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Ecstacy studied video


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A tv show sponsored a study trial on Ecstacy..the most watched show in England for this tv show.. 

a lot to learn from this not so much about the drug

but things they teach about how the brain works... I am still watching it... should have had a pen handy.

 

http://www.dailymotion.com/video/xtwdw1_drugs-live-the-ecstasy-trial-1of2-couchtripper_tech

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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Terms I learned watching these two videos:

 

Default mode network  http://en.wikipedia.org/wiki/Default_mode_network

It has been hypothesized to be relevant to disorders including Alzheimer's diseaseautismschizophrenia,depressionchronic pain and others.[5] In particular, a failure to deactivate default network activity during cognitively demanding tasks is associated with autism,[11] overactivity with schizophrenia,[12] and the default network is preferentially attacked by the buildup of beta-amyloid in Alzheimer's disease.[13] Lower connectivity was found across the default network in people who have experienced long term trauma, such as childhood abuse. Among people experiencing posttraumatic stress disorder, lower activation was found in the posterior cingulate gyrus compared to controls (Dr. Ruth Lanius, Brain Mapping conference, London, November 2010). Hyperconnectivity of the default network has been linked to rumination in depression[14] and chronic pain.[15]

 

 

posterior cingulate cortex (PCC)

http://brain.oxfordjournals.org/content/early/2013/07/18/brain.awt162

The posterior cingulate cortex (PCC) forms part of the posteromedial cortex. It is highly anatomically connected (Hagmann et al., 2008), has a high baseline metabolic rate (Raichle et al., 2001), and is a central part of the default mode network (DMN) (Buckner et al., 2008). Despite its importance in health and disease, the PCC is notably absent from many systems-level models of brain function, and there is no clear consensus about its function (Leech et al., 2012).

 

One influential hypothesis is that the PCC has a central role in supporting internally directed cognition (Raichle et al., 2001Buckner et al., 2008). The PCC shows increased activity when individuals retrieve autobiographical memories or plan for the future, as well as during unconstrained ‘rest’ when activity in the brain can be thought of as cognitively ‘free-wheeling’ (Gusnard et al., 2001Addis et al., 2007Mason et al., 2007). However, other evidence suggests that the PCC plays a more direct role in regulating the focus of attention (Gusnard and Raichle, 2001Hampson et al., 2006Hahn et al., 2007), perhaps controlling the balance between internally and externally focused thought (Leech et al., 2011). In addition, activity in the PCC varies with arousal state, and its interactions with other brain networks may be important for conscious awareness (Vogt and Laureys, 2005).

An important consideration is the degree to which the PCC is functionally homogeneous. Although it covers a relatively large area of cortex it is often discussed as having a unitary function. Functional MRI studies have repeatedly shown relative deactivation during many types of cognitively demanding tasks, such as a visual discrimination task (Singh and Fawcett, 2008). However, recent work suggests that focusing on overall changes in relative blood flow can be misleading as the region shows a complex functional organization (Vogt et al., 2006Margulies et al., 2009Dastjerdi et al., 2011Leech et al., 2011). For example, we have recently found evidence for ‘echoes’ or traces of the activity of multiple functionally discreet large-scale brain networks within the PCC (Leech et al., 2012).

The PCC also shows abnormal structure and function in many diseases (Zhang and Raichle, 2010). For example, early amyloid deposition and reduced metabolism is seen in Alzheimer’s disease (Johnson et al., 1998Greicius et al., 2004Buckner et al., 2005). Functional neuroimaging studies also show abnormalities in a range of neurological and psychiatric disorders including schizophrenia, autism, depression and attention deficit hyperactivity disorder (ADHD), as well as ageing (Buckner et al., 2008Greicius, 2008). Our own work has consistently shown abnormal PCC function following traumatic brain injury that relates to the pattern of cognitive impairment (Bonnelle et al., 20112012;Sharp et al., 2011). These results suggest that an accurate description of the function of the PCC will be important to the understanding of a wide range of diseases.

 

Here we review the anatomy and physiology of the PCC, including its atypical structural connectivity and elevated metabolism, before discussing its possible functions. We go on to discuss the impact of disease on the PCC, discussing this in the context of current theories of brain network function. We then synthesize key findings and propose a novel model of PCC function. We distinguish dorsal and ventral parts of the PCC and propose that the function of these subcomponents can be explained by considering: (i) arousal state; (ii) whether attention is focused internally or externally; and (iii) the breadth of attentional focus (ABBA: Arousal, Balance and Breadth of Attention model). We then outline a mechanistic explanation of elements of the model that uses a complex dynamic systems approach to studying brain function. We propose that the dorsal PCC plays a role in tuning the metastability of intrinsic connectivity networks, which allows control of how variable neural activity is across time in these networks, and so influences attentional focus.

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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