David S. Kozin

This is my workspace. I have until Monday to complete my HPPD series of papers. When complete, my faculty will call Dr. Henry David Abraham to be my formal reviewer and oral examination outside expert. So close...

HPPDonline.com used to be a first hit for Google, but I have made a few changes. Number 1: I made this board so items cannot be searched by google so our posts are not cached and owned elsewhere. So, the topics are not being recorded by Google Bots. HOWEVER, I do have Google Advertising money and there are other ways to do this. If anyone wants to take the Search engine optimization project as their own, I will work with you to make it listed up at top. The Erowid's are keeping the site on theirs and wikipedia continues to list it as well. Creating HPPD pages and domains pointing to this site, talking to other similar web site owners, and if our members agree to allow for advertisements/etc.... we can increase visibility. Trust me, there are doctors and researchers that are visiting and I know some are members. It will just take time, and if individuals participate in creating blogs/galleries and increasing hits and connections to web sites we can get this one back up. Thanks for the thoughts! David

Dear Community, I have a few minutes until I have a meeting with my faculty, but I wanted to make a quick message. The message board has been updated, and you should notice a new side bar that will help navigate updates to the web site. Additionally, Guest users are now no longer able to see certain sections that I want protected information for HPPD sufferers. I have upgraded a few accounts to become Administrators of the message board. Some other members can send me a message if interested in Moderating a specific area. Additionally, to protect the community I have a member reviewing the aspects of the software. Please, for the sake of the community, try to keep discussion of information on research or other treatments private if you are advised to do so. This is for safety reasons for the community and to ensure research continues. I expect my comprehensive series of papers on HPPD to be bound and published May 11th. Additionally, I hope to a have an audio or video tape of my oral exams that will include Dr. Henry David Abraham. I will be VERY AVAILABLE after graduation and working to build up this board. Lastly,. I am having non-HPPD individuals involved in the operation of the board to have non-biased reviews to ensure that the members are true to either understanding this complex set of disorders, and any members trying to sabotage the community will be removed. Be aware that some individuals may ask for information from you and not do so in good faith. If you are asked to be part of research or someone is asking questions you are uncomfortable with answering: PLEASE CONTACT ME AT HPPD@ME.COM. I will reply. I will set up an e-mail address for the Admins and Moderators. My best wishes, David Kozin, B.Sc. (May 11) Psychology/Neurophysiology

[ Wow Eric, I love your work! Thank you so much for sharing. I just "STARTED" my blog at blog.davidkozin.com, but have yet to play with it or add content. If anyone is a wordpress wizard and can pass a standard background check (or I already know you), I would love help with my work. My twitter page is slowly gathering reporters from Time Magazine, and I am getting press requests because of the MDMA research (I expect most of you will think it controversial, but it was based on a good science)... Visit and Support: erictiedt.blogspot.com quote name='eric' timestamp='1301328058' post='874'] ok let me start. thats my blog.i do some illustrations. erictiedt.blogspot.com in my worst hppd time i lost the good feelings i once had towards painting and being creative. but now as i get better(thanks to keppra) i step by step rediscover them. cheers, eric

