Madness and the Family (Part One): The History and Research of Family Dynamics and Psychosis

I was very lucky to have great family dynamics but there were non-family related stressors such as bullying and other traumas in my teenage years. Here’s part one of an interesting topic:

Madness and the Family (Part One): The History and Research of Family Dynamics and Psychosis

There are very few things considered more taboo in the world of mental health than the suggestion that problematic family dynamics can lead to a child developing a psychotic disorder. And yet, when we look honestly at the history and research of psychosis and the broader concept of “mental illness,” it becomes apparent that there are few subjects in the mental health field that are more important. I’d like to invite you, then, to join me on a journey into this taboo territory, dividing our trip into three legs. In the first leg (Part One), we’ll go back in time to explore how such a crucial topic has become so vilified, and then embark upon a flight for an aerial view of some of the most essential findings of the last 60 plus years of research that look at the links between problematic family dynamics and psychosis. In the second leg of the journey (Part Two), we’ll explore a framework that offers us the potential to unify the research on the various problematic family dynamics, trauma, and other factors associated with psychosis, locating the roots of psychosis within two core existential and relational dilemmas that I believe we all struggle with to greater or lesser degrees. Finally, in the third and last leg of our journey (Part Three), we will reap the fruits of our exploration, and consider how what we have learned may guide us as parents, as family members, and as society as a whole in offering genuine support to those who continue to grapple with these extreme states of mind.

Mindfulness and dissociation

I’m coping well with my ‘voices’ these days but still feel very ‘mindless’ and dissociated.

Dissociation and Mindfulness in Patients with Auditory Verbal Hallucinations.

The very few studies relating mindfulness and dissociation have found a negative association between them (depersonalization and absorption). However, all these studies have been done in non-clinical populations and there are no data on the relationship between these variables in psychiatric patients with auditory hallucinations. This study was designed to study the relationship between mindfulness and the two dissociative variables, absorption and depersonalization, as well as their predictive power for the severity of auditory hallucinations and the distress they cause in a clinical population. Fifty-five psychiatric patients with hallucinations were given the following tests: MAAS (Brown & Ryan, 2003), TAS (Tellegen & Atkinson, 1974), CDS (Sierra & Berrios, 2000), PSYRATS (Haddock, McCarron, Tarrier, & Faragher, 1999), and PANSS (Kay, Opler, & Lindenmayer, 1988). A significant negative correlation was found between mindfulness and the dissociative variables, and between mindfulness and the distress caused by the hallucinations. A positive correlation was also found between absorption and distress caused by hallucinations and between depersonalization and their severity. Finally, the variable with the most predictive power for severity of the voices was depersonalization, and the variable with the most predictive power for distress caused by the voices was mindfulness. Interventions addressing training in mindfulness techniques could diminish the distress associated with hearing voices.

Rufus May’s excellent site has interesting articles on mindfulness and dissociation.

I need to work on the following:

●    Acceptance – accepting what is present rather than denying it or wishing it was not there.
●    Non-judging – observing objects and events without evaluating them.
●    Patience – we stay with the present moment and don’t rush towards the next exciting event, we focus on the unique unfolding of what is happening now.
●    Beginners mind – seeing things with an open mind and noticing their unique qualities.
●    Letting go – developing the ability to switch attention and let go of one object of concentration and focus on another
●    Being with – as opposed to trying to fix or control things or achieve constantly
●    Non-striving – by accepting the present moment and its accompanying sensations we let go of constantly striving for better moments.  We focus on the journey rather than just the destination.
●    Non-attachment – this is about relating to things with kindness but not clinging onto them recognising that everything changes.

Mindfulness in schizophrenia: Associations with self-reported motivation, emotion regulation, dysfunctional attitudes, and negative symptoms.

Mindfulness and Metta-based Trauma Therapy (MMTT): Initial Development and Proof-of-Concept of an Internet Resource. 

