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Thread: PTSD ,Out of Darkness Into The Sun: My Recovery

  1. #11
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    Neuroendocrinology
    PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, which creates deep neurological patterns in the brain. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations.[49][56] During traumatic experiences the high levels of stress hormones secreted suppress hypothalamic activity which may be a major factor towards the development of PTSD.[57]

    PTSD causes biochemical changes in the brain and body that differ from other psychiatric disorders such as major depression. Individuals diagnosed with PTSD respond more strongly to a dexamethasone suppression test than individuals diagnosed with clinical depression.[58][59]

    In addition, most people with PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine,[60] with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.[61] This is in contrast to the normative fight-or-flight response, in which both catecholamine and cortisol levels are elevated after exposure to a stressor.[62]

    Brain catecholamine levels are high,[63] and corticotropin-releasing factor (CRF) concentrations are high.[64][65] Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.

    The HPA axis is responsible for coordinating the hormonal response to stress.[28] Given the strong cortisol suppression to dexamethasone in PTSD, HPA axis abnormalities are likely predicated on strong negative feedback inhibition of cortisol, itself likely due to an increased sensitivity of glucocorticoid receptors.[66] Some researchers have associated the response to stress in PTSD with long-term exposure to high levels of norepinephrine and low levels of cortisol, a pattern associated with improved learning in animals.[citation needed]

    Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis.[67]

    Low cortisol levels may predispose individuals to PTSD: Following war trauma, Swedish soldiers serving in Bosnia and Herzegovina with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms, following war trauma, than soldiers with normal pre-service levels.[68] Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained—that is, longer and more distressing—response, setting the stage for PTSD.

    Other studies indicate that people that suffer from PTSD have chronically low levels of serotonin which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity.[18] Serotonin also contributes to the stabilization of glucocorticoid production.

    Dopamine levels in patients with PTSD can help contribute to the symptoms associated. Low levels of dopamine can contribute to anhedonia, apathy, impaired attention, and motor deficits. Increased levels of dopamine can cause psychosis, agitation, and restlessness.[18]

    Hyperresponsiveness in the norepinephrine system can be caused by continued exposure to high stress. Overactivation of norepinephrine receptors in the prefrontal cortex can be connected to the flashbacks and nightmares frequently experienced by those with PTSD. A decrease in other norepinephrine functions (awareness of the current environment) prevents the memory mechanisms in the brain from processing that the experience, and emotions the person is experiencing during a flashback are not associated with the current environment.[18]

    However, there is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relationship between cortisol levels and PTSD. However the majority of reports indicate people with PTSD have elevated levels of corticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone.[28][69]

    Neuroanatomy

    Regions of the brain associated with stress and posttraumatic stress disorder[70]
    Three areas of the brain in which function may be altered in PTSD have been identified: the prefrontal cortex, amygdala, and hippocampus. Much of this research has utilised PTSD victims from the Vietnam War. For example, a prospective study using the Vietnam Head Injury Study showed that damage to the prefrontal cortex may actually be protective against later development of PTSD.[71] In a study by Gurvits et al., combat veterans of the Vietnam War with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans who suffered no such symptoms.[72] This finding could not be replicated in chronic PTSD patients traumatized at an air show plane crash in 1988 (Ramstein, Germany).[73][74]

    In human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD.[75] However during high stress times the hippocampus, which is associated with the ability to place memories in the correct context of space and time, and with the ability to recall the memory, is suppressed. This suppression is hypothesized to be the cause of the flashbacks that often plague PTSD patients. When someone with PTSD undergoes stimuli similar to the traumatic event the body perceives the event as occurring again because the memory was never properly recorded in the patients memory.[28]

    The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus particularly during extinction.[76] This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.[76][77] A study at the European Neuroscience Institute-Goettingen (Germany) found that fear extinction-induced IGF2/IGFBP7 signalling promotes the survival of 17–19-day-old newborn hippocampal neurons. This suggests that therapeutic strategies that enhance IGF2 signalling and adult neurogenesis might be suitable to treat diseases linked to excessive fear memory such as PTSD.[78] Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.

    The maintenance of the fear involved with PTSD has been shown to include the HPA axis, the locus coeruleus-noradrenergic systems, and the connections between the limbic system and frontal cortex. The HPA axis which coordinates the hormonal response to stress[79] which activates the LC-noradrenergic system is implicated in the over consolidation of memories that occurs in the aftermath of trauma.[80] This over consolidation increases the likelihood of developing PTSD. The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a threat.[28]

    The LC-noradrenergic system has been hypothesized to mediate the over-consolidation of fear memory in PTSD. High levels of cortisol reduces noradrenergic activity it is proposed that individuals with PTSD fail to regulate the increased noradrenergic response to traumatic stress.[81][clarification needed] It is thought that the intrusive memories and conditioned fear responses to associated triggers is a result of this response. Neuropeptide Y has been reported to reduce the release of norepinephrine and has been demonstrated to have anxiolytic properties in animal models. Studies have shown people with PTSD demonstrate reduced levels of NPY, possibly indicating their increased anxiety levels.[28]

    The basolateral nucleus (BLA) of the amygdala is responsible for the comparison and development of associations between unconditioned and conditioned responses to stimuli which results in the fear conditioning present in PTSD. The BLA activates the central nucleus (CeA) of the amygdala which elaborates the fear response, (including behavioral response to threat and elevated startle response). Descending inhibitory inputs from the medial prefrontal cortex (mPFC) regulate the transmission from the BLA to the CeA which is hypothesized to play a role in the extinction of conditioned fear responses.[28]

  2. #12
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    Today is a therapy day. Yay! I'm pretty happy about it. It was a month since the last one.

