Hysterical conversion and brain function

Laboratory for Behavioral Neurology and Imaging of Cognition, Clinic of Neurology, University University of Geneva, Geneva, Switzerland.
Progress in brain research (Impact Factor: 2.83). 02/2005; 150:309-29. DOI: 10.1016/S0079-6123(05)50023-2
Source: PubMed


Hysterical conversion disorders represent "functional" or unexplained neurological deficits such as paralysis or somatosensory losses that are not explained by organic lesions in the nervous system, but arise in the context of "psychogenic" stress or emotional conflicts. After more than a century of both clinical and theoretical interest, the exact nature of such emotional disorders responsible for hysterical symptoms, and their functional consequences on neural systems in the brain, still remain largely unknown. However, several recent studies have used functional brain imaging techniques (such as EEG, fMRI, PET, or SPECT) in the attempt to identify specific neural correlates associated with hysterical conversion symptoms. This article presents a general overview of these findings and of previous neuropsychologically based accounts of hysteria. Functional neuroimaging has revealed selective decreases in the activity of frontal and subcortical circuits involved in motor control during hysterical paralysis, decreases in somatosensory cortices during hysterical anesthesia, or decreases in visual cortex during hysterical blindness. Such changes are usually not accompanied by any significant changes in elementary stages of sensory or motor processing as measured by evoked potentials, although some changes in later stages of integration (such as P300 responses) have been reported. On the other hand, several neuroimaging results have shown increased activation in limbic regions, such as cingulate or orbitofrontal cortex during conversion symptoms affecting different sensory or motor modalities. Taken together, these data generally do not support previous proposals that hysteria might involve an exclusion of sensorimotor representations from awareness through attentional processes. They rather seem to point to a modulation of such representations by primary affective or stress-related factors, perhaps involving primitive reflexive mechanisms of protection and alertness that are partly independent of conscious control, and mediated by dynamic modulatory interactions between limbic and sensorimotor networks. A better understanding of the neuropsychobiological bases of hysterical conversion disorder might therefore be obtained by future imaging studies that compare different conversion symptoms and employ functional connectivity analyses. This should not only lead to improve clinical management of these patients, but also provide new insights on the brain mechanisms of self-awareness.