Dan, 21, was home from college in the middle of the winter, having dropped out after a miserable year and a half. His problems had begun about three years before, shortly after period of drug experimentation which had included three LSD trips. A few weeks after his final trip, newly abroad as an exchange student, he began experiencing spontaneous visual hallucinations including moving "dots" in the visual field, afterimages or "blurs" of moving objects, a sense of being able to "see the air," and other phenomena described by Abraham in 1983 (see also DSM-IV, pp.233-4) as "post-hallucinogen perception disorder." Neither his hosts nor the European physicians he eventually saw had any clue about what was wrong, and Dan sensed that they were beginning to think he was a hypochondriac, so he stopped complaining and endured this problem on his own for a year, fearing for his sanity. Not until he started college back in the U.S. did he find his way to a neurologist and eventually to Abraham himself, who made the definitive diagnosis and found "persistent activation of the right posterior temporal area" after visual evoked response testing. [The electrical activity in the brain's visual cortex, generated in response to a test stimulus, did not die away within the expected amount of time, but kept on going for much longer.] The symptoms were managed with clonazepam [trade name Klonopin, a potent relative of the familiar Valium] on the theory that their neurologic basis might resemble siezure activity. Dan seemed to require high and ever-increasing dosages, and became withdrawn and depressed. He stopped functioning in school and socially, drank alcohol more heavily, and, when he realized what was happening to him, finally decided to come home. My suspicion, when I began working with Dan, was that the clonazepam was a major contributor to his depression. But my initial efforts to taper the dose, while working in conventional psychotherapy on developmental issues behind his sense of being punished by his perceptual affliction, met with resistance and a florid worsening of the visual symptoms. Then, four months into the work, came the session when I spontaneously sat next to him on the couch, looking out the office window at a clear blue sky, and asked him to describe what he saw. As he began I tried to "suspend" my habitual state of consciousness and see whether any of his "hallucinations" were visible to me. To my surprise, I was immediately able to see irregular linear shapes floating slowly across the visual field. When I blinked, they would change shape or position. I began describing this to Dan in great detail so that he would have no doubt that I was not simply repeating his descriptions, but actually having my own similar experiences. Clearly, these "shooters" seemed to be generated by something on the surface of the eye to which we don't normally attend. I invite the reader to try this for him- or herself. In this and a few succeeding sessions I was able to experience with Dan most of the phenomena of his illness, including visual "trails" of moving objects, various line-shape illusions such as level bookshelves slanting, "aeropsia" (a sense of bright whiteness in the air between us and observed objects), and "dancing bright spots" originating between the letters and words on a printed page. With minimal information from him, I could describe these convincingly, at times even completing his sentences. We both found this a strangely exhilarating activity. It was clear to me, however, that I did not experience these visual phenomena as intensely and persistently as did he, and that I could ignore them at will. Whatever the physiological mechanism of this disorder may be, it is obvious that functionally a failure of a normal pre-conscious "editing" process was occurring, whereby additional irrelevant aspects of raw perceptual experience were reaching consciousness. Dan reported a great sense of relief and "normalization" as a result of these few sessions. Tapering of his clonazepam was now accomplished with relative ease down to a very minimal dosage. Predictably, the major depressive symptoms resolved. There was much else to talk about in a year of therapy, but we both agreed, and still agree several years later, that our perceptual experiment was the turning point. Before our mutual experiences, the symptoms "meant" that Dan was crazy, different from other people, alone forever in a distorted visual universe. This triggered a vicious cycle, or "positive feedback loop," in which Dan’s anxiety about this situation served to amplify the symptoms in his conscious awareness and continually re-focus his attention upon them. Thus the ordinary distractions of everyday experience were unable to perform their potentially useful role, powerless to divert him from an "illness" which became the center of his life and, expectably, a crystal nidus for fantasies of punishment which sprang from their usual developmental lairs. He was quite capable of understanding the sources of this hitherto-latent shame, but this did not impact his perceptual distortions one whit. After the "normalization," though, Dan had only the symptoms themselves with which to contend, and not the snowballing anxiety and sense of retribution. He became more distractible in the healthy sense, his conscious attention freer to roam, or focus elsewhere (studies, relationships). And through the experience (and perhaps, I'll allow, as a result of our developmental work as well-- sudden "miracles" usually have some amount of groundwork preceding them) he had found his way to a more thoroughgoing self-acceptance. Dan returned to a different college, did very well, and got his degree. He now works in the mental health field. For the past seven years the same low dose of clonazepam has been necessary, but with it, except in times of extreme stress or physical fatigue, he is rarely bothered by visual symptoms. A case of "post-hallucinogen perception disorder" by Paul Genova, M.D. (Adapted from author, The Thaw: 24 Essays in Psychotherapy; Pittsburgh: Dorrance Publishing Co., 2000, pp. 17-19. Used with permission from the author.) kozin 8032B.pdf

Proud member of a community of talented people sharing a common perception of our world since 1998. Cheers! David

