SBNI Lunch Lecture Series - The Neurobiology of PTSD

[Music] I'm going to talk about a post-traumatic stress disorder today and it's a very interesting topic Tom had sent me an article about PTSD that said it really may be the first psychiatric disorder that's beginning to be understood in terms of understanding at the level of the brain and I did a lot of reading and learning in preparing for this talk today and there is a lot of exciting research that's happened I have to say that there is so much research is a little overwhelming that many of the findings are inconsistent at times and in so it's a picture that is slowly coming into focus but has many parts that are not really clear yet but I think you'll find it very interesting to hear about the neurobiology I'm going to go through first a little bit of history about post traumatic stress disorder a little bit about the clinical presentation of the disorder and then go on to the neurobiology and some of the emerging treatments are very interesting I think the the treatments to date have had modest effectiveness but there's a lot of research and innovation happening in terms of understanding where there are places to intervene that really could make a big difference with post traumatic stress disorder so a few things you may not know originally post traumatic stress disorder was conceptualized as a traumatic event that was so severe that it kind of broke the stress management system and it was thought of as a universal response to an overwhelming stress but it's clear now that that's not the case most people exposed to trauma do not develop PTSD and those who do develop PTSD have underlying physiologic differences and those differences result in a failure to recover because most people recover and trauma unmasks this physiology that may not have been apparent prior to the traumatic event trauma itself also alters some of the physiology and not only are there genetic differences that translate into tissue differences and then hormonal and neuro endocrine and so on kinds of differences but there are significant epigenetic effects on the play a role in PTSD Rachel Yehuda is a psychologist who's one of the foremost researchers in PTSD and she looked at Holocaust survivors and she was studying PTSD in Holocaust survivors the children of these individuals came to her and said why aren't you studying us we all have PTSD too and she didn't really make too much of that at first but she began to talk with them and pay attention to them and in fact many of the Holocaust survivors children have PTSD and she has been able to do some research showing that there are epigenetic effects changes in gene expression that are passed on from parent to child so that a parent who's had PTSD can have a child who has that predisposition or that disorder based on the experience that the parent had had so mental was right but Lamarck was right as well that acquired experience can be inherited into the next generation I'm going to talk a little bit about treatments both current treatments and treatments that are in development and there's some very interesting findings there and talk a little bit in the next few slides about the scope of the problem with PTSD so post traumatic stress disorder didn't always have this name but there were other names for it and it's been recognized over centuries and I just picked a few of the more recent descriptions of PTSD in the franco-prussian war there was a physician who described it as soldier nostalgia in the Civil War it was called soldier's heart and it was thought to be a cardiac condition acquired in battle in late 19th century England the thought was that at the railway accidents people had their spines compressed and this was what led to trauma symptoms in World War one this was called shell shock until physicians began to see that even soldiers who weren't exposed to the new artillery shells were developing PTSD so it wasn't a cause from the artillery shells as first thought it was also called battle fatigue and the treatment then and this was true through World War Two as well was called PI proximity immediacy and exposure so soldiers were brought right back to their battalions put right back into the theater of war and there there's some wisdom in this in the sense that social support and camaraderie are protective for people who are recovering from trauma and reexpose you're Kennex can cause extinction in trauma memories in in the DSM 1 1952 the first description of this was gross stress reaction but really it was Vietnam that brought PTSD to the fore the original proposed name was post Vietnam syndrome and it's a good thing I think that people recognize this was in particular to Vietnam the conditions of warfare guerrilla warfare less lower morale less camaraderie around the soldiers who were working together bred conditions that led to a great deal of post-traumatic stress disorder more than 20% of the soldiers who served in the theater of war lifetime acquired PTSD the current rate is around 9% so that's a very high rate of persistence opposed to Vietnam and in the years since 1980 DSM 3 diagnosis the concept of PTSD has been enlarged so there's been a study of child abuse victims studies of domestic violence and rape victims and it's a it's a clearer concept now that this is a broad condition that applies to many kinds of trauma and you think about all the different settings now where we see trauma this week in the news from Brussels the Iraq and Afghanistan wars there's an estimate that the Syrian refugees one third of the country two to three million people those refugees who were in Turkey a third of them have a diagnosis of PTSD a child abuse domestic violence rates of very high inner-city violence is quite high and it's it's interpersonal violence and intimate violence that leads to the highest rates of PTSD so the rates are very high for child abuse rape those kinds of things and lower when it