Talk:Depersonalization: Difference between revisions

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==Neurological Analysis==

===Depersonalization may be a form of emotion processing disorder===

"To date, there have been two functional neuroimaging studies in depersonalization. One was a resting state single photon emission computed tomography SPECT case study showing left fronto-temporal activation (Hollander et al., 1992). The authors interpreted this as evidence . for a common neurobiological basis for depersonalization and OCD, in which increased frontal activation has been associated with the urge to ritualize (Breiter et al., 1996). The second study employed positron emission tomography PET to measure metabolism during performance of a verbal learning task, and demonstrated reduced activity in superior and middle temporal gyri in depersonalized patients compared with healthy volunteers (Simeon et al., 2000). The authors suggested that these findings indicated underlying functional abnormalities in brain regions important for an intact body schema in depersonalization disorder. No study has employed functional magnetic resonance imaging (fMRI), or examined neural responses to emotionally salient stimuli in patients with depersonalization disorder.

In the current study we employed fMRI to demonstrate the neural response to standardized emotionally salient stimuli aversive scenes, used previously in neuroimaging studies (Lane et al., 1997; Lang et al., 1998 ) in six depersonalized patients, in contrast to that in healthy volunteers and patients with OCD."

"Healthy volunteers and OCD patients, but not the depersonalized patients, activated the insula in response to the aversive scenes, and statistical

contrasts between the depersonalized patients and the other groups were significant. This brain region has been implicated previously in the neural response to disgust (Phillips et al., 1997), other negative moods (Reiman et al., 1997; Mayberg et al., 1999) and unpleasant visceral sensations such as pain (Ploghaus et al., 1999). Paradoxically, this area was activated in the depersonalized patients, and to a significantly greater extent compared

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Line 13:

"Symptoms like “feeling as though in a dream,” “feeling of detachment or separation from surroundings,” and “feeling detached or separated from body” have been reported before as evidence for derealization due to the failure of the sensory integration. They occur most frequently and best distinguish patients with vestibular disorders from healthy subjects [10–12, 30]. However, interestingly, we did not find any significant difference in the reports of these symptoms made by healthy subjects and vestibular patients without anxiety (Table 3). Quite the contrary, these symptoms distinguish the vestibular patient group with anxiety from both the vestibular patients without anxiety and from healthy subjects. Another group of symptoms such as “body feels numb,” “numbing of emotions,” “thoughts seem blurred,” “events seem to happen in slow motion,” “your emotions seem disconnected from yourself,” “feel as though in a trance,” “feel confused or bewildered,” and “feel isolated from the world” also indicate a difference between vestibular patients with anxiety and the other two groups studied. The frequency and severity of all these Dp/Dr symptoms apparently are influenced by the presence of anxiety in the vestibular patients."<ref>Kolev, O. I., Georgieva-Zhostova, S. O., & Berthoz, A. (2014). Anxiety changes depersonalization and derealization symptoms in vestibular patients. Behavioural Neurology, 2014. https://dx.doi.org/10.1155%2F2014%2F847054</ref>

===DP correlates with burning out of a medical profession===

"This study confirms the ability of two single item measures of emotional exhaustion and depersonalization to provide important information on the likelihood of high burnout among physicians and medical students."

"This study’s main strength is its large sample size, inclusion of participants from a variety of practice settings including national samples of physicians and medical students, and the striking consistency of the results across samples. Our aggregate sample of 10,525 physicians and medical students compares favorably with the original MBI validation sample of 1,104 physicians and nurses."<ref>West, C. P., Dyrbye, L. N., Sloan, J. A., & Shanafelt, T. D. (2009). Single item measures of emotional exhaustion and depersonalization are useful for assessing burnout in medical professionals. Journal of general internal medicine, 24(12), 1318. https://doi.org/10.1007/s11606-009-1129-z</ref>

===Acute stress/trauma triggers this effect in a certain way + pharmacotherapy notes===

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Atypical (or second generation) antipsychotic drugs that block both dopamine (D2) and serotonin (5HT2A) receptors may be of use in treating complex trauma cases with “psychotic features” although the psychiatrist should carefully evaluate symptoms that appear to be abnormal perceptions taking into account the dissociative symptoms reported by the patient. Opioid antagonists have also shown some promise in the treatment of dissociative symptoms;1 the mu and kappa systems in particular have been implicated in symptoms of depersonalization and analgesia. Naltrexone, an opioid antagonist, has exhibited some effect in reducing symptoms of DDD.1,13,14"<ref>Gentile, J. P., Snyder, M., & Gillig, P. M. (2014). STRESS AND TRAUMA: psychotherapy and pharmacotherapy for depersonalization/derealization disorder. Innovations in clinical neuroscience, 11(7-8), 37. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204471/</ref>

