psychopharmacologic interventions in the heterogeneous dissociative disorders. GABAA antagonism and 5-HT2a/2c agonism have induced psychotic and dissociative-like symptoms in healthy men,29 and alterations in enzymes such as catechol-O-methyltransferase (COMT) may explain individual vulnerability to trauma.30 Reports of dissociation related to ketamine31 and marijuana32 implicate other neurotransmitter systems in their etiology.

DID. Similar to guidelines for borderline personality disorder,33 guidelines for DID suggest using medications to treat the most prominent symptom clusters such as insomnia, affective instability, and posttraumatic intrusions.

Depersonalization disorder. Trials of fluoxetine and lamotrigine showed no benefit in depersonalization disorder.34,35 In an open trial of 14 patients, naloxone (mean 120 mg/d) reduced depersonalization symptoms by 30%, as measured by 3 validated scales.36

PTSD-related dissociation. If dissociative symptoms are associated with PTSD, selective serotonin reuptake inhibitors are considered first-line pharmacologic treatment.37 In a 10-week trial of 70 mostly minority adult outpatients with PTSD, paroxetine, ≤60 mg/d, was more effective than placebo in reducing dissociative symptoms, as shown by changes in DES scores.38

Related Resources

Drug Brand Names

  • Fluoxetine • Prozac
  • Lamotrigine • Lamictal
  • Naloxone • Narcan
  • Paroxetine • Paxil
Disclosure

Dr. MacDonald is a speaker for Eli Lilly and Company, Janssen, L.P., and Pfizer Inc.

References

1. Sar V, Akyuz G, Kundakci T, et al. Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. Am J Psychiatry 2004;161:2271-6.

2. Foote B, Smolin Y, Kaplan M, et al. Prevalence of dissociative disorders in psychiatric outpatients. Am J Psychiatry 2006;163:623-9.

3. Reuber M, Pukrop R, Bauer J, et al. Outcome in psychogenic nonepileptic seizures: 1 to 10-year follow-up in 164 patients. Ann Neurol 2003;53:305-11.

4. Spitzer C, Barnow S, Freyberger HJ, Grabe HJ. Dissociation predicts symptom-related treatment outcome in short-term inpatient psychotherapy. Aust N Z J Psychiatry 2007;41:682-7.

5. Allen JG, Console DA, Lewis L. Dissociative detachment and memory impairment: reversible amnesia or encoding failure? Compr Psychiatry 1999;40:160-71.

6. Dell PF. A new model of dissociative identity disorder. Psychiatr Clin North Am 2006;29:1-26.

7. Shalev AY, Freedman S. PTSD following terrorist attacks: a prospective evaluation. Am J Psychiatry 2005;162:1188-91.

8. Steinberg M, Rounsaville B, Cicchetti DV. The Structured Clinical Interview for DSM-III-R Dissociative Disorders: preliminary report on a new diagnostic instrument. Am J Psychiatry 1990;147:76-82.

9. Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York, NY: Harcourt, Inc; 1999.

10. Alkire MT, Miller J. General anesthesia and the neural correlates of consciousness. Prog Brain Res 2005;150:229-44.

11. Simeon D, Guralnik O, Knutelska M, Schmeidler J. Personality factors associated with dissociation: temperament, defenses, and cognitive schemata. Am J Psychiatry 2002;159(3):489-91.

12. Kihlstrom JF. Dissociative disorders. Annu Rev Clin Psychol 2005;1:227-53.

13. Isaac M, Chand PK. Dissociative and conversion disorders: defining boundaries. Curr Opin Psychiatry 2006;19(1):61-6.

14. Laney C, Loftus EF. Traumatic memories are not necessarily accurate memories. Can J Psychiatry 2005;50(13):823-8.

15. Loftus EF, Davis D. Recovered memories. Annu Rev Clin Psychol 2006;2:469-98.

16. Lyons-Ruth K, Dutra L, Schuder MR, Bianchi I. From infant attachment disorganization to adult dissociation: relational adaptations or traumatic experiences? Psychiatr Clin North Am 2006;29(1):63-86.

17. Morgan CA, 3rd, Hazlett G, Wang S, et al. Symptoms of dissociation in humans experiencing acute, uncontrollable stress: a prospective investigation. Am J Psychiatry 2001;158(8):1239-47.

18. Spiegel D. Recognizing traumatic dissociation. Am J Psychiatry 2006;163(4):566-8.

19. Scher CD, Stein MB, Asmundson GJ, et al. The childhood trauma questionnaire in a community sample: psychometric properties and normative data. J Trauma Stress 2001;14:843-57.

20. Teicher MH, Andersen SL, Polcari A, et al. The neurobiological consequences of early stress and childhood maltreatment. Neurosci Biobehav Rev 2003;27:33-44.

21. Bernstein EM, Putnam FW. Development, reliability, and validity of a dissociation scale. J Nerv Ment Dis 1986;174(12):727-35.

22. Steinberg M, Rounsaville B, Cicchetti D. Detection of dissociative disorders in psychiatric patients by a screening instrument and a structured diagnostic interview. Am J Psychiatry 1991;148(8):1050-4.

23. Devinsky O, Putnam F, Grafman J, et al. Dissociative states and epilepsy. Neurology 1989;39:835-40.

24. Schonenberg M, Reichwald U, Domes G, et al. Effects of peritraumatic ketamine medication on early and sustained posttraumatic stress symptoms in moderately injured accident victims. Psychopharmacology (Berl) 2005;182(3):420-5.

25. Hunter EC, Phillips ML, Chalder T, et al. Depersonalisation disorder: a cognitive-behavioural conceptualisation. Behav Res Ther 2003;41:1451-67.

26. Guidelines for treating dissociative identity disorder in adults (2005). J Trauma Dissociation 2005;6(4):69-149.

27. van der Hart O, Nijenhuis E. Generalized dissociative amnesia: episodic, semantic and procedural memories lost and found. Aust N Z J Psychiatry 2001;35:589-600.

28. Holmes EA, Brown RJ, Mansell W, et al. Are there two qualitatively distinct forms of dissociation? A review and some clinical implications. Clin Psychol Rev 2005;25(1):1-23.

29. D’Souza DC, Gil RB, Zuzarte E, et al. gamma-Aminobutyric acid-serotonin interactions in healthy men: implications for network models of psychosis and dissociation. Biol Psychiatry 2006;59(2):128-37.

30. Savitz JB, van der Merwe L, Newman TK, et al. The relationship between childhood abuse and dissociation. Is it influenced by catechol-O-methyltransferase (COMT) activity? Int J Neuropsychopharmacol 2008;11:149-61.

31. Curran HV, Morgan C. Cognitive, dissociative and psychotogenic effects of ketamine in recreational users on the night of drug use and 3 days later. Addiction 2000;95:575-90.

32. Mathew RJ, Wilson WH, Humphreys D, et al. Depersonalization after marijuana smoking. Biol Psychiatry 1993;33:431-41.

33. American Psychiatric Association. Practice guideline for the treatment of patients with borderline personality disorder. Am J Psychiatry 2001;158(10 suppl):1-52.

34. Sierra M, Phillips ML, Ivin G, et al. A placebo-controlled, cross-over trial of lamotrigine in depersonalization disorder. J Psychopharmacol 2003;17:103-5.

35. Simeon D, Guralnik O, Schmeidler J, Knutelska M. Fluoxetine therapy in depersonalisation disorder: randomised controlled trial. Br J Psychiatry 2004;185:31-6.

36. Simeon D, Knutelska M. An open trial of naltrexone in the treatment of depersonalization disorder. J Clin Psychopharmacol 2005;25:267-70.

37. Stein DJ, Ipser JC, Seedat S. Pharmacotherapy for post traumatic stress disorder (PTSD). Cochrane Database Syst Rev 2006(1):CD002795.-

38. Marshall RD, Lewis-Fernandez R, Blanco C, et al. A controlled trial of paroxetine for chronic PTSD, dissociation, and interpersonal problems in mostly minority adults. Depress Anxiety 2007;24:77-84.

References

1. Sar V, Akyuz G, Kundakci T, et al. Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. Am J Psychiatry 2004;161:2271-6.

2. Foote B, Smolin Y, Kaplan M, et al. Prevalence of dissociative disorders in psychiatric outpatients. Am J Psychiatry 2006;163:623-9.

3. Reuber M, Pukrop R, Bauer J, et al. Outcome in psychogenic nonepileptic seizures: 1 to 10-year follow-up in 164 patients. Ann Neurol 2003;53:305-11.

4. Spitzer C, Barnow S, Freyberger HJ, Grabe HJ. Dissociation predicts symptom-related treatment outcome in short-term inpatient psychotherapy. Aust N Z J Psychiatry 2007;41:682-7.

5. Allen JG, Console DA, Lewis L. Dissociative detachment and memory impairment: reversible amnesia or encoding failure? Compr Psychiatry 1999;40:160-71.

6. Dell PF. A new model of dissociative identity disorder. Psychiatr Clin North Am 2006;29:1-26.

7. Shalev AY, Freedman S. PTSD following terrorist attacks: a prospective evaluation. Am J Psychiatry 2005;162:1188-91.

8. Steinberg M, Rounsaville B, Cicchetti DV. The Structured Clinical Interview for DSM-III-R Dissociative Disorders: preliminary report on a new diagnostic instrument. Am J Psychiatry 1990;147:76-82.

9. Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York, NY: Harcourt, Inc; 1999.

10. Alkire MT, Miller J. General anesthesia and the neural correlates of consciousness. Prog Brain Res 2005;150:229-44.

11. Simeon D, Guralnik O, Knutelska M, Schmeidler J. Personality factors associated with dissociation: temperament, defenses, and cognitive schemata. Am J Psychiatry 2002;159(3):489-91.

12. Kihlstrom JF. Dissociative disorders. Annu Rev Clin Psychol 2005;1:227-53.

13. Isaac M, Chand PK. Dissociative and conversion disorders: defining boundaries. Curr Opin Psychiatry 2006;19(1):61-6.

14. Laney C, Loftus EF. Traumatic memories are not necessarily accurate memories. Can J Psychiatry 2005;50(13):823-8.

15. Loftus EF, Davis D. Recovered memories. Annu Rev Clin Psychol 2006;2:469-98.

16. Lyons-Ruth K, Dutra L, Schuder MR, Bianchi I. From infant attachment disorganization to adult dissociation: relational adaptations or traumatic experiences? Psychiatr Clin North Am 2006;29(1):63-86.

17. Morgan CA, 3rd, Hazlett G, Wang S, et al. Symptoms of dissociation in humans experiencing acute, uncontrollable stress: a prospective investigation. Am J Psychiatry 2001;158(8):1239-47.

18. Spiegel D. Recognizing traumatic dissociation. Am J Psychiatry 2006;163(4):566-8.

19. Scher CD, Stein MB, Asmundson GJ, et al. The childhood trauma questionnaire in a community sample: psychometric properties and normative data. J Trauma Stress 2001;14:843-57.

20. Teicher MH, Andersen SL, Polcari A, et al. The neurobiological consequences of early stress and childhood maltreatment. Neurosci Biobehav Rev 2003;27:33-44.

21. Bernstein EM, Putnam FW. Development, reliability, and validity of a dissociation scale. J Nerv Ment Dis 1986;174(12):727-35.

22. Steinberg M, Rounsaville B, Cicchetti D. Detection of dissociative disorders in psychiatric patients by a screening instrument and a structured diagnostic interview. Am J Psychiatry 1991;148(8):1050-4.

23. Devinsky O, Putnam F, Grafman J, et al. Dissociative states and epilepsy. Neurology 1989;39:835-40.

24. Schonenberg M, Reichwald U, Domes G, et al. Effects of peritraumatic ketamine medication on early and sustained posttraumatic stress symptoms in moderately injured accident victims. Psychopharmacology (Berl) 2005;182(3):420-5.

25. Hunter EC, Phillips ML, Chalder T, et al. Depersonalisation disorder: a cognitive-behavioural conceptualisation. Behav Res Ther 2003;41:1451-67.

26. Guidelines for treating dissociative identity disorder in adults (2005). J Trauma Dissociation 2005;6(4):69-149.

27. van der Hart O, Nijenhuis E. Generalized dissociative amnesia: episodic, semantic and procedural memories lost and found. Aust N Z J Psychiatry 2001;35:589-600.

28. Holmes EA, Brown RJ, Mansell W, et al. Are there two qualitatively distinct forms of dissociation? A review and some clinical implications. Clin Psychol Rev 2005;25(1):1-23.

29. D’Souza DC, Gil RB, Zuzarte E, et al. gamma-Aminobutyric acid-serotonin interactions in healthy men: implications for network models of psychosis and dissociation. Biol Psychiatry 2006;59(2):128-37.

30. Savitz JB, van der Merwe L, Newman TK, et al. The relationship between childhood abuse and dissociation. Is it influenced by catechol-O-methyltransferase (COMT) activity? Int J Neuropsychopharmacol 2008;11:149-61.

31. Curran HV, Morgan C. Cognitive, dissociative and psychotogenic effects of ketamine in recreational users on the night of drug use and 3 days later. Addiction 2000;95:575-90.

32. Mathew RJ, Wilson WH, Humphreys D, et al. Depersonalization after marijuana smoking. Biol Psychiatry 1993;33:431-41.

33. American Psychiatric Association. Practice guideline for the treatment of patients with borderline personality disorder. Am J Psychiatry 2001;158(10 suppl):1-52.

34. Sierra M, Phillips ML, Ivin G, et al. A placebo-controlled, cross-over trial of lamotrigine in depersonalization disorder. J Psychopharmacol 2003;17:103-5.

35. Simeon D, Guralnik O, Schmeidler J, Knutelska M. Fluoxetine therapy in depersonalisation disorder: randomised controlled trial. Br J Psychiatry 2004;185:31-6.

36. Simeon D, Knutelska M. An open trial of naltrexone in the treatment of depersonalization disorder. J Clin Psychopharmacol 2005;25:267-70.

37. Stein DJ, Ipser JC, Seedat S. Pharmacotherapy for post traumatic stress disorder (PTSD). Cochrane Database Syst Rev 2006(1):CD002795.-

38. Marshall RD, Lewis-Fernandez R, Blanco C, et al. A controlled trial of paroxetine for chronic PTSD, dissociation, and interpersonal problems in mostly minority adults. Depress Anxiety 2007;24:77-84.

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Interoceptive cues: When ‘gut feelings’ point to anxiety

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CASE: 'I don't know how I feel'

Ms. N, age 48, is seen in an outpatient clinic for episodic, impulsive aggression and evaluation of possible bipolar disorder. When you ask her to describe one of her episodes—which always involve a conflict with her partner or another loved one—Ms. N says, “I just lose control… I go blank.” You observe Ms. N’s deep, sighing respirations, trembling hands, and restless, fidgety leg movements. When you ask about her awareness of her physical state while she was recalling the incident, she immediately calms, looks at you quizzically, and states, “I don’t know how I feel.”

When assessing a patient who might have an anxiety disorder, don’t overlook the body. In addition to worry and avoidance, body-centered feelings are a vital component of anxiety and an important treatment target.1

This article:

  • highlights clinically relevant neurobiology of anxious feelings
  • discusses interoception—awareness of the physiologic state of one’s body—and its connection with anxiety
  • explains the use of interoceptive cues as an aid to diagnosing and treating anxiety.

Affective neuroscience and fear

Interoceptive cues are questions directed toward the somatic manifestations of anxiety. Because these questions encourage patients to consciously experience the physical symptoms of anxiety, using interoceptive cues essentially is an exposure-based intervention that may feel counterintuitive to practitioners who are more accustomed to trying to relieve anxiety.

Emotions are thought to be grounded in brain areas that receive and regulate somatic signals, such as the amygdala and insula.2 A feeling-focused approach to anxiety weds affective neuroscience—the study of emotions—with clinical assessment and treatment of anxiety disorders, and conceptualizes that fear is a core component of many anxiety-related disorders.3,4

Although the DSM-IV-TR views anxiety disorders as clinically heterogeneous, affective neuroscience emphasizes what these disorders have in common.5 This unifying perspective allows clinicians to anchor anxiety disorders and anxiety-related disorders—such as hypochondriasis—in core emotional systems that have 3 clinically important aspects—actions (behavior and body), brain, and consciousness (mind) (Figure).4 Two emotional systems related to anxiety disorders are fear (anxious anticipation) and panic (evolutionarily related to separation anxiety and suffocation alarm signals). Viewing anxiety disorders as rooted in core emotion systems allows you to incorporate recent advances in emotional neuroscience, including interoception, into your clinical practice.

Figure: A,B,C model for understanding emotions

Affective neuroscience is a broad-based scientific discipline that explores emotions from 3 vantages: actions (behaviors and bodily responses), brain bases, and conscious manifestations. Two core emotional systems related to anxiety disorders are fear and panic.
Source: Adapted with permission from Panksepp J. Affective neuroscience. New York: Oxford University Press; 1998:31.

Detecting ‘hidden’ anxiety

Conscious symptoms. Activity in the brain’s fear system can generate conscious experiences, including worry, heightened arousal, attentional biases, and body-based feelings of fear. Anxious feelings—by definition, sensory experiences—are an important component of an anxiety assessment and relatively easy to identify.

Kroenke et al6 evaluated a 2-item screening tool, the Generalized Anxiety Disorder scale (GAD-2) that highlights both cognitive (worry) and somatic (feeling) sides of anxiety. Researchers asked 965 randomly sampled primary care patients, “Over the past 2 weeks, how often have you been bothered by the following problems:

  • feeling nervous, anxious, or on edge
  • not being able to stop or control worrying.

Possible responses ranged from 0 (not at all) to 3 (nearly every day). The GAD-2 was as specific for detecting anxiety disorders as a 7-item scale, the GAD-7, (88%), though less sensitive (65% vs 77%).

Nonconscious symptoms. A challenge arises, however, when patients demonstrate signs of anxiety (stress-related physical symptoms such as stomach pains or avoidance-related behaviors) without conscious awareness of anxious feelings. Though patients may intellectually understand the concept of body-based “gut feelings,” these sensations are often reflexively ignored, avoided, or mislabeled. Patients may use terms such as “stressed,” “distressed,” or “tense,” focus on the external source of the fear (rather than their response to it), or reflexively engage in behaviors (avoidance, impulsive behaviors) without being aware of their internal responses.