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    Therapies I have done,
    CBT
    EXPOSURE THERAPY
    TALK THERAPY
    EMDR
    SOMATIC EXPERIENCING

    Phase 1: Achieving patient safety, reducing symptoms and increasing competencies
    This is the skills building phase and clinicians can use any evidence based therapy that has outcomes of improving emotion regulation, increasing distress tolerance, mindfulness, interpersonal effectiveness, cognitive restructuring, behavioral changes, and relaxation. This phase can also help move someone out of crisis to prepare for the next phase.

    Phase 2: Review and reappraisal of trauma memories
    There are different techniques for doing this, and they are described below, but the success of this phase hinges on someone’s ability to tolerate the discomfort of reviewing the memories. People with single incident trauma may be ready to withstand exposure with minimal distress tolerance training, while people with complex trauma may need months of skills building support in order to be ready to process their trauma.

    Phase 3: Consolidating the gains
    The therapist is helping the client apply new skills and adaptive understanding of themselves and their trauma experience. This phase can also include “booster” sessions to reinforce skills, increase professional and informal support systems, and create an ongoing care plan.

    Exploring One’s Trauma in Psychotherapy

    There are several different ways to explore one’s trauma:

    Exposure therapies

    The military has used Prolonged Exposure therapy for years to have the individual talk through the traumatic event over and over until the event is no longer activating. An evidence-based practice for children and adolescents is Trauma-Focused Cognitive Behavioral Therapy, which uses a trauma narrative to expose the individual to their trauma for the same result. Also, Cognitive Processing Trauma can sometimes include a trauma narrative.

    Exposure can be done all at once, called “flooding,” or gradually to build up tolerance, called “desensitization.”
    Trauma narratives can be done verbally, or with images or other forms of art.
    These therapies are most recommended for individuals who have experienced a single incident, or perhaps experienced several incidents but don’t have any other mental health complications.
    Reprocessing

    On SAMHSA’s National Registry of Evidence-Based Programs and Practices, Eye Movement Desensitization and Reprocessing (EMDR) is the only intervention that allows an individual to reprocess memories and events. Reprocessing means that an individual accesses the relevant memory and uses dual awareness with bilateral stimulation and images, thoughts, emotions and body sensations to move through the traumatic experiences that aren’t resolved. If storing memories is like putting away groceries, a traumatic event was stored by shoving a bunch of stuff in a cabinet and then any time it gets opened all the stuff falls on your head. EMDR allows you to pull everything out in a controlled manner and then put it away in the organized way that non-traumatic memories are stored.

    EMDR is highly recommended for individuals who have developmental or complex trauma, but also has evidence-based protocols for single incident trauma.
    EMDR has 8 phases of treatment, the first three of which don’t involve any bilateral stimulation, and are more about skills-building and resourcing in preparation for the processing phases.
    Somatic Therapies

    Therapies that use the body to process trauma are cutting edge and so far none of them are considered evidence based due to lack of research. Probably the most popular is Somatic Experiencing, based on Peter Levine’s observations of animals’ recovery from traumatic events. Another model is Sensorimotor Psychotherapy, which also uses the body to work through trauma.

    While all of the above treatments are designed to be used individually, most of them can be delivered in a group setting as well. Group therapy can be helpful for many people who have experienced trauma, since simply having experienced the type of event that can produce trauma symptoms can be isolating. Group members can help normalize a lot of the reactions and feelings that someone has.

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    So ,yeah I know what I want to discuss in therapy today. I can recognize more easily when my brain is really agitated. I can recognize when people are trying to gaslight me as opposed to I am just reacting. I can more easily deescalate a situation inside myself and with other people.

    That I'm not entirely responsible for the triggers but I am responsible for how I react to them. I cannot totally hide myself away from every single trigger but I can alter how I react. I am responsible for how I react.

    I am understanding more there has to be a boundary when my brain feels really agitated. And I need to articulate properly when I'm agitated. I need to tell people," I am agitated please just leave me be for the time being.This has nothing to do with you I am just very agitated. I need a timeout or I cannot act properly."

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    It is also exceedingly hard to articulate when I'm very agitated. So I have to do it before I get to that point. I just don't want people to take it as rejection because it's not. I just want them to understand that 99% of the time I am agitated. I am always at a heightened level ,waiting for that fight come my way. So my brain is almost in a permanent state of agitation 24/7 since I can ever remember. Most of the time I can control the agitation. And it is really hard to describe the physical sensations. It is almost like I can feel my brain tingling, the whole outside of it. That is when I know it is time for people to back off.

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    Counseling went really well today! She said with all the progress that I'm making and how much I figured myself out I've become my own counselor. Hahaha!
    But she did say that residential programme would help me to lean on myself more. I could learn to totally believe in myself and not need other people as much for emotional support.

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    [video=youtube_share;VrjYwl9sgow] ]

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    [video=youtube_share;byQBP7fq5vQ] ]

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    I was waiting to do the group therapy sessions again like I did a year and a half ago. Well they are finally available but they are on Friday mornings and I work on Friday mornings. I guess I will have to wait until the next session comes around.

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    [video=youtube_share;fYiZwSwdZTw]

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