The Neuroscience of Dissociation – Clinical Application in Trauma Disorders

CLINICAL CRITERIA FOR DISSOCIATION

The DSM-5 conceptualises that the disengagement, depersonalisation, and derealization of oneself is an attempt to psychologically separate themselves from the stressor.

• Dissociation is therefore suggested to reduce conscious awareness of trauma-related emotion and pain, particularly in those subjected to intense trauma. [Vonderlin et al 2018]
• However, some argue that dissociation is maladaptive and can increase the severity of PTSD by denying that individual the opportunity to process traumatic memories. [Ozer et al. 2003]

The dichotomisation of PTSD into dissociative and non-dissociative has, however, been challenged, particularly given how some dissociative symptoms are inherent to some of the symptom clusters of ‘classical’ PTSD. [Dorahy and van der Hart 2015]

• The DSM-5 diagnostic criteria for PTSD now include a Dissociative Subtype (PTSD-DS).
• The DSM indicates that for a patient to meet the criteria for the dissociative subtype (PTSD+DS), then they must show symptoms of depersonalisation and derealization.
• However, the DSM does not specify flashbacks or amnesia as symptoms of dissociative PTSD; as such, it may be that these criteria are not capturing all those who experience dissociative symptomatology.

In the DSM-5, dissociation is part of the following disorders

• Dissociative identity disorder (DID) 
• Dissociative amnesia, including Dissociative Fugue 
• Depersonalisation/Derealization disorder 
• Other Specified Dissociative Disorder 
• Unspecified Dissociative Disorder

Classification of Dissociative Disorders in ICD-11:

• Dissociative neurological symptom disorder
• Dissociative amnesia
• Depersonalisation- Derealization disorder
• Trance Disorder
• Possession Trance Disorder
• Complex dissociative intrusion disorder
• Dissociative Identity Disorder
• Other Dissociative Disorder

Commonly experienced symptoms of dissociation include: [Briere et al., 2005]

• Disengagement (“spacing out”)
• Emotional constriction (reduced ability to experience emotions)
• Memory disturbance (e.g., “blanks” in memory)
• Depersonalisation (feeling outside of or as if you do not belong to your own body)
• Derealization (feeling as though things around you are strange or unfamiliar)
• Identity dissociation (e.g., feeling as though there is more than one person inside of you)

Steinberg outlined five core features of Dissociation included in the Semi-Structured Clinical Interview for Dissociative Symptoms and Disorders (SCID-D).

The SCID-D is a semi-structured interview intended to elicit patients’ experiences of five core symptoms : [Steinberg, 1995]

1. Amnesia

• Recurrent memory problems (often described as losing time).
• Gaps in memory can vary from several minutes to years. 

2. Depersonalization

• Sense of detachment or disconnection from one’s self
• Feeling like a stranger to yourself.
• Feeling detached from your emotions.
• Feeling robotic or like you are on autopilot.
• Feeling like a part of your body does not belong to you.
• Some people self-injure when depersonalised to feel “real”.

3. Derealization 

• Sense of disconnection from familiar people or one’s surroundings (e.g. family members or familiar surroundings, may seem unreal or foreign.
• Episodes of derealization may happen during flashbacks.

4. Identity confusion

• An inner struggle about one’s sense of self/identity.
• Severe identity confusion regarding sexual identity has been reported in people who have been sexually abused.

5. Identity alteration 

• Sense of acting like a different person sometimes (e.g., using other names in different situations).

Risk Factors for Dissociation: [Lanius et al., 2018]

• Chronic, inescapable stress occurring within the context of prolonged, repeated traumatic experiences (e.g., childhood neglect or abuse)
• Exposure to childhood abuse or neglect than among non-abused or neglected samples
• Younger age of onset
• Longer duration of abuse
• Parental abuse was associated with higher levels of dissociative symptoms.

CONCEPT OF DISSOCIATION

In general, dissociation can be understood in three distinct ways: [Schauer and Elbert, 2010]

Conceptual perspective:

• Lack of integration of mental modules or systems
• Altered state of consciousness
• Defence mechanism.

Behavioural perspective:

In the context of an escalating threat to life, the cascade involves:

• Complete functional sensory deafferentation.
• Decline of and finally absence of efferent motor commands.
• Reduction of and ultimately lack of speech perception and production.

Evolutionary perspective:

• Analgesia and numbing of panic and fear are adaptive when the victim is about to be attacked.

In human beings, tonic immobility can be understood as a defensive strategy, developed during an extended period of evolution in which human beings had to face predators in much the same way many animals do today, and designed to maximize the individual’s chances of surviving a potentially lethal attack, for example, a murderous killing. An immobile prey animal is less likely to be killed and eaten.

Tonic immobility or ‘‘thanatosis’’ is a process by which mammals feign death in order to evade unwelcome attention.