Anxiety symptoms that occur without corresponding awareness can be called occult, nonconscious, or unconscious anxiety. These symptoms, unique to each patient, can be used as:

  • cues to the patient that he or she is anxious
  • stimuli to be desensitized (via exposure-based interventions)
  • markers of treatment progress.

Patients who experience occult anxiety often have a deficit in interoception (Box).2,7-11 Using interoceptive cues to foster awareness of these unrecognized body-based symptoms can provide insight into formerly unrecognized manifestations of anxiety.

 

 

Neurobiology of anxiety

The fear system. Dynamic changes in stimulus-specific physical sensations—anxious feelings—are linked to activity of the brain’s fear system. This system, which detects and rapidly learns to anticipate danger or distress, can exhibit low-level tonic activity (chronic, generalized anxiety), phasic high-amplitude reactivity (spikes of anxiety), and combinations of the 2.4,12

This precognitive, primary-process alarm system can generate:

  • behaviors, often centered around avoidance—though other types (such as impulsive) can occur
  • physiologic responses, which may or may not become conscious
  • states of mind, including attention (hypervigilance, dissociation), cognitive contents (specific worries), and viscerosomatic awareness (“feelings”).

Through learning—and under the influence of temperamental/genetic predispositions—the fear system can be linked to internal and external stimuli, yielding a spectrum of clinical disorders that includes anxiety disorders.5

Box

Interoception: Looking inside the mind and body

Consciously experiencing an emotion, attending to an emotionally arousing external stimulus, and remembering an emotionally arousing event all involve overlapping mental and neurobiologic processes in brain areas that process and regulate sensations from the body.2,7 Therefore, one does not need to remember “how one felt in the past” to elicit similar neurobiologic and physiologic responses in the present. These responses are recreated in the present when one consciously activates the memory. This understanding underlies the use of interoceptive cues.

Interoception is intentional, mindful awareness of the physiologic state of one’s body. Consciously directing attention to one’s internal state actively unifies the activity of the attending mind and brain with ongoing visceromotor sensations from the body.8,9 These body-based somatic markers often lie at the border of consciousness and can be brought into awareness via interoceptive cues.9 Awareness of and exposure to these often private, physiologic symptoms is an important part of many evidence-based therapies for anxiety disorders.10,11

Brain basis of fear. The amygdala and insula are 2 key components of the brain basis of fearful feelings.

The amygdala processes internal or external stimuli, alerts other brain areas that a threat is present, and triggers a fear or anxiety response (Table 1).13-16 Early, nonconscious threat detection by the amygdala may be a core component of the brain basis of many anxiety disorders.17

Amygdala activity has been associated with automatic fear perception, associative fear learning, trauma,18 and (on the treatment side) extinction of learned fears via active coping.19 The amygdala provides an extremely rapid response to fearful stimuli—within milliseconds—and can be active without conscious awareness of the stimuli (which may take several hundred milliseconds to develop).20,21

Inputs into the amygdala can come from:

  • inside the brain (memories, images, emotions, predictions of the future)
  • or outside (contemporary stimuli).

In treatment, the amygdala may be one site of activity of serotonergic medications.22 It is partially regulated by orbitofrontal and medial prefrontal areas that may be target sites of “top-down” psychotherapeutic interventions.23

The insula—a sector of cortex tucked beneath the fissure between the temporal and parietal lobesis involved in interoception, modulation of emotional processing, and emotional learning, especially as related to aversive internal states.24,25

Paulus24 proposes that in anxiety-prone individuals the insula may create a negatively valenced, preattentive, body-centered warning of negative things to come—in a sense, a somatic semaphore that signals danger ahead. In a related study, Stein et al26 presented college students with emotion-provoking faces. Students prone to anxiety had elevated activity in the amygdala and insula compared with normal controls.

The insula also may respond to mindful mental exercise. Lazar et al27 found increased cortical thickness in prefrontal and anterior insula in 20 subjects with extensive experience in insight meditation, which involves focusing attention on internal states.

Table 1

Amygdala output pathways that result in anxiety symptoms

Link to specific brain areaClinically important responses
HypothalamusSympathetic activation: increased heart rate, sweating, dilated pupils, striated muscle tension, strained breathing
Dorsal motor nucleus of vagusParasympathetic activation: slowed heart rate, bladder and bowel symptoms—frequent urination, diarrhea—via smooth muscle activity, gastric acid secretion
Parabrachial nucleusIncreased respiratory rate: sighing respirations
Ventral tegmental area/locus ceruleusGeneralized arousal, perceptual vigilance (excessive stimulation leads to disruption of attention/dissociation, via prefrontal cortical connections)
Nucleus reticularis pontis caudalisStartle response, jumpiness
Periaqueductal gray matterAutomatic coping patterns, from passive (freeze, collapse) to active (confrontation, fight)
Trigeminal facial motor nucleiJaw tension, facial expressions of fear
Source: Adapted with permission from references 13 with additional information from references 14-16

CASE CONTINUED: Using focused interoception

You help Ms. N become aware of her somatic symptoms of anxiety by using a series of questions to direct her attention to her physical responses in a “head-to-toe” approach: “Do you notice the tension in your jaw?” “Is your neck tense?” “How is your breathing now?” Though Ms. N had been unaware of these symptoms, she easily agrees: “Yes, now that you mention it, I am aware of that, but I never knew it was anxiety. I thought it was just stress.”

 

 

This exercise reveals marked generalized muscle tension, sweating, and a brief period of going “blank” in her mind when she recalled one of her impulsive, aggressive episodes. You explain that these physical reactions are part of the normal biologic fear response. Apart from these symptoms, Ms. N denies any prototypical manic symptoms and does not meet bipolar disorder criteria.

Using interoceptive cues

To frame an interoceptive inquiry, discuss with patients how the brain’s fear system is connected to the body, and explain that investigating these physical symptoms can assist diagnosis and treatment. For example, you might ask, “Could we look into your physical responses in these situations to help us better understand your difficulties?”

To actively explore somatic markers of anxiety (anxious feelings), encourage the patient to describe a specific stressful or avoided situation in detail. While he or she does this, direct the patient’s attention to objective physiologic markers of anxiety, such as strained breathing or increased heart rate. Use body-directed questions (interoceptive cues) to foreground these sensory experiences in the patient’s mind. For example:

  • “As we are discussing this issue, I notice your breathing becomes more strained. Do you notice it?”
  • “As you picture this incident in your mind, are you aware of what happens in your body?”
  • “When you perceive her in that way, what do you notice about your physical response?”

You can further inquire into these somatic symptoms and their effect on the patient by asking, “How long have you been having these particular symptoms?” “How frequently do they occur?” or “How distressing are these symptoms?” These questions can separate transient physiologic arousal (normal) from pathologic (recurrent, disabling) responses that may respond to treatment. These cues and their responses can be used as person-specific biomarkers to assay a patient’s:

  • ability to attend to his or her somatic state
  • baseline level of autonomic arousal
  • internal state before problematic behaviors (such as impulsive or self-harming behaviors, substance use)
  • tendency toward anxiety-related perceptual disturbances (such as dissociation).

When the patient actively attends to and carefully describes his or her somatic sensations, the immediate outcome typically is anxiolytic. A shared awareness of the anxiolytic nature of this exercise—“It’s interesting that paying attention to these feelings actually reduces anxiety”—creates a positive first step toward further exploration. Patients can feel the power of the mind to regulate distress.

Overcoming barriers to interoception

Many patients—including those with dissociative disorders, impulse control disorders, or disorders with significant obsessive features—have difficulty using their attention to bring physical symptoms to mind. Some develop automatic, phobic patterns of disattention to contemporaneous somatic feelings of anxiety. This experiential avoidance is the fear of fear itself—fear of the conscious experience of fearful feelings. Their typical responses to interoceptive cues include:

  • lack of awareness (“I don’t know,” “I wasn’t aware of anything”)
  • perceptions, phrased as feelings (“I feel as if he doesn’t like me”)
  • action tendencies or impulses, phrased as feelings (“I feel like I want to get out of there”)
  • a verbal explanation of why they are anxious (“I’m worried about what might happen”).

Depending on the context of your inquiry, if the patient does not respond to an interoceptive cue with actual body-centered feelings, you can:

  • reframe the question: “OK, but when you perceive him in that way, if you focus your mind on your physical reactions, what do you notice?”
  • point out observable symptoms: “Did you notice as we were talking about this issue that your breathing got very shallow, and your hands got tense?”

Some patients may look transiently “spacey” or report “checking out” during the exercise. Inquire specifically about this because they may be demonstrating dissociative symptoms: “Does this sometimes happen when you are stressed, that you lose touch with your sense of your body, you go numb or your mind goes blank?” These symptoms warrant attention, as they may preclude effective retention of the exercise.