Mindfulness & Metta Trauma Therapy (MMTT) is a self-help therapy for improving self-regulation in people suffering from trauma and stressor-related disorders that can be practiced online. The therapy was developed by Dr. Paul Frewen, a psychologist at Western University, Canada. MMTT involves learning to apply 6 therapeutic principles to your everyday life through the practice of a reflective journaling exercise we call Mindful and Metta Moments, as well as through the practice of guided meditations. The 6 therapeutic principles of MMTT are: 1) Presence, 2) Awareness, 3) Letting-Go, 4) Metta, 5) Re-Centering and De-Centering, and 6) Acceptance and Change.

Trauma and Stressor-related Disorders

Trauma and stressor-related disorders are psychological problems that are caused by the experience of one or more traumatic life events or relationships. Different researchers and clinicians define traumatic life events in different ways; some definitions are very broad and general, whereas others are more specific. For the purposes of this website, we define traumatic life events and relationships somewhat broadly as any life event or relationship that caused a person psychological harm that continues to be experienced long after the event occurred or the relationship ended. Examples of traumatic life events include:

  • rejection, abandonment or betrayal following the ending of a close and loving relationship;
  • experiences of complicated or extended grieving following the loss of a loved one (complicated bereavement);
  • being physically or sexually assaulted, or witnessing or finding out that this happened to another person you care about;
  • being verbally or emotionally abused or bullied, including as a child;
  • being abused, mistreated or neglected by caregivers when you were a child;
  • being in a life threatening or physically disabling event, for example, as in military combat, a serious car accident, or a fire, workplace accident or natural disaster;
  • experiences of guilt and shame for physical or psychological harm that you have caused another person.

Post-Traumatic Growth Follow Up: What It Takes To Grow From Tough Times

Compassion and the Voice of the Tormentor

See more at Voice Hearers Connect

Auditory verbal hallucinations in schizophrenia and post-traumatic stress disorder: common phenomenology, common cause, common interventions? (2015)

I’ve been thinking along similar lines…

Auditory verbal hallucinations in schizophrenia and post-traumatic stress disorder: common phenomenology, common cause, common interventions?

Auditory verbal hallucinations (AVH: ‘hearing voices’) are found in both schizophrenia and post-traumatic stress disorder (PTSD). In this paper we first demonstrate that AVH in these two diagnoses share a qualitatively similar phenomenology. We then show that the presence of AVH in schizophrenia is often associated with earlier exposure to traumatic/emotionally overwhelming events, as it is by definition in PTSD. We next argue that the content of AVH relates to earlier traumatic events in a similar way in both PTSD and schizophrenia, most commonly having direct or indirect thematic links to emotionally overwhelming events, rather than being direct re-experiencing. We then propose, following cognitive models of PTSD, that the reconstructive nature of memory may be able to account for the nature of these associations between trauma and AVH content, as may threat-hypervigilance and the individual’s personal goals. We conclude that a notable subset of people diagnosed with schizophrenia with AVH are having phenomenologically and aetiologically identical experiences to PTSD patients who hear voices. As such we propose that the iron curtain between AVH in PTSD (often termed ‘dissociative AVH’) and AVH in schizophrenia (so-called ‘psychotic AVH’) needs to be torn down, as these are often the same experience. One implication of this is that these trauma-related AVH require a common trans-diagnostic treatment strategy. Whilst antipsychotics are already increasingly being used to treat AVH in PTSD, we argue for the centrality of trauma-based interventions for trauma-based AVH in both PTSD and in people diagnosed with schizophrenia.

Another recent article highlights how “interventions specifically targeting aspects of self-experience, including self-affection, self-reflection, self-schema and self-concept, may be sufficient to reduce distress and disruption in the context of hearing voices” [1].

See also:

Are some Auditory Verbal Hallucinations trauma/fear memories that are amendable via therapy & pharmacologically enhanced reconsolidation/extinction?

Clinical perspectives on the relationship between psychosis and dissociation: utility of structural dissociation and implications for practice (2015)

Trauma-related dissociation and altered states of consciousness: a call for clinical, treatment, and neuroscience research (2015)

Hallucinations: New interventions supporting people with distressing voices and/or visions

Hallucinations as a trauma-based memory: Implications for psychological interventions.