comes to natural disasters here are the current dsm-5 criteria for PTSD it requires exposure to a traumatic event that involves actual or threatened death serious injury or sexual violence in one or more of the following ways directly experiencing witnessing the events occurring to others learning that traumatic events occurred to a close family member or experiencing extreme or repeated exposures of trauma to others such first responders would see this is a broader definition than the 1980 dsm 3 definition that really required direct experience of trauma and an experience of threatened death or serious injury and really the criteria has become broader to capture more of the trauma events that people suffer and realizing that PTSD applies to a broader group than combat veterans or people who've directly experienced violence the criteria require four types of symptoms used to be three under DSM three REE experiencing which are intrusive memories flashbacks nightmares reacting to cues that bring back the experience of the trauma avoidance and numbing which is kind of a reaction to this overwhelmingly experiencing where people avoid the thoughts reminders of the trauma and also restrict their activities and interpersonal life as well the new condition in dsm-5 is negative cognitions and mood associated with the trauma and the last is hyper arousal so hyper vigilance irritability insomnia when people can't sleep is one of the things that comes to my mind is is this related to trauma since it's a very common accompaniment of trauma so currently I'm working with an individual who is in a program here who after her alcohol and heroin binge which happened along with her boyfriend she found her boyfriend dead in the bathroom from an overdose of heroin and in the program she has constant anxiety she can't concentrate she feels jumpy she startles easily she can't sleep she's having flashbacks and really can't participate in the program so she has acute stress disorder in the first month these symptoms are called acute stress disorder after one month they're called post-traumatic stress disorder and and the question was what to do for her and one of the more recent medication treatments has been praise us in an alpha 2 blocker which was studied at the University of Washington among combat veterans who had severe insomnia and nightmares and had really quite good effects for helping combat veterans with their sleep problems so this is now more widely used she's taking a small dose in the morning and a larger dose at bedtime and for her it's had a marked effect of she's much calmer much more able to sleep much more able to participate in the program I'm not going to spend a lot of time on the clinical aspects of treatment of PTSD but this is one book I would recommend by Judy Herrmann she was a psychiatrist and actually a teacher of mine at Cambridge Hospital who started off hearing many stories of incest that were being dismissed by others and wrote a burke book first about incest but then went on to write about trauma and recovery and this is just an excellent overview of what happens as a consequence of trauma and how do people get better the burden from trauma is not just in the immediate symptoms that people experience but people become ill with chronic illnesses as a consequence of trauma cardiovascular disease rates are higher diabetes obesity hypertension so trauma and and the continuing stress of trauma predisposes people to develop chronic illness and also psychiatric and addiction problems so the rates of psychiatric and Addiction comorbidity with post-traumatic stress disorder exceed 80% it's very unusual to see someone with PTSD who doesn't have comorbid disorders and usually both psychiatric and medical doctor Frawley and i have talked about how many chronic pain patients have a background of trauma and there's a connection there that I don't think is well understood but I think many traumatized individuals go on to develop chronic pain conditions addiction alcoholism is very common one of the things to counsel people when they've been exposed to severe trauma is not to turn to alcohol because that's a very common response rates of depression and anxiety and overall poor self-care are very high for individuals have PTSD and if you look at lifetime what percent of the u.s. population is exposed to a trauma that's in the definition of PTSD it's about 75% so over the course of a lifetime most people are going to be exposed to a significant trauma but the rates of PTSD lifetime are only about 7% higher in women and the prevalence the current 12-month prevalence of PTSD in the population is about three and a half four percent so you can see that there's a very large percentage of people who are exposed to trauma but it's a much smaller percentage of people who go on to develop post-traumatic stress disorder surveys in other countries have found lower rates and as I mentioned comorbid conditions are the rate of comorbid medical and psychiatric conditions are very high and so why is it that most people do not get PTSD well what's become clear is that there are specific underlying physiologic differences in individuals who are vulnerable to developing post-traumatic stress disorder and their physiological management of a severe stress is different from other people there are other kinds of FAC there's people for instance who suffered child abuse and haven't developed PTSD but then are exposed to trauma as adults are going to be much more at risk and there are genetic differences that underlie DIF the risk for developing it but the usual course of trauma is to get better it's not uncommon for symptoms to last one month up to three months but most individual symptoms resolved by three months so PTSD symptoms are normal in the short term and people will meet the definition of PTSD after one month at a very high rate but most individual symptoms are going to resolve and they're not going