Explaining occult anxiety

Regardless of how far you choose to pursue an interoceptive inquiry, uncovering an interoceptive deficit—an inability to describe one’s somatic experience—may be diagnostically helpful. Doing so identifies a potentially modifiable component of self-awareness. So-called mindfulness-based and emotion-focused therapies assist patients in developing a more robust awareness and understanding of their emotions, including the somatic sensations of emotion (see Related Resources).

With appropriate psychoeducation, an interoceptive exploration makes anxiety a real, physical event anchored in brain-body function, and facilitates a nonshaming, organ-based explanation of anxiety. Psychoeducation about fear grounds physical symptoms of anxiety in a brain-based, evolutionarily selected neural system whose activity has a variety of inputs and outputs (Table 2).

 

 

An organ-based, body-centered discussion also may reduce defensiveness in patients who feel (or have been told) that anxiety is “not real” or signals personality weakness. This model may help trainees and medical colleagues avoid outdated distinctions between real/organic problems and functional/emotional problems and find a more conciliatory construct based in emotional neuroscience.

Serotonergic medications and psychotherapy—both of which work on the brain—have demonstrated broad efficacy for anxiety disorders.5 Several national organizations offer information about evidence-based psychotherapeutic treatments grounded in emotional awareness and neuroscience (see Related Resources).

Table 2

Activity of the fear system

Inputs
Contemporary situations
Memories (visual and sensory)
Anticipated future situations
Other nonconscious body and brain processes (including the physiologic symptoms of emotions and anxiety—a ‘fear of fear’ or ‘fear of feelings’)
Outputs
Physical symptoms
Thoughts
Perceptions
Behaviors
States of attention

CASE CONTINUED: Putting interoception to work

Your psychotherapeutic work with Ms. N focuses on attending to and consciously modulating her newly labeled anxiety For example, after an inquiry into a “stressful” situation, you help her use careful interoceptive attention—and when necessary, mindful relaxation and breathing—to regulate her fear symptoms.

She finds that these simple “exposure/regulation” exercises are enough to rapidly resolve her impulsive behaviors. In distressing situations, she can now be aware of her reactions and make a conscious choice of how to react. Your psychotherapeutic work now proceeds toward more effective interpersonal expression of other emotions.

Related Resources

  • Barrett LF, Mesquita B, Ochsner K, Gross JJ. The experience of emotion. Annu Rev Psychol 2007;58:373-403.
  • Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York: Harcourt; 1999.
  • International Experiential Dynamic Therapy Association. www.iedta.net.
  • International Center for Excellence in Emotionally Focused Therapy. www.eft.ca.

Disclosure

Dr. MacDonald reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

References

1. Katon W, Lin EH, Kroenke K. The association of depression and anxiety with medical symptom burden in patients with chronic medical illness. Gen Hosp Psychiatry 2007;29(2):147-55.

2. Niedenthal PM. Embodying emotion. Science 2007;316(5827):1002-5.

3. McClure EB, Monk CS, Nelson EE, et al. Abnormal attention modulation of fear circuit function in pediatric generalized anxiety disorder. Arch Gen Psychiatry 2007;64(1):97-106.

4. Panksepp J. Affective neuroscience. New York: Oxford University Press; 1998:31.

5. Stein DJ. Advances in understanding the anxiety disorders: the cognitive-affective neuroscience of ‘false alarms’. Ann Clin Psychiatry 2006;18(3):173-82.

6. Kroenke K, Spitzer RL, Williams JBW, et al. Anxiety disorders in primary care: prevalence, impairment, comorbidity, and detection. Ann Intern Med 2007;146(5):317-25.

7. Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York: Harcourt; 1999.

8. Wiens S. Interoception in emotional experience. Curr Opin Neurol 2005;18(4):442-7.

9. Cameron OG. Interoception: the inside story—a model for psychosomatic processes. Psychosom Med 2001;63(5):697-710.

10. Wald J, Taylor S. Interoceptive exposure therapy combined with trauma-related exposure therapy for post-traumatic stress disorder: a case report. Cognit Behav Ther 2005;34(1):34-40.

11. Wells A, Papageorgiou C. Social phobic interoception: effects of bodily information on anxiety, beliefs and self-processing. Behav Res Ther 2001;39(1):1-11.

12. Davidson RJ. Anxiety and affective style: role of prefrontal cortex and amygdala. Biol Psychiatry 2002;51(1):68-80.

13. Kandel ER, Squire LR. Memory: from mind to molecules. New York: Henry Holt and Company, 1999.

14. Fokkema DS. The psychobiology of strained breathing and its cardiovascular implications: a functional system review. Psychophysiology 1999;36(2):164-75.

15. Arnsten AF. Fundamentals of attention-deficit/hyperactivity disorder: circuits and pathways. J Clin Psychiatry 2006;67 (suppl 8):7-12.

16. Keay KA, Bandler R. Parallel circuits mediating distinct emotional coping reactions to different types of stress. Neurosci Biobehav Rev 2001;25(7-8):669-78.

17. Garakani A, Mathew SJ, Charney DS. Neurobiology of anxiety disorders and implications for treatment. Mt Sinai J Med 2006;73(7):941-9.

18. Phelps EA. Emotion and cognition: insights from studies of the human amygdala. Annu Rev Psychol 2006;57:27-53.

19. LeDoux JE, Gorman JM. A call to action: overcoming anxiety through active coping. Am J Psychiatry 2001;158(12):1953-5.

20. LeDoux JE. The emotional brain. New York: Simon and Schuster, 1996.

21. Liddell BJ, Brown KJ, Kemp AH, et al. A direct brainstemamygdala-cortical ‘alarm’ system for subliminal signals of fear. Neuroimage 2005;24(1):235-43.

22. Harmer CJ, Mackay CE, Reid CB, et al. Antidepressant drug treatment modifies the neural processing of nonconscious threat cues. Biol Psychiatry 2006;59(9):816-20.

23. Hariri AR, Mattay VS, Tessitore A, et al. Neocortical modulation of the amygdala response to fearful stimuli. Biol Psychiatry 2003;53(6):494-501.

24. Paulus MP, Stein MB. An insular view of anxiety. Biol Psychiatry 2006;60(4):383-7.

25. Simmons A, Strigo I, Matthews SC, et al. Anticipation of aversive visual stimuli is associated with increased insula activation in anxiety-prone subjects. Biol Psychiatry 2006;60(4):402-9.

26. Stein MB, Simmons AN, Feinstein JS, et al. Increased amygdala and insula activation during emotion processing in anxiety-prone subjects. Am J Psychiatry 2007;164(2):318-27.

27. Lazar SW, Kerr CE, Wasserman RH, et al. Meditation experience is associated with increased cortical thickness. Neuroreport 2005;16(17):1893-7.

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CASE: 'I don't know how I feel'

Ms. N, age 48, is seen in an outpatient clinic for episodic, impulsive aggression and evaluation of possible bipolar disorder. When you ask her to describe one of her episodes—which always involve a conflict with her partner or another loved one—Ms. N says, “I just lose control… I go blank.” You observe Ms. N’s deep, sighing respirations, trembling hands, and restless, fidgety leg movements. When you ask about her awareness of her physical state while she was recalling the incident, she immediately calms, looks at you quizzically, and states, “I don’t know how I feel.”

When assessing a patient who might have an anxiety disorder, don’t overlook the body. In addition to worry and avoidance, body-centered feelings are a vital component of anxiety and an important treatment target.1

This article:

  • highlights clinically relevant neurobiology of anxious feelings
  • discusses interoception—awareness of the physiologic state of one’s body—and its connection with anxiety
  • explains the use of interoceptive cues as an aid to diagnosing and treating anxiety.

Affective neuroscience and fear

Interoceptive cues are questions directed toward the somatic manifestations of anxiety. Because these questions encourage patients to consciously experience the physical symptoms of anxiety, using interoceptive cues essentially is an exposure-based intervention that may feel counterintuitive to practitioners who are more accustomed to trying to relieve anxiety.

Emotions are thought to be grounded in brain areas that receive and regulate somatic signals, such as the amygdala and insula.2 A feeling-focused approach to anxiety weds affective neuroscience—the study of emotions—with clinical assessment and treatment of anxiety disorders, and conceptualizes that fear is a core component of many anxiety-related disorders.3,4

Although the DSM-IV-TR views anxiety disorders as clinically heterogeneous, affective neuroscience emphasizes what these disorders have in common.5 This unifying perspective allows clinicians to anchor anxiety disorders and anxiety-related disorders—such as hypochondriasis—in core emotional systems that have 3 clinically important aspects—actions (behavior and body), brain, and consciousness (mind) (Figure).4 Two emotional systems related to anxiety disorders are fear (anxious anticipation) and panic (evolutionarily related to separation anxiety and suffocation alarm signals). Viewing anxiety disorders as rooted in core emotion systems allows you to incorporate recent advances in emotional neuroscience, including interoception, into your clinical practice.

Figure: A,B,C model for understanding emotions

Affective neuroscience is a broad-based scientific discipline that explores emotions from 3 vantages: actions (behaviors and bodily responses), brain bases, and conscious manifestations. Two core emotional systems related to anxiety disorders are fear and panic.
Source: Adapted with permission from Panksepp J. Affective neuroscience. New York: Oxford University Press; 1998:31.

