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Fig. 3 | The Egyptian Journal of Neurology, Psychiatry and Neurosurgery

Fig. 3

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

Fig. 3

A process diagram showing how reflex memory is formed as a result of neuronal perturbation. As depicted, healthy memory formation is on the left side, and pathological memory (reflex memory) on the right side. The rectangles marked in red prints indicate potential areas of therapeutic targets. Drugs aimed at inhibiting the formation of, or erasing, the pathological memory may be targeted at phases marked red. Glutamate is most implicated, and upregulated, in neural perturbations of hyperexcitatory nature like TD, PTSDs, phantom syndromes, and similar disorders. Excess glutamate may be mopped up quickly from the synaptic cleft at the memory acquisition phase by enhancing the function of excitatory amino acid transporters (EAATs). Sustained excitotoxicity can lead to calcium overload with consequent neurodegeneration. CaV1.3 isoform-specific blocker may be helpful in any recommended combination therapy. The author thinks that extant theories overlooked the possible role of pathological memory in these phenomena states, and this may have accounted for the resistance of these disorders to extant therapies. A combination therapy that includes memory inhibition and/erasure is therefore advocated

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