Social defeat models of schizophrenia

It’s nice to have a growing sense of friendship and social inclusion these days. Reflecting back, I can definitely relate to strong feelings of ‘social defeat’ and I know the negative consequences it carries. I’ve internalised a lot of things that my ‘voices’ still try to ‘socially defeat’ me with everyday, so it’s a constant struggle to keep positive and not let ‘them’ (or me…) emotionally defeat myself, or impact on the progress I’m making socially and with returning to study.

Epidemiological data suggest that the experience of being excluded from the majority group (or social defeat) may be the common denominator of social risks associated with schizophrenia [1].

Here are a few recent articles relating to social defeat that I found interesting [see an extensive review here]:

The dopaminergic system:

“Dopamine dysregulation involving striatal dopamine sensitization may represent a common mechanism, linking multiple environmental exposures to underlying biological mechanisms of psychosis (Yuii et al., 2007 and Collip et al., 2008). Additionally, previous research suggests a reciprocal relationship between prefrontal and striatal dopaminergic dysfunction in schizophrenia. A number of researchers have suggested that prefrontal dopaminergic dysfunction may partly be the result of dysregulated input from the midbrain dopamine system (Braver et al., 1999, Braver and Cohen, 2000 and Tanaka, 2006). On the other hand, according to the tonic-phasic dopamine theory introduced by Grace (1991), when the tonic activity is low, stressful stimuli are not optimally regulated by the PFC, resulting in increased phasic dopamine release in the striatum.”

The social defeat (SD) hypothesis of schizophrenia posits that repeated experiences of SD may lead to sensitisation of the mesolimbic dopaminergic system and to precipitation of psychosis. When exposed to social threat, defeated rats have elevated levels of extracellular dopamine in the nucleus accumbens and repeated experiences of SD lead to behavioral sensitisation and enhanced behavioral response to dopamine agonists [2]:

“…If the results of the animal studies can be extended to humans, chronic exposure to SD may lead to sensitization of the mesolimbic dopamine system and/or overactivity of this system, and thus foster the development of psychosis “

Schizophrenia: an integrated sociodevelopmental-cognitive model.

Schizophrenia remains a major burden on patients and society. The dopamine hypothesis attempts to explain the pathogenic mechanisms of the disorder, and the neurodevelopmental hypothesis the origins. In the past 10 years an alternative, the cognitive model, has gained popularity. However, the first two theories have not been satisfactorily integrated, and the most influential iteration of the cognitive model makes no mention of dopamine, neurodevelopment, or indeed the brain. In this Review we show that developmental alterations secondary to variant genes, early hazards to the brain, and childhood adversity sensitise the dopamine system, and result in excessive presynaptic dopamine synthesis and release. Social adversity biases the cognitive schema that the individual uses to interpret experiences towards paranoid interpretations. Subsequent stress results in dysregulated dopamine release, causing the misattribution of salience to stimuli, which are then misinterpreted by the biased cognitive processes. The resulting paranoia and hallucinations in turn cause further stress, and eventually repeated dopamine dysregulation hardwires the psychotic beliefs. Finally, we consider the implications of this model for understanding and treatment of schizophrenia. [full text]

“Position in the social hierarchy affects the recovery of the dopamine
system after isolated animals are returned to the social group; dominant, but not subordinate, monkeys show reversal of the striatal dopamine changes”

“Stress also increases striatal dopamine release in human beings, although not in all studies. This inconsistency could be related to the severity of the stressor—findings from animal studies suggest that mild stressors do not always increase striatal dopamine concentrations. Furthermore, increased dopamine release is associated with greater cortisol response to a challenge.”

Adolescent social defeat stress produces deficits in adult mPFC DA activity and corresponding behavioral and cognitive dysfunction [3].

See more here.

The opioid system:

Research indicates that the mu opioid receptor is an important mediator of behavioural flexibility and responses to psychosocial stress [4]. Kappa-opioid receptors expressed in DAergic systems regulate the effects of acute, but not chronic, social stress in mice [5].

