What’s going on in the brain with DID? Biological markers in DID

Since a few of us are rabidly into facts and physical proof, I’ve done some research to understand the biological and physiological changes that accompany DID and PTSD. While those with mental disorders may disparagingly be called “head cases,” it turns out that in the physical sense, that’s actually true .

Summary of findings

1. Normal factual memories are stored in one part of the brain, while traumatic emotional memories are stored somewhere else.

2. Chemicals in the brain that communicate among brain structures are significantly altered during trauma, and can remain so through years of PTSD. These changes can lead to long-term mood/behavior changes, depression, fear, impulsive aggression, inability to perceive/process events correctly, and dissociation.

2. After trauma (especially prolonged), the size of these brain structures decreases. The imbalance of chemicals affects storage of regular memories (causing amnesia).

3. The communication between these structures can be compromised. This prevents normal processing of the traumatic memories (stored separately), because now there is no “story” to connect the intense emotions to. So these emotions remain raw, explode at times, and seem to have no source. This causes a vicious cycle of triggers, flashbacks, and inappropriate activation of the fight-or-flight response.

4. In individuals with DID, the communication pathway between both sides of the brain can shrink. DID may be caused by extreme reduced communications between the hemispheres. Switches between alters may be associated with switches between left-to-right brain activation.

Scientific research has shown that it is possible to forget memories and experiences. That raw emotional trauma never goes away without processing. That dissociation is a powerful coping mechanism for the individual to survive during the trauma, and in some cases, for the rest of their lives.

That PTSD and DID may not really be “disorders” but just the normal consequence of abnormal situations.

There’s a lot to cover. Let’s get started.

What prompted this long researched post? I knew it would be complicated, but I had promised to write about research and findings related to the brain in DID. It was on the back burner until I read an interesting post by a woman with autism who met a woman with DID, and they found many similarities in their experiences. It really got me thinking about the many components that fall into place to foster the development of DID in childhood and to cement it through childhood and adulthood. It’s not all in our head, it’s in our brains.

There are studies coming up with a variety of neurochemical, neurological and patterning differences in those who develop DID. [Williams]

[P]sychological trauma may in fact induce neurological damage in humans [Gilbertson]

There are several areas we need to cover to be true to this topic, including how the brain develops in young children, how trauma affects this development, some basics of memory storage and how traumatic memories are stored in different places in the brain than regular memories, and how continued trauma or secondary traumas make matters worse. Because of the complexity of the topic, I will summarize and provide references for the interested reader to pursue more. Please forgive any oversimplications.

Lotsa ground to cover, so let’s get started.

Some basic stuff about memories

To do this topic justice, I need to talk a bit about types of memories, and the structures in the brain associated with each. This is because amnesia, flashbacks, and DID are associated with lack of integration of different types of memories, and/or changes in the associated brain structures.

Declarative memory (long term memory) is the autobiographical stuff. The “movie” of your life. It is conscious memory and the ability to reason and recall events. Two types of declarative memory exist – episodic, which is your memory of events, and semantic, which is your memory for facts. The hippocampus is involved in filing away these memories.

Non-declarative memory is implicit memory related to storage of senses and emotions and “our ability to recall smells, feelings, images, sounds, and tastes”. It is related to fear conditioning and unconscious fight-of-flight responses. This processing takes place mainly in the amygdala.

A major problem that arises with PTSD and DID are amnesia for events, and extreme emotional responses and hypervigilance often related to triggering. Research has shown that trauma interferes with declarative memory – recall of events – but does not inhibit non-declarative memory – the part that stores emotional responses and sensations related to those events. [van der Kolk] Therefore, the feelings of trauma do not fade over time as normal memories do, due to the disconnect between the autobiographical elements. These disconnected feelings of high arousal and terror are never processed, and so remain vivid to be triggered in response to minor stress. [van der Kolk]

Changes in brain chemistry

It appears that the problems with the disconnect in the declarative and non-declarative memories is associated with a barrage of chemicals in the brain. So let’s talk about some of these chemicals that are involved in stress and the response to stress. [Kendell] An overview will help see how changes in these chemicals can affect growing brain function, which I will talk about in the next section.

Neurotransmitters are chemicals that neurons use to communicate with one another. This list is not comprehensive, but includes the major players.

Cortisol: a stress-regulating hormone.

Serotonin, dopamine: neurotransmitters affecting mood and behavior.

Norepinephrine and epinephrine : neurotransmitters affecting mood and behavior, creating the familiar fight/flight/freeze trauma response.