"We begin today's program on psychedelics with a young man, David. He says his use of LSD and the club drug ecstasy, properly called MDMA, or methylenedioxy-n-methylamphetamine has left him literally unable to see straight. DAVID: I was mainly using ecstasy once every two weeks. There is a certain type of pill, they're called Lucky Sevens. I took them, and the next morning when I woke up, my vision was completely different. I mean, I can see objects, it's just my vision's now blurry. I had 20/20 vision, and up till later, I can't read street signs that are at a distance. And, you know, driving at night is a problem for me. You know, it's difficult to, you know, tell an employer or a family member, `I'm sorry, I can't drive tonight because I hallucinate all the time because I used to take a bunch of drugs when I was young.' A way to describe hallucinogen persisting perception disorder is if you're in a room and there's a breeze coming through and your window or shades are moving and your clothes are moving because of the breeze, imagine that without having any wind coming through and having that constantly. So it's like everything's in a breeze, constantly moving. The studio I'm in is not HPPD friendly. As I sit here, I just--the entire room is constantly shifting, the shadows are creeping in, clock is moving, the black speaker in front of me that's turning to a purplish color. That's very common for me, having black turn to purple. We have what we call trails. People who've taken LSD are very--understand this, is if you wave objects past you, that object leaves a visual translucent trail of itself behind, and so a-- as people move throughout, out the window, I see trails of their bodies. The one thing I wish I could do, the one thing that makes me the craziest, is I would like to be able to look at a blank--like a solid cud--color wall and not have it change colors, not have it shift, not have it do anything, just have it be plain black, plain red, plain pink, plain something, but not have it sparkle, or not have it have static over it or not be able to see patterns and see faces in it, just have it be a blank wall.” From the transcript of guest, David S. Kozin, from syndicated radio show, The Infinite Mind, National Public Radio, 2003.

Oops, the section was available in barebones but no user group had permissions to use it. I opened it up and moved around the categories. Thanks Jay, David

Functional Segregation of Visual Inputs to the LGN The primary ganglion cells involved in visual perception with projections mapped to the lateral geniculate nucleus (LGN) are: The midget ganglion cells. Small receptive fields Project to layers 3–6 of the parvocellular LGN. L2V1.pdf The parasol cells Extensive receptive fields Project to layers 1 and 2 of the magnocellular LGN The bistratified ganglion projects to the koniocellular layers of the LGN. The parvocellular system (P-pathway) is a static firing system that conveys information from the retina to the LGN concerning wavelength selectivity and low-contrast retinal imagery with high spatial resolution High band-pass resolution perimetry (ring perimetry) is an attempt to selectively evaluate the P-pathway In contrast, the magnocellular system (M-pathway) conveys high-contrast, low-resolution information that is color blind. The magnocellular system is a phasic system, thus is well suited for the analysis of moving stimuli. Perimetric techniques, such as frequency-doubled perimetry and motion-detection automated perimetry, are used in an attempt to isolate the M-pathway. The koniocellular system (K-pathway) conveys information concerning blue-yellow color opponency. The visual cortex in the macaque was initially divided into six sub-regions named visual areas 1–6 (Areas V1–V6). Area V1 is the primary visual cortex, and it corresponds to the striate cortex in both humans and lower primates. Areas V2–V6 are extensively interconnected visual areas that lie anterior to V1 and contain specialized maps of the visual field. Based on numerous studies of lesions in humans, functional imaging of normal subjects, and experiments in monkeys, it is clear that the information processed by the striate cortex and visual associative areas is projected through two occipitofugal pathways: a ventral occipitotemporal pathway and a dorsal occipitoparietal pathway. The ventral pathway, often called the “what” pathway, is involved in processing the physical attributes of a visual image that are important to the perception of color, shape, and pattern. These, in turn, are crucial for object identification and object-based attention. The ventral pathway originates in V1 and projects through V2 and V4 to specific inferior temporal cortical areas, the angular gyrus, and limbic structures. It provides visual information to areas involved in visual identification, language processing, memory, and emotion. Thus, a lesion in this pathway may cause a variety of associative defects, including visual alexia and anomia, visual agnosia, visual amnesia, and visual hypoemotionality. The dorsal, or “where” pathway, begins in V1 and projects through V2 and V3 to V5. From V5, this pathway continues to additional areas in the parietal and superior temporal cortex. These projections are involved in visuospatial analysis, in the localization of objects in visual space, and in modulation of visual guidance of movements toward these objects. Thus, lesions of this pathway may cause a variety of visuospatial disorders, such as Bálint’s syndrome and hemispatial neglect. Although the ventral and dorsal pathways are clearly involved in the analysis of different aspects of the visual environment, they are extensively interconnected laterally and in feedback and feed forward directions, indicating that the flow of perceptual processing does not necessarily proceed in a stepwise, hierarchic manner. This “what” and “where” dichotomy of visual processing is an oversimplification of how these cortical areas function, but it serves as a useful framework in which to develop a clinical model of cortical visual processing. A number of specific syndromes in humans involving the central processing of visual information can be localized primarily to one of the six visual cortical areas or one of the two occipitofugal pathways and thus are of clinical value. These are discussed below. Both primate and human studies have demonstrated that area V2 may play a role in the detection of illusionary contours. This perceptual task is of great importance in the detection of obscured objects, such as a camouflaged predator. Patients with early posterior Alzheimer’s disease demonstrate impaired detection of illusionary contours, possibly due to degeneration of area V2. The reticular nucleus is of particular interest here because it is thought to serve as a sort of gate for processing signals to the cortex. Synaptic inputs to the reticular nucleus arise from the other thalamic nuclei, and it sends inhibitory projections back into the thalamus, apparently serving a negative-feedback regulatory role in thalamic function. It has been proposed to serve as a sort of ‘‘searchlight’’ of attention (Crick, 1984; Sherman & Guillery, 1996) and to control elements of signal-to-noise or the quality of information being sent to the cortex (see Vollenweider & Geyer, 2001, and references therein).

