Talk:Depersonalization: Difference between revisions

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==Neurological Analysis==

===Various neurobiological correlates===

"Like researchers quoted above, we endorse the view that depersonalization is a “hard wired” vestigial response for dealing with extreme anxiety combining a state of increased alertness with a profound inhibition of the emotional response system."

"In addition to its function as an emotional executive, the medial prefrontal cortex is also thought to be the seat of an emotion-working memory system that plays an important role in the conscious experience of emotions (Reiman et al 1997) (...) We propose that in depersonalization the above inhibitory mechanism (on the amygdala and possibly other structures of the emotional system) leads to a state of hypoemotionality and disables the process by means of which perception and cognition become emotionally colored. The latter will result in a “qualitative change” in the experiencing of perception and cognition, which is then reported by the subject as “unreal or detached”. One possibility is that these feelings of reduced emotional coloring are partially mediated (a` la James-Lange) by the marked reduction in autonomic output seen in depersonalization. Thus, there is evidence that emotional feelings are, at least partially, determined by awareness of the body changes brought about by emotional responses (LeDoux 1996; Damasio 1994). In nonemotional contexts (as occurs in the spontaneous onset of depersonalization), the same inhibitory mechanism will dampen the constant flow of body signals (i.e., body “background feelings”) that are thought to contribute to the experience of the self (Damasio 1994; Tye 1995). Such a reduction will lead to feelings of “not being there, or the feeling as if one didn’t have a body.”

"The “epilepsy model” of depersonalization has lingered on to the present day. For example, Locatelli et al (1993) reported temporal lobe electroencephalographic abnormalities in panic disorder patients with depersonalization as compared with those with panic disorder without depersonalization. In particular, patients with depersonalization showed increased slow activity and bilateral lack of fast alpha frequency response to odor stimulation. The validity of this finding is uncertain, however, as the same researchers were unable to replicate it (Locatelli et al 1995). In a single case study of a patient with ongoing depersonalization, Hollander et al (1992) reported theta activity and increased evoked potential negativities in left temporal areas suggesting temporal lobe dysfunction. Clinical associations have been reported between depersonalization and phenomena ordinarily related to the temporal lobes."

"From what has been said so far, it would seem that knowledge about the neurobiology of emotions may be an important element in the understanding of depersonalization. In this regard, converging evidence suggests that the amygdala, anterior cingulate, and medial prefrontal cortex are salient components of a parallel distributed network that integrates emotional responses (LeDoux 1994; Devinsky et al 1995). Indeed, converging evidence suggests that the amygdala plays a crucial role in assigning emotional significance to stimuli (Davis 1992; LeDoux 1992); this would not only determine type of emotional response but also “color” perceptual and cognitive experiences."

"Right or bilateral basal occipitotemporal lesions may also render patients incapable of experiencing feelings in response to visual stimuli. It has been proposed that such lesions disrupt the inferior longitudinal fasciculus, thereby disconnecting the visual association cortex (Broadmann

areas 18 and 19) from temporal limbic structures. As expected, narratives by these patients are redolent of those uttered by some depersonalized subjects"

"Also supporting the analogy of depersonalization with corticolimbic disconnections is the finding that feelings of unreality may be modality specific (Sierra and Berrios 1997), and the observation has been made that the visual modality is the most frequently affected (Mayer-Gross 1935; Schilder 1935). Mayer-Gross (1935) reported patients who “only derealized as to sight”, one noting that upon closing his eyes the experience of unreality disappeared: “If I close my eyes the world seems beautiful [again] and I am quite happy” (p 111). This latter feature suggests that the putative disconnection occurs at an early stage of emotional processing, i.e., at a stage at which the different modalities are still segregated. Since the amygdala is known to receive polymodal sensory input (Amaral 1992), it might be possible to predict that the disconnection should be between inferior temporal lobes and amygdala rather than between amygdala and other limbic structures (e.g., anterior cingulate). The same view can be held in regard to the Capgras phenomenon, where the delusion is often only maintained in the visual modality (Hirstein and Ramachandran 1997)."

