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  3. Date: February 22, 2021 Source: University of Michigan Summary: When you slip into sleep, it's easy to imagine that your brain shuts down, but new research suggests that groups of neurons activated during prior learning keep humming, tattooing memories into your brain. https://www.sciencedaily.com/releases/2021/02/210222164216.htm When you slip into sleep, it's easy to imagine that your brain shuts down, but University of Michigan research suggests that groups of neurons activated during prior learning keep humming, tattooing memories into your brain. U-M researchers have been studying how memories associated with a specific sensory event are formed and stored in mice. In a study conducted prior to the coronavirus pandemic and recently published in Nature Communications, the researchers examined how a fearful memory formed in relation to a specific visual stimulus. They found that not only did the neurons activated by the visual stimulus keep more active during subsequent sleep, sleep is vital to their ability to connect the fear memory to the sensory event. Previous research has shown that regions of the brain that are highly active during intensive learning tend to show more activity during subsequent sleep. But what was unclear was whether this "reactivation" of memories during sleep needs to occur in order to fully store the memory of newly learned material. "Part of what we wanted to understand was whether there is communication between parts of the brain that are mediating the fear memory and the specific neurons mediating the sensory memory that the fear is being tied to. How do they talk together, and must they do so during sleep? We would really like to know what's facilitating that process of making a new association, like a particular set of neurons, or a particular stage of sleep," said Sara Aton, senior author of the study and a professor in the U-M Department of Molecular, Cellular and Developmental Biology. "But for the longest time, there was really no way to test this experimentally." Now, researchers have the tools to genetically tag cells that are activated by an experience during a specific window of time. Focusing on a specific set of neurons in the primary visual cortex, Aton and the study's lead author, graduate student Brittany Clawson, created a visual memory test. They showed a group of mice a neutral image, and expressed genes in the visual cortex neurons activated by the image. To verify that these neurons registered the neutral image, Aton and her team tested whether they could instigate the memory of the image stimulus by selectively activating the neurons without showing them the image. When they activated the neurons and paired that activation with a mild foot shock, they found that their subjects would subsequently be afraid of visual stimuli that looked similar to the image those cells encode. They found the reverse also to be true: after pairing the visual stimulus with a foot shock, their subjects would subsequently respond with fear to reactivating the neurons. "Basically, the precept of the visual stimulus and the precept of this completely artificial activation of the neurons generated the same response," Aton said. The researchers found that when they disrupted sleep after they showed the subjects an image and had given them a mild foot shock, there was no fear associated with the visual stimulus. Those with unmanipulated sleep learned to fear the specific visual stimulus that had been paired with the foot shock. "We found that these mice actually became afraid of every visual stimulus we showed them," Aton said. "From the time they go to the chamber where the visual stimuli are presented, they seem to know there's a reason to feel fear, but they don't know what specifically they're afraid of." This likely shows that, in order for them to make an accurate fear association with a visual stimulus, they have to have sleep-associated reactivation of the neurons encoding that stimulus in the sensory cortex, according to Aton. This allows a memory specific to that visual cue to be generated.The researchers think that at the same time, that sensory cortical area must communicate with other brain structures, to marry the sensory aspect of the memory to the emotional aspect. Aton says their findings could have implications for how anxiety and post-traumatic stress disorder are understood. "To me this is kind of a clue that says, if you're linking fear to some very specific event during sleep, sleep disruption may affect this process. In the absence of sleep, the brain seems to manage processing the fact that you are afraid, but you may be unable to link that to what specifically you should be afraid of," Aton said. "That specification process may be one that goes awry with PTSD or generalized anxiety." Story Source: Materials provided by University of Michigan. Note: Content may be edited for style and length. Journal Reference: Brittany C. Clawson, Emily J. Pickup, Amy Ensing, Laura Geneseo, James Shaver, John Gonzalez-Amoretti, Meiling Zhao, A. Kane York, Femke Roig Kuhn, Kevin Swift, Jessy D. Martinez, Lijing Wang, Sha Jiang, Sara J. Aton. Causal role for sleep-dependent reactivation of learning-activated sensory ensembles for fear memory consolidation. Nature Communications, 2021; 12 (1) DOI: 10.1038/s41467-021-21471-2