The thalamic filter and integrator model. The thalamus, within limbic cortico–striato–(pallido)–thalamo–cortical (CSTC) feedback loops, is proposed to function as a filter in the gating of extero- and interoceptive sensory and cognitive information to the cortex and, within cortico–thalamo–cortical (CTC) re-entrant pathways, it is proposed to be crucial in integrating cortically categorized exteroceptive perception with internal stimuli of the memory and value system. Thalamic gating is under the control of glutamatergic cortico–striatal pathways projecting to the dorsomedial (MD) and reticular nuclei of the thalamus and under the modulatory influence of serotonergic and dopaminergic projections arising from the raphe and ventral tegmentum (VTA) to several components of the CSTC loops (for details, see Ref. [22]). The model predicts that serotonergic hallucinogens disrupt thalamic gating and produce sensory overload of the prefrontal cortex by excessive stimulation of 5-HT2A receptors located in several components of the CSTC loop, including the prefrontal cortex (i and ii), limbic striatum (iii) and thalamus (iv). The blockade of NMDA-mediated glutamatergic (Glu) cortico–striatal neurotransmission (v) (e.g. by ketamine) or the increase of mesolimbic dopaminergic (DA) neurotransmission (vi) (e.g. by D-amphetamine) could lead to a similar neurotransmitter imbalance in CSTC loops, which again results in an opening of the thalamic filter, sensory overload of the cortex and psychosis. In addition, the excessive stimulation of thalamic and/or cortical 5-HT2A receptors located on GABAergic interneurons by hallucinogens could lead to a disruption of CTC or cortico–cortical integration of distributed neuronal activity (‘binding’) (vii), which, in turn, might underlie the more anxious and fragmented experience of egodissolution that is often reported after high doses of hallucinogens. Although application of serotonergic hallucinogens into the frontal cortex in rodents has been demonstrated to increase pyramidal-cell activity via stimulation of 5-HT2A receptors located on apical dendrites of pyramidal cells (i) and/or GABAergic neurons (ii), it remains unclear whether such a local activation without a subsequent disruption of thalamic gating or integration of information processing leads to psychosis in humans or simply to excitation and/or increased sensory awareness. Abbreviations: VTA, ventral tegmental area; AMY, amygdala; HPC, hippocampus; 5-HT, serotonin, DA,dopamine, Glu, glutamate; receptors: 2A, 5-HT2A; 1A, 5-HT1A; mGlu2/3, metabotropic glutamate receptor subtypes 2 and 3; NMDA, N-methyl-D-aspartate; D2, dopamine D2.