Such catatonia can be understood as an evolutionary-based fear response with features such as immobility, decreased vocalization, analgesia, ‘‘waxy flexibility,’’ and evidence of alertness as well as the fixed eye gaze, reducing visual input from the offender and thereby decreasing distress and arousal. At a later stage, a ‘‘waxy flexibility’’ is present. [Schauer and Elbert, 2010]

PSYCHOLOGICAL MODELS OF DISSOCIATION

The Trauma Model of Dissociation (TM)

• According to this model, dissociation is a psychobiological response that enhances individuals’ survival during and after a traumatic event. [Myrick & Brand, 2015]

Fantasy Model of Dissociation (FM)

• The relationship between reported trauma and dissociation is due to fantasy proneness, suggestibility, and cognitive failures.
• Evidence overwhelmingly suggests that trauma is causal in dissociation. [Myrick & Brand, 2015]

NEUROBIOLOGICAL MODELS OF DISSOCIATION

From a neurobiological perspective, the major models have been described in the context of PTSD.

PTSD is neurobiologically dichotomised into two phenotypes :

1. Emotional undermodulation [PTSD + Hyperarousal]
2. Emotional overmodulation [PTSD + DS]

The emotional overmodulation phenotype is associated with dissociative phenomenon.

In this section, we will predominantly focus on the pathophysiology of PTSD + DS.

1. Corticolimbic inhibition model:

PTSD+DS has been described as an overmodulation of limbic reactivity by the medial prefrontal cortex (PFC) and is also referred to as the corticolimbic inhibition model of PTSD and is directly in contrast to non-dissociative PTSD [undermodulation of emotional reactivity, i.e., a failure of the PFC to regulate limbic activity]. [Lanius et al. 2010]

• Neuroimaging studies have highlighted that experiences of intrusion and hyperarousal occur in 70% of patients with PTSD, whilst the remaining 30% exhibit dissociative symptoms. [Lanius et al. 2006]
• Those who meet the criteria of PTSD+DS may instead cycle between over and undermodulation [Lanius et al. 2010] as opposed to those with PTSD without DS, who tend to remain predominantly in the hyperarousal state.

2. Threat imminence continuum

• Neuroimaging studies utilising high-resolution functional MRI have suggested that these alterations between modulatory states are a function of threat processing and the proximity to that threat. [Mobbs et al. 2007]; [Mobbs et al. 2009]
• When the threat is remote in time, it is linked to passive freezing.
• When the threat is imminent, it is exemplified by fear and active avoidance.

3. Response Inhibition Model / Threat Processing Model: [Mobbs et al., 2009]

Both models are similar and link the prefrontal brain regions (orbitofrontal cortex, vmPFC) to subcortical structures (amygdala, PAG). Differential connectivity between these brain regions is responsible for varied PTSD phenotypes and associated symptoms.

The critical brain areas involved are:

PAG:

• Propagation and modulation of pain
• Sympathetic responses
• The learning and action of defensive and aversive behaviours
• Dorsolateral and lateral PAG (dl-PAG and l-PAG) are associated with emotional undermodulation and activate the sympathetic nervous system in response to threats and active defence responses.
• The ventrolateral PAG (vl-PAG) promotes emotional overmodulation via activation of the parasympathetic nervous system serving as the “brake” for the dl-PAG and l-PAG and is associated with passive defensive responses.

The basolateral amygdala (BLA)

• Evaluates sensory information
• It has projections to the thalamus, striatum, and PFC for subsequent cortical processing of sensory information.
• This subregion of the amygdala is moderated by top-down inhibition from the vmPFC.

Centromedial amygdala (CMA)

• Activation of nociception
• Execution of fear responses via projections to the PAG and other subcortical brain regions.

Bed Nucleus of Stria Terminalis (BNST):

• Recent evidence suggests a more significant role of the BNST in threat responses.
• The BNST is a subcortical brain structure considered an extension of the amygdala.
• Involved in anticipation of threat and worry about the future (as compared to the amygdala, involved in evaluation and response to immediate threat)

PTSD with hyperarousal symptoms [Bottom-up processing of threat]: Emotional Undermodulation

• Associated with reduced modulation of the amygdala and dl-PAG by the vmPFC leading to chronic activation of these brain regions and persistent hyperemotionality and hyperarousal.
• Subcortical regions (PAG and amygdala) drive responses that lead to chronic hyperarousal and defensive posturing towards the perception of imminent threat.
• Chronic posttraumatic stress promotes BNST activity via the amygdala and brainstem arousal networks.
• Chronic BNST activation leads to HPA axis dysfunction with a shift towards cortical dysexecutive processing of negative emotions. [Awasthi et al., 2020].
• Hyperarousal symptoms are associated with a loss of functional connectivity between the BNST and dorsolateral prefrontal and ventromedial orbitofrontal cortex, reflecting a loss of top-down inhibition.
• Noradrenergic projections to the BNST mediate hyperarousal
• Negative valence is mediated by serotonergic inputs abundant in the BNST. [Lebow & Chen, 2016] 

PTSD+DS [Dominant top-down processing]: Emotional Overmodulation

• Associated with increased modulation of the amygdala, BNST and PAG regions by the vmPFC i.e. over-regulation of defensive processing by PFC regions, as seen in healthy controls during early detection of threat.
• Associated with passive defensive responding and chronic emotional detachment (symptoms of depersonalisation and derealization).

