In my opinion your ideas on learned non-use are completely wrong. It is much more likely that you are slowly losing functionality because your doctor DID NOTHING to stop the neuronal cascade of death in the first week.
You are losing billions of neurons, miles of myelinated fibers, and tons of dead synapses that first week. I'd suggest charging your stroke hospital $1,000 a dead neuron, that might finally get your stroke hospital to solve stroke.
I only lost 5.4 billion neurons that first week. If I had only lost 177 million neurons, the 90 minutes it took to deliver tPA, then I would be completely recovered by now.
A First Step Toward the Operationalization of the Learned Non-Use Phenomenon: A Delphi Study
Abstract
Background
The negative discrepancy between residual functional capacity and reduced use of the contralesional hand, frequently observed after a brain lesion, has been termed Learned Non-Use (LNU) and is thought to depend on the interaction of neuronal mechanisms during recovery and learning-dependent mechanisms.
Objective
Albeit the LNU phenomenon is generally accepted to exist, currently, no transdisciplinary definition exists. Furthermore, although therapeutic approaches are implemented in clinical practice targeting LNU, no standardized diagnostic routine is described in the available literature. Our objective was to reach consensus regarding a definition as well as synthesize knowledge about the current diagnostic procedures.
Methods
We used a structured group communication following the Delphi method among clinical and scientific experts in the field, knowledge from both, the work with patient populations and with animal models.
Results
Consensus was reached regarding a transdisciplinary definition of the LNU phenomenon(Where the fuck is that definition then? Not publicly available, then it doesn't exist. Useless.). Furthermore, the mode and strategy of the diagnostic process, as well as the sources of information and outcome parameters relevant for the clinical decision making, were described with a wide range showing the current lack of a consistent universal diagnostic approach.
Conclusions
The need for the development of a structured diagnostic procedure and its implementation into clinical practice is emphasized. Moreover, it exists a striking gap between the prevailing hypotheses regarding the mechanisms underlying the LNU phenomenon and the actual evidence. Therefore, basic research is needed to bridge between bedside and bench and eventually improve clinical decision making and further development of interventional strategies beyond the field of stroke rehabilitation.
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