Table of Contents for the Initial Review Paper as Part of Senior Thesis for Graduation <br style="page-break-before: always;" clear="all"> A REVIEW OF HALLUCINOGEN PERSISTING PERCEPTION DISORDER I. DEFINITION OF HALLUCINOGEN PERSISTING PERCEPTION DISORDER<a name="_Toc286895037"><br style=""> A. Visual Perceptual Abnormalities: Hallucinations and Illusions II. DISTINCTION BETWEEN TRANSIENT “FLASHBACKS” AND ACUTE ALTERED PERCEPTION DISORDER III. DISTINCTION BETWEEN ALTERED PERCEPTION DISORDER AND RELATED PERMANENT VISION DISORDERS IV. ROLE OF DISSOCIATION IN HALLUCINOGEN PERSISTING PERCEPTION DISORDER V. ROLE OF SUBJECTIVE EMOTIONAL STRESSORS IN HPPD VI. CROSS-CULTURAL CONSIDERATIONS FOR HPPD VII. TIMEFRAME FOR DIAGNOSING HPPD VIII. DISTINCTION BETWEEN NORMALAND PATHOLOGICAL STRESS REACTIONS IX. UTILITY OF A CORRECT HPPD DIAGNOSIS X. LITERATURE-INFORMED RECOMMENDATIONS TO THE DIAGNOSTIC CRITERIA OF HPPD XI. PROPOSED HPPD DIAGNOSTIC CRITERIA FOR DSM-V XII. PROPOSED ALTERED PERCEPTION SUBTYPES OF SUBSTANCE-INDUCED DISORDERS XIII. PROPOSED RESEARCH FOR IMPROVING DIAGNOSTIC VALIDITY XIV. CONCLUSION: ACHIEVING A VALID SERIES OF DIAGNOSTIC CRITERIA

Current Opinion in Psychiatry: May 2010 - Volume 23 - Issue 3 - p 278–283 doi: 10.1097/YCO.0b013e3283387ab4 Neuropsychiatry: Edited by Perminder Sachdev and Francine M. Benes Depersonalization disorder Reutens, Sharona; Nielsen, Olavb; Sachdev, Perminderc Abstract Purpose of review: There is increasing interest in depersonalization disorder, in part because of the increased community awareness of the condition via the Internet. The disorder may be more prevalent than schizophrenia but is often misdiagnosed; hence, an update is timely. Recent findings: Recent research has included characterization of the nosology and phenomenology of the disorder, whereas emerging evidence demonstrates a neurophysiological dampening down in addition to psychological dampening in the face of emotional stimulation. Summary: Greater understanding of the clinical characteristics of this disorder will improve the reliability of diagnosis and aid the development of neurobiological and psychological models for empirical testing. Although response to current treatments has been disappointing, recent research has identified the basis for the development of new pharmacological and psychological treatments © 2010 Lippincott Williams & Wilkins, Inc. Colleague's E-mail is Invalid Your Name: (optional) Your Email: Colleague's Email: Separate multiple e-mails with a (. Message: Thought you might appreciate this item(s) I saw at Current Opinion in Psychiatry. Send a copy to your email Your message has been successfully sent to your colleague. Some error has occurred while processing your request. Please try after some time. Add Item(s) to: An Existing Folder A New Folder Folder Name: Description: The item(s) has been successfully added to "".

