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Fig. 4 | The Egyptian Journal of Neurology, Psychiatry and Neurosurgery

Fig. 4

From: Reflex memory theory of acquired involuntary motor and sensory disorders

Fig. 4

A process diagram showing stages of reflex memory formation, and their provoking factors. As expressed in the figure, stages of neural events are presented on the left of the diagram and to the right are provoking factors. When neurons are perturbed by either physical injury or chemical insult, there is usually an attempt to remodel by reestablishing connectivity or regrow the neurons. When the process fails or is poorly done, a defect occurs in the circuit. This defect may provoke upregulation of excitatory neurotransmitters (ENTs), mostly ionotropic glutamate NMDA receptor complexes leading to Ca2+ influx and excessive calcium loading, and then excitotoxic stimulation of the neurons with consequent homeostatic failure. Maladaptive synaptic plasticity is induced with consequent formation of abnormal memory, the “reflex memory.” Consolidation of the memory occurs as the abnormal process continues. When retrieval or recall occurs, the abnormal memory becomes unstable and fragile. In normal acquired implicit memory, reconsolidation occurs after retrieval, but in this abnormal acquired implicit memory, no reconsolidation occurs because this memory remains in persistent retrieval/recall mode. Because this memory is in a persistent retrieval/recall mode, it is said to have “lost inhibition control” or “disobeyed the inhibition rule.” The “loss of inhibition control” is what makes the retrieval uncontrollable. This state of fragility and instability, and persistent recall mode makes this memory vulnerable to interventions using pharmacological, molecular, optogenetic, or behavioral manipulations, and so, can even be erased

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