Posted by: Steve Andreas in: Articles
The Structural Patterns of Change:
(A reorganization of reframing patterns)
Note: I have revised this presentation repeatedly since I first offered it several years ago, trying to make it clearer and more “user-friendly.” It is an attempt to summarize what I presented in my two-volume book, Six Blind Elephants (578 pp.) but which I failed to provide in those books. So it inevitably leaves out a lot of detail—and almost all of the examples. Please consider this a “work in progress” to be further refined in the future.
You can download this article as a PDF here:
Reframing is usually thought of as a relatively small part of NLP, originally divided into content reframing and context reframing, and later further divided into the 14 “sleight of mouth” patterns. However, I think that all change can be usefully described using one or more patterns of reframing, and all of these different patterns derive from only three variables. Every change of experience changes one or more of the following:
NLP is often defined as “The study of the structure of subjective experience.” The main difficulty in describing the structure of an experience of scope is that usually a scope is immediately categorized, and that nearly all the words we have to use to describe a scope indicate categories (except for proper nouns such as “John Smith” or “New York City”). Scope is what is experienced (seen, heard, felt, smelled, or tasted) before it is categorized or identified.
An example of this is hearing someone speaking a language you don’t understand; you can hear the sounds perfectly well, but you don’t know how to punctuate the stream of sounds into separate scopes of sounds, or what those scopes indicate. Or think of a time when you didn’t know what you were seeing or hearing; you could see it or hear it, but you couldn’t immediately categorize it. Usually an experience of this kind is immediately followed by a vigorous effort to identify what it is, because that is so useful in responding appropriately.
For simplicity, let’s first explore scope in a moment in time, as if the flow of time were stopped:
Each modality provides information that is different from the other modalities—though there is some overlap, such as location. (If there were no overlap, we wouldn’t be able to integrate the scopes from the different senses into the unitary experience we usually enjoy.)
Every still image will have submodalities, but only some will have partial enhancement that “highlights” one (or more) aspects of an image, drawing attention to it. This effect is often a factor in internal representations of importance or values, which are motivating (toward or away from) and if out of balance, may result in compulsions or addictions.
Even the shortest movie changes the scope of time, and this usually changes the scope of space. We typically punctuate our experience of time into segments of different length, with somewhat arbitrary beginnings and endings. The span of an “event” can vary from a “split-second” to days or months, or even a lifetime, before categorizing it, as in “That was a tough interview,” or “He had a good life.” A longer scope in time provides a larger context, similar to that provided by a larger context in space, the “bigger picture.” However, a larger context in either space or time usually makes it harder to notice the smaller details, unless you “zoom in” to magnify a part of the image.
Summary: Researchers have identified a link between traumatic brain injury and intestinal changes. A new study reports the intestinal changes may contribute to increased risk of developing infections and could worsen brain damage in TBI patients.
Source: University of Maryland School of Medicine.
University of Maryland School of Medicine (UMSOM) researchers have found a two-way link between traumatic brain injury (TBI) and intestinal changes. These interactions may contribute to increased infections in these patients, and may also worsen chronic brain damage.
This is the first study to find that TBI in mice can trigger delayed, long-term changes in the colon and that subsequent bacterial infections in the gastrointestinal system can increase posttraumatic brain inflammation and associated tissue loss. The findings were published recently in the journal Brain, Behavior, and Immunity.
“These results indicate strong two-way interactions between the brain and the gut that may help explain the increased incidence of systemic infections after brain trauma and allow new treatment approaches,” said the lead researcher, Alan Faden, MD, the David S. Brown Professor in Trauma in the Departments of Anesthesiology, Anatomy & Neurobiology, Psychiatry, Neurology, and Neurosurgery at UMSOM, and director of the UMSOM Shock, Trauma and Anesthesiology Research Center.
Researchers have known for years that TBI has significant effects on the gastrointestinal tract, but until now, scientists have not recognized that brain trauma can make the colon more permeable, potentially allowing allow harmful microbes to migrate from the intestine to other areas of the body, causing infection.. People are 12 times more likely to die from blood poisoning after TBI, which is often caused by bacteria, and 2.5 times more likely to die of a digestive system problem, compared with those without such injury.
In this study, the researchers examined mice that received an experimental TBI. They found that the intestinal wall of the colon became more permeable after trauma, changes that were sustained over the following month.
It is not clear how TBI causes these gut changes. A key factor in the process may be enteric glial cells (EGCs), a class of cells that exist in the gut. These cells are similar to brain astroglial cells, and both types of glial cells are activated after TBI. After TBI, such activation is associated with brain inflammation that contributes to delayed tissue damage in the brain. Researchers don’t know whether activation of ECGs after TBI contributes to intestinal injury or is instead an attempt to compensate for the injury.
The researchers also focused on the two-way nature of the process: how gut dysfunction may worsen brain inflammation and tissue loss after TBI. They infected the mice with Citrobacter rodentium, a species of bacteria that is the rodent equivalent of E. coli, which infects humans. In mice with a TBI who were infected with this the bacteria, brain inflammation worsened. Furthermore, in the hippocampus, a key region for memory, the mice who had TBI and were then infected lost more neurons than animals without infection.
This suggests that TBI may trigger a vicious cycle, in which brain injury causes gut dysfunction, which then has the potential to worsen the original brain injury. “These results really underscore the importance of bi-directional gut-brain communication on the long-term effects of TBI,” said Dr. Faden.
Other authors of this paper include Elise Ma, a doctoral student; Terez Shea-Donahue PhD, professor of radiation oncology; Bogdan A. Stoica, MD, associate professor of anesthesiology ; and David Loane, PhD, associate professor of anesthesiology- all at UMSOM.
Source: David Kohn – University of Maryland School of Medicine
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