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Increased muscle tension occurs during states of high stress or fear to prepare the physical body for fighting or fleeing . If an animal carries out a survival-oriented action to completion, the system receives vestibular and somatosensory feedback. A thwarted or incomplete motor response to a threatening situation may explain how traumatized individuals often experience their body reflexively enters exaggerated reactive motor patterns and/or defensive states such as tonic immobility or collapse in the face of everyday stressors or trauma triggers. Exaggeratedly heightened tonicity and decreased postural sway create a tonic immobility or “freeze” response, exhibited by animals.
Likewise, tonic immobility in humans is more common under fear-inducing conditions of somatosensory restraint, such as rape
High muscle tonicity (tonic immobility) (Figure 6).
Alternatively, hypo-arousal and decreased muscle tone occur during emotional shut-down or feign death as a passive defensive response to inescapable or prolonged threat (Hofer, 1970; Depaulis et al., 1994; Bracha, 2004). Here, drastically reduced arousal and tonicity diminish the conscious experience of further injury and psychic distress during inevitable or prolonged attack, sometimes to the point of an out-of-body experience or complete loss of consciousness
Muscle flaccidity (dissociation)(Figure 7)
Accordingly, those with trauma-related dissociative disorders are thought to exhibit top-down overmodulation of subcortical brain activity (Lanius et al., 2010b; Nicholson et al., 2017; Terpou et al., 2020), which putatively suppresses somatic sensory information from reaching higher-order regions involved in its integration into awareness
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When the execution of movement to self- or other-protect is disrupted, states of psychic anger or rumination may be disconnected from the body, or bodily activation may be disconnected from awareness (Corrigan and Christie-Sands, 2020). This disrupted subcortico-cortical information flow engenders pervasive senses of defectiveness and defenselessness, and may contribute to unintegrated traumatic memory manifesting at somatic or affective levels
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a rape victim experiences aversive touch, imposed bodily movement and somatosensory restraint
Given that extreme stress activates an individual’s innate attachment system (Bowlby, 1973), an inability to seek co-regulation from another or engage neural circuitry related to self-regulatory mechanisms due to a history of insecure attachment and somatic sensory disintegration results in persisting trauma-related symptoms. In more extreme cases where the individual experiences tonic immobility(note: high muscle tonicity) or emotional shutdown (note: muscle flaccidity), a sensory feedback-motor action plan for survival is thwarted and intention to obtain survival needs is decoupled from expected or intended action. This sensory-motor mismatch is experienced by the body as an inadequate response to existential threat (Fischer and Riedesser, 1999; Sar and Öztürk, 2008), and corresponds with a disrupted sense of agency and connectedness to/trust in the body.
note: muscle flaccidity (dissociation)^
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Relatedly, those with trauma-based dissociative disorders may have adapted to chronic traumatization by suppressing lower-level survival responses and maintaining cortico-cortical hyperconnectivity, resulting in disembodiment and a lack of connection to raw emotion and sensorimotor experience. Indeed, upstream alterations in functional connectivity have been found at the level of the vestibular nuclei
Without a grounded, stable, and physiologically regulated soma generated through somatic sensory integration, exteroceptive input such as bright lights, sudden noises, and unexpected touch can over-activate the SN, disturb the DMN, and throw multisensory integrative balance off kilter (Figure 9A). Here, one “feels too much” and lacks the ability to self-regulate resulting in aggression, emotional/physical overwhelm, and startle hyperresponsivity. Alternatively, chronic detachment from bodily sensations and emotions in conjunction with fluctuating hypoarousal presents in PTSD + DS. A vicious cycle of overwhelm and shutdown occurs in a desperate attempt to attenuate chronically overbearing feelings. Over-modulation of arousal and affect by prefrontal structures dampens sensory experiences as a protective mechanism, resulting in emotional numbness or feeling “dead inside”
Further, chronic childhood traumatization may alter development of SN and DMN circuitry, where highly activating or threatening sensory stimuli feel familiar or normal (Lanius et al., 2020). These individuals may seek to engage the SN and thus gain access to the DMN through intense or primally threatening somatic sensory experiences, such as car racing, extreme sports, and promiscuous sex (van der Kolk, 1989, 2015; Lanius et al., 2020). For severe and lifelong overmodulation, any experience of bodily sensation feels foreign, threatening to flood the cortical defense mechanism created to protect the brain from overwhelm. Those who are overcome by any experience of bodily sensation may avoid certain environments, physical activity, and intimacy which elicit too triggering of sensations. Consideration of pre-reflective sensorimotor brainstem regions in therapeutic attempts to restore, or in the case of chronic childhood trauma, primarily establish, the capacity for safety and trust in the body is crucial.