Glutamate: The above neurotransmitters are inhibitory, while glutamate is excitatory. A balance of these are required for organized perception of events.

In normal stress, these chemicals allow an individual to mobilize and “with greater endurance, strength, immunity, and clarity”. [Diehl]

So what goes wrong?

However, overwhelming stress, especially early in life, alters the production of these chemicals. Levels of cortisol are decreased in veterans and rape victims with PTSD. Norepinephrine and epinephrine are elevated, serotonin is decreased.

Prolonged exposure to cortisol and its derivatives causes “behavioral consequences of changes in social behavior, insufficiency of active avoidance learning” [Chundler], and changes have been observed with depression, trauma, fear, etc. Abuse can also lower serotonin levels, “leading to depression and impulsive aggression.”

High levels of glutamate during trauma lead to “impaired perception at the time of trauma, as well as altered coding of memory” [Banks] “Drugs that block one subtype of glutamate (N-methyl-d-aspartate, or NMDA) produce dissociative symptoms.” [Morgan]

New research shows that neurotransmitters that stimulate the release of GABA (gamma amino butyric acid) also increase dissociation.

With trauma, the imbalance of these chemicals interferes with the storage of declarative memories (the story of what happened).

Therefore, traumatic memories are stored in the implicit form, as emotions and senses. As practitioners, we have become accustomed to our clients remembering their experiences in pieces, and virtually “shutting down” as they attempt to re-tell their stories. Survivors become haunted by feelings and senses they know are related to the trauma, but have great difficulty clearly identifying the source(s).

This promotes a vicious cycle in which the body is unable to assess danger signals and reacts to any direct or indirect reminder of the trauma as a potential re-victimization, even if the reminder is completely non-threatening. These triggers bring overwhelming emotions and sometimes flashbacks and panic attacks which in-turn cause the body to return to the emergency chemical response. These continual “flight or fight” reactions bring base-level psychobiological changes [Diehl]

Developmental neurobiology and changes with trauma

We talked about chemicals, now let’s talk about some structures in the brain that are associated with memory storage and retrieval, and how they are affected by these changes in brain chemistry. The structure of the brain changes with the accumulation of memories and experiences, both good and bad. It also has the amazing ability to connect multiple aspects of a specific experience – the sight, sounds, smell, etc., and generalize the effects for use in current or future events. [Perry] But this amazing ability relies on appropriate communications among several brain structures.

A leader in research in this area is Martin Teicher, who has provided physical evidence childhood trauma “dramatically affects both the structure and chemistry of the developing brain.” He reported in 1993 that brain abnormalities were found in 54% of children with histories of physical abuse, but only in 27 of non-abused children. Add sexual abuse to the equation, and the number jumps to 72%. His theory is based on the “cascade effect” of how trauma and stress (including changes in the chemicals listed above) lead to brain abnormalities.

So, to the major structures in the brain:

1. The hippocampus – helps process the declarative memories and emotions and critical for learning. It is part of the limbic system and allows individuals to “process normal memories and manage the emotions associated with them. [Spiegel] WIth PTSD, reduced activation in the hippocampus leads to improper storage and/or processing and recall of these autobiographical memories – amnesia for traumatic events. [Chapman] In addition, increased levels of glutamate may cause cell damage in the hippocampus [Banks]. To corroborate this, left-hippocampus is smaller in abuse victims who are diagnosed with DID. [Tiecher] (More on this later.)

2 The amygdala – is associated with unconscious storage and processing of emotions and initiating the flight-or-flight response. It is a cluster of nuclei near the brain’s emotional control center. It is part of the limbic system and is associated with fear in response to sensory inputs (visual, auditory, etc). It can stimulate in a near instant in response in the sympathetic nervous system.

The amygdala doesn’t appear to activate with recall of normal events. However, when the amygdala modulates hippocampal activity, memories can be enhanced. Lesions in the amygdala have eliminated conditioned fear. Fear conditioning actually causes changes in plasticity of the amygdala. With PTSD the amygdala becomes hypersensitive, explaining why memories can feel so powerful. [Chapman]

Additionally, the hippocampus does interact with the amygdala, so events with a strong emotional content involve both the hippocampus and the amygdala. A great example is when you heard about 9-11. You remember where you were, what happened, and the emotions you felt. A normal stress response was activated, but not abnormal enough to cause the facts to be separated from the emotional recall (unless you were at the scene or somehow very intimately involved).