Mind emptiness is explored. '''Good figure in this paper'''

===Additional neurobiology===

"Depersonalization can be induced in subjects not suffering from the disorder by means of a pharmacological challenge with tetrahydrocannabinol (THC) (3) or the partial serotonin agonist m-CPP (4). Attempts at localizing depersonalization, although not in depersonalization disorder per se (5–12), have yielded contradictory results regarding activation, laterality, and regional involvement."

"Some lines of evidence are consistent with this temporal lobe hypothesis of depersonalization. The epilepsy literature describes depersonalization with seizures. In a series of 32 cases, 11 manifested depersonalization, four with a left-sided focus, three with a right-sided focus, and four with general dysrhythmia (5). In another series of 71 epileptic patients in whom dissociative symptoms were quantified, depersonalization was most commonly induced by partial complex seizures, more so with left-sided foci,"

"The temporal lobe was subdivided into medial and lateral regions, each with five Brodmann’s areas. There was a significant group-by-hemisphere-by-region interaction and a significant group-by-hemisphere-by-region-byBrodmann’s area interaction (Table 2). Post hoc comparisons revealed that the depersonalization disorder group had significantly lower metabolic rates in area 22 of the right superior temporal gyrus (subjects with depersonalization disorder: mean=1.06, SD=0.06; healthy comparison subjects: mean=1.11, SD=0.06; t=2.24, df=30, p<0.05) and in area 21 of the middle temporal gyrus (subjects with depersonalization disorder: "

"The main findings of this first (to our knowledge) functional imaging study of depersonalization disorder point to metabolic abnormalities primarily in the posterior cortex. Subjects with depersonalization disorder differed in relative glucose metabolic rate from comparison subjects in portions of the sensory cortex in the temporal, parietal, and occipital lobes. These specifically included right temporal area 22 (auditory association area), parietal areas 7B (somatosensory association area) and 39 (multimodal association area), and left occipital area 19 (visual association area). Depersonalization disorder subjects were characterized by greater activity than comparison subjects in all these areas, with the exception of area 22, where activity was lower. Analyses of the relative glucose metabolic rate in whole brain sensory cortex confirmed an extensive pattern of significant between-group differences.

These data do not support the primacy of temporal lobe phenomena in depersonalization, described in the introduction (5, 6, 13, 14), but rather, they implicate more extensive associational brain networks, given the prominent occipital and parietal findings. The perceptual alterations that are hallmark symptoms of depersonalization primarily involve two sensory modalities, visual and somatosensory, although auditory disturbances can also be described. There is a hierarchy of sensory processing in the brain, from primary sensory areas to unimodal and then polymodal association areas and finally to the prefrontal cortex (27). Unimodal association areas showed more activity in depersonalization disorder subjects, both in occipital area 19 of the prestriate visual cortex and parietal area 7B, which is believed to be central to high-order integration within the somatosensory system (28). Dissociation and depersonalization scores showed a strong positive correlation with area 7B activity. Multimodal sensory integration occurs in the region of the parietal-temporal-occipital junction or the inferior parietal lobule (27, 29). Area 39, which corresponds to the angular gyrus and is implicated in somatosensory-visual-auditory integration, was again more active in depersonalization disorder subjects"<ref>Simeon, D., Guralnik, O., Hazlett, E. A., Spiegel-Cohen, J., Hollander, E., & Buchsbaum, M. S. (2000). Feeling unreal: a PET study of depersonalization disorder. American Journal of Psychiatry, 157(11), 1782-1788. https://doi.org/10.1176/appi.ajp.157.11.1782</ref>

'''Good figure in this paper (good neurology paper in general)'''