Detecting ‘hidden’ anxiety

Conscious symptoms. Activity in the brain’s fear system can generate conscious experiences, including worry, heightened arousal, attentional biases, and body-based feelings of fear. Anxious feelings—by definition, sensory experiences—are an important component of an anxiety assessment and relatively easy to identify.

Kroenke et al6 evaluated a 2-item screening tool, the Generalized Anxiety Disorder scale (GAD-2) that highlights both cognitive (worry) and somatic (feeling) sides of anxiety. Researchers asked 965 randomly sampled primary care patients, “Over the past 2 weeks, how often have you been bothered by the following problems:

  • feeling nervous, anxious, or on edge
  • not being able to stop or control worrying.

Possible responses ranged from 0 (not at all) to 3 (nearly every day). The GAD-2 was as specific for detecting anxiety disorders as a 7-item scale, the GAD-7, (88%), though less sensitive (65% vs 77%).

Nonconscious symptoms. A challenge arises, however, when patients demonstrate signs of anxiety (stress-related physical symptoms such as stomach pains or avoidance-related behaviors) without conscious awareness of anxious feelings. Though patients may intellectually understand the concept of body-based “gut feelings,” these sensations are often reflexively ignored, avoided, or mislabeled. Patients may use terms such as “stressed,” “distressed,” or “tense,” focus on the external source of the fear (rather than their response to it), or reflexively engage in behaviors (avoidance, impulsive behaviors) without being aware of their internal responses.

Anxiety symptoms that occur without corresponding awareness can be called occult, nonconscious, or unconscious anxiety. These symptoms, unique to each patient, can be used as:

  • cues to the patient that he or she is anxious
  • stimuli to be desensitized (via exposure-based interventions)
  • markers of treatment progress.

Patients who experience occult anxiety often have a deficit in interoception (Box).2,7-11 Using interoceptive cues to foster awareness of these unrecognized body-based symptoms can provide insight into formerly unrecognized manifestations of anxiety.

 

 

Neurobiology of anxiety

The fear system. Dynamic changes in stimulus-specific physical sensations—anxious feelings—are linked to activity of the brain’s fear system. This system, which detects and rapidly learns to anticipate danger or distress, can exhibit low-level tonic activity (chronic, generalized anxiety), phasic high-amplitude reactivity (spikes of anxiety), and combinations of the 2.4,12

This precognitive, primary-process alarm system can generate:

  • behaviors, often centered around avoidance—though other types (such as impulsive) can occur
  • physiologic responses, which may or may not become conscious
  • states of mind, including attention (hypervigilance, dissociation), cognitive contents (specific worries), and viscerosomatic awareness (“feelings”).

Through learning—and under the influence of temperamental/genetic predispositions—the fear system can be linked to internal and external stimuli, yielding a spectrum of clinical disorders that includes anxiety disorders.5

Box

Interoception: Looking inside the mind and body

Consciously experiencing an emotion, attending to an emotionally arousing external stimulus, and remembering an emotionally arousing event all involve overlapping mental and neurobiologic processes in brain areas that process and regulate sensations from the body.2,7 Therefore, one does not need to remember “how one felt in the past” to elicit similar neurobiologic and physiologic responses in the present. These responses are recreated in the present when one consciously activates the memory. This understanding underlies the use of interoceptive cues.

Interoception is intentional, mindful awareness of the physiologic state of one’s body. Consciously directing attention to one’s internal state actively unifies the activity of the attending mind and brain with ongoing visceromotor sensations from the body.8,9 These body-based somatic markers often lie at the border of consciousness and can be brought into awareness via interoceptive cues.9 Awareness of and exposure to these often private, physiologic symptoms is an important part of many evidence-based therapies for anxiety disorders.10,11

Brain basis of fear. The amygdala and insula are 2 key components of the brain basis of fearful feelings.

The amygdala processes internal or external stimuli, alerts other brain areas that a threat is present, and triggers a fear or anxiety response (Table 1).13-16 Early, nonconscious threat detection by the amygdala may be a core component of the brain basis of many anxiety disorders.17

Amygdala activity has been associated with automatic fear perception, associative fear learning, trauma,18 and (on the treatment side) extinction of learned fears via active coping.19 The amygdala provides an extremely rapid response to fearful stimuli—within milliseconds—and can be active without conscious awareness of the stimuli (which may take several hundred milliseconds to develop).20,21

Inputs into the amygdala can come from:

  • inside the brain (memories, images, emotions, predictions of the future)
  • or outside (contemporary stimuli).

In treatment, the amygdala may be one site of activity of serotonergic medications.22 It is partially regulated by orbitofrontal and medial prefrontal areas that may be target sites of “top-down” psychotherapeutic interventions.23

The insula—a sector of cortex tucked beneath the fissure between the temporal and parietal lobesis involved in interoception, modulation of emotional processing, and emotional learning, especially as related to aversive internal states.24,25

Paulus24 proposes that in anxiety-prone individuals the insula may create a negatively valenced, preattentive, body-centered warning of negative things to come—in a sense, a somatic semaphore that signals danger ahead. In a related study, Stein et al26 presented college students with emotion-provoking faces. Students prone to anxiety had elevated activity in the amygdala and insula compared with normal controls.

The insula also may respond to mindful mental exercise. Lazar et al27 found increased cortical thickness in prefrontal and anterior insula in 20 subjects with extensive experience in insight meditation, which involves focusing attention on internal states.

Table 1

Amygdala output pathways that result in anxiety symptoms

Link to specific brain areaClinically important responses
HypothalamusSympathetic activation: increased heart rate, sweating, dilated pupils, striated muscle tension, strained breathing
Dorsal motor nucleus of vagusParasympathetic activation: slowed heart rate, bladder and bowel symptoms—frequent urination, diarrhea—via smooth muscle activity, gastric acid secretion
Parabrachial nucleusIncreased respiratory rate: sighing respirations
Ventral tegmental area/locus ceruleusGeneralized arousal, perceptual vigilance (excessive stimulation leads to disruption of attention/dissociation, via prefrontal cortical connections)
Nucleus reticularis pontis caudalisStartle response, jumpiness
Periaqueductal gray matterAutomatic coping patterns, from passive (freeze, collapse) to active (confrontation, fight)
Trigeminal facial motor nucleiJaw tension, facial expressions of fear
Source: Adapted with permission from references 13 with additional information from references 14-16

CASE CONTINUED: Using focused interoception

You help Ms. N become aware of her somatic symptoms of anxiety by using a series of questions to direct her attention to her physical responses in a “head-to-toe” approach: “Do you notice the tension in your jaw?” “Is your neck tense?” “How is your breathing now?” Though Ms. N had been unaware of these symptoms, she easily agrees: “Yes, now that you mention it, I am aware of that, but I never knew it was anxiety. I thought it was just stress.”

 

 

This exercise reveals marked generalized muscle tension, sweating, and a brief period of going “blank” in her mind when she recalled one of her impulsive, aggressive episodes. You explain that these physical reactions are part of the normal biologic fear response. Apart from these symptoms, Ms. N denies any prototypical manic symptoms and does not meet bipolar disorder criteria.

Using interoceptive cues

To frame an interoceptive inquiry, discuss with patients how the brain’s fear system is connected to the body, and explain that investigating these physical symptoms can assist diagnosis and treatment. For example, you might ask, “Could we look into your physical responses in these situations to help us better understand your difficulties?”

To actively explore somatic markers of anxiety (anxious feelings), encourage the patient to describe a specific stressful or avoided situation in detail. While he or she does this, direct the patient’s attention to objective physiologic markers of anxiety, such as strained breathing or increased heart rate. Use body-directed questions (interoceptive cues) to foreground these sensory experiences in the patient’s mind. For example:

  • “As we are discussing this issue, I notice your breathing becomes more strained. Do you notice it?”
  • “As you picture this incident in your mind, are you aware of what happens in your body?”
  • “When you perceive her in that way, what do you notice about your physical response?”

You can further inquire into these somatic symptoms and their effect on the patient by asking, “How long have you been having these particular symptoms?” “How frequently do they occur?” or “How distressing are these symptoms?” These questions can separate transient physiologic arousal (normal) from pathologic (recurrent, disabling) responses that may respond to treatment. These cues and their responses can be used as person-specific biomarkers to assay a patient’s:

  • ability to attend to his or her somatic state
  • baseline level of autonomic arousal
  • internal state before problematic behaviors (such as impulsive or self-harming behaviors, substance use)
  • tendency toward anxiety-related perceptual disturbances (such as dissociation).

When the patient actively attends to and carefully describes his or her somatic sensations, the immediate outcome typically is anxiolytic. A shared awareness of the anxiolytic nature of this exercise—“It’s interesting that paying attention to these feelings actually reduces anxiety”—creates a positive first step toward further exploration. Patients can feel the power of the mind to regulate distress.

Overcoming barriers to interoception

Many patients—including those with dissociative disorders, impulse control disorders, or disorders with significant obsessive features—have difficulty using their attention to bring physical symptoms to mind. Some develop automatic, phobic patterns of disattention to contemporaneous somatic feelings of anxiety. This experiential avoidance is the fear of fear itself—fear of the conscious experience of fearful feelings. Their typical responses to interoceptive cues include:

  • lack of awareness (“I don’t know,” “I wasn’t aware of anything”)
  • perceptions, phrased as feelings (“I feel as if he doesn’t like me”)
  • action tendencies or impulses, phrased as feelings (“I feel like I want to get out of there”)
  • a verbal explanation of why they are anxious (“I’m worried about what might happen”).

