The term deafferentiation is indebted to the Latin words de (away from, 'negation'), and affere (to take somewhere, to bring somewhere). The deafferentiation hypothesis of hallucinatory activity is a hypothetical model that seeks to explain the mediation of some types of hallucination by reference to an endogenous type of " sensory deprivation attributed to disruptions in neural connectivity. It postulates that spontaneous hallucinatory activity can be mediated by sensory cortical areas when these are deafferentiated, i.e. when they are cut off from the neurons and/or axons conducting afferent sensory impulses. This hallucinatory activity is attributed to massive degeneration and subsequent reorganization taking place in the cortical termination zones, as well as in the primary non-affected subfields of the sensory cortex.It is generally held that deafferentiation of primary sensory cortical areas may entail the spontaneous mediation of relatively "simple hallucinations, whereas deafferentiation of cortical association areas may entail the spontaneous mediation of "complex hallucinations. The deaf-ferentiation hypothesis has been employed as an explanatory model for various types of hallucinations, including the "visual hallucinations occurring in the context of " Charles Bonnet syndrome, "hemianopic hallucinations, "verbal auditory hallucinations, " musical hallucinations, "olfactory hallucinations, "deafferentiation pain, " anaesthesia dolorosa, and " phantom limb illusion. Conceptually, the deafferentiation hypothesis of hallucinatory activity is indebted to early 19th-century deafferentiation models of sleep, such as those of the Italian anatomist Luigi Rolando (1773-1831).
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