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

"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

with normal control subjects, when they were shown neutral scenes. Regions important for visual object and spatial perception middle and superior temporal gyri, and the inferior parietal lobe were also activated to a significantly greater extent in normal control subjects and OCD patients compared with depersonalized patients when they viewed the aversive scenes. These findings are similar to those of a previous study, in which depersonalized patients demonstrated reduced metabolism within middle and superior temporal gyri during performance of a variant of the California Verbal Learning Test (Simeon et al., 2000). Activation of occipito-temporal cortex has been demonstrated in the response to expressions of fear and disgust (Morris et al., 1996; Phillips et al., 1997), and to the same unpleasant scenes we used (Lane et al., 1997; Lang et al.,1998). The increased activation in these regions in both normal control subjects and OCD patients, in particular, middle and superior temporal gyri, may reflect the heightened visual attention and processing induced by aversive stimuli in these subjects but not the depersonalized patients. The normal control subjects also demonstrated significantly greater activation in bilateral anterior cingulate gyri and the left posterior cingulate gyrus in response to the aversive scenes compared with the depersonalized patients. These areas have been previously associated with the experience of negative mood (Mayberg et al., 1999) and emotional appraisal (Maddock, 1999), respectively."<ref>Phillips, M. L., Medford, N., Senior, C., Bullmore, E. T., Suckling, J., Brammer, M. J., ... & David, A. S. (2001). Depersonalization disorder: thinking without feeling. Psychiatry Research: Neuroimaging, 108(3), 145-160. https://doi.org/10.1016/S0925-4927(01)00119-6</ref>

===Skin conductive response measured emotional differences in response to stimuli===

"our findings support the view that depersonalization disorder is characterized by reduced emotional reactivity to emotional stimuli"<ref>Sierra, M., Senior, C., Dalton, J., McDonough, M., Bond, A., Phillips, M. L., ... & David, A. S. (2002). Autonomic response in depersonalization disorder. Archives of General Psychiatry, 59(9), 833-838. https://doi.org/10.1001/archpsyc.59.9.833</ref>

===Sensory integration dysfunction promotes feelings of unreality, with anxiety affecting some of these functions===

