Dr Selma Aybek completed her Medical training and Neurology residency in Lausanne, Switzerland. After she received her specialist title in 2007, she did a 3-year fellowship at the Institute of Psychiatry in London (King's College University) where she trained in Neuroimaging and in Cognitive Neuropsychiatry with Professor Anthony David. Her main research and clinical interest focuses on Conversion Disorder (Functional neurological Symptom), a paradigmatic neuropsychiatric disorder. She currently runs a clinic dedicated to patients suffering from Conversion Disorder at Geneva University Hospital in Switzerland and leads a research program aimed at underpinning the neural correlates if this disorder, in collaboration with the Laboratory for Behavioral Neurology and Imaging of Cognition (Geneva University). She authored several clinical and neurosciences papers in the field and has been awarded the Lishman Prize from the British Neuropsychiatry Association in 2010 and 2013 as well as the Boursière d'Excellence award from Geneva University in 2013.
Functional Neurological Symptoms (FNS) are now considered as a consequence of cerebral dysfunction but two main previous explanations have been hypothesized in the course of human medicine: first a role of an unstable uterus and then of a psychological trauma being responsible for- or converted into- the physical manifestation. If the theory of the uterus has been abandoned more than a century ago, the hypothesis of a major role for psychological trauma is still debated. Many epidemiological data support a link between psychological stressor and FNS with systematic reviews and meta-analysis reporting a 3-fold increase rate of childhood and recent life adverse events in FNS patients compared to various control groups (other neurological or psychiatric conditions). However, what emerges from this literature is that a percentage (even is small) of patients still do not report any kind of trauma. The model of a trauma acting as a cause, therefore, doesn't hold and the term “psychogenic” (suggesting the origin has to be found in psychological factors) should be abandoned. If it is now clear in the in the clinical setting that the importance of psychological factors in FNS should be downgraded (which is reflected by the new DSM-5 definition, which deleted in 2013 the B. criteria “the presence of a psychological factor”), it is still relevant, in the research setting, to try and refine the link between such stressors and physical symptoms.
Several recent studies in FNS have highlighted a dysfunction in emotion regulation, in threat responses and in traumatic memories recall. Among them, some fMRI studies suggest an abnormal limbic-motor interaction in these patients as anomalous functional connectivity has been found between the amygdala and the premotor cortex (supplementary motor area). Moreover, abnormal automatic motor responses, known to correspond in animals to defence mechanisms to threat (such as the freeze response), have been observed in a study in FNS patients, alongside increased activity in the periaqueducal gray area (a key region for the freeze response) under negative emotions in another. These preliminary work suggest that the physical symptoms of FNS may have correlates of automatic defence mechanisms and further research need to establish why certain individuals are more prone to others to display this -usually physiological- pattern in an abnormal way. In particular, the role of genetic factors and/or gene-environment interaction should be clarified so that we may be able to integrate psychological factors as predisposing risk factors or modulating factors in our understanding of FNS and no longer as causal factors.
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