===DP has been proposed as a defence mechanism for anxiety although there are some fundamental differences + neural correlates + emotional processing dysfunction + sensory integration dysfunction===

"Depersonalization has been shown to correlate with anxiety measures (Trueman, 1984), and patients with a diagnosis of DPD, a condition characterised by chronic depersonalization are often found to have high levels of anxiety (Baker et al., 2003). Additionally, it has been observed that the onset of depersonalization often coincides with stressing life-events or even life threatening situations. This has been interpreted as suggesting that depersonalization represents an anxiety triggered ‘hard wired’ inhibitory response intended to ensure the preservation of adaptative behaviour during situations normally associated with overwhelming and potentially disorganizing anxiety (Sierra & Berrios, 1998). It has been proposed that such inhibitory response is mediated by a fronto-limbic suppressive mechanism, which would generate a state of emotional numbing, and disable the process by means of which perception (including that of one’s own body), as well as cognition become emotionally coloured. Such ‘decolouring’ will result in a ‘‘qualitative change’’ of conscious awareness, which is then reported by the subject as ‘‘unreal or detached’’. In patients with DPD this response would become abnormally persistent and dysfunctional (Sierra & Berrios, 1998). Studies carried out during the last decade seem supportive of this model."

"the highest basal autonomic activity was observed in the chronic anxiety group (almost four times higher than observed in the depersonalization group), both groups had similarly high subjective anxiety. The authors concluded: ‘‘The evidence suggests that the discrepancy between subjective and objective signs of anxiety is the fundamental characteristic of patients with depersonalization. In physiological terms, anxiety is experienced but is not translated into defence reaction arousal’’ (Kelly & Walter, 1968)."

"These findings suggested the presence of both inhibitory and facilitatory mechanisms on autonomic arousal, which suggests a specific disruption in emotion processing rather than a non-specific dampening effect on autonomic reactivity."

"Interestingly, one of the most significant findings was that of an abnormally increased activation in the angular gyrus of the right parietal lobe, which correlated (r = 0.7) with ratings of depersonalization intensity. The potential significance of abnormal parietal functioning in depersonalization is further suggested by a recent open label trial using low frequency repetitive transcranial magnetic stimulation (TMS) on the right temporoparietal junction in 12 patients with DPD (Mantovani et al., 2010). It was found that after 3 weeks treatment half of the patients showed significant improvement"

"Experimental neuroimaging studies on the neural correlates of embodiment and agency feelings, have identified a network of parietal regions, which appear to play an important role in the generation of embodiment and agency feelings: the inferior parietal cortex, the temporoparietal junction, and the posterior insula. Increased activation in the angular gyrus has been observed in patients experiencing a lack of agency feelings regarding movement or the experience that movements are being controlled by an external agency (Farrer et al., 2004; Frith, Blakemore, & Wolpert, 2000)."

Etc.<ref>Sierra, M., & David, A. S. (2011). Depersonalization: a selective impairment of self-awareness. Consciousness and cognition, 20(1), 99-108. https://doi.org/10.1016/j.concog.2010.10.018</ref>

===The opioid system plays a role in the psychopathology of this disorder===

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Line 47:

Our data do not provide sufficient evidence to conclude whether the therapeutic effect of naloxone is only related to the blockade of the opioid receptors or to some other factors that affect the opioid system. In most patients, the positive action of naloxone developed during the first hours after the infusion and, in many, the improvement lasted more than 24 h. Because the half-life of naloxone is approximately 60 min, this suggests that naloxone increased the patients’ therapeutic sensitivity to the drugs that were previously not very effective for these particular patients"<ref>Nuller, Y. L., Morozova, M. G., Kushnir, O. N., & Hamper, N. (2001). Effect of naloxone therapy on depersonalization: a pilot study. Journal of Psychopharmacology, 15(2), 93-95. https://doi.org/10.1177%2F026988110101500205</ref>

===Marijuana intoxication induces this effect with no experience of anxiety or dysphoric mood===