Neuroimmune effects:

Preexisting individual differences in the sensitivity of the peripheral immune system may predict and promote vulnerability to social stress [6]. Interleukin-1β was rapidly increased in key limbic structures (paraventricular nucleus of the hypothalamus, PVN; amygdala) in response to stress challenges that involve application of an aversive/noxious stimulus but not in response to social stress. On the contrary, social stressors appear to increase release of another pro-inflammatory cytokine, interleukin-6 (IL-6), in both plasma and brain [7]:

“Although IL-1, IL-6, and TNF-α are considered to be the classic proinflammatory cytokines – and all appear to be modulated in the CNS by stressor exposure – these are by no means the only neuroimmune factors impacted by stress. For example, monocyte chemoattractive protein-1 (MCP1/CCL2) is a chemokine expressed in the CNS in response to a number of stress challenges and likely plays a key role in recruitment of monocytes from the blood into the CNS (Blandino et al., 2009; Wohleb et al., 2013). Prostaglandins also appear to be highly active in cortical regions after stress (Garcia-Bueno et al., 2008). Thus, a multitude of distinct neuroimmune signaling pathways appear to be activated in response to stressful circumstances, and these effects often depend upon specific individual subject characteristics such as sex, age, strain and prior stress history.”

“In addition to stress-related increases in expression of cytokines and other inflammatory signaling molecules, stress exposure is often accompanied by other cellular manifestations of neuroimmune activation, such as dynamic changes in microglial activation state. Microglia play a prominent role in immune surveillance within the CNS, and are often viewed as the “first responders” in response to infection and/or damage. Prior studies have shown that microglia are highly responsive to stress, with evidence to date suggesting that microglia exhibit priming-like effects following stress exposure as evidenced by enhanced or accelerated activational responses to subsequent immune challenge either in vivo (Johnson et al., 2002) or ex vivo (Frank et al., 2010). An enhanced functional activation state of microglia is also associated with altered expression of cell surface markers that are known to modify or regulate microglia reactivity to antigens (Blandino et al., 2009; Frank et al., 2007). Other studies have shown that chronic stress enhanced microglial proliferation (Nair & Bonneau, 2006) and migration into the CNS (Wohleb et al., 2013). Although it is not clear whether these changes in microglia are the cause or consequence of cytokine expression, it is clear that microglial activation is associated with increased cytokine expression, and exogenous cytokine administration often enhances microglial activation. In this sense, it is notable that IL-1 in particular is often described in the neuroinjury literature as an immediate early gene indicative of microglial activation state. “

Microglia from mice exposed to repeated social defeat had higher mRNA expression of IL-6, TNF-α, and IL-1β, and these increases were reversed by imipramine treatment [8].

Infliximab (a TNF-α inhibitor) decreased anhedonia and despair-like behavior in the rat unpredictable chronic mild stress (UCMS) model of depression [9].

Lorazepam and clonazepam, aside from exerting anxiolytic and antidepressant effects, may have therapeutic potential as neuroimmunomodulators during psychosocial stress [10].

Central immune alterations in passive strategy following chronic defeat stress have been studied [11].

Social defeat causes long lasting anxiety behaviour :

Microglia and CD11b+/CD45 MCs contribute to social defeat-induced prolonged anxiety. The response to social defeat activates fear/threat appraisal circuitry in the brain. Activation of microglia in these areas results in the release proinflammatory cytokines including IL-1β and CCL2. In turn, these cytokine responses contribute to the development of a reactive endothelium in the regional neurovasculature. Social defeat also activates the HPA axis and SNS which stimulate the production of primed CD11+/CD45+MCs in the bone marrow. Release of MCs into circulation results in trafficking of these cells to the reactive neurovasculature which is followed by adhesion and diapedesis into the brain. The activation of microglia and the trafficking of primed MCs results in the development of prolonged anxiety-behavior.
Microglia and CD11b+/CD45 MCs contribute to social defeat-induced prolonged anxiety. The response to social defeat activates fear/threat appraisal circuitry in the brain. Activation of microglia in these areas results in the release proinflammatory cytokines including IL-1β and CCL2. In turn, these cytokine responses contribute to the development of a reactive endothelium in the regional neurovasculature. Social defeat also activates the HPA axis and SNS which stimulate the production of primed CD11+/CD45+MCs in the bone marrow. Release of MCs into circulation results in trafficking of these cells to the reactive neurovasculature which is followed by adhesion and diapedesis into the brain. The activation of microglia and the trafficking of primed MCs results in the development of prolonged anxiety-behavior. [source]
Directions for future therapeutics:

” …administration of specific pathway inhibitors such as IL-1 receptor antagonist (intra-cerebroventricular; i.c.v.) has been shown to block behavioral deficits indicative of learned-helplessness (Maier & Watkins, 1995), and the enhanced HPA axis response produced by inescapable tailshock (Johnson et al., 2002a). In our hands, IL-1 receptor antagonist reversed the suppression of social interaction produced by prior stressor exposure, and blocked the release of aversive odor cues emitted by stressed rats (Arakawa et al., 2009). Agents with more global anti-inflammatory properties, such as alpha-melanocyte stimulating hormone (α-MSH), have been shown to rescue stress-induced reductions in food intake and HPA axis aberrations (Milligan et al., 1998). IL-10, a potent anti-inflammatory cytokine, has also been shown to reverse sickness-like behavioral responses in a guinea pig model of maternal separation (Hennessy et al., 2011), and sensitization of febrile responses produced by this maternal separation experience was reversed with naproxen, a relatively selective inhibitor of cyclooxygenase-2 activity (i.e. the enzyme responsible for production of mature prostaglandin E2 synthesis) – a final common mediator of many inflammation-related effects (Hennessy et al., 2015). Although there is some recent evidence suggesting that antagonists to the P2X7 (purinergic) receptor can reverse some stress-related effects (presumably due to blocking IL-1 release), these effects are generally modest, perhaps because they are blocking only one cytokine within the context of many (Catanzaro et al., 2014; Lord et al., 2014). Thus, one very fruitful avenue of future studies will be the development of novel therapeutics targeting inflammatory signaling pathways that can be used to ameliorate adverse health consequences of stress. The key challenge for production of these therapeutics will be the formulation of agents that either (a) readily cross the blood-brain barrier (BBB) or (b) can be coupled to some form of vector (viruses, nanoparticles, etc.) in order to promote CNS penetration of the drugs.”

See more:

Effect of chronic social defeat stress on behaviors and dopamine receptor in adult mice.

Resilience to the effects of social stress: Evidence from clinical and preclinical studies on the role of coping strategies

Social Stress and Psychosis Risk: Common Neurochemical Substrates?

Inflammation in schizophrenia: A question of balance (2015)

Inflammation and microglia

Role of Inflammation in Psychiatric Disease (2015)

Trauma-related dissociation and altered states of consciousness: a call for clinical, treatment, and neuroscience research (2015)

Trauma-related dissociation and altered states of consciousness: a call for clinical, treatment, and neuroscience research

The primary aim of this commentary is to describe trauma-related dissociation and altered states of consciousness in the context of a four-dimensional model that has recently been proposed (Frewen & Lanius, 2015). This model categorizes symptoms of trauma-related psychopathology into (1) those that occur within normal waking consciousness and (2) those that are dissociative and are associated with trauma-related altered states of consciousness (TRASC) along four dimensions: (1) time; (2) thought; (3) body; and (4) emotion. Clinical applications and future research directions relevant to each dimension are discussed. Conceptualizing TRASC across the dimensions of time, thought, body, and emotion has transdiagnostic implications for trauma-related disorders described in both the Diagnostic Statistical Manual and the International Classifications of Diseases. The four-dimensional model provides a framework, guided by existing models of dissociation, for future research examining the phenomenological, neurobiological, and physiological underpinnings of trauma-related dissociation.

A summary of the 4-D model that categorizes symptoms of trauma-related psychopathology into (1) those that occur within normal waking consciousness and (2) those that are dissociative and are associated with trauma-related altered states of consciousness (TRASC) along four dimensions: (1) time; (2) thought; (3) body; and (4) emotion. The bottom pink part of the boxes indicates non-dissociative processes and normal waking consciousness, whereas the orange part of the boxes denote dissociative processes and TRASC. The first arrow (infrequency) indicates that the experience of TRASC is hypothesized to be less common than presentations of normal waking consciousness given that states of normal waking consciousness, by definition, are the most common phenomenological state of human beings. It should be noted that the four dimensions of consciousness are not mutually exclusive, but may refer to the same phenomena viewed from different perspectives (e.g., depersonalisation can manifest itself both in the dimension body and emotion). From Frewen and Lanius (2015).