OLD DIAGNOSTIC CRITERIA (DSM-IV-TR) Depersonalization Disorder A. Persistent or recurrent experiences of feeling detached from, and as if one is an outside observer of, one's mental processes or body (e.g., feeling like one is in a dream). B. During the depersonalization experience, reality testing remains intact. C. The depersonalization causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. D. The depersonalization experience does not occur exclusively during the course of another mental disorder, such as Schizophrenia, Panic Disorder, Acute Stress Disorder, or another Dissociative Disorder, and is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., temporal lobe epilepsy). UPDATED DIAGNOSTIC CRITERIA FOR DSM-V Depersonalization/Derealization Disorder Either (1), (2), or both: A1. Depersonalization: Persistent or recurrent experiences of feeling detached from, and as if one is an outside observer of, one’s mental processes or body (e.g., feeling as though one is in a dream; sense of unreality of self or body; or time moving slowly) A2. Derealization: Persistent or recurrent experiences of unreality of surroundings (e.g., world around the person is experienced as unreal, dreamlike, distant, or distorted) B. During the depersonalization or derealization experience, reality testing remains intact C. The depersonalization or derealization symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. D. The depersonalization or derealization symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., complex partial seizures). E. The depersonalization or derealization symptoms are not restricted to the symptoms of another mental disorder (e.g.,schizophrenia, panic disorder, acute stress disorder, posttraumatic stress disorder, major depressive disorder, or another dissociative disorder). Specify if: a) Depersonalization only Derealization only THE RATIONALE FOR THE CHANGES D and E: Changes allow comorbid diagnoses to be made when warranted. Reference: Spiegel D et al. (Depression & Anxiety; in preparation) The group also proposes that depersonalization disorder should retain its classification as a dissociative disorder in its current form. However, it is problematic that chronic derealization is not included in the diagnosis. In the DSM-IV-TR derealization is classified with DDNOS, which is not in line with the ICD which has depersonalization-derealization as a single disorder. There is recent empirical evidence that individuals with prominent derealization alone do not significantly differ from those with depersonalization accompanied with derealization in any respect, including demographics, precipitants, illness characteristics, and comorbidity (Simeon 2009) Simeon D. 2009. Depersonalization disorder. In: Dell PF, O'Neil JA, editors. Dissociation and dissociative disorders: DSM-V and beyond. New York: Routledge. 2009. p 441-442.

I think the 12-step model has a lot of utility for HPPD... David

My disclaimer: This application could induce seizures, panic attacks, worsen symptoms, etc. That being said, I have used it with people who do not have HPPD as a way to demonstrate "perceptual movement" symptoms. http://www.neave.com/strobe/ You have probably seen this before (YouTube has this illusion), but on Retina display it is a handheld way to induce temporary hallucinatory symptoms in anyone. HOWEVER, read the disclaimer: WARNING: Do not use this application if you suffer from photosensitive epilepsy or are sensitive to flashing lights. Strobe Illusion By Neave Interactive View More By This Developer Open iTunes to buy and download apps. Description Stare into the Strobe Illusion and begin to hallucinate! After watching for 30 seconds your vision will distort and things around you will appear to move as if you're underwater or tripping out. The walls around you will appear to breathe, expanding and shrinking. This is a very effective optical illusion that will distort your vision! It is not a prank or 'scare' application - it really does work. You can even customize the size, direction and speed of the illusion to experience different kinds of hallucinogenic effects! WARNING: Do not use this application if you suffer from photosensitive epilepsy or are sensitive to flashing lights.