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The experience of inhabiting one’s own body, or embodiment, is an ineffable, subconscious perception rooted in sensorimotor processes (Ciaunica et al., 2021a). Embodiment is a state in which the mind is oriented in physical space, giving rise to a first-person perspective (Lenggenhager et al., 2006, 2007; Blanke and Metzinger, 2009). This spatial union of the mind with the physical body (Ferrè et al., 2014) provides a fundamental reference point for higher-order cortical function as it directs our attention and intentions in volitional thought and action (Panksepp, 1998). Ultimately, it provides us with an anchor to who we are, where we are, and what we want.
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An ineffable disconnection from a sense of self is extensively reported in PTSD, such as “I am not myself,” and “I feel like an object, not a person” (Foa et al., 1999; Bluhm et al., 2009; Lanius et al., 2011, 2020). Experiences of deep emotion and perceptions of being terrestrially grounded, socially connected, and/or emotionally intuitive are often dulled or completely lost in trauma’s aftermath. Trauma engenders the sense that one’s body is not safe, is not under one’s own control, and/or is a cauldron of disgust and shame- particularly when it is chronic, interpersonal, and early in onset (Frewen and Lanius, 2015). Traumatogenic dissociative symptomology manifests as severe distortions in how the bodily self is perceived and experienced in relation to the outside world and often corresponds with trauma during critical periods of sensorimotor development (van der Hart et al., 2005; van der Kolk, 2005; Schmahl et al., 2010). Without adequate somatic sensory integration, we do not know where our body begins or where it ends; statements such as “I feel as if I am outside my body,” and “I feel like there is no boundary around my body,” highlight how alterations to the bodily self is a common experience in dissociative individuals
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Eye Movement Desensitization and Reprocessing (EMDR) therapy utilizes saccadic eye movements to elicit an innate relaxation response and integrate maladaptively stored trauma memories (Shapiro, 1995; Oren and Solomon, 2012). Although the mechanism behind EMDR’s therapeutic benefits remains unclear, oculomotor muscles have extensive reciprocal connections with the brainstem reticular formation, vestibular nuclei, and superior colliculi (Horn and Adamzyk, 2012; Harricharan et al., 2019) influencing arousal and multisensory integration. Reduced physiological arousal is reported during EMDR sessions (Aubert-Khalfa et al., 2008; Sack et al., 2008; Söndergaard and Elofsson, 2008), which then attenuates the intensity of negative affect (Oren and Solomon, 2012). Significant reductions in PTSD symptoms have been found in as few as three to eight sessions (Rothbaum, 1997; Wilson et al., 1997; Marcus et al., 2004) although longer durations are recommended for severe and chronic early life traumatization (van der Kolk et al., 2007).
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(not included in this study)
Key mechanisms behind forgetting trauma include:
State-dependent learning: Memories formed during high stress or altered states (e.g., fear, panic) are best retrieved when the brain returns to that same state. This can make traumatic memories inaccessible unless triggered by similar emotional or physiological conditions.
Altered brain function: Trauma affects key brain regions:
The amygdala (emotion and fear processing) becomes hyperactive.