"The physiological basis for anxiety and euphoria is believed to be increased levels of brain arousal (4648). Arousal refers to levels of generalized, diffuse activation of the brain mediated by the brain stem reticular activating system (49-51). The frontal lobe is believed to be the cortical representative of the arousal chain (52). Evidence from a variety of sources indicates that frontal blood flow may also be sensitive to levels of brain activation (53). Several lines of evidence support a THCinduced increase in brain activation. After marijuana smoking, the EEG shifts in favour of fast frequencies, especially over the frontal lobes (54, 55). After marijuana intoxication, cerebral blood flow shows a diffuse increase, especially over the frontal lobes (56). Although marijuana use increases brain arousal, the associated mood change is not one of dysphoria, but of euphoria. Excitement, although associated with increased brain arousal, is not always unpleasant. In the present study, post-THC increases in CBF were observed all over the cortex. However, the changes were most marked over the frontal lobes. As expected, marijuana intoxication correlated positively with most regional CBFs. When level of intoxication was included in the model, depersonalization showed a positive correlation with most brain regions, which reached the level of significance in two of them. This would support the notion that depersonalization is a mechanism triggered by increased activation levels."

"The mechanism of dissociation associated with depersonalization may, indeed, be related to malfunction of the anterior cingulate. According to Papez, the cingulate gyrus is the ‘seat of dynamic vigilance by which emotional experiences are endowed with an emotional consciousness.’ This brain region, which is transposed between the subcortical and cortical structures, may be responsible for integrating the subcortical and cortical mechanisms which contribute to the composite feeling of self."<ref>Mathew, R. J., Wilson, W. H., Chiu, N. Y., Turkington, T. G., DeGrado, T. R., & Coleman, R. E. (1999). Regional cerebral blood flow and depersonalization after tetrahydrocannabinol adrninistration. Acta Psychiatrica Scandinavica, 100(1), 67-75. https://doi.org/10.1111/j.1600-0447.1999.tb10916.x</ref>

===There was a very strong association between increasing dissociation severity and declining norepinephrine===

"Norepinephrine plays a central role in arousal, attention and emotional memory. In PTSD, basal catecholamine, noradrenergic challenge and receptor binding studies have revealed heightened noradrenergic tone, consistent with the hyperarousal and intrusive symptomatology characteristic of the disorder

(Southwick et al., 1999). In contrast, given the ‘shut-down’ symptomatology typically characteristic of dissociative states, one might predict autonomic hyporesponsivity"

"Within the dissociative group there was a very strong association between increasing dissociation severity and declining norepinephrine, independent of anxiety; indeed dissociation and anxiety were not intercorrelated. We speculate that this noradrenergic blunting might partly explain the hypoarousal, attentional difficulties and short-term memory deficits characteristic of depersonalization (Guralnik et al., 2000). Our finding is in good accordance with other reports describing autonomic physiologic blunting in dissociation (Griffin et al., 1997; Sierra et al., 2002). The present finding is also very similar to the single published study, to our knowledge, which has examined norepinephrine and dissociation (Delahanty et al., 2003). This study found that in the immediate aftermath of motor vehicle accidents, 15-h urinary norepinephrine was inversely correlated to the severity of peritraumatic dissociation."<ref>Simeon, D., Guralnik, O., Knutelska, M., Yehuda, R., & Schmeidler, J. (2003). Basal norepinephrine in depersonalization disorder. Psychiatry Research, 121(1), 93-97. https://doi.org/10.1016/S0165-1781(03)00205-1</ref>

===DP is inversely related with mindfulness and childhood trauma===

"In confirmation of our hypothesis, we found a strong negative relationship between DP severity and mindfulness. This pronounced connection between CDS-9 and MAAS is explained significantly by strong correlations with MAAS items concerning being on “autopilot,” which account for almost 40% of the variance of DP severity."

"With respect to the relevance of childhood adversities, we found a significant association between DP severity and emotional abuse and neglect in the nonpatients. This result is in line with findings from a mixed sample of patients with DP disorder and healthy controls, where emotional abuse was found to be specifically related to DP severity (Simeon et al., 2001). In this context, it is interesting that we also found a strong inverse correlation between emotional abuse/neglect during childhood and mindfulness in the nonpatient sample."<ref>Michal, M., Beutel, M. E., Jordan, J., Zimmermann, M., Wolters, S., & Heidenreich, T. (2007). Depersonalization, mindfulness, and childhood trauma. The Journal of nervous and mental disease, 195(8), 693-696. https://doi.org/10.1097/NMD.0b013e31811f4492</ref>