to continue to meet that diagnostic criteria so here's one example at the World Trade Center attack on 9/11 there was a look at individuals who are in close proximity to the World Trade Center and at one month 7.5% of the residents met criteria for PTSD but as you can see over the subsequent months it dropped to 0.6 percent of residents continuing to meet that criteria after six months what are some of the risk factors the dosage of trauma matters history of childhood adversity or trauma plays puts a person at significant risk a history of poor coping leads to a higher risk low social support family history of trauma and then the physiologic variables low heart rate variability as a predictor low cortisol as a predictor and I'll talk about some of the the neurobiology that that that underlies this so in fear processing the amygdala plays a central role and the amygdala can cause a person to sense fear and react to it without even any awareness it bypasses the cortical circuits so if you see a cue that is dangerous or frightened your body can be reacting before you have any awareness of what that danger might be about and in PTSD many of the memories or many of the re-experiencing ZAR amygdala type memories so people will find themselves re-experiencing trauma or reacting with a high rate of anxiety or autonomic response and not really know why one example is a veteran who every time his wife baked would get into a highly hyper-vigilant highly aroused distressed state and he realized after a while that one of the smells from baking reminded him of the smell of an explosive when he had been in combat but his body was reacting he didn't have the awareness so the amygdala is involved in conditioned fear response just as in Pavlov's model you you tie a cue to a painful stimulus and people will continue to react to the cue as though the painful stimulus is going to come and it's the amygdala that puts these things together so when people suffer a trauma all of the context of the trauma all of the cues associated with it get associated with the trauma and the amygdala starts reacting to this and has outputs to the hypothalamus to the brainstem to other areas so amygdala is the threat processing Center and in PTSD patients the amygdala is hyperactive compared to non-exposed controls so the amygdala for for reacting to fear or to threats and developing fear and anxiety is hyperactive before people are exposed to traumatic events and develop PTSD at a in those individuals who are going to go on to develop PTSD and there's some debate about is this a pre-existing condition or is this a consequence of trauma exposure but it really seems to be a pre-existing condition in individuals now a partner of the amygdala is the prefrontal cortex and in particular the anterior cingulate cortex so this is a part of the brain that talks to the amygdala and evaluates the threat and provides some context for it and can dampen the response of the amygdala if the threat is not really something that's going to be dangerous it exerts inhibitory control over the stress response in over emotional reactivity it modulates the signals from the amygdala and condition fear responses can be reduced or extinguished by the prefrontal cortex so so for most people after trauma they're going to be hyper reactive to cues that associate with the trauma but as they go through experiences where they see that they have the cues but there's no trauma that follows afterwards their anterior cingulate cortex is working with the amygdala to dampen the response and to take away that hyper reactivity that was there originally and most of the time in individuals exposed to trauma this partnership is able to work and people are no longer frightened of going out to the car if they were assaulted there or no longer afraid of other contexts in which the trauma occurred so conditioned fear responses typically are reduced or extinguished it's an active learning process it's impaired in PTSD so individuals who develop PTSD are simply not able to use this fear extent action process that is available normally to most individuals and and this is a little illustration of some of the fear circuits and post-traumatic stress disorder the amygdala is at the center that's where anxiety and fear signals are processed the medial prefrontal cortex the anterior cingulate cortex is down below and is talking with the amygdala the hippocampus is also involved in this fear circuitry and plays a key role in contextualizing and in putting into a framework and understanding of the trauma so what happens to the hippocampus and individuals who develop PTSD for one thing there was a finding in Vietnam combat veterans that the hippocampus was smaller in individuals who develop post-traumatic stress disorder than in individuals who did not develop PTSD and it was thought at first that this was a result of the trauma that high levels of glucocorticoids can cause damage to the hippocampus until there was a study of twins one of whom had served in combat in Vietnam and one of whom had not served in combat and what they found was the twin who had not been in combat had a smaller hippocampus as well so it became clear that this was a pre-existing condition it's associated with lower intellectual ability when people have a smaller hippocampus so the ability to process cognitively what's happening with the trauma to put it in context to make sense of it is impaired in somebody with a smaller hippocampus individuals have less cognitive flexibility so these three systems also interact with the hypothalamic pituitary adrenal axis and this is another circuitry that's neuro and endocrine based that's involved in post-traumatic stress disorder and that has inputs from the hippocampus and from the amygdala and is dysregulated in individuals who have post-traumatic stress disorder so the usual stress response is that in the hypothalamus under inputs from the amygdala that are