“Psychological trauma may not only affect the perspective of an individual’s narrative but also the plot and the structure of the narrative. Although often able to maintain first-person perspective, trauma survivors may exhibit distinctly negative self-referential thinking, including “I am a bad person” or “I do not deserve to live”

Traumatized individuals may, however, occasionally exhibit alterations in the perspective of their narrative. These alterations can lead survivors to experience voices in the second-person perspective, for example, telling them, “you are bad” or “you deserve to die,” an experience thought to reflect a dissociative process associated with TRASC. When this occurs, the person is no longer the only storyteller of his/her lived experience but rather another or other narrative voice(s) also speak inside his/her head. These voices may present distinctly different goals, motivations, and affects, in the extreme case creating the experience of possessing multiple selves. Research in the area of voice hearing has suggested that this phenomenon is elevated significantly in individuals suffering from trauma-related disorders, including in individuals diagnosed with PTSD, dissociative disorders, and borderline personality disorders as compared to patients with other psychiatric disorders; voice hearing is also related to the experience of dissociative symptomatology and a history of early life adversity”

“From a clinical perspective on trauma-related voice hearing, it is crucial to create a shared narrative by identifying the strengths of each voice or self state in the present and by encouraging awareness and communication among different voices or self states, thereby facilitating collaboration between or among distinctly compartmentalized and contradictory goals, motivations, and affects associated with each voice or self state. The latter is also critical in fostering of self-compassion, which is sorely lacking in many survivors of chronic trauma due to ongoing conflict among different voices or self states.”

“…while remembering an event, mental time travel is “partial” in that the present self voluntarily directs attention to the past self, thus maintaining awareness of the present self in the present time. In this case, the “I” is proposed to exist in the present self, which outweighs the representation of the past self in past time. In contrast, during a reliving experience, mental time travel occurs “fully,” generally not by choice, and is usually triggered by internal and/or external stimuli that bear some resemblance to a past self-state. In this case, the “I” is thought to inhabit the past self, which is thought to outweigh the presence of the present self, thus lacking a mental time traveler and the ability to voluntarily position oneself in the past or in the future.”

“…it may be critical to strengthen the self among survivors of trauma, in order to facilitate the emergence of a mental time traveler that is able to remember rather than to relive the past. Processes relevant to this development across all four dimensions of consciousness include the encouragement of safe relationships, including the therapeutic relationship, enhancing mindful awareness of the present through mindfulness exercises, emotion regulation, distress tolerance skills, and building capacity for positive affect tolerance. Based on the theoretical assumptions reviewed here, strengthening the sense of self through the use of present-centered therapies in combination with exposure-based treatments may be crucial to successfully overcoming severe dissociative flashbacks.”

“…among individuals who suffer from the aftermath of trauma, the mind/body connection is often severed, leading to the subjective experience of feeling partially or fully detached from one’s body, or alternatively, as if one’s body does not belong to oneself.”

“It is critical for clinicians to understand the subjective experience from which the traumatized individual experiences his/her body and its relation to the surrounding world. Body-scan meditations, intended to facilitate awareness and the monitoring bodily sensations, form a central part of the mindfulness-based stress reduction program developed by Kabat-Zinn (1990) and provide an important means of assessing states of full or partial depersonalization, while at the same time enhancing the capacity for interoceptive awareness and diminishing detachment from bodily states. It is critical to note, however, that body scans must be carried out in a trauma-sensitive way in order to prevent the traumatized individual from becoming overwhelmed during this exercise”

“In the aftermath of trauma, however, it is well documented that emotion dysregulation can range from states of emotional undermodulation during which the individual experiences painful states of fear, anger, guilt, and shame to states of emotional overmodulation, during which the individual experiences emotional detachment such as states of depersonalization, derealization, emotional numbing, and affective shut-down.”

