Hi everyone ^_^
I was wondring if there is a specific technique to study the chemical change responsible for DID and I want to know if I could follow a specific procedure to the neurochemicals behinde this disorder and how the alteration vary between a normal person and a DID patient? also, the most important thing is finding a specific drug to cure this disorder. I know that there are drugs that help the patients endure anixty and depression come with this disorder but there is no direct and specific cure for DID.
I read that contextual treatment helped the patient somehow to know themselves and some of them return the control and can change from one personlaity to the other when they want but it didn't work for most of them although it benfits them somehow but not cure them. So; I read a lot of artiles and reviews from the litreture but most of them focused in the contextual treatment not chemical based treatment!!
I don't know if this is right or not but I think this return to neuropsychopharmacology and I'm a chemistry master student so I want to know if there is a possibility to study this in my thesis project and if I need a high tech equipments to do that?
Sar, V., S. N. Unal, and E. Ozturk. “Frontal and Occipital Perfusion Changes in Dissociative Identity Disorder.” Psychiatry Research: Neuroimaging 156.3 (2007): 217–23. /z-wcorg/. Web. Schore, Allan. “Attachment and the Regulation of the Right Brain.” Attachment & Human Development 2.1 (2000): 23. /z-wcorg/. Web. Vermetten, Eric, et al. “Hippocampal and Amygdalar Volumes in Dissociative Identity Disorder.” The American Journal of Psychiatry. 163.4 (2006): 630. /z-wcorg/. Web. Weniger, G., et al. “Amygdala and Hippocampal Volumes and Cognition in Adult Survivors of Childhood Abuse with Dissociative Disorders.” Acta Psychiatrica Scandinavica 118.4 (2008): 281–90. /z-wcorg/. Web.
Dissociative Identity Disorder - Neuroscience News https://neurosciencenews.com/ai-did-brain-10312/ Dec 7, 2018 - Summary: Machine learning algorithms were able to distinguish, with 73% accuracy, neurobiological differences between those with ...
Dissociation and Alterations in Brain Function and Structure - NCBI - NIH https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5283511/ by A Krause-Utz - 2017 - Cited by 14 - Related articles Jan 30, 2017 - In this article, we provide an overview of neurobiological models of dissociation, primarily based on research in DDD, DID, and D-PTSD.
PDF) The Neuropsychiatry of Dissociative Identity Disorder: Why Split ... https://www.researchgate.net/.../316428531_The_Neuropsychiatry_of_Dissociative_Ide... May 16, 2017 - This reviews suggests that the patients of DID have structural changes in the limbic system ... about the possible causes and mechanism behind this disorder. ..... e study concluded - that on a neurobiological level, the.
SOMATOFORM & DISSOCIATIVE DISORDERS www2.hawaii.edu/~heiby/Somatoform_and_Dissociative_DX.html May have physical cause that is not understood. Cannot prove null ... Dissociative Identity Disorder .... Biological/medical : stress related neurotransmitter
Fascinating research to come, I believe. There is still so much debate.
If you want to specifically measure chemicals in the brain, then you cannot do it when the subject was alive. Psychiatry is still clouded in mystery, as we cannot objectively measure many things we theorize. It was likely easier to measure brain wave or structural abnormalities from X-ray or MRI. However, even those do not provide reliable outcome, as the changes vary depending on the individuals and specific cut off to determine which is normal and which is not is still debatable. I'd like to brief you about the difficulty faced when measuring chemicals, hoping that one day any one can overcome it.
When we measure chemicals in the brain, we cannot use chemicals in the blood. The problem is because there is a tight clutter of cells preventing large chemicals to pass through, which is termed blood brain barrier. As neurotransmitter (neurochemicals in the brain) cannot pass through this junction, even if we measure it's concentration in the blood, it's hard to make connection with it's level in the brain. It might even be possible that the level in the blood increases while the level in the brain decreases. There are already methods to measure neurotransmitter in urine as representative of it's concentration in the blood, but it's very much debatable as there is no reliable argument of how it reflects anything in the brain.
The second problem is that the neurotransmitter in the brain mainly exists inside neurons (neural cells). When a neuron is active, it would then release neurotransmitter to the next neuron to pass electrical signals. It was a very quick release through junction between neurons, which is called synapse. Once the neuron goes inactive, the excess neurotransmitter in the synapse get recollected (reuptake). Even if we measure the neurotransmitter inside the neuron, it might not be a good clue about how much the chemical is used during neuron activation. And measuring it when it was in synapse for a very brief time is quite an obstacle. Instead, we may be able to measure the amount of neurotransmitter receptors the neuron has. As receptor is necessary during release of neurotransmitter, the increasing amount of receptors reflect the increasing activitty of neurotransmitter. However, receptor is not soluble and remain attached to the neuron. One of the way to visualize it is by sending "dummy neurotransmitter" attached with radioluscent materials visible in X-ray or MRI (so that they attach to the receptors and we can see how much receptor is there). but even then, the result is variable as we mostly use animal study, which may or may not have psychiatric disorder (animal model is yet another obstacle as we cannot diagnose animal with interview).
The third problem is that many neurons use the same neurotransmitter, while they may convey completely unrelated information. Let's assume that we see three neuron and name it neuron A, neuron B, and neuron C. Increase of total amount of neurotransmitter in a single place does not necessarily mean all individual pathways got more active. Even if certain neurotransmitter increases by two-fold the concentration, it doesn't mean the activity of neuron A is increased as well. And each of these three neurons may govern completely different pathways and completely different inputs, even when the target area is close by.
Wow!! It is really difficult 😐 thanks so much because you gave me a glance at the difficulties which is very important to me. I will read more Insha'allah. I hope one day we can overcome those barriers 🤗
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