The top-down connection from the vmPFC to the amygdala and the bottom-up connection from the amygdala to the PAG underlies flight-or-fight inhibition and enables a passive defence response. As threat approaches and is perceived as more imminent, defensive processing shifts from prefrontal brain regions (e.g., to subcortical brain regions involved in primitive defensive responses (e.g., amygdala and PAG).

Mobb’s threat processing model:

PTSD + DS:

• Predominant top-down connectivity from the vmPFC to the amygdala to PAG is consistent with overmodulation of fear processing.
• Greater functional connectivity of both CMA and BLA with frontal regions, supporting previous findings of increased top-down inhibition and, thus, reduced defensive responding via the CMA.
• Among individuals with PTSD+DS, increased insula-BLA connectivity across insula subregions was reported in a recent study when compared to patients with PTSD or with controls. [Nicholson et al., 2016].
• Increased functional connectivity of the claustrum with the bed nucleus of the stria terminalis (BNST) was found among individuals with PTSD+DS compared to those with PTSD and healthy controls. [Rabellino et al, 2017].

Phenotypes in individuals with DID: [Krause-Utz and Elzinga, 2018]

Traumatic identity state (State with access to traumatic memories):

• Increased activity in limbic regions
• Decreased activity in prefrontal regions
• Increased perfusion in the thalamus in comparison to their “normal functioning identity state” (a state where dissociative amnesia is present)

Normal identity state (State with Dissociative amnesia):

• Increased activity in prefrontal regions
• Decreased activity in limbic regions
• Emotional overmodulation.

4. The Defence Cascade: [Schauer and Elbert, 2010]

The defence cascade consists of a sequence of six somatomotor responses mediated by descending neural networks:

“Freeze-Flight-Fight-Fright-Flag-Faint” [Volchan et al. 2017]

Freeze: (Attentive Immobility)

• Mediated via the superior colliculus and PAG
• Allows the organism to determine the presence and location of threat in the environment at a subcortical level.

Fight or flight: (Hyperarousal and Hypervigilance) – Toward the Arousal Peak of the Alarm Response.

• Activation of the sympathetic nervous system and the dorsolateral PAG (dlPAG) activates motor patterns of fight or flight via the PAG, amygdala, and limbic forebrain.
• Accompanied by the release of endocannabinoids, leading to analgesia.

Fright: (Tonic Immobility -Unresponsive Immobility) –  Peak of Arousal and Physical immobility 

• If fleeing is not possible, the animal may enter the fright stage (also known as tonic immobility), where the sympathetic and parasympathetic nervous systems are simultaneously activated to decrease hyperarousal.
• Characterised by inhibition of aggression through muscle restraining when being overwhelmed by a threat.

Flag and Faint: (Unresponsive immobility / Shutdown response) – Flaccid immobility and/or fainting

• When escape and/or chance of survival is low.
• Profoundly dissociative state (flag) or even faint as a response to the overwhelming life threat.
• Mediated by the ventrolateral PAG (brake to the lateral PAG), which activates vagal parasympathetic activity.
• Sensation, perception, and motor abilities are significantly altered (mirrored by symptoms of depersonalisation and derealization) associated with cortical-sensory deafferentation, where reduced integration of sensory stimuli via the thalamus to the cortex allows the individual to reduce response to external stimuli.
• In a more progressed flag state, emotional involvement fades away, memory consolidation becomes weak, and later rehearsal becomes more difficult. As a result, the patient may take minutes to hours for a patient to be oriented in reality. [Schauer and Elbert, 2010]
• From a neurotransmitter perspective, opioid-mediated analgesia accompanies the shutdown response, with perceptual and mood alterations (e.g., dysphoria) mediated by the kappa (K)-opioid (dynorphin) system.
• Flaccid immobility up to fainting (a response also seen in blood-injection-injury phobia) is also explained by the ‘heart defence hypothesis’, which postulates that the response is a defence against the danger of cardiac failure during inescapable attacks to reduce myocardial oxygen consumption when cardiac strain is expected to be excessive. Hypotension and bradycardia due to excessive parasympathetic activity as part of this stage lead to cerebral hypoperfusion and loss of consciousness; the horizontal position induced by fainting restores blood supply to the brain. [Alboni & Alboni,2017]

In summary, response inhibition and the defence cascade have signature neural patterns that involve the extended amygdala, hypothalamus, and PAG.

In cases of PTSD+DS, the available data suggests that this involves amygdala deactivation, parasympathetic activation, and stress-induced opioid-mediated analgesia. [Lanius et al 2003]; [Lanius et al 2006]; [Lanius et al 2010]

5. Polyvagal theory: [Porges, 2011]

When the heart is affected, it reacts on the brain; and the state of the brain again reacts through the pneumo-gastric [vagus] nerve on the heart; so that under any excitement there will be much mutual action and reaction between these, the two most important organs of the body [Darwin, 1872]

Three vagal circuits provide adaptive responses to safe, dangerous, and life-threatening events and contexts. [Porges, 2009]

1. The Sympathetic-Adrenal Vagus branch – The Fight and Flight Branch

• Active during mobilisation behaviours (e.g. fight/flight) when under attack.