Depending on the context of your inquiry, if the patient does not respond to an interoceptive cue with actual body-centered feelings, you can:

  • reframe the question: “OK, but when you perceive him in that way, if you focus your mind on your physical reactions, what do you notice?”
  • point out observable symptoms: “Did you notice as we were talking about this issue that your breathing got very shallow, and your hands got tense?”

Some patients may look transiently “spacey” or report “checking out” during the exercise. Inquire specifically about this because they may be demonstrating dissociative symptoms: “Does this sometimes happen when you are stressed, that you lose touch with your sense of your body, you go numb or your mind goes blank?” These symptoms warrant attention, as they may preclude effective retention of the exercise.

Explaining occult anxiety

Regardless of how far you choose to pursue an interoceptive inquiry, uncovering an interoceptive deficit—an inability to describe one’s somatic experience—may be diagnostically helpful. Doing so identifies a potentially modifiable component of self-awareness. So-called mindfulness-based and emotion-focused therapies assist patients in developing a more robust awareness and understanding of their emotions, including the somatic sensations of emotion (see Related Resources).

With appropriate psychoeducation, an interoceptive exploration makes anxiety a real, physical event anchored in brain-body function, and facilitates a nonshaming, organ-based explanation of anxiety. Psychoeducation about fear grounds physical symptoms of anxiety in a brain-based, evolutionarily selected neural system whose activity has a variety of inputs and outputs (Table 2).

 

 

An organ-based, body-centered discussion also may reduce defensiveness in patients who feel (or have been told) that anxiety is “not real” or signals personality weakness. This model may help trainees and medical colleagues avoid outdated distinctions between real/organic problems and functional/emotional problems and find a more conciliatory construct based in emotional neuroscience.

Serotonergic medications and psychotherapy—both of which work on the brain—have demonstrated broad efficacy for anxiety disorders.5 Several national organizations offer information about evidence-based psychotherapeutic treatments grounded in emotional awareness and neuroscience (see Related Resources).

Table 2

Activity of the fear system

Inputs
Contemporary situations
Memories (visual and sensory)
Anticipated future situations
Other nonconscious body and brain processes (including the physiologic symptoms of emotions and anxiety—a ‘fear of fear’ or ‘fear of feelings’)
Outputs
Physical symptoms
Thoughts
Perceptions
Behaviors
States of attention

CASE CONTINUED: Putting interoception to work

Your psychotherapeutic work with Ms. N focuses on attending to and consciously modulating her newly labeled anxiety For example, after an inquiry into a “stressful” situation, you help her use careful interoceptive attention—and when necessary, mindful relaxation and breathing—to regulate her fear symptoms.

She finds that these simple “exposure/regulation” exercises are enough to rapidly resolve her impulsive behaviors. In distressing situations, she can now be aware of her reactions and make a conscious choice of how to react. Your psychotherapeutic work now proceeds toward more effective interpersonal expression of other emotions.

Related Resources

  • Barrett LF, Mesquita B, Ochsner K, Gross JJ. The experience of emotion. Annu Rev Psychol 2007;58:373-403.
  • Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York: Harcourt; 1999.
  • International Experiential Dynamic Therapy Association. www.iedta.net.
  • International Center for Excellence in Emotionally Focused Therapy. www.eft.ca.

Disclosure

Dr. MacDonald reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: 'I don't know how I feel'

Ms. N, age 48, is seen in an outpatient clinic for episodic, impulsive aggression and evaluation of possible bipolar disorder. When you ask her to describe one of her episodes—which always involve a conflict with her partner or another loved one—Ms. N says, “I just lose control… I go blank.” You observe Ms. N’s deep, sighing respirations, trembling hands, and restless, fidgety leg movements. When you ask about her awareness of her physical state while she was recalling the incident, she immediately calms, looks at you quizzically, and states, “I don’t know how I feel.”

When assessing a patient who might have an anxiety disorder, don’t overlook the body. In addition to worry and avoidance, body-centered feelings are a vital component of anxiety and an important treatment target.1

This article:

  • highlights clinically relevant neurobiology of anxious feelings
  • discusses interoception—awareness of the physiologic state of one’s body—and its connection with anxiety
  • explains the use of interoceptive cues as an aid to diagnosing and treating anxiety.

Affective neuroscience and fear

Interoceptive cues are questions directed toward the somatic manifestations of anxiety. Because these questions encourage patients to consciously experience the physical symptoms of anxiety, using interoceptive cues essentially is an exposure-based intervention that may feel counterintuitive to practitioners who are more accustomed to trying to relieve anxiety.

Emotions are thought to be grounded in brain areas that receive and regulate somatic signals, such as the amygdala and insula.2 A feeling-focused approach to anxiety weds affective neuroscience—the study of emotions—with clinical assessment and treatment of anxiety disorders, and conceptualizes that fear is a core component of many anxiety-related disorders.3,4

Although the DSM-IV-TR views anxiety disorders as clinically heterogeneous, affective neuroscience emphasizes what these disorders have in common.5 This unifying perspective allows clinicians to anchor anxiety disorders and anxiety-related disorders—such as hypochondriasis—in core emotional systems that have 3 clinically important aspects—actions (behavior and body), brain, and consciousness (mind) (Figure).4 Two emotional systems related to anxiety disorders are fear (anxious anticipation) and panic (evolutionarily related to separation anxiety and suffocation alarm signals). Viewing anxiety disorders as rooted in core emotion systems allows you to incorporate recent advances in emotional neuroscience, including interoception, into your clinical practice.

Figure: A,B,C model for understanding emotions

Affective neuroscience is a broad-based scientific discipline that explores emotions from 3 vantages: actions (behaviors and bodily responses), brain bases, and conscious manifestations. Two core emotional systems related to anxiety disorders are fear and panic.
Source: Adapted with permission from Panksepp J. Affective neuroscience. New York: Oxford University Press; 1998:31.

Detecting ‘hidden’ anxiety

Conscious symptoms. Activity in the brain’s fear system can generate conscious experiences, including worry, heightened arousal, attentional biases, and body-based feelings of fear. Anxious feelings—by definition, sensory experiences—are an important component of an anxiety assessment and relatively easy to identify.

Kroenke et al6 evaluated a 2-item screening tool, the Generalized Anxiety Disorder scale (GAD-2) that highlights both cognitive (worry) and somatic (feeling) sides of anxiety. Researchers asked 965 randomly sampled primary care patients, “Over the past 2 weeks, how often have you been bothered by the following problems:

  • feeling nervous, anxious, or on edge
  • not being able to stop or control worrying.

Possible responses ranged from 0 (not at all) to 3 (nearly every day). The GAD-2 was as specific for detecting anxiety disorders as a 7-item scale, the GAD-7, (88%), though less sensitive (65% vs 77%).

Nonconscious symptoms. A challenge arises, however, when patients demonstrate signs of anxiety (stress-related physical symptoms such as stomach pains or avoidance-related behaviors) without conscious awareness of anxious feelings. Though patients may intellectually understand the concept of body-based “gut feelings,” these sensations are often reflexively ignored, avoided, or mislabeled. Patients may use terms such as “stressed,” “distressed,” or “tense,” focus on the external source of the fear (rather than their response to it), or reflexively engage in behaviors (avoidance, impulsive behaviors) without being aware of their internal responses.

Anxiety symptoms that occur without corresponding awareness can be called occult, nonconscious, or unconscious anxiety. These symptoms, unique to each patient, can be used as:

  • cues to the patient that he or she is anxious
  • stimuli to be desensitized (via exposure-based interventions)
  • markers of treatment progress.

Patients who experience occult anxiety often have a deficit in interoception (Box).2,7-11 Using interoceptive cues to foster awareness of these unrecognized body-based symptoms can provide insight into formerly unrecognized manifestations of anxiety.

 

 

Neurobiology of anxiety

The fear system. Dynamic changes in stimulus-specific physical sensations—anxious feelings—are linked to activity of the brain’s fear system. This system, which detects and rapidly learns to anticipate danger or distress, can exhibit low-level tonic activity (chronic, generalized anxiety), phasic high-amplitude reactivity (spikes of anxiety), and combinations of the 2.4,12

This precognitive, primary-process alarm system can generate:

  • behaviors, often centered around avoidance—though other types (such as impulsive) can occur
  • physiologic responses, which may or may not become conscious
  • states of mind, including attention (hypervigilance, dissociation), cognitive contents (specific worries), and viscerosomatic awareness (“feelings”).

Through learning—and under the influence of temperamental/genetic predispositions—the fear system can be linked to internal and external stimuli, yielding a spectrum of clinical disorders that includes anxiety disorders.5

Box

Interoception: Looking inside the mind and body

Consciously experiencing an emotion, attending to an emotionally arousing external stimulus, and remembering an emotionally arousing event all involve overlapping mental and neurobiologic processes in brain areas that process and regulate sensations from the body.2,7 Therefore, one does not need to remember “how one felt in the past” to elicit similar neurobiologic and physiologic responses in the present. These responses are recreated in the present when one consciously activates the memory. This understanding underlies the use of interoceptive cues.