The hippocampus (memory formation and context) may shrink or function poorly, impairing the ability to integrate traumatic events into a coherent narrative.
The prefrontal cortex (executive control) may show reduced activity, limiting emotional regulation and memory retrieval.
Memory distortion and amplification: While some memories are forgotten, others may be distorted or amplified—people may remember more trauma than occurred due to intrusive imagery or emotional re-experiencing, often seen in PTSD.
why now? why does it come back now? i don't know what triggered it. everything was normal and fine but suddenly at night i start crying because i couldnt stop thinking about it. i woke up the next day and it doesnt go away. why now? what caused this? no way it was random. i remembered my pre-psychosis. i'm too afraid of reaching that low again. i'm so scared of getting bad again. but what was i scared of? i'm having the same thoughts as before. is it going to be hard to live again? this is so sudden. i'm suddenly reminded that i feel pain and stress and dread. i suddenly remember life was hard barely a year ago. i thought everything was over. i thought i would never have to think about it again. i thought i was cured. now my head won't shut up and the split between my body and my mind is happening . again. i'm scared of writing and splitting like i did before. suddenly i'm reminded of fear. it's been less than 20 hours fighting against it and i'm already exhausted.
no bluesky eu postei:
madrugada de sexta, 6 de fevereiro
meu cerebro decide me lembrar da minha (pre)psicose de 3 anos atrás (apenas 2, namverdade). é como se eu tivesse recaído tudo de novo instantaneamente e sinto aquele pedacinho de insanidade que ainda existe em mim e se eu prestar atenção eu facilmente enlouqueço.
Por quê? Eu tava tão bem.
Preciso muito voltar a escrever, mas tenho medo de acontecer ne novo. Tenho medo do episódio bravo que eu tive enquanto escrevia. Eu sinto que se provocado ele volta. Tenho estado bem há quase 2 anos. Achei que tinha me trivado disso. Tem muitas coisas que eu escondo de mim mesmo. Meu dia foi bom;
apaguei quando acordei mas tirei print
espero que eu esteja mais forte do que antes
False trauma memories occur when individuals develop vivid, emotionally charged recollections of events that never happened. These are not deliberate lies but genuine beliefs formed due to memory distortions, often influenced by psychological, neurological, and social factors.
1. Associative Activation and Spreading Networks
People with PTSD or a history of trauma have highly interconnected emotional memory networks. When exposed to trauma-related cues, their brains rapidly activate associated concepts—even if those events weren’t experienced. This spreading activation can generate false memories. For example, someone with trauma might falsely recall "being cut" after hearing words like "knife" or "blood," due to strong internal associations.
isso me tranquiliza muito. memórias falsas realmente existem e não sou eu que sou uma exagerada. realmente não aconteceu. acho que achei uma resposta definitiva. nossa. que bom. mas por que isso? daonde veio esse medo tão extremo? que eventos minha cabeça está exagerando?
https://www.sciencedirect.com/science/article/abs/pii/S0165178122001500
In general, memories are prone to alterations, like insertions or deletions. After the retrieval or reactivation of a memory, it becomes labile and modifiable (Alberini, 2011; Nader et al., 2000). This implies that intrusions or flashbacks, which are characteristic for PTSD, could further modify memory contents. For example, Brewin et al. (2012) asked individuals with PTSD to write a narrative of their trauma. One week later, the participants were presented with words and phrases of these narratives, but also with words and phrases of the narrative of another person (foil stimuli). Some participants reported flashbacks during stimuli presentation that were other participants' narratives. This increased the probability that the foil stimuli were later inaccurately ascribed as part of their own narrative. Therefore, the question arises whether PTSD is associated with a tendency to form false memories, leading to the incorrect assumption that a certain stimulus had been experienced. As a consequence, individuals might be certain that the altered memory is how they experienced the situation (Bremner et al., 2000). Therefore, altered memories, especially false memories, might be a sustaining factor of PTSD, preventing habituation during re-experiencing the traumatic event.
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