  4. Date: January 31, 2018 Source: University of Zurich Summary: Trauma-related disorders were previously classified under one single diagnosis -- post-traumatic stress disorder. Now, a representative survey carried out by a psychopathologist has shown for the first time how often such disorders are present in a more severe form. According to the findings, more than 0.5 percent of people in Germany suffer from complex post-traumatic stress disorder. ____________________________________________________________________________________________________________________________________ FULL STORY Post-traumatic stress disorder (PTSD) can sometimes occur in a particularly severe form, known as complex post-traumatic stress disorder. In both forms of PTSD, patients suffer from an over-activation of the memories of traumatic events -- in the form of images, smells, and sounds. In complex PTSD, patients also undergo personality changes and have difficulties with interpersonal relationships, in particular suffering from deep-seated mistrust, incapacity for intimacy, and greatly impaired self-worth. 1.5 percent suffering from classic PTSD Andreas Maercker, professor of psychopathology at the University of Zurich, together with researchers from Germany, carried out a representative survey. Around 2,500 adults across all age groups from more than 250 places in Germany completed the survey, which included questions about traumatic experiences such as war, rape, childhood sexual abuse, serious accidents, violence, natural disasters, kidnapping, witnessing a traumatic event, or other traumatic experiences. The researchers diagnosed around 0.5 percent of the women and men questioned as having complex PTSD, and 1.5 percent were found to have classic PTSD. Childhood sexual abuse is the critical factor "We found that the complex form of PTSD was most often present in people who had experienced sexual abuse in childhood or repeated sexual assaults as adolescents or adults," explains Andreas Maercker. Meanwhile, the more well-known classic form of PTSD was most often reported in people who had had serious accidents or directly witnessed a traumatic event. The results of Maercker's study are comparable with findings in Central Europe, where complex PTSD has been found to be mainly caused by experiences of sexual violence such as child abuse. "In other regions of the world where it is estimated that there is higher incidence of complex PTSD, causes also include prolonged experience of war, persecution, being held hostage, and torture," adds the UZH professor. Further research needed for better therapies "The creation of the new diagnosis of complex PTSD as distinct from the previously known form of PTSD was necessary because the two disorders require different therapeutic strategies," says Andreas Maercker. While for the classic form of PTSD, often just called "psychological trauma," there are good therapeutic options that can alleviate patients' suffering within several weeks or months, there are still few therapies offering successful outcomes for complex psychological trauma -- and further research is required. Academics from UZH are currently involved in studies into complex PTSD in refugees in Switzerland, as well as international studies in partnership with other researchers to look into new therapy options. Inclusion in the WHO classification of diseases (ICD) In 2013, Andreas Maercker, together with an international working group, made a proposal to the World Health Organization (WHO) to include the additional diagnosis of complex PTSD in the ICD. The disorder will be added to the WHO disorder classification in spring 2018. Story Source: Materials provided by University of Zurich. Note: Content may be edited for style and length. Journal Reference: Andreas Maercker, Tobias Hecker, Mareike Augsburger, Sören Kliem. ICD-11 Prevalence Rates of Posttraumatic Stress Disorder and Complex Posttraumatic Stress Disorder in a German Nationwide Sample. The Journal of Nervous and Mental Disease, 2018; 1 DOI: 10.1097/NMD.0000000000000790
  5. Hei Lars og beklager et svært sent svar. For å komme i kontakt med en psykomotorisk fysioterapeut, bør du forhøre deg om det finnes noen i området ditt f.eks. via psykologer eller ordinære fysioterapeuter. Pr. i dag trenger man ingen henvisning så vidt jeg vet, heller ikke til psykomotorisk fysioterapi, men det kan være opptil ett års venteliste. Forsøk å forhør deg om den enkelte fysioterapeuts kompetanse og se om denne har erfaring på din problemstilling/lidelse. Det kan variere en hel del. Lykke til!
