From Hysteria to Functional Neurological Symptom Disorder: Developments in Clinical Diagnosis and Neurobiology

Abstract

Changes in the nomenclature of functional neurological symptom disorders (FND) from the past to the present represent historical changes in understanding etiology. Today, there is still difficulty in excluding potential underlying neurological disorders. In addition, there is no consensus on the psychological mechanism leading to the disorder. As a result, diagnostic problems continue to exist. While functional neuroimaging studies show that suppression and conversion mechanisms, which are the concepts of the psychoanalytical theory, may have neural counterparts, neurobiological data suggests that the conversion model cannot be explanatory for every patient. The dorsolateral prefrontal cortex (dlPFC), amygdala, temporoparietal junction (TPJ), insula, anterior cingulate structures, and their connections come to the fore. The fact that the connections between the dlPFC and the hippocampus can prevent the recall of an unwanted memory, as well as the changes detected in the amygdala in these disorders and the increased connectivity between the amygdala and the motor areas, suggest an abnormal connection between emotions and the motor system. It is addressed how changes in the TPJ are related to the loss of the sense of agency. However, it is unclear whether the findings of these studies suggest a "predisposition", "onset of disorder", or "compensatory changes secondary to disorder". Exploring FND to learn how the brain and mind react to psychosocial stressors can be a turning point in understanding the brain-mind connection. The goal of this review is to present the history of the changes in terminology and perspective on this disorder that followed the establishment of psychoanalysis, as well as what kind of evidence has been presented regarding hysteria in light of advances in neuroscience