# I found a very interesting medical study and a medication(PRAZOSIN) PLEASE READ



## nocturnalman (Nov 15, 2017)

Before I got DR/DP out of curiosity I used to read about the functions of the brain.I mostly read about the prefrontal lobe of the brain ,how a lie detector detecs if a person is lying or not.The prefrontal lobe is also responsible for complex cognitive behavior, personality expression, decision making, and moderating social behavior.

It is well known that traumatized people have problems with social interactions.Why do many people who are traumatized like to keep to themselves ? Also trauma greatly affects the personality of a person ,as we can read here a lot ,many of us feel that their personality has changed ,that they can't identify or enjoy what they used to like and do in the past.

Now I have found this research study https://www.sciencedirect.com/science/article/pii/S2352289514000101 with the title

"The effects of stress exposure on prefrontal cortex: Translating basic research into successful treatments for post-traumatic stress disorder"

The whole study says :

"Research on the neurobiology of the stress response in animals has led to successful new treatments for Post-Traumatic Stress Disorder (PTSD) in humans. Basic research has found that high levels of catecholamine release during stress rapidly impair the top-down cognitive functions of the prefrontal cortex (PFC), while strengthening the emotional and habitual responses of the amygdala and basal ganglia. Chronic stress exposure leads to dendritic atrophy in PFC, dendritic extension in the amygdala, and strengthening of the noradrenergic (NE) system. High levels of NE release during stress engage low affinity alpha-1 adrenoceptors, (and likely beta-1 adrenoceptors), which rapidly reduce the firing of PFC neurons, but strengthen amygdala function. In contrast, moderate levels of NE release during nonstress conditions engage higher affinity alpha-2A receptors, which strengthen PFC, weaken amygdala, and regulate NE cell firing. Thus, either alpha-1 receptor blockade or alpha-2A receptor stimulation can protect PFC function during stress. Patients with PTSD have signs of PFC dysfunction. Clinical studies have found that blocking alpha-1 receptors with prazosin, or stimulating alpha-2A receptors with guanfacine or clonidine can be useful in reducing the symptoms of PTSD. Placebo-controlled trials have shown that prazosin is helpful in veterans, active duty soldiers and civilians with PTSD, including improvement of PFC symptoms such as impaired concentration and impulse control. Open label studies suggest that guanfacine may be especially helpful in treating children and adolescents who have experienced trauma. Thus, understanding the neurobiology of the stress response has begun to help patients with stress disorders."

SO ,since this study says that chronic stress releases catecholamine (adrenaline ,noradrenaline ,dopamine) that rapidly impair cognitive functions how profound is the release of those catecholamies during a long phase of panic attacks ,lets say on a bad weed trip ?

The study also says Chronic stress exposure leads to dendritic atrophy ,so I think this is an important point in weed/panic attack induced DR/DP.

After I read this study I strongly believe that the high anxiety caused by weed or a panic attack ,has caused some damage (dont worry ,the brain can repair itself) in the above mentioned receptors.Therefore we might have a hint that we need to fix this issue.

I might become a geniua pig and try this medication.I will discuss this with a good doctor and report back to you.


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## nickcb96 (Jun 27, 2017)

Keep us updated on how it goes!


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## Broken (Jan 1, 2017)

Interesting, I also compare DPD to PTSD (or complex PTSD in my case), but think of it as more dissociative and related to personality traits AND trauma (or multiple trauma/abuse), as opposed to just one trauma causing PTSD.

Another study of a DTI scan in DPD also implicated the basal ganglia as a cause for symptoms. Perhaps as dopamine is involved with reward, pleasure and alertness which are numb. There isn't a lot of studies that include the hippocampus of amygdala but I think they are without a doubt involved.


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## TDX (Jul 12, 2014)

> which rapidly reduce the firing of PFC neurons, but strengthen amygdala function


There is just one catch about your idea: This is the *inverse* pattern of what was actually found in depersonalization. In depersonalization disorder areas of the prefrontal cortex were found to be overactive and the amygdala underactive. PTSD patients with depersonalization symptoms also show a somewhat similar pattern.



> Another study of a DTI scan in DPD also implicated the basal ganglia as a cause for symptoms.


Which one do you mean?


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## Broken (Jan 1, 2017)

http://www.dpselfhelp.com/forum/index.php?/topic/73882-dti-study-been-waiting-a-while-for-this/

Unbelievably the study seems to have vanished from the Internet. I can't find it at all and the link on the website says the page is missing. It's a depersonalization conspiracy I tells ya!

It was a hard study to decipher but it said there were less connections to the basal ganglia and parietal cortex from what I could make out. Pretty annoyed I can't find it now


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