modulated by other circuits corticotropin-releasing hormone goes up under stress that's a signal to the pituitary to then increase the output of ACTH which is in turn a signal to the adrenal medulla to release cortisol and and the cortisol exerts a negative feedback loop to the hypothalamus so that's that that's the typical functioning of this stress response system that normally is self regulating and one where things return to a homeostasis normally now what happens in post-traumatic stress disorder din dividuals well again at first the finding that cortisol was lower in people with PTSD was thought to be a consequence of exposure to the trauma but it's become clearer now over time that individuals who are vulnerable to developing PTSD have lower cortisol to begin with so they're individuals who maybe don't have the ability to have the feedback to the hypothalamus to turn down CRF it's it's a it's a feedback system that compared to depression is is very different in depression CRF results in increased cortisol decreased glucocorticoid responsiveness back at the hypothalamus weaker negative cortisol feedback but in PTSD the the rate of CRF is elevated which he would lead you would think to a signal to the adrenal glands to increase the output of cortisol but in fact the cortisol level is lower in PTSD so it's a pre-existing vulnerability in a study with motor vehicle accident victims those who develop PTSD had lower cortisol within hours of the trauma compared with those who did not so you look at all the individuals who'd been in motor vehicle accidents you measured their cortisol levels several hours after the trauma exposure and the lower cortisol level predicted those would be the individuals who go on to develop PTSD another example is in mothers who develop PTSD after the 9/11 attacks in New York City their infants had lower cortisol levels compared with mothers who did not develop PTSD and this may be another instance of an epigenetic effect where there's a physiologic difference between those mothers who went on to develop PTSD and then a difference in their infants as well cortisol contains the sympathetic nervous system response and facilitates the return to homeostasis or hollow stasis as that this dynamic system is sometimes called so the deficiency of cortisol seems to play a significant role in the vulnerability there's also a disturbance in the HPA axis that the feedback loop from hypothalamus to pituitary to thyroid individuals with PTSD have higher levels in the acute phase of both t3 and t4 but Vietnam combat veterans even decades later have circulating levels of tea four and this is thought to be maybe a contributor to the increased rates of anxiety and sympathetic symptoms so so just to go through some of the neurotransmitters that are involved with these various circuits corticotropin-releasing hormone which comes from the hippocampus to the pituitary is elevated in individuals with PTSD and corticotropin-releasing hormone is the name of it makes it sound as though it is primarily involved in signaling the pituitary but in fact there are CRH neurons throughout the brain that project to many of the circuits involved in PTSD and corticotropin-releasing hormone promotes many of the cardinal features of PTSD so startle responses condition fear responses hyper arousal anxiety are all higher when people have higher CNS levels of CRH and there's been an interest in seeing if there could be the development of a medication that could block CRH because this seems to be such a central feature in PTSD but that's that's still in the research arena catecholamines are higher in PTSD norepinephrine is the principal driver of autonomic stress responses both in the CNS and in the periphery the locus coeruleus has norepinephrine neurons that project to the prefrontal cortex to the amygdala to the hippocampus to the hypothalamus and the flood of norepinephrine that happens after a traumatic event is he in encoding those memories and one of the ideas and people into who develop PTSD is that they encode the trauma memories more strongly than people who don't develop pts they have more norepinephrine that floods their system they have less of the feedback break that glucocorticoids cortisol provide so these fear memories become highly encoded in in their memory systems and very powerful than in coming back as reacts perience incurring or norepinephrine is comes from the adrenal gland and all of the sympathetic responses of elevated heart rate blood pressure skin conductance are increased and a higher rate of peripheral norepinephrine is a constant in PTSD so these are individuals who continue to have elevations in their heart rate and blood pressure and their sympathetic system generally a serotonin plays a role in modulating these brain circuits the dorsal and median Rafi neurons and the brainstem have projections to all of the circuitry that I was talking about earlier and different subtypes of receptors have different effects in the serotonin system so 5-htt to receptors are involved in modulating anxiety Enic effects so they turn up the effects of anxiety and fear and so on the next one down should say five ht1 receptors mediate exile it effects and they facilitate extinction and suppress encoding of trauma memories so again there's there's interest in developing medicines that would target these sub receptors that might be more useful to stimulate in treating PTSD and overall serotonin plays a significant role in symptoms of impulsivity hostility aggression and suicidality there are other neurotransmitters that also are dysregulated in PTSD so if you look at GABA receptors there are fewer gaba receptors in in various parts of the brain in individuals who develop PTSD that's the inhibitory system that can quiet transmission the glutamate system is also dysregulated and there are increased levels of glutamate which can be cytotoxic some of the damage that seems to happen to the