2. The Myelinated Vagus Branch / The Ventral Vagal Complex (VVC) – The Regulatory Branch

• Only mammals have a myelinated vagus.
• Regulates cardiac vagal activity and withdrawal via inhibition of the sympathetic branch associated with decreased arousal, social engagement and self-soothing behaviours.

3. The Unmyelinated Vagus Branch / The Dorsal Vagal Complex (DVC) – The Shut-Down branch

• Associated with immobilisation (e.g. fainting, shutdown, dissociation), bradycardia and decreased muscle tone.

The polyvagal theory postulates dissociation as a defensive immobilisation response modulated by the dorsal vagal complex and associated with significant heart rate decreases.

When the environment is perceived as safe, homeostasis is achieved through increase in the influence of mammalian myelinated vagal motor pathways on the cardiac pacemaker that slows the heart, inhibits the fight-flight mechanisms of the sympathetic nervous system, dampens the stress response system of the HPA axis (e.g., cortisol), and reduces inflammation by modulating immune reactions (e.g., cytokines).

Second, through the process of evolution, the brainstem nuclei that regulate the myelinated vagus became integrated with the nuclei that regulate the muscles of the face and head. This link results in the bidirectional coupling between spontaneous social engagement behaviours and bodily states. [Porges, 2009]

The assumptions and premises underpinning the polyvagal theory have recently been refuted and described as untenable based on past & present evidence. [Grossman, 2023]

DISSOCIATION, THE STRESS RESPONSE AND THE HPA AXIS

Stress regulation in response to a threat is characterised by reciprocal and synchronised interactions between the HPA axis, the sympathetic nervous system, and the immune system.

Whilst the HPA axis is tightly regulated by glucocorticoid feedback mechanisms that restrain the endocrine portion of the stress response, the regulation of neural stress-response circuits is mediated by neuromodulators such as neuropeptide Y, endocannabinoids, and endogenous opioids. [Bowers et al 2012]; [Crowe et al 2014]

• HPA axis dysregulation in PTSD+DS is characterised by autonomic blunting, which has been demonstrated by reductions in heart rate and skin conductance reactivity. [Simeon et al. 2007]
• Furthermore, recent findings have shown enhanced negative feedback in PTSD+DS, i.e., significant hypercortisolemia and an inverse relationship between morning cortisol levels and dissociation severity.[Lee et al., 2022]

NEUROTRANSMITTERS AND DISSOCIATION

The neurochemical processes that are related to PTSD have been difficult to establish; however, what is known is that each defence cascade response is associated with changes in pain processing, e.g., non-opioid analgesia accompanies active responses (fight or flight) whilst opioid analgesia accompanies passive defence responses (freezing or fainting). [Keay et al 2001]; [da Silva et al 2012]

Endogenous opioid system:

PTSD is associated with chronic downregulation of the endogenous opioid system, leading to a conditioned passive defence response when opioids are released. [Baker et al. 1997]

• Inescapable shock is also associated with altered responses of the endogenous opioid system, particularly initial upregulation followed by chronic down-regulation of opioid signalling.
• Patients may counteract this chronic downregulation of the endogenous opioid system by engaging in self-destructive behaviour that leads to an upregulation of opioid release in response to stress (e.g., self-harm, involvement in future abusive relationships)
• The mu-opioid and kappa-opioid systems are linked to dissociative symptoms, with the mu-opioid system mediating analgesic effects, whilst the kappa-opioid system is responsible for alterations in consciousness. [Van der Kolk 2001]
• As the BNST contains kappa opioid receptors (KORs), increased activation of the kappa-opioid system in response to chronic inescapable stress may increase functional connectivity between the claustrum and BNST in PTSD + DS, leading to dissociative symptoms and secondary dysphoria. [Rabellino et al, 2017].

Endocannabinoid (ECB) deficiency hypothesis of PTSD: [Steardo et al., 2021]. 

• Individuals with PTSD show reduced endocannabinoid levels associated with increased threat sensitivity and hyperarousal symptoms.
• Individuals with PTSD show an increased availability of cannabinoid receptor type 1 (CB1 receptors) in the amygdala, indicative of reduced bioavailability of endocannabinoids, linked to an increased attentional bias to threat.
• The ECB deficiency hypothesis may explain the use of cannabis for self-medication in PTSD and anxiety.
• ECB signalling at CB1 receptors helps promote adaptation to repeated stress exposure by dampening the release of catecholamines counteracting excessive sympathetic activity.
• Functionally, cannabinoids reduce neuronal activity within the amygdala, increase neuronal activity within the vmPFC, and increase the functional coupling of these structures.
• Exogenous cannabinoids, including THC, exert opposing dose-dependent effects. THC and cannabis can reduce HPA-axis function in response to stress and show anxiolytic properties; however, they can increase HPA-axis function and be anxiogenic at higher doses.

In summary, augmenting ECB signalling:

• Reduces reactivity of the amygdala
• Enhances activation of the mPFC
• Increases the vmPFC coupling to the amygdala, thus reducing hyperarousal.
• Suppresses the recall and enhances the extinction of emotionally aversive memories.
• Modulates HPA Axis signalling.
• Inhibits excessive sympathetic activity.
• Reduces inflammatory processes
• Reduces the occurrence of REM sleep and arousal, thus increasing time spent sleeping.