===References===

@@ Line 3: / Line 3: @@
 ==Neurological Analysis==
 ===Depersonalization may be a form of emotion processing disorder===
-"To date, there have been two functional neuroimaging studies in depersonalization. One was a resting state single photon emission computed tomography SPECT case study showing left fronto-temporal activation (Hollander et al., 1992). The authors interpreted this as evidence . for a common neurobiological basis for depersonalization and OCD, in which increased frontal activation has been associated with the urge to ritualize (Breiter et al., 1996). The second study employed positron emission tomography PET to  measure metabolism during performance of a verbal learning task, and demonstrated reduced activity in superior and middle temporal gyri in depersonalized patients compared with healthy volunteers (Simeon et al., 2000). The authors suggested that these findings indicated underlying functional abnormalities in brain regions important for an intact body schema in depersonalization disorder. No study has employed functional magnetic resonance imaging (fMRI), or examined neural responses to emotionally salient stimuli in patients with depersonalization disorder.
-In the current study we employed fMRI to demonstrate the neural response to standardized emotionally salient stimuli aversive scenes, used previously in neuroimaging studies (Lane et al., 1997; Lang et al., 1998 ) in six depersonalized patients, in contrast to that in healthy volunteers and patients with OCD."
 "Healthy volunteers and OCD patients, but not the depersonalized patients, activated the insula in response to the aversive scenes, and statistical
 contrasts between the depersonalized patients and the other groups were significant. This brain region has been implicated previously in the neural response to disgust (Phillips et al., 1997), other negative moods (Reiman et al., 1997; Mayberg et al., 1999) and unpleasant visceral sensations such as pain (Ploghaus et al., 1999). Paradoxically, this area was activated in the depersonalized patients, and to a significantly greater extent compared
@@ Line 17: / Line 13: @@
 "Symptoms like “feeling as though in a dream,” “feeling of detachment or separation from surroundings,” and “feeling detached or separated from body” have been reported before as evidence for derealization due to the failure of the sensory integration. They occur most frequently and best distinguish patients with vestibular disorders from healthy subjects [10–12, 30]. However, interestingly, we did not find any significant difference in the reports of these symptoms made by healthy subjects and vestibular patients without anxiety (Table 3). Quite the contrary, these symptoms distinguish the vestibular patient group with anxiety from both the vestibular patients without anxiety and from healthy subjects. Another group of symptoms such as “body feels numb,” “numbing of emotions,” “thoughts seem blurred,” “events seem to happen in slow motion,” “your emotions seem disconnected from yourself,” “feel as though in a trance,” “feel confused or bewildered,” and “feel isolated from the world” also indicate a difference between vestibular patients with anxiety and the other two groups studied. The frequency and severity of all these Dp/Dr symptoms apparently are influenced by the presence of anxiety in the vestibular patients."<ref>Kolev, O. I., Georgieva-Zhostova, S. O., & Berthoz, A. (2014). Anxiety changes depersonalization and derealization symptoms in vestibular patients. Behavioural Neurology, 2014. https://dx.doi.org/10.1155%2F2014%2F847054</ref>
+===DP correlates with burning out of a medical profession===
+"This study confirms the ability of two single item measures of emotional exhaustion and depersonalization to provide important information on the likelihood of high burnout among physicians and medical students."
+"This study’s main strength is its large sample size, inclusion of participants from a variety of practice settings including national samples of physicians and medical students, and the striking consistency of the results across samples. Our aggregate sample of 10,525 physicians and medical students compares favorably with the original MBI validation sample of 1,104 physicians and nurses."<ref>West, C. P., Dyrbye, L. N., Sloan, J. A., & Shanafelt, T. D. (2009). Single item measures of emotional exhaustion and depersonalization are useful for assessing burnout in medical professionals. Journal of general internal medicine, 24(12), 1318. https://doi.org/10.1007/s11606-009-1129-z</ref>
 ===Acute stress/trauma triggers this effect in a certain way + pharmacotherapy notes===
@@ Line 26: / Line 27: @@
 Atypical (or second generation) antipsychotic drugs that block both dopamine (D2) and serotonin (5HT2A) receptors may be of use in treating complex trauma cases with “psychotic features” although the psychiatrist should carefully evaluate symptoms that appear to be abnormal perceptions taking into account the dissociative symptoms reported by the patient. Opioid antagonists have also shown some promise in the treatment of dissociative symptoms;1 the mu and kappa systems in particular have been implicated in symptoms of depersonalization and analgesia. Naltrexone, an opioid antagonist, has exhibited some effect in reducing symptoms of DDD.1,13,14"<ref>Gentile, J. P., Snyder, M., & Gillig, P. M. (2014). STRESS AND TRAUMA: psychotherapy and pharmacotherapy for depersonalization/derealization disorder. Innovations in clinical neuroscience, 11(7-8), 37. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204471/</ref>