“Clinical efforts to assist individuals in overcoming emotional numbing and affective shutdown may center around assisting the traumatized individual to shift out of his/her shut-down state in order to be able to feel a full range of emotions, particularly pleasure and joy”

Future directions for research are covered:

“Future research is needed to identify more precisely the neurobiology underlying voice hearing and negative self-referential processing in trauma-related disorders as compared to that underlying voice hearing in psychotic-spectrum and other psychiatric disorders. This will be important to facilitate more accurate diagnosis, thereby guiding the most appropriate treatment interventions. Here, it will also be critical to examine how emotional triggers, for example, positive or negative self-related statements, may affect differently the presentation and underlying neurobiology of voice hearing in trauma-related disorders as compared to psychotic and other psychiatric disorders. Moreover, it will be important to examine the integrity of neural networks, such as the default mode network, which has been associated with an integrated sense of self across time , pre- and post-treatment interventions that target specifically the creation of a shared narrative between or among voices that may be associated with different self states.

From a clinical perspective, treatment outcome studies that focus specifically on interventions designed to affect voice hearing in trauma-related disorders should also be urgent foci of investigation”

See also:

Auditory Hallucinations in Chronic Trauma Disorders: Phenomenology and Psychological Mechanisms

Clinical perspectives on the relationship between psychosis and dissociation: utility of structural dissociation and implications for practice (2015)

Are some Auditory Verbal Hallucinations trauma/fear memories that are amendable via therapy & pharmacologically enhanced reconsolidation/extinction?

A pilot study exploring compassion in narratives of individuals with psychosis: implications for an attachment-based understanding of recovery

‘Hearing voices’, ‘pseudohallucinations’ and ‘lucid dreams’

Journaling as Therapy (2015)

‘Hearing voices’, ‘pseudohallucinations’ and ‘lucid dreams’

Expanding on the post: Clinical perspectives on the relationship between psychosis and dissociation: utility of structural dissociation and implications for practice (2015)

‘Pseudohallucinations versus hallucinations: wherein lies the difference?’ [1]:

“Pseudohallucination has been variously defined in the literature as an experience similar to hallucinations but falling short in some formal characteristics. The concept has achieved greater relevance in psychiatry with the introduction of the Hearing Voices Network in Australia by Richmond Fellowship in 2005. In this program, voices are understood as part of the individual’s life experience with an emphasis on acceptance and respect. However, there does appear to be a blurring of phenomenological differentiation in hallucinosis that has significant relevance to the psychiatric profession.

The term pseudohallucinations was first used by the German psychiatrist Hagen to refer to a perceptual phenomenon that could be mistaken for a hallucination. Kadinsky built on this definition as he had experienced both hallucinations and pseudohallucinations himself. He defined pseudohallucinations as subjective stimulation of sensory areas giving rise to concrete perceptions that lacked the objectivity or the realness of the hallucinatory experience.

Jaspers, who built on Kadinsky’s work, emphasized the concept of the inner subjective space, where vivid, subjective sensory images occurred spontaneously but lacked the realness of hallucinations. Blueler viewed pseudohallucinations as perceptions with full sensory clarity, internal localization and intact reality testing.

The theme in these early writings is that pseudohallucinations could be differentiated from hallucinations in that the experience occurred in the subjective inner space and lacked the sensory realness of hallucinations.

Van der Zwaard and Polak did a comprehensive review on pseudohallucinations and found that internal localization of voices and subjective insight did not discriminate pseudohallucinations from hallucinations. They broke down the concept of pseudohallucinations into categories. Nonpsychotic hallucinations represented isolated experiences of external voices such as hearing a loved one’s voice after death. Partial hallucinations were those having reduced sensory vividness with the presence of insight. Lastly, transient hallucinations represented lack of insight as in brief reactive psychoses.”

Comparing schizophrenia with PTSD, the authors found several differences:

  • Delusions differed significantly between the groups, with schizophrenia subjects scoring significantly higher than PTSD subjects. By any measure of effect size this difference was large.
  • PTSD subjects reported more negative content than schizophrenia subjects, including verbal abuse or personal threats to self. The effect size for this difference was moderate to high.
  • The groups differed significantly in terms of their experience of abuse.