Cannabinoids, thus, may target the emotional undermodulation phenotype of PTSD.

Chronic cannabis use, however, has been associated with a reversible downregulation of CB1 receptors in the brain leading to impairments in fear extinction which can lead to poorer outcomes in PTSD.

CLINICAL APPLICATION AND IMPLICATIONS FOR THE DIAGNOSIS AND MANAGEMENT OF DISSOCIATION

As trauma is a significant aetiological factor for dissociation, in this article, we focus on the treatment of dissociation in Trauma-related disorders (PTSD/ C-PTSD / BPD).

As dissociation (and individuals with dissociative disorders) is used as an exclusionary criterion for PTSD outcome studies and in studies of chronic childhood abuse, the generalisability of the PTSD outcome studies may not apply to patients with dissociation. [Cloitre,2002]

Treatment of Dissociative identity disorder (DID), Dissociative amnesia including Dissociative Fugue, Depersonalization/Derealization disorder and other Specified Dissociative Disorders are outside the scope of this article; however, some of the following principles may apply.

Diagnosis:

Clinicians should assess dissociative symptoms before engaging patients in any exposure-based treatments. [Lanius et al., 2010]

Failure to do so can lead to an actual increase in PTSD and related symptoms.

Scales for assessing dissociative symptoms:

• Dissociative Experiences Scale (DES)
• Multidimensional Inventory of Dissociation (MID) [Dell, 2006]
• Multiscale Dissociation Inventory (MDI)
• Somatoform Dissociation Scale

Dissociation as a conditioned learned response to stress:

Dissociative responses are learned responses that involve both classical and reward learning. [survival as a reward due to the ‘‘shut-down’’ during the severe threat]

Thus, exposure to trauma reminders in trauma survivors can activate a strong vasovagal dissociative response, even decades later [Schauer and Elbert, 2010]

Why clinicians should assess for dissociation: 

• The presence of dissociation is linked to treatment outcome.
• Those with complex trauma histories are at risk of being misclassified as malingering, feigning or exaggerating. This misclassification can be due to; some malingering scales, including dissociative and other trauma-related symptoms and; due to the high number of psychiatric symptoms, comorbid with DD being considered rare on some psychological tests.
• Dissociation inhibits amygdala-based emotional learning in patients with borderline personality disorder (BPD) and may interfere with treatment, particularly during treatment sessions. [Brand and Lanius, 2014]
• Self-harming behaviours can interfere with treatment, and the differential mechanisms for self-harm are essential to understand. The pathophysiology of self-harming behaviour in DD differs from self-harming behaviours in BPD. In DD, self-harming behaviour is a compensatory strategy to interrupt unwanted hypoarousal and numbing in contrast to BPD, where self-mutilating behaviour facilitates tension relief by setting the shut-down flag state in motion. [Rossi et al., 2019].

Self-mutilating behaviour serves to initiate dissociation in the form of flaccid immobility. When mutilating the skin surface (i.e., cutting), a vasovagal reaction is launched. During this ‘‘shut-down’’ blood pressure and heart rate are down, together with a fading emotional tension and a termination of ruminating thoughts, worries, troubles, etc. The potentially reinforcing effects of self-injurious behaviour may account for the failure of some treatment regimens. We conclude that borderline patients induce their own relaxing dissociative shut-down response (type 2) as a learned response.

KEY PRINCIPLES IN THE MANAGEMENT OF REDUCING HYPERAROUSAL AND INTERVENTIONS TARGETING STAGES OF THE DEFENCE CASCADE

Trauma treatment must differentiate between patients on two dimensions:

• Patients with peritraumatic sympathetic activation
• Patients who went down the whole defence cascade in the context of reminders, leading to parasympathetic dominance and dissociative responding, in the context of reminders.

Clinicians should be aware that individuals with PTSD+DS do not experience only static symptoms of depersonalisation and derealization but oscillate between symptoms of emotion under and overmodulation, with emotion overmodulation predominating. [Lanius et al., 2018]

By contrast, individuals with PTSD without the dissociative subtype do not usually experience symptoms of depersonalisation and derealization.

Since trauma can activate the body’s arousal systems, which subsequently trigger the defence cascade, interventions that reduce hyperarousal states can prevent the progress of the cascade, thus addressing dissociation indirectly. [Kozlowska et al, 2015]

The differential management of dissociative stages (“fright” and “faint”) has important treatment implications. [Schauer and Elbert, 2010]

Key Arousal Reduction Targets:

1. Modulating the sympathetic-vagal balance.
2. Downregulation of the hypothalamic-pituitary-adrenal (HPA) axis.
3. Downregulation of limbic activity or reactivity.

Interventions broadly may be divided into those:

1. Utilising a somatic approach:

• Targeting the body via enhancing interoceptive and sensory awareness.
• This approach has its roots in evolution. with soothing interventions mothers use for their infants, e.g. patting, rocking, singing, rely on the activation of interoceptive, proprioceptive, and classic sensory afferents.