anterior cingulate or other regions may be due to this elevated level of glutamate neuropeptide Y if you look at combat veterans who did not develop PTSD in Vietnam they have higher levels of circulating neuropeptide Y and individuals who develop PTSD lower and then endogenous opioids also seem to play a role so for instance individuals in combat who have a serious injury and receive morphine are more likely to not develop PTSD than individuals who didn't receive morphine so when it comes to genetics what what are some of the underlying differences that are known at this point that lead to smaller hippocampal volume increased amygdala reactivity so there are a number of findings that are linked to individuals who develop PTSD there's a lower expression of Sara point serotonin transporter gene so serotonin levels are lower and individuals who have this gene variant are at increased risk to develop PTSD have increased amygdala reactivity there are gene variants in the glucocorticoid receptor that put people at risk for PTSD so there's there's one particular GCR variant that's been studied wild widely and seems to moderate risk for PTSD in childhood abuse as well as in adults the C MOT gene variant is also linked to an increased risk for PTSD so all of these systems that are regulating an imbalance can have norepinephrine disturbances dopamine disturbances glucocorticoid disturbances that are evident in the genes and then in addition to genetics there's a very significant role for epigenetics and PTSD so and in I think in mental health disorders generally epigenetics is coming into view as a phenomenon that plays a very significant role in the development of mental health disorders so so what is epigenetics um the genes that an individual is born with can be expressed or not and epigenetics is the modulation of gene expression that happens that leads to consequences for proteins that are made and neurotransmitters that are made and the main mechanism that seems to be at work in epigenetics is methylation of DNA so for a gene to be expressed it needs to be active the promoter regions need to be active DNA methylation typically silences the expression of expression of certain genes there are other methods as well through modifying histones and even some micro RNA expression that seemed to be involved in epigenetics but this seems to play a significant role in trauma so as I mentioned before Rachael Yehuda was studying Holocaust survivors and had their children talking with her saying you need to study us as well and what she found was that a glucocorticoid receptor gene had a higher rate of methylation in survivors of the Holocaust but also in their children compared with controls so she studied individuals who had been through the Holocaust and their children and then other Jewish individuals who live had lived outside Europe at that time and their children and the survivors of the Holocaust had a higher rate of methylation of this gene silencing it but their children did as well if their father was a Holocaust survivor this is a fellow Kessler at Emory in Georgia where there's a lot of PTSD research that's very exciting going on exposed mice to the smell of cherry blossoms and then gave them a mild electric shock so the mice came to fear that smell then he looked at that phenomenon in the offspring of the mice and the offspring feared the smell of cherry blossoms as well even though they had never been exposed to it to a stimulus another finding in epigenetics in terms of a protective effect are that rat pups who have better maternal care are licked and groomed more develop a more robust glucocorticoid receptor expression than rat pups who don't receive that treatment and when they're exposed to trauma they develop PTSD at a lower rate than individuals who didn't receive that kind of maternal care and there's other findings as well that there may be a kind of optimal exposure to trauma so rap pups who experience a relatively mild degree of maternal deprivation seemed to develop into individuals who are PTSD resistant compared to rap pups that don't have that maternal deprivation so you know what what is going on that there are these protective effects and resilience effects as well as vulnerability effects based on experience that animals or humans may have and then the consequences of gene expression or silencing that goes on so here's one other study of childhood maltreatment so this is a study where three groups were looked at everybody was trauma exposed as an adult but the first group was trauma exposed and didn't develop PTSD the second grow group was trauma exposed and developed PTSD but had never been traumatized in childhood the third group developed PTSD but did have a history of childhood trauma and when the comparison was made between those who were trauma exposed never developed PTSD and the other two groups there were many different gene expression developments that were changed in the individuals who developed PTSD but what was interesting is the patterns were completely different between individuals who had a history of childhood trauma and individuals who did not have a history of childhood trauma so there was a whole pattern of gene expression or silencing in those with childhood trauma that didn't overlap with the individuals who did not have the childhood trauma these are these are the common current therapies cognitive behavioral therapy where the context of the trauma the thinking around the current danger compared to what happened in the past people's thinking about the trauma is addressed and usually eight to twelve sessions of CBT if done properly can have a significant helpful effect for individuals who have PTSD the other kind of psychotherapy that's proven effective is exposure therapy so individuals are brought back to but they're the trauma that they experienced and asked to endure what they experienced while they go through it again and over time their