While some stress strengthens the system, “childhood sexual abuse does the opposite: it sensitizes the individual to subsequent stressors decades later.” [Spiegel] Repeated abuse causes increased irritability of the limbic system, which causes the amygdala to signal danger even when there is no apparent threat. Temper tantrums and crying spells are symptoms of a constantly firing amygdala. Decreased size correlates with increased depression and irritability. Dr. Bruce Perry, a neuroscientist who heads the nonprofit research center, the Child Trauma Academy in Houston reports,

”A maladaptive amygdala makes an abused child recoil in fear at the drop of a hat.”

3. Cerebellar vermis – structure between the cerebellar lobes that is linked proprioception and the information regarding the body’s movement through space. Trauma causes reduced activity in this area.

4. The cortex – associated with rational thinking and critical for learning. Includes the medial pre-frontal cortex (orbitofrontal cortex and anterior cingulate): Exerts some regulatory control over the amygdala. [Banks] Damage causes a decrease in self-reflection and self-awareness, and an increase in emotional instability and apathy.

5. Corpus collosum – thick “highway” band of neurons connecting the left and right hemispheres of the brain. Decreased myelination (sheath around neural axons that is required for proper signaling among neurons) decreases the thickness of the corpus collosum and decreases the integration of these two hemispheres. So what does this mean?

” In one study, adults with no history of abuse showed bilateral involvement in memory of both neutral and traumatic memories, while adults with a childhood trauma history showed activation of the left hemisphere during neutral memories with a marked shift to right hemisphere activation with disturbing memories”

Early exposure to stress causes the following, according to Teicher’s cascade model:

1. Stress-response systems are activated. This changes their molecular organization by changing their sensitivity and response bias. This means normal responses to stressors can be exaggerated. “Increased fearfulness and anxiety and enhanced hormonal response to stress.” (See full article for the gory details.)

2. Changes in stress hormones affects normal childhood development (e.g., myelination, programmed cell death, and genesis of new neurons and synapses).

3. Different brain regions have different sensitivity, partly due to genetics, gender, timing, rate of development and density of glucocorticoid receptors.

And finally, he proposes that these changes “increase vulnerability to neuropsychiatric consequences, including dissociative identity disorder.”

So what about this left brain/right brain stuff?

Since one aspect of the development of DID involves decreased communication between the left and right hemispheres of the brain, let’s recall a bit about that first.

Some of these topics can get complicated, and I am amused and pleased to find that there are a few websites that explain some complicated science ideas for kids. Chundler’s Neuroscience for kids – Hemispheres is just such a page. It explains split-brain experiments and summarize the basic functions of each hemisphere.

The dominant functions for the left hemisphere include language, math and logic. Right brain dominant functions include spatial abilities, face recognition, visual imagery, and music. Now, these are not set in stone, and surgeons will often test for specific areas for language, for example, before performing brain surgery to make sure they avoid damaging important areas. [Chundler]

Why is this important? Well, during development of the brain from birth through about five years old, extensive changes to the size of the brain, the number of neurons, and their connectivity occur. Myelination increases brain size – this is the creation of layers around neural cells which increase the speed of information processing. Neurons connect to one another for communication (synaptic connections), and the connectivity is dependent upon our experiences in childhood. We start with many more neurons than we need, and about 50% are programmed to die as connections are established. [Chunder]

These changes that occur in the brain during development are called plasticity, and this nature decreases over time. An interesting and important aspect is that the decrease in plasticity over time is different for different systems in the brain. Some areas of the cortex continue to reorganize with experience until late in life, while others such as language centers are less likely to change. [Perry]

Trauma affects this normal development. These changes are not easily reversed, which is why trauma that occurs before the age of about five tends to facilitate the development of DID.

Dissociative identity disorder may be a result of an extreme of reduced hemispheric integration. One study indicated that patients diagnosed with DID had a much greater degree of left hemisphere activation. It is theorized that switches between identities may be related to transition to a right hemisphere dominant mode. [Teicher]

Another proposal

Putnum proposes a different model that the orbitalfrontal cortex (OFC) is the locus of this fragmented consciousness, or dissociative states. She bases this on the idea that normally children integrate different behavioral states to create an integrated “sense of self.” But, trauma affects this integration and consolidation.

Forrest adds to this. She proposes that because dopamine and norepinephrine are primary neurotransmitters in the OFC, that their disregulation affects the OFC’s role in “healthy adult humans to be conscious of and have mental representations of their past, present and future subjective experiences.”