2. Utilising a brain-first approach

• Bottom-up: Targeting limbic areas
• Top-down: Targeting cortical areas involved in emotion/somatic regulation

SOMATIC APPROACHES TO DECREASE AROUSAL:

The fundamental principle in somatic approaches is to enhance vagal tone.

Breathing interventions:

• Hyperarousal is associated with central vagal respiratory-gating mechanism dysregulation.
• Reduction in breathing rate results in automatic upregulation of vagal activity.
• Thus, training in slow breathing may reset the mechanism by strengthening the vagal tone.

Other breathing interventions, e.g. use of resistance or vibrations, increase peripheral activation of vagal lung afferents.

Types of breathing interventions:

• Controlled breathing
• Slow-breathing techniques (from yoga and other Eastern disciplines)
• Coherence breathing
• Brahmari (Sanksrit for bee) breathing. This breath practice is named after a type of black Indian bee due to the bee-like buzzing sound produced during the exhale.
• Breathing at one’s resonant frequency: utilising a decrease in respiratory rate, prolonged expiration (pranayama), breathing against airway resistance, or vibration of the airway to reduce physiological arousal.

Acupuncture

• Downregulates HPA axis
• Sympatholytic

Voluntary regular exercise

• Reduces amygdala reactivity

BOTTOM-UP BRAIN APPROACHES TO DECREASE AROUSAL 

Pharmacological agents (see later) to reduce amygdala activity.

• Benzodiazepines
• Clonidine
• Propranolol
• SSRIs and SNRIs

TOP-DOWN BRAIN APPROACHES TO DECREASING AROUSAL 

Mindfulness and meditation

• Enhances prefrontal cortex (PFC) activity and downregulates amygdala activity.

Somatic micro-tracking Mindfulness

• Helps patients attend to minute shifts in somatic state and to allow themselves to experience defensive action patterns or to finish enacting them in an accepting and nonjudgmental way.

EEG Biofeedback “open focus”: 

• Utilising shifts in attention to induce high-amplitude alpha waves in the EEG, which are associated with reduced brain-body arousal.
• Alpha range (8-12 Hz) is produced during alert, relaxed states, including mindfulness and other states characterised by open-focus attention.

Clinical Interventions:

• Since a critical trigger for hyperarousal is the reactivation of traumatic memories, interventions targeting memory processing and desensitising the individual to the traumatic memories are an integral component of treatment. E.g., Cognitive-behavioural therapy (CBT), Eye movement desensitisation and reprocessing (EMDR), and tapping.

Interventions for PTSD and cPTSD have been covered previously.

Post Traumatic Stress Disorder (PTSD) – A Primer on Neurobiology and Management

Complex Post Traumatic Stress Disorder (cPTSD)- Impact of Childhood Trauma | Assessment and Management Principles

SPECIFIC INTERVENTIONS FOR DEFENCE CASCADE STAGES [Kozlowska et al, 2015]

1. MANAGING TONIC IMMOBILITY:

• Tonic immobility can be conceptualised as an action response that occurred in response to the original trauma and is now a fixed action response that is incompletely processed and automatically reactivated by trauma reminders.
• Patients in a tonic immobility state are often disconnected from self and therapist.
• The aim is to help patients shift out of a tonic immobility state by using bottom-up somatic strategies combined with mindfulness to heighten somatosensory signals by focusing on interoceptive, proprioceptive, or touch sensations allowing the patient to become aware of their body.
• Patients in this state, however, are most likely to shift into a state of flight or fight or extreme arousal (as arousal immediately precedes tonic immobility)

Grounding interventions:

• Sensorimotor interventions help patients focus attention on interoceptive, proprioceptive, and classic sensory sensations to orient them back to the here and now.
• Examples include putting one hand on the abdomen and the other hand over the heart, feeling one’s feet on the ground (which can be accentuated by having patients stomp their feet, massage their legs, or shift the body’s weight to the toes, heels, and sides of the feet), feeling the chair pressing on one’s back, and feeling the firmness of the wall with one’s hands.

Motor interventions:

• They can be used to help patients shift out of tonic immobility or to prevent its activation.
• Standing up (to increase proprioceptive signals, walking, raising the arms or stretching the body in some way, conducting therapy while the patient is sitting on a ball (which requires constant attention to proprioceptive signals to keep one’s balance),

2. MANAGING FREEZING

• Freezing is a mind-body state characterised by a narrow focus of attention, i.e. the individual is focused on the threat.

Mindful observation and tracking of body sensations:

• Assist the patient in mindfully observing their body sensations and tracking them or ” breathing into” them until they have subsided and transformed.

Expanding the focus of attention:

• These interventions are usually considered if the patient cannot tolerate the intensity of body sensations.
• e.g. Meditation exercises that practice narrowing and widening the focus of attention
• Open-focus biofeedback exercises.
• Freezing states are generally transitory, and one can use the above strategies to prepare the patient to deal with freezing.