response is extinguished so it's in a way it's like mobilizing the fear extinction response it may be exercising that prefrontal cortex area more and more exposure therapy has a very high dropo rate that's one of the problems with it so when you bring individuals who've been through combat back into an experiencing of the combat it's very distressing and a lot of people just can't do this there are now new video game type exposures that you you can turn up and down to try to help people have a level of exposure therapy that's manageable EMDR also has evidence that's eye movement descents what is it I'm movement reorganization so I don't understand what AMDR is it's a rhythmic physical experience typically or and rapid eye movement it seems to me what happens is people are asked to read to retell the story about their trauma while they do this and it seems to me a kind of exposure therapy but it has proven effective and here's an interesting new approach so a Grady Hospital which is a really a trauma center they're not only doing bench research but they went into the ER and they selected trauma patients and they had those individuals who had been shot or salted or whatever trauma they had experienced go through imaginal exposure immediately after the trauma so it's like fear extinction immediately after the trauma at three months there was a 50% reduction in the rate of PTSD diagnosis compared with controls so it used to be thought you know there was this this movement to do critical incident debriefing after trauma where individuals would talk about the trauma and studies of critical incident debriefing showed that there was no value in it it didn't really had anything in terms of how people did in developing PTSD and so for a long time that kind of immediate work on trauma really kind of went by the wayside but this imaginal exposure right after the time of trauma has proved effective there are medications that are effective the mainstays have been serotonin medicines beta blockers and now alpha 2 blockers these medications sometimes have modest benefits sometimes more dramatic than that there was a look at using beta blockers in individuals who were exposed to trauma as a preventive approach and it does seem to prevent some of the memory consolidation of trauma memories but it did not have the effect that was hoped for in terms of dampening the norepinephrine surge and the consequent brain effects here's another interesting study of morphine after combat this was in the Iraq theater there were 696 patients about a third of whom had developed PTSD and there was a look at the records of the use of morphine during early resuscitation so those who had a PTSD diagnosis 61% had received morphine those without a pts diagnosis had at a higher rate received morphine and the odds ratio for that difference was very small it seemed that morphine had a protective effect there since been a look at the use of low dose cortisol treatment for PTSD because murmur of PTSD individuals have a lower baseline level of cortisol this was a three-month study double-blind crossover looking at patient ratings and clinician ratings and cortisol reduced the rate of re-experiencing symptoms and seemed to have some carryover effect into the months when people were not on cortisol so was it inhibiting retrieval of trauma memories because that's what glucocorticoids do or was it having a broader effect in reducing PTSD symptoms there is a study now of how to improve fear extinction processes and individuals with PTSD so if you look at the anterior cingulate in individuals who have PTSD there the ACC is smaller in volume less physiologically impaired by other measures and the reduction in volume actually tracks the severity of the trauma experience so the more trauma the more impact on the anterior cingulate and the more impairment in an individual's ability to extinguish trauma memories this was a study of D cyclo serine which is an NMDA partial agonist and NMDA is involved or glutamate receptors are involved in in the learning and the extinction combining this with exposure therapy was known to help with anxiety conditions but was studied in 25 patients with PTSD after the World Trade Center attack in 12 sessions and there was a difference substantial improvement in clinician administered scales that was evident by six weeks and was sustained over six months this is a very recent study at Emory of using dexamethasone to facilitate fear extinction so this was an animal study rats were subjected to immobilization followed by fear conditioning they developed PTSD symptoms and dexamethasone was administered for hours before fear extinction training so reexpose a and produced a dose related enhancement of fear extinction and retention and the kind of gene level finding was that in the amygdala when dexamethasone was used to facilitate fear extinction there was a change in a glucocorticoid receptor messenger RNA expression and also there was DNA methylation of this gene that occurred in a dose-dependent manner so simply administering the dexamethasone facilitating extinction fear extinction resulted in measurable methylation of a glucocorticoid receptor gene in the amygdala that was correlated with this improvement in PTSD so I think I'll I'll stop there [Applause] you

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Keywords: Santa Barbara Neuroscience Institute, Cottage Health, Santa Barbara, California, PTSD, Post Traumatic Stress Disorder, Trauma, Veterans, SBNI, Research, Lecture, seminar, talk, presentation, psychiatric disorder, brain, neurobiology, treatments, stress, trauma, physiology, genetics, shell shock, soldiers heart, war neurosis, proximity immediacy and exposure, gross stress reaction, post-vietnam syndrome, symptoms, re-experiencing, avoidance, numbing, child abuse, rape, insomnia, traumatic events, exposure

Id: hrIUPOtmeyQ

Length: 50min 49sec (3049 seconds)

Published: Thu Apr 07 2016