Interoception is intentional, mindful awareness of the physiologic state of one’s body. Consciously directing attention to one’s internal state actively unifies the activity of the attending mind and brain with ongoing visceromotor sensations from the body.8,9 These body-based somatic markers often lie at the border of consciousness and can be brought into awareness via interoceptive cues.9 Awareness of and exposure to these often private, physiologic symptoms is an important part of many evidence-based therapies for anxiety disorders.10,11

Brain basis of fear. The amygdala and insula are 2 key components of the brain basis of fearful feelings.

The amygdala processes internal or external stimuli, alerts other brain areas that a threat is present, and triggers a fear or anxiety response (Table 1).13-16 Early, nonconscious threat detection by the amygdala may be a core component of the brain basis of many anxiety disorders.17

Amygdala activity has been associated with automatic fear perception, associative fear learning, trauma,18 and (on the treatment side) extinction of learned fears via active coping.19 The amygdala provides an extremely rapid response to fearful stimuli—within milliseconds—and can be active without conscious awareness of the stimuli (which may take several hundred milliseconds to develop).20,21

Inputs into the amygdala can come from:

  • inside the brain (memories, images, emotions, predictions of the future)
  • or outside (contemporary stimuli).

In treatment, the amygdala may be one site of activity of serotonergic medications.22 It is partially regulated by orbitofrontal and medial prefrontal areas that may be target sites of “top-down” psychotherapeutic interventions.23

The insula—a sector of cortex tucked beneath the fissure between the temporal and parietal lobesis involved in interoception, modulation of emotional processing, and emotional learning, especially as related to aversive internal states.24,25

Paulus24 proposes that in anxiety-prone individuals the insula may create a negatively valenced, preattentive, body-centered warning of negative things to come—in a sense, a somatic semaphore that signals danger ahead. In a related study, Stein et al26 presented college students with emotion-provoking faces. Students prone to anxiety had elevated activity in the amygdala and insula compared with normal controls.

The insula also may respond to mindful mental exercise. Lazar et al27 found increased cortical thickness in prefrontal and anterior insula in 20 subjects with extensive experience in insight meditation, which involves focusing attention on internal states.

Table 1

Amygdala output pathways that result in anxiety symptoms

Link to specific brain areaClinically important responses
HypothalamusSympathetic activation: increased heart rate, sweating, dilated pupils, striated muscle tension, strained breathing
Dorsal motor nucleus of vagusParasympathetic activation: slowed heart rate, bladder and bowel symptoms—frequent urination, diarrhea—via smooth muscle activity, gastric acid secretion
Parabrachial nucleusIncreased respiratory rate: sighing respirations
Ventral tegmental area/locus ceruleusGeneralized arousal, perceptual vigilance (excessive stimulation leads to disruption of attention/dissociation, via prefrontal cortical connections)
Nucleus reticularis pontis caudalisStartle response, jumpiness
Periaqueductal gray matterAutomatic coping patterns, from passive (freeze, collapse) to active (confrontation, fight)
Trigeminal facial motor nucleiJaw tension, facial expressions of fear
Source: Adapted with permission from references 13 with additional information from references 14-16

CASE CONTINUED: Using focused interoception

You help Ms. N become aware of her somatic symptoms of anxiety by using a series of questions to direct her attention to her physical responses in a “head-to-toe” approach: “Do you notice the tension in your jaw?” “Is your neck tense?” “How is your breathing now?” Though Ms. N had been unaware of these symptoms, she easily agrees: “Yes, now that you mention it, I am aware of that, but I never knew it was anxiety. I thought it was just stress.”

 

 

This exercise reveals marked generalized muscle tension, sweating, and a brief period of going “blank” in her mind when she recalled one of her impulsive, aggressive episodes. You explain that these physical reactions are part of the normal biologic fear response. Apart from these symptoms, Ms. N denies any prototypical manic symptoms and does not meet bipolar disorder criteria.

Using interoceptive cues

To frame an interoceptive inquiry, discuss with patients how the brain’s fear system is connected to the body, and explain that investigating these physical symptoms can assist diagnosis and treatment. For example, you might ask, “Could we look into your physical responses in these situations to help us better understand your difficulties?”

To actively explore somatic markers of anxiety (anxious feelings), encourage the patient to describe a specific stressful or avoided situation in detail. While he or she does this, direct the patient’s attention to objective physiologic markers of anxiety, such as strained breathing or increased heart rate. Use body-directed questions (interoceptive cues) to foreground these sensory experiences in the patient’s mind. For example:

  • “As we are discussing this issue, I notice your breathing becomes more strained. Do you notice it?”
  • “As you picture this incident in your mind, are you aware of what happens in your body?”
  • “When you perceive her in that way, what do you notice about your physical response?”

You can further inquire into these somatic symptoms and their effect on the patient by asking, “How long have you been having these particular symptoms?” “How frequently do they occur?” or “How distressing are these symptoms?” These questions can separate transient physiologic arousal (normal) from pathologic (recurrent, disabling) responses that may respond to treatment. These cues and their responses can be used as person-specific biomarkers to assay a patient’s:

  • ability to attend to his or her somatic state
  • baseline level of autonomic arousal
  • internal state before problematic behaviors (such as impulsive or self-harming behaviors, substance use)
  • tendency toward anxiety-related perceptual disturbances (such as dissociation).

When the patient actively attends to and carefully describes his or her somatic sensations, the immediate outcome typically is anxiolytic. A shared awareness of the anxiolytic nature of this exercise—“It’s interesting that paying attention to these feelings actually reduces anxiety”—creates a positive first step toward further exploration. Patients can feel the power of the mind to regulate distress.

Overcoming barriers to interoception

Many patients—including those with dissociative disorders, impulse control disorders, or disorders with significant obsessive features—have difficulty using their attention to bring physical symptoms to mind. Some develop automatic, phobic patterns of disattention to contemporaneous somatic feelings of anxiety. This experiential avoidance is the fear of fear itself—fear of the conscious experience of fearful feelings. Their typical responses to interoceptive cues include:

  • lack of awareness (“I don’t know,” “I wasn’t aware of anything”)
  • perceptions, phrased as feelings (“I feel as if he doesn’t like me”)
  • action tendencies or impulses, phrased as feelings (“I feel like I want to get out of there”)
  • a verbal explanation of why they are anxious (“I’m worried about what might happen”).

Depending on the context of your inquiry, if the patient does not respond to an interoceptive cue with actual body-centered feelings, you can:

  • reframe the question: “OK, but when you perceive him in that way, if you focus your mind on your physical reactions, what do you notice?”
  • point out observable symptoms: “Did you notice as we were talking about this issue that your breathing got very shallow, and your hands got tense?”

Some patients may look transiently “spacey” or report “checking out” during the exercise. Inquire specifically about this because they may be demonstrating dissociative symptoms: “Does this sometimes happen when you are stressed, that you lose touch with your sense of your body, you go numb or your mind goes blank?” These symptoms warrant attention, as they may preclude effective retention of the exercise.

Explaining occult anxiety

Regardless of how far you choose to pursue an interoceptive inquiry, uncovering an interoceptive deficit—an inability to describe one’s somatic experience—may be diagnostically helpful. Doing so identifies a potentially modifiable component of self-awareness. So-called mindfulness-based and emotion-focused therapies assist patients in developing a more robust awareness and understanding of their emotions, including the somatic sensations of emotion (see Related Resources).

With appropriate psychoeducation, an interoceptive exploration makes anxiety a real, physical event anchored in brain-body function, and facilitates a nonshaming, organ-based explanation of anxiety. Psychoeducation about fear grounds physical symptoms of anxiety in a brain-based, evolutionarily selected neural system whose activity has a variety of inputs and outputs (Table 2).

 

 

An organ-based, body-centered discussion also may reduce defensiveness in patients who feel (or have been told) that anxiety is “not real” or signals personality weakness. This model may help trainees and medical colleagues avoid outdated distinctions between real/organic problems and functional/emotional problems and find a more conciliatory construct based in emotional neuroscience.

Serotonergic medications and psychotherapy—both of which work on the brain—have demonstrated broad efficacy for anxiety disorders.5 Several national organizations offer information about evidence-based psychotherapeutic treatments grounded in emotional awareness and neuroscience (see Related Resources).

Table 2

Activity of the fear system

Inputs
Contemporary situations
Memories (visual and sensory)
Anticipated future situations
Other nonconscious body and brain processes (including the physiologic symptoms of emotions and anxiety—a ‘fear of fear’ or ‘fear of feelings’)
Outputs
Physical symptoms
Thoughts
Perceptions
Behaviors
States of attention

CASE CONTINUED: Putting interoception to work

Your psychotherapeutic work with Ms. N focuses on attending to and consciously modulating her newly labeled anxiety For example, after an inquiry into a “stressful” situation, you help her use careful interoceptive attention—and when necessary, mindful relaxation and breathing—to regulate her fear symptoms.

