Dissociative Fugue especially shares a lot of traits with my MLCer.
I can pick out immediately from this list the ones that I know for sure (it's a given there are things he didn't tell me):
gaps in your memory
distorted views of your body
forgetting important personal information
a sense of detachment from your emotion
internal voices and dialogue
feeling detached from the world
feeling that a customary environment is unfamiliar
a sense that what is happening is unreal
forgetting a talent or learned skill
a sense that people you know are strangers
feeling you don’t know who you are
acting like different people, including child-like behaviour
being unsure of the boundaries between yourself and others
feeling like a stranger to yourself
referring to yourself as ‘we’
being told by others that you have behaved out of character
writing in different handwriting
And just to geek out a bit on it (I think the thread title would allow for that
):
http://en.wikibooks.org/wiki/Textbook_of_Psychiatry/Dissociative_Disorders/PathogenesisIn the area of neurobiological research, multiple studies were done that confirm the presence of physiological changes associated with dissociative symptoms. As already mentioned, there is a hypothesis that early psychological trauma or abuse (i.e., stress) can mediate the development of those changes. To date, several neurotransmitter systems have been implicated in the development of Dissociative Disorders: Hypothalamo-Pituitary-Adrenal Dysfunction (HPA), Glutamate/N-methyl-D-aspartate (NMDA) receptor, Serotonin 5-HT2a, 5-HT2c, ?-aminobutyric acid (GABA), and Opioid receptors.
The HPA axis is known to play a central role in medicating the stress response. Several studies on this have been done to date. Most of them presented similar findings showing that individuals with dissociative symptoms have basal HPA-axis hyperactivity with elevated cortisol and diminished pituitary negative-feedback inhibition (Simeon, 2006).
As an extension of this dysregulation due to stress, some research was performed using neuroimaging. In both animal and human studies, stress at a young age has been shown to be associated with changes in the structure of the hippocampus. Smaller hippocampal and amygdalar volumes in patients with dissociative symptoms have been reported by some researchers (Vermetten, 2006). Decreased hippocampal volume may be explained by stress exposure; the hippocampus is a major target organ for glucocorticoids, which are released during stressful experiences, and prolonged exposure to glucocorticoids can lead to progressive atrophy of the hippocampus. The exact mechanism that can lead to smaller amygdalar volume is unclear. It is possible that other neurotransmitters play a role in this change. In their study, D’Souza et al. (2006) proposed that dissociative symptoms, similar to psychosis, may be related to the inhibitory (GABAergic) deficits that cause unopposed stimulation of serotonin receptors. Lysergic acid diethylamide (LSD), dimethyltryptamine (DMT) work as agonists of serotonin 5-HT2a and 5-HT2c receptors, again suggesting a possible mediating role for serotonin in dissociation.
This throws a lot of thoughts my way about the effectiveness of supplements in a case like this (luckily most that I've read says talk therapy, not pharma, is the preferred treatment. Not a fan of pharma here!). Found this from
http://www.psychforums.com/dissociative-identity/topic116258.htmlso the difference between DID and schizophrenia could be that in DID, the brain produces strong and coherent semantic models (alters) that correspond to different appreciations of the outside world. In schizophrenia, on the other hand, the semantic coherence breaks down altogether.
the interesting thing is, schizophrenia, according to some researchers, is characterised by an excess of dopamine in the brain. Certain drugs that massively boost dopamine in the brain (such as cocaine) can temporarily induce schizophrenia-like symptoms in healthy subjects, such as semantic disintegration, paranoia and delusions.
I'm not sure about the dopamine factor in DID, but I know that I, personally, am frequently low on dopamine. Now here's the thing: I have also noticed that once I increase my dopamine levels (through drugs or supplements), my mental fragmentation (i.e. separateness from alters) becomes less.
So this leads me to think: what if there is some kind of continuum, the extreme points of which are DID and schizophrenia, that is mediated by dopamine? so:
low dopamine - rigid semantic structures that can appear difficult to dissolve (e.g. amnestic walls between alters, difficulty integrating different structures/alters)
high dopamine - fluid and 'soft' semantic structure with a tendency to completely disintegrate.
I bring this up here because my xH had a marked period of cycling forward in spring 2012 after I'd suggested he take l-tyrosine, which is an amino acid that works to increase dopamine. It cut off abruptly when he stopped (I suspect at OW's urging based on a few clues).
All interesting data that just gives us a little more possible insight, I think.