+===DP has been proposed as a defence mechanism for anxiety although there are some fundamental differences + neural correlates + emotional processing dysfunction + sensory integration dysfunction===
+"Depersonalization has been shown to correlate with anxiety measures (Trueman, 1984), and patients with a diagnosis of DPD, a condition characterised by chronic depersonalization are often found to have high levels of anxiety (Baker et al., 2003). Additionally, it has been observed that the onset of depersonalization often coincides with stressing life-events or even life threatening situations. This has been interpreted as suggesting that depersonalization represents an anxiety triggered ‘hard wired’ inhibitory response intended to ensure the preservation of adaptative behaviour during situations normally associated with overwhelming and potentially disorganizing anxiety (Sierra & Berrios, 1998). It has been proposed that such inhibitory response is mediated by a fronto-limbic suppressive mechanism, which would generate a state of emotional numbing, and disable the process by means of which perception (including that of one’s own body), as well as cognition become emotionally coloured. Such ‘decolouring’ will result in a ‘‘qualitative change’’ of conscious awareness, which is then reported by the subject as ‘‘unreal or detached’’. In patients with DPD this response would become abnormally persistent and dysfunctional (Sierra & Berrios, 1998). Studies carried out during the last decade seem supportive of this model."
+"the highest basal autonomic activity was observed in the chronic anxiety group (almost four times higher than observed in the depersonalization group), both groups had similarly high subjective anxiety. The authors concluded: ‘‘The evidence suggests that the discrepancy between subjective and objective signs of anxiety is the fundamental characteristic of patients with depersonalization. In physiological terms, anxiety is experienced but is not translated into defence reaction arousal’’ (Kelly & Walter, 1968)."
+"These findings suggested the presence of both inhibitory and facilitatory mechanisms on autonomic arousal, which suggests a specific disruption in emotion processing rather than a non-specific dampening effect on autonomic reactivity."
+"Interestingly, one of the most significant findings was that of an abnormally increased activation in the angular gyrus of the right parietal lobe, which correlated (r = 0.7) with ratings of depersonalization intensity. The potential significance of abnormal parietal functioning in depersonalization is further suggested by a recent open label trial using low frequency repetitive transcranial magnetic stimulation (TMS) on the right temporoparietal junction in 12 patients with DPD (Mantovani et al., 2010). It was found that after 3 weeks treatment half of the patients showed significant improvement"
+"Experimental neuroimaging studies on the neural correlates of embodiment and agency feelings, have identified a network of parietal regions, which appear to play an important role in the generation of embodiment and agency feelings: the inferior parietal cortex, the temporoparietal junction, and the posterior insula. Increased activation in the angular gyrus has been observed in patients experiencing a lack of agency feelings regarding movement or the experience that movements are being controlled by an external agency (Farrer et al., 2004; Frith, Blakemore, & Wolpert, 2000)."
+Etc.<ref>Sierra, M., & David, A. S. (2011). Depersonalization: a selective impairment of self-awareness. Consciousness and cognition, 20(1), 99-108. https://doi.org/10.1016/j.concog.2010.10.018</ref>
 ===The opioid system plays a role in the psychopathology of this disorder===
@@ Line 33: / Line 47: @@
 Our data do not provide sufficient evidence to conclude whether the therapeutic effect of naloxone is only related to the blockade of the opioid receptors or to some other factors that affect the opioid system. In most patients, the positive action of naloxone developed during the first hours after the infusion and, in many, the improvement lasted more than 24 h. Because the half-life of naloxone is approximately 60 min, this suggests that naloxone increased the patients’ therapeutic sensitivity to the drugs that were previously not very effective for these particular patients"<ref>Nuller, Y. L., Morozova, M. G., Kushnir, O. N., & Hamper, N. (2001). Effect of naloxone therapy on depersonalization: a pilot study. Journal of Psychopharmacology, 15(2), 93-95. https://doi.org/10.1177%2F026988110101500205</ref>
+===Marijuana intoxication induces this effect with no experience of anxiety or dysphoric mood===
