Abstract

ReceivedMarch 24, 2013; revised June 8, 2013; accepted June 10, 2013. From Neurology Department, Guglielmo da Saliceto Hospital, AUSL Piacenza, Piacenza, Italy (ER, NM); Ophthalmology Department, Mondovi-Ceva, ASL CN1, Cuneo, Italy (AG, EB); Nuclear Medicine Department, S. Croce Hospital, Cuneo, Italy (AP). Send correspondence and reprint requests to Eugenia Rota, Department of Neurology, Guglielmo da Saliceto Hospital, Via Taverna 49, 29121 Piacenza, Italy; e-mail: eugeniarota.md@gmail.com & 2014 The Academy of Psychosomatic Medicine. Published by Elsevier Inc. All rights reserved. Hysteria has long been a puzzling and intriguing issue in neuropsychology. This old and complex term refers to conditions otherwise described as “somatoform” or “conversion” disorder. Conversion disorder refers to a hypothesis based on psychoanalytic theory: it involves sensory or motor symptoms, which cannot be explained by any known medical condition, that are not consciously produced and are considered to be associated with psychologic factors. The Diagnostic and Statistical Manual of Mental Disorders-5 (DSM 5) proposed renaming conversion disorder as “functional neurologic disorder.” Neurology outpatient clinics report 10%–30% of patients complaining of medically unexplained symptoms, which are, therefore, thought to be “nonorganic,” “functional” in nature and bear a poor prognosis for recovery. As far back 1870, Jean-Martin Charcot first hypothesized that hysteria may reflect some sort of dynamic, functional brain abnormality. The last decade has witnessed a number of functional neuroimaging studies that have provided support for Charcot's theory, revealing abnormal brain perfusional patterns in patients with functional symptoms. These studies showed a selective decreased activity of frontal, prefrontal, and subcortical circuits involved in motor control during hysterical paralysis, reduced activity of somatosensory cortices during hysterical anesthesia, and a reduced visual cortex activity during functional visual loss. However, increased activation has been detected by functional neuroimaging studies in limbic regions, including the cingulate and orbitofrontal cortex, during conversion symptoms involving different sensory or motor modalities. However, the neural mechanisms that

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