Since DID is associated with amnesia and splitting off of experiences, the OFC is involved. [Forrest]


In the quest for more facts and concrete evidence, researchers have turned to brain imaging techniques to look for differences in individuals with and without DID, and also for the same individual in different alter states.

Neuroimaging studies such as PET scans and fMRI studies have purported to show the brain areas involved in personality switching and differential access of different personality states to autobiographical memories of childhood trauma.

Tsai reported fMRI (functional magnetic imaging) study with one woman who could control a switch between two personalities. fMRI allows imaging of the brain during functional tasks, to see what areas of the brain change, in real time. While the study is small and the woman had a dual diagnosis of PTSD and DID, he observed a significantly smaller hippocampal volume than normal.

This study suggests that personality switches in DID may be produced by alterations in hippocampal and temporal function.

Another study by Reinders use a PET (positive emission tomography) scanner to study the patterns of brain activation in 11 women with DID. Each could switch between one of two personalities – one that was “traumatic” and the other “neutral”. A traumatic personality was defined as one with access to the trauma, while the neutral personality was either amnesic to the event, or reacted “as if the event did not happen to them.”

Scripts of traumatic and nontraumatic events were read to each participant and personality. The trauma scripts produced an inhibition of activity in several areas of the brain, including the temperal lobes, suggesting that the neutral personalities had difficulty recognizing the trauma as their own. This “blocking”, as Reinders reiterates, is a normal defense mechanism to allow survivors to function somewhat normally. In addition, a difference in cerebral blood flow was noted. The authors conclude:

Our results indicate the possibility of one human brain to generate at least two distinct states of self-awareness, each with its own access to autobiographical trauma-related memory, with explicit roles for the medial prefrontal cortex and the posterior associative cortices in the representation of these different states of consciousness.

Individuals who are dissociating have lower activity in areas of the brain surrounding the hippocampus when they listen to accounts of their traumas. Processing of the memories and incorporating the emotional content are hindered. [Lanius]

Using MRI, a decrease in both hippocampal volume (19.2%) and amygdalar volume (31.6%) was observed in subjects with dissociative identity disorder as compared to the healthy subjects. The difference was statistically significant. [Vermetten]


Regarding these experiments – several researchers have commented that cause and effect has not been established. It may be possible that stress causes smaller hippocampal and amygdala volumes, or that smaller hippocampal and amygdalavolumes make an individual more susceptible to PTSD [Gilbertson] and DID. Or even that larger volumes may be associated with a protective effect. [Vermetten]

Two heads are not better than one when they share the same brain. The fragmentation of mental function that can occur after a series of traumatic experiences may both protect a person from distress and make it harder for the individual to put the trauma into perspective. As we come to appreciate the complexity of neural development, we also understand that early life experiences have a profound effect on the developing brain. [Spiegel]

Can these changes be undone?

Ta da! There is a biological basis for this psychological disorder! But can they be undone?

Wow – the question of the century.

I read an interesting article in Discover this month about the renewed interest in the use of Schedule 1 drugs such as psilocybin (the psychoactive ingredient in the hallucinogenic mushrooms), LSD, and MDMA (3,4-methylenedioxymethamphetamine or Ecstasy) on people with severe PTSD. [Marsa]

The cornerstone of PTSD treatment involves reliving the trauma in a way that enables patients to process their fears in a rational way. But by definition, revisiting the experience can be frightening, and people often become locked in the grip of intense anxiety.

The drug MDMA, a chemical cousin of mescaline and methamphetamine, can kindle intense euphoria or sublime seren­ity, creating a calming therapeutic environment in which to revisit trauma. [Marsa]

Studies have shown positive effects with individuals with trauma, reducing symptoms dramatically in a little as two sessions. [Marsa, Newton]

This idea is not new and was explored with some great success in the 1960’s and 70’s with veterans. LSD and other psychedelics were legally sanctioned for use to treat individuals with a range of psychiatric issues such as “schizophrenia, autism, drug addiction, alcoholism, and chronic depression…heroin addition, alcoholism.”

While the exact effect is not known, these drugs simulate the release of seratonin, dopamine, and norepinephrine, stimulate an array of brain structures: “the prefrontal cortex, which is the center of executive functioning; limbic regions such as the amygdala that govern our emotional life and the formation of memories” [Marsa]

Are we just fragmented computer systems?