I am very pleased to announce that our research has now been recognized in publications and by the American Psychiatric Association DSM-V Task Force as contributing to the proposed revision of the previously clinically vague criteria of Depersonalization Disorder. Research manuscripts and textbooks have cited our research 18 times, including supporting the primary citation on DSM5.org. The proposed change: Updated May-20-2010 Depersonalization/Derealization Disorder Either (1), (2), or both: A1. Depersonalization: Persistent or recurrent experiences of feeling detached from, and as if one is an outside observer of, one’s mental processes or body (e.g., feeling as though one is in a dream; sense of unreality of self or body; or time moving slowly) A2. Derealization: Persistent or recurrent experiences of unreality of surroundings (e.g., world around the person is experienced as unreal, dreamlike, distant, or distorted) B. During the depersonalization or derealization experience, reality testing remains intact C. The depersonalization or derealization symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. D. The depersonalization or derealization symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., complex partial seizures). E. The depersonalization or derealization symptoms are not restricted to the symptoms of another mental disorder (e.g.,schizophrenia, panic disorder, acute stress disorder, posttraumatic stress disorder, major depressive disorder, or another dissociative disorder). Specify if: a) Depersonalization only Derealization only ------ The listed rationale for change: Updated February-14-2011 D and E: Changes allow comorbid diagnoses to be made when warranted. Reference: Spiegel D et al. (Depression & Anxiety; in preparation) The group also proposes that depersonalization disorder should retain its classification as a dissociative disorder in its current form. However, it is problematic that chronic derealization is not included in the diagnosis. In the DSM-IV-TR derealization is classified with DDNOS, which is not in line with the ICD which has depersonalization-derealization as a single disorder. There is recent empirical evidence that individuals with prominent derealization alone do not significantly differ from those with depersonalization accompanied with derealization in any respect, including demographics, precipitants, illness characteristics, and comorbidity (Simeon 2009) Simeon D. 2009. Depersonalization disorder. In: Dell PF, O'Neil JA, editors. Dissociation and dissociative disorders: DSM-V and beyond. New York: Routledge. 2009. p 441-442. Congratulations to our collegues in this field and the tremendous advocacy of the International Society for the Study of Trauma and Dissociation. The largest thanks to Dr. Daphne Simeon for her work and expertise on the project and the members who participated in our research. This revision was posted today. Cheers, David

PPI occurs when a relatively weak sensory event (the prepulse) is presented 30–500 ms before a strong startle-inducing stimulus, and this reduces the magnitude of the startle response. In humans, PPI occurs in a robust, predictable manner when the prepulse and startling stimuli occur in either the same or different sensory modalities (acoustic, visual, or cutaneous). Our objective is to examine if visual persisting perception disorder influences on PPI related to the underlying construct of sensori- (prepulse) motor gating (startle reflex; measured with electromygraphy). We can compare our results with past PPI studies with other psychopathological and neurological disorders, which form a group of related gating disorders. Lastly, we will note any effects correlated with different medications that individuals may be taking that could influence PPI in individuals with HPPD. Notably, others (Pouretemad et al. 1998) reported PPI deficits in individuals with “non-epileptic seizures”, which may constitute a variant of Temperal Lobe Epilepsy. This latter observation suggests that psychosis per se is not a requirement for deficient PPI in seizure disorder patients. Study findings of PPI deficits in non-psychotic individuals for reduced PPI in non-psychotic patients with bipolar affective disorder will be reduced with JH’s differential diagnosis. In humans, Abduljawad et al. (1997) assessed the effects of clonidine and diazepam on startle and PPI in normal male volunteers. Subjects were tested in a within-subject design in which they received oral doses of placebo, 10 mg diazepam, and 0.2 mg clonidine in a balanced double-blind protocol. EMG recordings from the right eye were obtained during each drug’s peak plasma level for maximal CNS effect. Both drugs dramatically reduced the magnitude of startle responses, neither drug significantly altered PPI calculated as a percent score. Hallucinogenic serotonin agonists, such as 2,5-dimethoxy-4-iodoamphetamine (DOI), disrupt PPI in rats (Geyer et al. 2001), psilocybin, however, does not appear to disrupt PPI in rats reliably, perhaps because it is less selective as a serotonin agonist relative to DOI. As discussed in Geyer et al. 2001, this 5-HT1A agonists increase PPI in mice despite the fact that they decrease PPI in rats. Thus, the 5-HT1A agonist actions of psilocybin, which are not shared by DOI, may be responsible for the increased PPI observed in human subjects by Gouzoulis-Mayfrank et al. (1998). PPI’s unique actions will help support information related to the neurobiological pathways and receptor sites potentially implicated in the cause of the disorder.