She finds that these simple “exposure/regulation” exercises are enough to rapidly resolve her impulsive behaviors. In distressing situations, she can now be aware of her reactions and make a conscious choice of how to react. Your psychotherapeutic work now proceeds toward more effective interpersonal expression of other emotions.

Related Resources

  • Barrett LF, Mesquita B, Ochsner K, Gross JJ. The experience of emotion. Annu Rev Psychol 2007;58:373-403.
  • Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York: Harcourt; 1999.
  • International Experiential Dynamic Therapy Association. www.iedta.net.
  • International Center for Excellence in Emotionally Focused Therapy. www.eft.ca.

Disclosure

Dr. MacDonald reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

References

1. Katon W, Lin EH, Kroenke K. The association of depression and anxiety with medical symptom burden in patients with chronic medical illness. Gen Hosp Psychiatry 2007;29(2):147-55.

2. Niedenthal PM. Embodying emotion. Science 2007;316(5827):1002-5.

3. McClure EB, Monk CS, Nelson EE, et al. Abnormal attention modulation of fear circuit function in pediatric generalized anxiety disorder. Arch Gen Psychiatry 2007;64(1):97-106.

4. Panksepp J. Affective neuroscience. New York: Oxford University Press; 1998:31.

5. Stein DJ. Advances in understanding the anxiety disorders: the cognitive-affective neuroscience of ‘false alarms’. Ann Clin Psychiatry 2006;18(3):173-82.

6. Kroenke K, Spitzer RL, Williams JBW, et al. Anxiety disorders in primary care: prevalence, impairment, comorbidity, and detection. Ann Intern Med 2007;146(5):317-25.

7. Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York: Harcourt; 1999.

8. Wiens S. Interoception in emotional experience. Curr Opin Neurol 2005;18(4):442-7.

9. Cameron OG. Interoception: the inside story—a model for psychosomatic processes. Psychosom Med 2001;63(5):697-710.

10. Wald J, Taylor S. Interoceptive exposure therapy combined with trauma-related exposure therapy for post-traumatic stress disorder: a case report. Cognit Behav Ther 2005;34(1):34-40.

11. Wells A, Papageorgiou C. Social phobic interoception: effects of bodily information on anxiety, beliefs and self-processing. Behav Res Ther 2001;39(1):1-11.

12. Davidson RJ. Anxiety and affective style: role of prefrontal cortex and amygdala. Biol Psychiatry 2002;51(1):68-80.

13. Kandel ER, Squire LR. Memory: from mind to molecules. New York: Henry Holt and Company, 1999.

14. Fokkema DS. The psychobiology of strained breathing and its cardiovascular implications: a functional system review. Psychophysiology 1999;36(2):164-75.

15. Arnsten AF. Fundamentals of attention-deficit/hyperactivity disorder: circuits and pathways. J Clin Psychiatry 2006;67 (suppl 8):7-12.

16. Keay KA, Bandler R. Parallel circuits mediating distinct emotional coping reactions to different types of stress. Neurosci Biobehav Rev 2001;25(7-8):669-78.

17. Garakani A, Mathew SJ, Charney DS. Neurobiology of anxiety disorders and implications for treatment. Mt Sinai J Med 2006;73(7):941-9.

18. Phelps EA. Emotion and cognition: insights from studies of the human amygdala. Annu Rev Psychol 2006;57:27-53.

19. LeDoux JE, Gorman JM. A call to action: overcoming anxiety through active coping. Am J Psychiatry 2001;158(12):1953-5.

20. LeDoux JE. The emotional brain. New York: Simon and Schuster, 1996.

21. Liddell BJ, Brown KJ, Kemp AH, et al. A direct brainstemamygdala-cortical ‘alarm’ system for subliminal signals of fear. Neuroimage 2005;24(1):235-43.

22. Harmer CJ, Mackay CE, Reid CB, et al. Antidepressant drug treatment modifies the neural processing of nonconscious threat cues. Biol Psychiatry 2006;59(9):816-20.

23. Hariri AR, Mattay VS, Tessitore A, et al. Neocortical modulation of the amygdala response to fearful stimuli. Biol Psychiatry 2003;53(6):494-501.

24. Paulus MP, Stein MB. An insular view of anxiety. Biol Psychiatry 2006;60(4):383-7.

25. Simmons A, Strigo I, Matthews SC, et al. Anticipation of aversive visual stimuli is associated with increased insula activation in anxiety-prone subjects. Biol Psychiatry 2006;60(4):402-9.

26. Stein MB, Simmons AN, Feinstein JS, et al. Increased amygdala and insula activation during emotion processing in anxiety-prone subjects. Am J Psychiatry 2007;164(2):318-27.

27. Lazar SW, Kerr CE, Wasserman RH, et al. Meditation experience is associated with increased cortical thickness. Neuroreport 2005;16(17):1893-7.

References

1. Katon W, Lin EH, Kroenke K. The association of depression and anxiety with medical symptom burden in patients with chronic medical illness. Gen Hosp Psychiatry 2007;29(2):147-55.

2. Niedenthal PM. Embodying emotion. Science 2007;316(5827):1002-5.

3. McClure EB, Monk CS, Nelson EE, et al. Abnormal attention modulation of fear circuit function in pediatric generalized anxiety disorder. Arch Gen Psychiatry 2007;64(1):97-106.

4. Panksepp J. Affective neuroscience. New York: Oxford University Press; 1998:31.

5. Stein DJ. Advances in understanding the anxiety disorders: the cognitive-affective neuroscience of ‘false alarms’. Ann Clin Psychiatry 2006;18(3):173-82.

6. Kroenke K, Spitzer RL, Williams JBW, et al. Anxiety disorders in primary care: prevalence, impairment, comorbidity, and detection. Ann Intern Med 2007;146(5):317-25.

7. Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York: Harcourt; 1999.

8. Wiens S. Interoception in emotional experience. Curr Opin Neurol 2005;18(4):442-7.

9. Cameron OG. Interoception: the inside story—a model for psychosomatic processes. Psychosom Med 2001;63(5):697-710.

10. Wald J, Taylor S. Interoceptive exposure therapy combined with trauma-related exposure therapy for post-traumatic stress disorder: a case report. Cognit Behav Ther 2005;34(1):34-40.

11. Wells A, Papageorgiou C. Social phobic interoception: effects of bodily information on anxiety, beliefs and self-processing. Behav Res Ther 2001;39(1):1-11.

12. Davidson RJ. Anxiety and affective style: role of prefrontal cortex and amygdala. Biol Psychiatry 2002;51(1):68-80.

13. Kandel ER, Squire LR. Memory: from mind to molecules. New York: Henry Holt and Company, 1999.

14. Fokkema DS. The psychobiology of strained breathing and its cardiovascular implications: a functional system review. Psychophysiology 1999;36(2):164-75.

15. Arnsten AF. Fundamentals of attention-deficit/hyperactivity disorder: circuits and pathways. J Clin Psychiatry 2006;67 (suppl 8):7-12.

16. Keay KA, Bandler R. Parallel circuits mediating distinct emotional coping reactions to different types of stress. Neurosci Biobehav Rev 2001;25(7-8):669-78.

17. Garakani A, Mathew SJ, Charney DS. Neurobiology of anxiety disorders and implications for treatment. Mt Sinai J Med 2006;73(7):941-9.

18. Phelps EA. Emotion and cognition: insights from studies of the human amygdala. Annu Rev Psychol 2006;57:27-53.

19. LeDoux JE, Gorman JM. A call to action: overcoming anxiety through active coping. Am J Psychiatry 2001;158(12):1953-5.

20. LeDoux JE. The emotional brain. New York: Simon and Schuster, 1996.

21. Liddell BJ, Brown KJ, Kemp AH, et al. A direct brainstemamygdala-cortical ‘alarm’ system for subliminal signals of fear. Neuroimage 2005;24(1):235-43.

22. Harmer CJ, Mackay CE, Reid CB, et al. Antidepressant drug treatment modifies the neural processing of nonconscious threat cues. Biol Psychiatry 2006;59(9):816-20.

23. Hariri AR, Mattay VS, Tessitore A, et al. Neocortical modulation of the amygdala response to fearful stimuli. Biol Psychiatry 2003;53(6):494-501.

24. Paulus MP, Stein MB. An insular view of anxiety. Biol Psychiatry 2006;60(4):383-7.

25. Simmons A, Strigo I, Matthews SC, et al. Anticipation of aversive visual stimuli is associated with increased insula activation in anxiety-prone subjects. Biol Psychiatry 2006;60(4):402-9.

26. Stein MB, Simmons AN, Feinstein JS, et al. Increased amygdala and insula activation during emotion processing in anxiety-prone subjects. Am J Psychiatry 2007;164(2):318-27.

27. Lazar SW, Kerr CE, Wasserman RH, et al. Meditation experience is associated with increased cortical thickness. Neuroreport 2005;16(17):1893-7.

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Interoceptive cues: When ‘gut feelings’ point to anxiety
Display Headline
Interoceptive cues: When ‘gut feelings’ point to anxiety
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anxiety disorder; interoception; body-centered feelings; Kai MacDonald MD
Legacy Keywords
anxiety disorder; interoception; body-centered feelings; Kai MacDonald MD
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