“PTSD clients appeared to experience the voices in isolation rather than as part of a complex delusional system. The voices were also more likely to be critical and negative towards the individual, consistent with the experience of abuse.”

On the contrary:

“PTSD subjects were just as likely as schizophrenic subjects to perceive voices as loud, occurring outside the head and having no control over them. There was no difference between groups in the duration and frequency of hallucinations with both groups reporting the phenomena occurring daily or hourly and lasting over time.”

To conclude:

“It is important to note that neither this study nor the literature support the traditional view of pseudohallucinations necessarily occurring in the internal subjective space or retaining insight. The experience of hearing voices could not be easily differentiated in terms of loudness, position, control, frequency or duration of voices.”

Some guidelines are provided:

“Experienced clinicians are highly sensitive to the extreme suggestibility of the dissociated individual and may appropriately minimize discussion of the experience of hallucination to avoid exacerbating the situation. Informal feedback however from individuals taking part in this study, were that their clinicians tended to avoid discussion of their experiences, and they perceived themselves as not being believed with regards to these distressing experiences. The term pseudohallucination was seen as negative and critical of their experience.

Some of the experiences of pseudohallucinations are far more persistent than transitory, as shown in the above individuals with PTSD with dissociation. The diagnosis of brief psychotic disorder does not appropriately describe the phenomenology. The term trauma-intrusive hallucinations has been recognized as occurring along a continuum with hallucinations and could be added to a dimensional system, as a symptom of PTSD associated with dissociation. It would be significantly less pejorative than pseudohallucination, which associates with being “unreal” or “not severe”

subtyping of pseudohallucinations

“…the standard of care when the disorder is more complicated, such as with complex PTSD, trauma-related borderline personality disorder, and complex dissociative disorders, is phase-oriented treatment. The treatment phases are (a) safety, stabilization, symptom reduction, and skills training; (b) treatment of traumatic memories; and (c) personality (re)integration and (re)habilitation. Their application often takes the form of a spiral, in which different phases can be alternated according to the client’s needs. Phase-oriented treatment models have developed based on consistent clinical observations that the majority of patients with complex trauma-related disorders need to develop specific skills prior to meeting the challenges of integrating traumatic memories and their personality. Empirical support is developing for this clinical standard of care.” [2]

Lucid dreams responding to a novel intervention have also reported [3].

“Lucid Dreams are a form of dream life, during which the dreamer may be aware that he/she is dreaming, can stop/re-start the dreams, depending on the pleasantness or unpleasant nature of the dream, and experiences the dream as if he/she were fully awake. Depending on their content, they may be pleasant, un-pleasant or terrifying, at least in the context of patients, who also exhibit characteristics of Reward Deficiency Syndrome (RDS) and Posttraumatic Stress Disorder (PTSD). We present eight clinical cases, with known substance abuse, childhood abuse and diagnosed PTSD/RDS. The administration of a putative dopamine agonist, KB200Z™, was associated with the elimination of unpleasant and/or terrifying, lucid dreams in 87.5% of the cases presented, whereas one very heavy cocaine abuser showed a minimal response. These results required the continuous use of this nutraceutical. The lucid dreams themselves were distinguishable from typical, PTSD nightmares insofar as their content did not appear to reflect a symbolic rendition of an originally-experienced, historical trauma. Each of the cases was diagnosed with a form of RDS, i.e., ADHD, ADD, and/or Tourette’s syndrome. They all also suffered from some form of Post-Traumatic-Stress-Disorder (PTSD) and other psychiatric diagnoses as well. The reduction or elimination of terrifying Lucid Dreams seemed to be dependent on KB220Z, whereby voluntary stopping of the agent results in reinstatement of the terrifying non-pleasant nature of the dreams. Following more required research on a much larger population we anticipate confirmation of these seemingly interesting observations. If these results in a small number of patients are indeed confirmed we may have found a frontline solution to a very perplexing and complicated symptom known as lucid dreams.”