@@ Line 2: / Line 2: @@
 ==Neurological Analysis==
+===Various neurobiological correlates===
+"Like researchers quoted above, we endorse the view that depersonalization is a “hard wired” vestigial response for dealing with extreme anxiety combining a state of increased alertness with a profound inhibition of the emotional response system."
+"In addition to its function as an emotional executive, the medial prefrontal cortex is also thought to be the seat of an emotion-working memory system that plays an important role in the conscious experience of emotions (Reiman et al 1997) (...) We propose that in depersonalization the above inhibitory mechanism (on the amygdala and possibly other structures of the emotional system) leads to a state of hypoemotionality and disables the process by means of which perception and cognition become emotionally colored. The latter will result in a “qualitative change” in the experiencing of perception and cognition, which is then reported by the subject as “unreal or detached”. One possibility is that these feelings of reduced emotional coloring are partially mediated (a` la James-Lange) by the marked reduction in autonomic output seen in depersonalization. Thus, there is evidence that emotional feelings are, at least partially, determined by awareness of the body changes brought about by emotional responses (LeDoux 1996; Damasio 1994). In nonemotional contexts (as occurs in the spontaneous onset of depersonalization), the same inhibitory mechanism will dampen the constant flow of body signals (i.e., body “background feelings”) that are thought to contribute to the experience of the self (Damasio 1994; Tye 1995). Such a reduction will lead to feelings of “not being there, or the feeling as if one didn’t have a body.”
+"The “epilepsy model” of depersonalization has lingered on to the present day. For example, Locatelli et al (1993) reported temporal lobe electroencephalographic abnormalities in panic disorder patients with depersonalization as compared with those with panic disorder without depersonalization. In particular, patients with depersonalization showed increased slow activity and bilateral lack of fast alpha frequency response to odor stimulation. The validity of this finding is uncertain, however, as the same researchers were unable to replicate it (Locatelli et al 1995). In a single case study of a patient with ongoing depersonalization, Hollander et al (1992) reported theta activity and increased evoked potential negativities in left temporal areas suggesting temporal lobe dysfunction. Clinical associations have been reported between depersonalization and phenomena ordinarily related to the temporal lobes."
+"From what has been said so far, it would seem that knowledge about the neurobiology of emotions may be an important element in the understanding of depersonalization. In this regard, converging evidence suggests that the amygdala, anterior cingulate, and medial prefrontal cortex are salient components of a parallel distributed network that integrates emotional responses (LeDoux 1994; Devinsky et al 1995). Indeed, converging evidence suggests that the amygdala plays a crucial role in assigning emotional significance to stimuli (Davis 1992; LeDoux 1992); this would not only determine type of emotional response but also “color” perceptual and cognitive experiences."
+"Right or bilateral basal occipitotemporal lesions may also render patients incapable of experiencing feelings in response to visual stimuli. It has been proposed that such lesions disrupt the inferior longitudinal fasciculus, thereby disconnecting the visual association cortex (Broadmann
+areas 18 and 19) from temporal limbic structures. As expected, narratives by these patients are redolent of those uttered by some depersonalized subjects"
+"Also supporting the analogy of depersonalization with corticolimbic disconnections is the finding that feelings of unreality may be modality specific (Sierra and Berrios 1997), and the observation has been made that the visual modality is the most frequently affected (Mayer-Gross 1935; Schilder 1935). Mayer-Gross (1935) reported patients who “only derealized as to sight”, one noting that upon closing his eyes the experience of unreality disappeared: “If I close my eyes the world seems beautiful [again] and I am quite happy” (p 111). This latter feature suggests that the putative disconnection occurs at an early stage of emotional processing, i.e., at a stage at which the different modalities are still segregated. Since the amygdala is known to receive polymodal sensory input (Amaral 1992), it might be possible to predict that the disconnection should be between inferior temporal lobes and amygdala rather than between amygdala and other limbic structures (e.g., anterior cingulate). The same view can be held in regard to the Capgras phenomenon, where the delusion is often only maintained in the visual modality (Hirstein and Ramachandran 1997)."
+Mind emptiness is explored. '''Good figure in this paper'''
+===Additional neurobiology===
+"Depersonalization can be induced in subjects not suffering from the disorder by means of a pharmacological challenge with tetrahydrocannabinol (THC) (3) or the partial serotonin agonist m-CPP (4). Attempts at localizing depersonalization, although not in depersonalization disorder per se (5–12), have yielded contradictory results regarding activation, laterality, and regional involvement."
+"Some lines of evidence are consistent with this temporal lobe hypothesis of depersonalization. The epilepsy literature describes depersonalization with seizures. In a series of 32 cases, 11 manifested depersonalization, four with a left-sided focus, three with a right-sided focus, and four with general dysrhythmia (5). In another series of 71 epileptic patients in whom dissociative symptoms were quantified, depersonalization was most commonly induced by partial complex seizures, more so with left-sided foci,"