Some researchers are attempting to show reversal of these observed psychobiological changes in animal studies after anectodal evidence with patients suggests this may be possible. [Kendell]

The brains of adult survivors are fragmented and resemble a hard drive on a computer that has crashed. [Oak]

Ouch. I agree with the reference up to the part where the hard drive “crashes.” That implies that the data cannot be recovered. Instead, I’d like to suggest an alternative analogy which may be more “techyy” but I think more descriptive:

The brains of adult survivors are fragmented and resemble a hard drive on a computer that needs to be defragmented. Clusters may be forever lost, but some files can be reconstructed.

Too bad, though, that we can’t be defragged as easily and quickly as our computers by selecting Accessories -> System Tools -> Disk Defragmenter.


Chudler EH. (2006). Neuroscience for kids – Hemispheres. Accessed from http://faculty.washington.edu/chudler/split.html

Banks A (Summary by Patricia Papernow) (2004). Relational Approach to the Neurobiology of PTSD and Dissociation: Can medications enhance therapeutic effectiveness? Presentation to NESTTD Society for the Treatment of Trauma and Dissociation’s Annual Meeting, accessed from http://www.nesttd.org/Amy%20Bank%20Summary.htm

The Biological Psychology of Dissociative Identity Disorder: Developmental Neurobiology of DID, accessed from http://home.earthlink.net/~maiziekelly/DevNeuro.htm

The Biological Psychology of Dissociative Identity Disorder: Neurobiologial Etiology of DID, accessed from http://home.earthlink.net/~maiziekelly/EtiolDID.htm

Chapman H. (???) Emotion and memory. Guest Lecture, University of Toronto, accessed from http://www.psych.utoronto.ca/users/ferber/Emotionandmemory.pdf

Diehl ES (). Psychobiology of Trauma, from the Florida Council of Sexual Abuse Services newsletter, accessed from http://www.healing-arts.org/tir/n-r-diehl.htm

Donna William’s Blog. (2006). Losing Time – Dissociative Identity Disorder and the real time travellers, accessed from http://blog.donnawilliams.net/2006/03/16/losing-time-dissociative-identity-disorder-and-the-real-time-travellers/

Forrest KA. (2001). Toward an etiology of dissociative identity disorder: a neurodevelopmental approach. Consciousness and Cognition, 10, 259-293.

Gilbertson MW. (2002). Smaller Hippocampal Volume Predicts Pathologic Vulnerability to Psychological Trauma, Nature Neuroscience, 2002, 5 (11), 1242-1247, accessed from http://www.trauma-pages.com/a/gilbertson-2002.php

Kendell J. (2002). How child abuse and neglect damage the brain, Boston Globe, accessed from http://www.snapnetwork.org/psych_effects/how_abuse_andneglect.htm

Lanius, RA, et al. Brain Activation during Script-Driven Imagery Induced Dissociative Responses in PTSD: A Functional Magnetic Resonance Imaging Investigation. Biological Psychiatry 2002; 52(4): 305-311.

Marsa L. (2008). Could an Acid Trip Cure Your OCD? Researchers are again using mind-bending drugs as a means of treating mental disorders. Discovery Magazine, 5-16-2008, accessed from http://discovermagazine.com/2008/jun/16-could-an-acid-trip-cure-your-ocd/article_view?b_start:int=0&-C=

Newton C. (2001). FDA OKs Clinical Testing of Ecstasy, The Associated Press, Tuesday, Nov. 6, 2001; 9:52 p.m. EST, accessed from http://www.washingtonpost.com/wp-srv/aponline/20011106/aponline215233_000.htm

Morgan, CA, et al. Symptons of Dissociation in Healthy Military Populations: Why and How Do War Fighters Differ in Responses to Intense Stress? In E Vermetten, MJ Dorahy, and D Spiegel, eds., Traumatic Dissociation Neurobiology and Treatment, 157-179. Washington, DC: American Psychiatric Publishing, 2007.

Oak A. (2002), Survivors Project, Greenfield, MA

Perry D. (1999). Memories of Fear: How the Brain Stores and Retrieves Physiologic States, Feelings, Behaviors and Thoughts from Traumatic Events, Trauma Child Academy, originally from “Splintered Reflections: Images of the Body in Trauma” (Edited by J. Goodwin and R. Attias) Basic Books (1999), accessed from http://www.childtrauma.org/ctamaterials/memories.asp

Putnam FW, Zahn TP, Post RM (1990). “Differential autonomic nervous system activity in multiple personality disorder”. Psychiatry research 31 (3): 251-60. doi:10.1016/0165-1781(90)90094-L . PMID 2333357.