+"The physiological basis for anxiety and euphoria is believed to be increased levels of brain arousal (4648). Arousal refers to levels of generalized, diffuse activation of the brain mediated by the brain stem reticular activating system (49-51). The frontal lobe is believed to be the cortical representative of the arousal chain (52). Evidence from a variety of sources indicates that frontal blood flow may also be sensitive to levels of brain activation (53). Several lines of evidence support a THCinduced increase in brain activation. After marijuana smoking, the EEG shifts in favour of fast frequencies, especially over the frontal lobes (54, 55). After marijuana intoxication, cerebral blood flow shows a diffuse increase, especially over the frontal lobes (56). Although marijuana use increases brain arousal, the associated mood change is not one of dysphoria, but of euphoria. Excitement, although associated with increased brain arousal, is not always unpleasant. In the present study, post-THC increases in CBF were observed all over the cortex. However, the changes were most marked over the frontal lobes. As expected, marijuana intoxication correlated positively with most regional CBFs. When level of intoxication was included in the model, depersonalization showed a positive correlation with most brain regions, which reached the level of significance in two of them. This would support the notion that depersonalization is a mechanism triggered by increased activation levels."
+"The mechanism of dissociation associated with depersonalization may, indeed, be related to malfunction of the anterior cingulate. According to Papez, the cingulate gyrus is the ‘seat of dynamic vigilance by which emotional experiences are endowed with an emotional consciousness.’ This brain region, which is transposed between the subcortical and cortical structures, may be responsible for integrating the subcortical and cortical mechanisms which contribute to the composite feeling of self."<ref>Mathew, R. J., Wilson, W. H., Chiu, N. Y., Turkington, T. G., DeGrado, T. R., & Coleman, R. E. (1999). Regional cerebral blood flow and depersonalization after tetrahydrocannabinol adrninistration. Acta Psychiatrica Scandinavica, 100(1), 67-75. https://doi.org/10.1111/j.1600-0447.1999.tb10916.x</ref>
+===There was a very strong association between increasing dissociation severity and declining norepinephrine===
+"Norepinephrine plays a central role in arousal, attention and emotional memory. In PTSD, basal catecholamine, noradrenergic challenge and receptor binding studies have revealed heightened noradrenergic tone, consistent with the hyperarousal and intrusive symptomatology characteristic of the disorder
+(Southwick et al., 1999). In contrast, given the ‘shut-down’ symptomatology typically characteristic of dissociative states, one might predict autonomic hyporesponsivity"
+"Within the dissociative group there was a very strong association between increasing dissociation severity and declining norepinephrine, independent of anxiety; indeed dissociation and anxiety were not intercorrelated. We speculate that this noradrenergic blunting might partly explain the hypoarousal, attentional difficulties and short-term memory deficits characteristic of depersonalization (Guralnik et al., 2000). Our finding is in good accordance with other reports describing autonomic physiologic blunting in dissociation (Griffin et al., 1997; Sierra et al., 2002). The present finding is also very similar to the single published study, to our knowledge, which has examined norepinephrine and dissociation (Delahanty et al., 2003). This study found that in the immediate aftermath of motor vehicle accidents, 15-h urinary norepinephrine was inversely correlated to the severity of peritraumatic dissociation."<ref>Simeon, D., Guralnik, O., Knutelska, M., Yehuda, R., & Schmeidler, J. (2003). Basal norepinephrine in depersonalization disorder. Psychiatry Research, 121(1), 93-97. https://doi.org/10.1016/S0165-1781(03)00205-1</ref>
+===DP is inversely related with mindfulness and childhood trauma===
+"In confirmation of our hypothesis, we found a strong negative relationship between DP severity and mindfulness. This pronounced connection between CDS-9 and MAAS is explained significantly by strong correlations with MAAS items concerning being on “autopilot,” which account for almost 40% of the variance of DP severity."
+"With respect to the relevance of childhood adversities, we found a significant association between DP severity and emotional abuse and neglect in the nonpatients. This result is in line with findings from a mixed sample of patients with DP disorder and healthy controls, where emotional abuse was found to be specifically related to DP severity (Simeon et al., 2001). In this context, it is interesting that we also found a strong inverse correlation between emotional abuse/neglect during childhood and mindfulness in the nonpatient sample."<ref>Michal, M., Beutel, M. E., Jordan, J., Zimmermann, M., Wolters, S., & Heidenreich, T. (2007). Depersonalization, mindfulness, and childhood trauma. The Journal of nervous and mental disease, 195(8), 693-696. https://doi.org/10.1097/NMD.0b013e31811f4492</ref>
 ===References===
 <references />