+"The temporal lobe was subdivided into medial and lateral regions, each with five Brodmann’s areas. There was a significant group-by-hemisphere-by-region interaction and a significant group-by-hemisphere-by-region-byBrodmann’s area interaction (Table 2). Post hoc comparisons revealed that the depersonalization disorder group had significantly lower metabolic rates in area 22 of the right superior temporal gyrus (subjects with depersonalization disorder: mean=1.06, SD=0.06; healthy comparison subjects: mean=1.11, SD=0.06; t=2.24, df=30, p<0.05) and in area 21 of the middle temporal gyrus (subjects with depersonalization disorder: "
+"The main findings of this first (to our knowledge) functional imaging study of depersonalization disorder point to metabolic abnormalities primarily in the posterior cortex. Subjects with depersonalization disorder differed in relative glucose metabolic rate from comparison subjects in portions of the sensory cortex in the temporal, parietal, and occipital lobes. These specifically included right temporal area 22 (auditory association area), parietal areas 7B (somatosensory association area) and 39 (multimodal association area), and left occipital area 19 (visual association area). Depersonalization disorder subjects were characterized by greater activity than comparison subjects in all these areas, with the exception of area 22, where activity was lower. Analyses of the relative glucose metabolic rate in whole brain sensory cortex confirmed an extensive pattern of significant between-group differences.
+These data do not support the primacy of temporal lobe phenomena in depersonalization, described in the introduction (5, 6, 13, 14), but rather, they implicate more extensive associational brain networks, given the prominent occipital and parietal findings. The perceptual alterations that are hallmark symptoms of depersonalization primarily involve two sensory modalities, visual and somatosensory, although auditory disturbances can also be described. There is a hierarchy of sensory processing in the brain, from primary sensory areas to unimodal and then polymodal association areas and finally to the prefrontal cortex (27). Unimodal association areas showed more activity in depersonalization disorder subjects, both in occipital area 19 of the prestriate visual cortex and parietal area 7B, which is believed to be central to high-order integration within the somatosensory system (28). Dissociation and depersonalization scores showed a strong positive correlation with area 7B activity. Multimodal sensory integration occurs in the region of the parietal-temporal-occipital junction or the inferior parietal lobule (27, 29). Area 39, which corresponds to the angular gyrus and is implicated in somatosensory-visual-auditory integration, was again more active in depersonalization disorder subjects"<ref>Simeon, D., Guralnik, O., Hazlett, E. A., Spiegel-Cohen, J., Hollander, E., & Buchsbaum, M. S. (2000). Feeling unreal: a PET study of depersonalization disorder. American Journal of Psychiatry, 157(11), 1782-1788. https://doi.org/10.1176/appi.ajp.157.11.1782</ref>
+'''Good figure in this paper (good neurology paper in general)'''
 ===Depersonalization may be a form of emotion processing disorder===
 "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
 with normal control subjects, when they were shown neutral scenes. Regions important for visual object and spatial perception middle and superior temporal gyri, and the inferior parietal lobe were also activated to a significantly greater extent in normal control subjects and OCD patients compared with depersonalized patients when they viewed the aversive scenes. These findings are similar to those of a previous study, in which depersonalized patients demonstrated reduced metabolism within middle and superior temporal gyri during performance of a variant of the California Verbal Learning Test (Simeon et al., 2000). Activation of occipito-temporal cortex has been demonstrated in the response to expressions of fear and disgust (Morris et al., 1996; Phillips et al., 1997), and to the same unpleasant scenes we used (Lane et al., 1997; Lang et al.,1998). The increased activation in these regions in both normal control subjects and OCD patients, in particular, middle and superior temporal gyri, may reflect the heightened visual attention and processing induced by aversive stimuli in these subjects but not the depersonalized patients. The normal control subjects also demonstrated significantly greater activation in bilateral anterior cingulate gyri and the left posterior cingulate gyrus in response to the aversive scenes compared with the depersonalized patients. These areas have been previously associated with the experience of negative mood (Mayberg et al., 1999) and emotional appraisal (Maddock, 1999), respectively."<ref>Phillips, M. L., Medford, N., Senior, C., Bullmore, E. T., Suckling, J., Brammer, M. J., ... & David, A. S. (2001). Depersonalization disorder: thinking without feeling. Psychiatry Research: Neuroimaging, 108(3), 145-160. https://doi.org/10.1016/S0925-4927(01)00119-6</ref>
+===Skin conductive response measured emotional differences in response to stimuli===
+"our findings support the view that depersonalization disorder is characterized by reduced emotional reactivity to emotional stimuli"<ref>Sierra, M., Senior, C., Dalton, J., McDonough, M., Bond, A., Phillips, M. L., ... & David, A. S. (2002). Autonomic response in depersonalization disorder. Archives of General Psychiatry, 59(9), 833-838. https://doi.org/10.1001/archpsyc.59.9.833</ref>
 ===Sensory integration dysfunction promotes feelings of unreality, with anxiety affecting some of these functions===