Reinders, A.A.T.S., Nijenhuis, E.R.S., Paans, A.M.J., Korf, J., Willemsen, A.T.M., and den Boer, J.A. (2003). One brain, two selves. Neuroimage, 20, 2119-2125.

Reinders, A.A.T.S., Nijenhuis, E.R.S., Quak J, et al. (2006). Psychobiological Characteristics in Dissociative Identity Disorder: A symptom provocation study, BIOL PSYCHIATRY 2006;60:730–740, accessed from http://hal.psych.uw.edu.pl/2006zalaczniki/did%20pet.pdf

Spiegel D. (2008). Coming Apart: Trauma and the Fragmentation of the Self, The Dana Foundation, accessed from http://www.dana.org/news/cerebrum/detail.aspx?id=11122

Teicher MH. (2002). Developmental neurobiology of childhood stress and trauma. Psychiatric Clinics of North America, 25, 397-426.

Tsai, Guochuan E. MD PhD, Condie, Donald MD, Wu, Ming-Ting MD, Chang, I-Wen BA. (1999). Functional magnetic resonance imaging of personality switches in a woman with dissociative identity disorder. Harvard Review of Psychiatry, 7, 119-122.

van der Kolk B (2002). The Body Keeps The Score: Memory & the Evolving Psychobiology of Post Traumatic Stress, Harvard Review of Psychiatry, 1994, 1(5), 253-265, accessed from http://www.trauma-pages.com/a/vanderk4.php

Vermetten E. (2006). Hippocampal and Amygdalar Volumes in Dissociative Identity Disorder, Am J Psychiatry 163:630-636, accessed online from http://ajp.psychiatryonline.org/cgi/content/full/163/4/630



  emilylonelygirl wrote @

Karen posted a comment here that I managed to delete in my spam filter, but she emailed the information to me:
You can do a search in http://www.pubmed.org for hippocampus volume PTSD.

I am pleased to see how much more information and research has been done in the past three or four years.

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA. jdbremn@emory.edu
Posttraumatic stress disorder (PTSD) is associated with long-term changes in neurobiology. Brain areas involved in the stress response include the medial prefrontal cortex, hippocampus, and amygdala. Neurohormonal systems that act on the brain areas to modulate PTSD symptoms and memory include glucocorticoids and norepinephrine. Dysfunction of these brain areas is responsible for the symptoms of PTSD. Brain imaging studies show that PTSD patients have increased amygdala reactivity during fear acquisition. Other studies show smaller hippocampal volume. A failure of medial prefrontal/anterior cingulate activation with re-experiencing of the trauma is hypothesized to represent a neural correlate of the failure of extinction seen in PTSD. The brain has the capacity for plasticity in the aftermath of traumatic stress. Antidepressant treatments and changes in environment can reverse the effects of stress on hippocampal neurogenesis, and humans with PTSD showed increased hippocampal volume with both paroxetine and phenytoin.
PMID: 18037014 [PubMed – indexed for MEDLINE]
Related Articles

* Stress and brain atrophy. [CNS Neurol Disord Drug Targets. 2006]
* Traumatic stress: effects on the brain. [Dialogues Clin Neurosci. 2006]
* Alterations in brain structure and function associated with post-traumatic stress disorder. [Semin Clin Neuropsychiatry. 1999]
* Neural correlates of declarative memory for emotionally valenced words in women with posttraumatic stress disorder related to early childhood sexual abuse. [Biol Psychiatry. 2003]
* Circuits and systems in stress. II. Applications to neurobiology and treatment in posttraumatic stress disorder. [Depress Anxiety. 2002]
* » See all Related Articles…

  Comment: Emotional Flashbacks « Emily First Girl wrote @

[…] body remembers. And now that I did the research to understand how emotional memories of trauma are stored differently than normal narrative […]

  ClinicallyClueless wrote @

This was an excellent post and it is exactly the type of information that I have been looking into. My therapist has been teaching me about this which has been helpful in not blaming myself for the things and thoughts that I have now. It is gaining awareness enough to try a different neuro pathway to form. Thank you. I love your site.

  neural bases of language wrote @

[…] PTSD because the conditions travel as a group: 1. Normal factual memories are stored in one part ofhttps://emilyfirstgirl.wordpress.com/2008/05/22/whats-going-on-in-the-brain-with-did-biological-marke…Top Scoops Scoop.co.nzThe most potent weapon in the hands of the oppressor is the mind of the […]

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