  6. Hei. Jeg lurer på om dere har noen PMF-terapeuter med kompetanse innen PTSD-behandling i Oslo. Mvh Lars
  7. https://www.youtube.com/watch?v=MTwKja28Fzs dina handleder talar för det flaouapaoua så här får du en låt ifrån panda så du förstår att du inte är ensam längre och att det finns hopp att du ska sluta vända på dig ut och in för jag har också mått så och jag vet jag vet hur du mår jag stod med knytna nävar framför spegelen och jag slog mot mig själv jag tog en sax och skar mig över axelen jag brände mig med en varm skruvmejsel sen låg jag där på mattan sen låg jag där på mattan och nu när jag tänker tillbaka på allt har jag ett leende på läpparna för det gjorde mig stark kallar dem dig emo eller att du gör det för att va cool dem har ingen aning nej dem har ingen aning om hur det känns att inte veta vad som e fel vad som e fel jag stod med knytna nävar framför spegelen och jag slog mot mig själv jag tog en sax och skar mig över axelen jag brände mig med en varm skruvmejsel sen låg jag där på mattan sen låg jag där på mattan och nu när jag tänker tillbaka på allt har jag ett leende på läpparna för det gjorde mig stark så ta mitt ord istället för ditt blod så ta mitt ord istället för ditt blod jag stod med knytna nävar framför spegelen och jag slog mot mig själv jag stod med knytna nävar framför spegelen och jag slog mot mig själv jag tog en sax och skar mig över axelen jag brände mig med en varm skruvmejsel sen låg jag där på mattan... fa.an
  8. https://www.sciencedaily.com/releases/2020/05/200518145008.htm Scientists find brain center that 'profoundly' shuts down pain Date: May 18, 2020 Source: Duke University Summary: A research team has found a small area of the brain in mice that can profoundly control the animals' sense of pain. Somewhat unexpectedly, this brain center turns pain off, not on. It's located in an area where few people would have thought to look for an anti-pain center, the amygdala, which is often considered the home of negative emotions and responses, like the fight or flight response and general anxiety. A Duke University research team has found a small area of the brain in mice that can profoundly control the animals' sense of pain. Somewhat unexpectedly, this brain center turns pain off, not on. It's also located in an area where few people would have thought to look for an anti-pain center, the amygdala, which is often considered the home of negative emotions and responses, like the fight or flight response and general anxiety. "People do believe there is a central place to relieve pain, that's why placebos work," said senior author Fan Wang, the Morris N. Broad Distinguished Professor of neurobiology in the School of Medicine. "The question is where in the brain is the center that can turn off pain." "Most of the previous studies have focused on which regions are turned ON by pain," Wang said. "But there are so many regions processing pain, you'd have to turn them all off to stop pain. Whereas this one center can turn off the pain by itself." The work is a follow-up to earlier research in Wang's lab looking at neurons that are activated, rather than suppressed, by general anesthetics. In a 2019 study, they found that general anesthesia promotes slow-wave sleep by activating the supraoptic nucleus of the brain. But sleep and pain are separate, an important clue that led to the new finding, which appears online May 18 in Nature Neuroscience. The researchers found that general anesthesia also activates a specific subset of inhibitory neurons in the central amygdala, which they have called the CeAga neurons (CeA stands for central amygdala; ga indicates activation by general anesthesia). Mice have a relatively larger central amygdala than humans, but Wang said she had no reason to think we have a different system for controlling pain. Using technologies that Wang's lab has pioneered to track the paths of activated neurons in mice, the team found the CeAga was connected to many different areas of the brain, "which was a surprise," Wang said. By giving mice a mild pain stimulus, the researchers could map all of the pain-activated brain regions. They discovered that at least 16 brain centers known to process the sensory or emotional aspects of pain were receiving inhibitory input from the CeAga. "Pain is a complicated brain response," Wang said. "It involves sensory discrimination, emotion, and autonomic (involuntary nervous system) responses. Treating pain by dampening all of these brain processes in many areas is very difficult to achieve. But activating a key node that naturally sends inhibitory signals to these pain-processing regions would be more robust." Using a technology called optogenetics, which uses light to activate a small population of cells in the brain, the researchers found they could turn off the self-caring behaviors a mouse exhibits when it feels uncomfortable by activating the CeAga neurons. Paw-licking or face-wiping behaviors were "completely abolished" the moment the light was switched on to activate the anti-pain center. "It's so drastic," Wang said. "They just instantaneously stop licking and rubbing." When the scientists dampened the activity of these CeAga neurons, the mice responded as if a temporary insult had become intense or painful again. They also found that low-dose ketamine, an anesthetic drug that allows sensation but blocks pain, activated the CeAga center and wouldn't work without it. Now the researchers are going to look for drugs that can activate only these cells to suppress pain as potential future pain killers, Wang said. "The other thing we're trying to do is to (transcriptome) sequence the hell out of these cells," she said. The researchers are hoping to find the gene for a rare or unique cell surface receptor among these specialized cells that would enable a very specific drug to activate these neurons and relieve pain. This research was supported by the National Institutes of Health (DP1MH103908, R01 DE029342, R01 NS109947, R01 DE027454), the Holland-Trice Scholar Award, the W.M. Keck Foundation, and a predoctoral fellowship from the National Science Foundation. Story Source: Materials provided by Duke University. Original written by Karl Leif Bates. Note: Content may be edited for style and length. Journal Reference: Thuy Hua, Bin Chen, Dongye Lu, Katsuyasu Sakurai, Shengli Zhao, Bao-Xia Han, Jiwoo Kim, Luping Yin, Yong Chen, Jinghao Lu, Fan Wang. General anesthetics activate a potent central pain-suppression circuit in the amygdala. Nature Neuroscience, 2020; DOI: 10.1038/s41593-020-0632-8
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