3. MANAGING FIGHT AND FLIGHT

Prevention:

• Aim to identify early somatic precursors (movements or sensations that herald the emergence of fight and flight patterns), for example, the furrowing of the eyebrows, the tensing of the jaw, or the clenching of a fist.
• Interrupt the patient’s narrative when precursors are identified and occurring in therapy.
• Assist the patient in considering mindful observation and tracking of body sensations, putting aside emotions, memories, and cognitions until the defence state resolves.
• If the patient cannot tolerate the intensity of body sensations, use interventions that expand the focus of attention.
• Sometimes, the patient may need to implement breathing or grounding interventions to downregulate arousal.

4. MANAGING FLAG (FLACCID OR UNRESPONSIVE IMMOBILITY) AND FAINT (COLLAPSED IMMOBILITY)

Collapsed immobility presents as episodes of fainting (syncope) or alternately as a loss of muscle tone accompanied by a compromised level of consciousness (presyncope).

• Exclude medical causes (e.g., cardiac pathology, hypoglycemia, orthostatic problems).
• Interventions to increase the patient’s safety.
• Some patients may know their early warning signs, e.g. visual blurring, sweating, nausea, warmth, light-headedness, and fatigue and may be able to prevent syncope by positioning themselves on the floor and lifting their feet. Other patients can identify specific trauma-related triggers and may be able to take appropriate precautions.
• Stress-related hyperventilation can increase the susceptibility to episodes of fainting.
• Implement arousal-decreasing interventions to reduce the probability of dorsal cardiac vagal pathway activation since the dorsal pathway is activated in high-arousal contexts.
• Pharmacological interventions, e.g. SSRIs, SNRIs, beta-blockers, to decrease arousal.
• Address trauma related triggers-past or present.

KEY PRINCIPLES IN MANAGEMENT OF DISSOCIATION

Directly addressing dissociative symptoms is necessary for improved outcomes.

Implications for treatment: [Myrick & Brand, 2015]

• Emotional engagement in traumatic memory is necessary for successfully processing the event and resultant recovery.
• In trauma survivors with dissociative responses, exposure may reactivate the flag state or even result in fainting. [Schauer and Elbert, 2010]
• In treating patients with a peritraumatic response of vasovagal shut-down or fainting, replicating these responses and emotions during treatment can quickly lead to therapeutic failure.
• Thus, during treatment, patients with the dissociative shut-down form of PTSD ( complex trauma patients) need assistance to actively fight the replay risk of vasovagal dominance.
• Activation (active motoric engagement) may help to maintain arousal and prevent immobility.
• Relaxation techniques are contraindicated since they would aggravate vasovagal responses and support fainting.
• In the initial stages of exposure, recall of the trauma material should be combined with forced reality testing, with the therapist actively providing directive guidance at the first signs of flagging or fainting.

Recommendations are to consider a staged approach to treatment which is in line with the complex trauma/DD literature, which recommends a trauma-informed, staged approach to treatment [Myrick et al., 2015] [Brand et al., 2012].

A staged approach to treatment:

Phase 1 – Safety | Symptom Reduction | Enhance Emotional, Psychological and Social Competencies

• It focuses on psychoeducation, enhancing control over symptoms through developing affect tolerance skills, understanding the function of SIB and suicidality, and building a collaborative therapeutic relationship.

Phase 2 – Review and Reappraisal of Trauma memories | Integration of traumatic memories into an Adaptive Representation of Self, Relationships and World  

• Developing a narrative including nontraumatic and traumatic experiences. Patients strive to gain mastery over memories and resolve trauma-related cognitive distortions. Contrary to traditional exposure therapy for PTSD, however, trauma processing is carefully paced to provide patients with time to understand and integrate memories while continuing to focus on safety and stability. Experts do not recommend exploring traumatic memories every session, even during the trauma-processing stage.

Phase 3- Consolidation -Transition out of therapy to greater engagement in relationships, work or education and community life. 

• Reconnection with self and others and focuses on improved social functioning, among other topics.

Expert consensus has identified a core set of interventions to be implemented in a staged manner. [Brand et al., 2012].

• Targeting diagnosis
• Psychoeducation
• Affect modulation
• Impulse control
• Interpersonal skills
• Stabilisation from crises

DIFFERENCES IN INTERVENTIONS IN PTSD WITH HYPERAROUSAL VS PTSD + DS

KEY PRINCIPLES IN THE MANAGEMENT OF PTSD WITH HYPERAROUSAL SUBTYPE:

Aim:

• Activation of the fear network elements in relation to their autobiographical context (space and time when the event happened).

Techniques: 

Sensory afferent:

• Emphasise the exploration of sensory details of the past traumatic event, comparing/contrasting with sensations and emotions in the present during recall.

Narrative:

• Emphasise the narration of the past traumatic scene.

Emotional expression:

• Support full emotional expression.

Avoid

• Termination of exposure before contextualisation and integration can take place (i.e., avoidance).

KEY PRINCIPLES IN TREATMENT OF PTSD DISSOCIATIVE SUBTYPE

Nutritional aspects:

• Ensure normal blood sugar level and electrolytes
• Ensure sufficient nutrition intake.

Aim:

• Activation of elements of the fear network in relation to their autobiographical context
• Support and interrupt the activation by continuous reality testing, cardiovascular activation, and sensory stimulation.
• Encourage speech production until trauma material can be processed without shut-down.

Techniques:

Sensory afferent:

• Emphasise the exploration of sensory details of the past traumatic event, comparing/contrasting with sensations and emotions in the present during recall as in hyperarousal phenotype.
• Combine the above with stimulation of the senses in the here and now (e.g. present positive fragrances (e.g., lemon) or tasting samples (peppermint oil or chilli gum), switch on a bright light, present tactile information (e.g., texture, ice-packs) etc.

Motor afferent:

• Emphasise skeletal muscle activation and muscle tonus which should increase blood pressure.
• Techniques include applied tension, physical exercises, leg crossing, and body balancing tasks.

Narrative:

• Emphasise the narration of the past traumatic scene, supported by the facilitation of continuous narrative engagement in the here and now (e.g., active communication; enhance speech production).

Emotional expression:

• Support the full emotional expression, allowing and promoting specifically anger affect that has been inhibited peritraumatically.

Nutritional demands:

• Ensure attention to adequate nutrition (caution for malnutrition/eating disorders)
• Increase dietary salt and fluid intake in daily life
• Advise drinking water (approx. 500 ml, if tolerated) before trauma exposure.

Avoid:

• Termination of exposure before contextualisation and integration could take place.
• Disengagement from the here and now.
• Relaxation (instead of activation).
• Sensory similarities between the trauma context and the therapeutic setting.
• Stimuli associated with disgust or similar to body fluids and faeces.
• Threat cues in the here and now (instead: present safety signals).
• Semi-darkness in the room and objects for hiding behind (e.g., large plants, furniture).

PHARMACOTHERAPY PRINCIPLES IN DISSOCIATION

Pharmacotherapy: [Gentile et al., 2013]

This section should be read in conjunction with pharmacotherapy in PTSD.

Antidepressants/ Anxiolytics:

• SSRIs
• SNRIs
• TCAs
• MAOIs 
• Antidepressants treat co-morbid symptoms, stabilise mood, and reduce intrusive symptoms, hyperarousal, and anxiety through their differing actions on reducing amygdala reactivity and strengthening PFC function.

Simplified Guide to 21 Common Antidepressants – Mechanisms of Action, Side effects and Indications

Antipsychotic agents: 

• Atypical (or second-generation) antipsychotic (APs) agents are useful in treating agitation and hypervigilance, reducing intrusion symptoms, and treating complex trauma cases with psychotic features.
• Clinicians should distinguish auditory hallucinations, which originate from an external locus, from pseudohallucinations which can occur as “internal” voices and may be less responsive to AP agents.  Hallucinations – What are Hallucinations? The Neurobiology of Hallucinations

A Simplified Guide to Oral Antipsychotic Medications – Mechanism of Action, Side Effects, and Need to Know Points

Benzodiazepines

• Use with caution to decrease anxiety.
• They may exacerbate dissociation.

Beta-blockers / Clonidine:

• Propranolol, a beta blocker, is effective in reducing PTSD symptoms when administered before trauma reactivation as part of therapy.
• Clonidine (alpha-2 agonist) and prazosin are effective in reducing hyperarousal and nightmares.

Mood stabilisers:

Lamotrigine, topiramate etc., reduce aggression, intrusive symptoms and hyperarousal through GABAergic modulation. Pharmacotherapy in PTSD.

Naltrexone and Naloxone:

• Since stress-induced analgesia, a form of dissociation, is mediated by the mu-opioid system; Naltrexone has shown some promise in treating dissociative symptoms.

• Naloxone reversed stress-induced analgesia among veterans with PTSD compared to those without PTSD, suggesting upregulation of the opioid response following exposure to trauma cues. [Pitman, 1990].

• Naltrexone may also reduce self-injurious behaviour.

Paroxetine and Naloxone are the only pharmacological agents studied through RCTs and found modest evidence for controlling depersonalisation symptoms and dissociative symptoms co-morbid with PTSD and BPD. [Sutar and Sahu, 2019]

Essential aspects in prescribing: 

Discontinuation of medication and the subsequent removal of limbic inhibition can predispose the individual to strong limbic reactivity to new stressors.

Hence, in treating trauma-related disorders with hyperarousal, clinicians should consider two important aspects.

1. Gradual discontinuation to avoid significant limbic rebound
2. Consider appropriate psychological treatments in combination with pharmacological treatments (in a staged approach as necessary) to facilitate long-term changes in information processing, which can ease medication reduction and /or cessation over time.

Endocannabinoids (ECBs): 

SUMMARY

The response inhibition and defence cascade models describe different responses to threat and their perceived imminence and time proximity; these complementary models are posited to underlie the neurobiology of dissociative symptomatology in PTSD.

Neuroimaging studies suggest top-down structural changes to circuits connecting the amygdala, hypothalamus, and PAG, consistent with emerging evidence of emotional overmodulation in PTSD+DS.

In clinical practice, clinicians must differentiate between the peritraumatic state of hyperarousal vs those that have gone further down the defence cascade as the treatment modalities differ.

Directly addressing dissociative symptoms is essential for improved outcomes in trauma-related disorders.