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Available from: Patrik Vuilleumier, Feb 04, 2015
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    • "Importantly, complex behavior, such as pseudo-labor, Genser syndrome, anorexia nervosa and catatonia, has been attributed to conversion (Jensen, 1984; Lyman, 2004; Jiménez Gómez and Quintero, 2012; Shah et al., 2012; Goldstein et al., 2013) implicating also higher order processes. Moreover, de facto organic findings in conversion disorder (Ballmaier and Schmidt, 2005; Vuilleumier, 2005 Vuilleumier, , 2014 García-Campayo et al., 2009) indicate, contrary to the traditional conception, the possibility of a neurocognitive mechanism answering to symptom generation, and conversion disorder thus being a phenomenon, also, of the brain. Reflecting the multitude of mechanisms and etiologies suggested, current DSM and ICD nosology is ''widely regarded as unsatisfactory'' (Gelder, 2001) in particular with regards to clinical overlap between conversion, dissociation and somatization (Brown and Lewis-Fernández, 2011; North, 2015), and mechanistic as well as etiological bias involving unconscious mental states and psychological stress or trauma, with undecided, little, or no empirical relation to symptoms (Roelofs and Spinhoven, 2007; Brown and Lewis-Fernández, 2011). "
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    ABSTRACT: Resignation syndrome (RS) designates a long-standing disorder predominately affecting psychologically traumatised children and adolescents in the midst of a strenuous and lengthy migration process. Typically a depressive onset is followed by gradual withdrawal progressing via stupor into a state that prompts tube feeding and is characterised by failure to respond even to painful stimuli. The patient is seemingly unconscious. Recovery ensues within months to years and is claimed to be dependent on the restoration of hope to the family. Descriptions of disorders resembling RS can be found in the literature and the condition is unlikely novel. Nevertheless, the magnitude and geographical distribution stand out. Several hundred cases have been reported exclusively in Sweden in the past decade prompting the Swedish National Board of Health and Welfare to recognise RS as a separate diagnostic entity. The currently prevailing stress hypothesis fails to account for the regional distribution and contributes little to treatment. Consequently, a re-evaluation of diagnostics and treatment is required. Psychogenic catatonia is proposed to supply the best fit with the clinical presentation. Treatment response, altered brain metabolism or preserved awareness would support this hypothesis. Epidemiological data suggests culture-bound beliefs and expectations to generate and direct symptom expression and we argue that culture-bound psychogenesis can accommodate the endemic distribution. Last, we review recent models of predictive coding indicating how expectation processes are crucially involved in the placebo and nocebo effect, delusions and conversion disorders. Building on this theoretical framework we propose a neurobiological model of RS in which the impact of overwhelming negative expectations are directly causative of the down-regulation of higher order and lower order behavioural systems in particularly vulnerable individuals.
    Full-text · Article · Jan 2016 · Frontiers in Behavioral Neuroscience
    • "Several authors have suggested that basal and thalamic areas would control emotional movement modulation and that its deafferentation would be the key in the integration impairments underlying these kinds of disorders (Vuilleumier et al., 2001; Lanius et al., 2014a). Previous studies have found alterations in other regions such as the frontal cortex and the lower OFC ( Vuilleumier, 2005). Studies based on various paradigms suggest that there may be a disconnection between the dorsolateral prefrontal cortex (dlPFC) and motor areas (Marshall et al., 1997; Spence et al., 2000; De Lange et al., 2010). "
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    ABSTRACT: Previous reviews have focused on neurobiological and physiological mechanisms underlying conversion disorder, but they do not usually distinguish between negative and positive conversion symptoms. Some authors have proposed that different phenomena should underlie both situations and that diverse emotion regulation strategies (under- vs. overregulation of affect) should be related to different internal experiences (excitatory experiences with hyperarousal manifestations vs. inhibitory experiences coexisting with hypoarousal states, respectively). After a careful review of the literature, we conclude that there is not a unique theory comprising all findings. Nevertheless, we have also collected some replicated findings that should be salient. Patients manifesting positive conversion symptoms tended to present with limbic hyperfunction, not sufficiently counteracted by prefrontal control. This leads to underregulation of affect mechanisms, increased emotional reactivity and autonomic hyperarousal. The opposite pattern (with a prefrontal overfunction working as a cognitive brake over the limbic system) has been described during negative conversion manifestations. We also highlight the influence of fronto-limbic circuits over cortico-striato-thalamo-cortical circuits' regulation, whose horizontal and vertical synchronization has been at the spotlight of the genesis of conversion and dissociative disorders.
    No preview · Article · Aug 2015 · Reviews in the neurosciences
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    • "It is distinguished from other " non-organic " movement disorders by a lack of conscious intention to deceive (Bass, 2001). Symptoms are thought to arise from underlying psychological stressors such as trauma or conflict, but the neural mechanisms remain unknown (Scott & Anson, 2009; Vuilleumier, 2005). The neurobiology underpinning conversion paresis and other conversion disorders remains mysterious. "
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    ABSTRACT: Conversion paresis is the presence of unexplained weakness without detectable neuropathology that is not feigned. To examine the 'abnormal preparation' and 'disrupted execution' hypotheses proposed to explain the movement deficits in conversion paresis, electroencephalographic, electromyographic and kinematic measures were recorded during motor preparation and execution. Six patients with unilateral upper limb conversion weakness, 24 participants feigning weakness and 12 control participants performed a 2-choice precued reaction time task. Precues provided advance information about the responding hand or finger. Patients and feigners demonstrated similar diminished force, longer movement time and extended duration of muscle activity in their symptomatic limb. Patients showed significantly suppressed contingent negative variation (CNV) amplitudes, but only when the symptomatic limb was precued. Despite the similarity in performance measures, this CNV suppression was not seen in feigners. Diminished CNV for symptomatic hand precues may reflect engagement of an inhibitory mechanism suppressing cortical activity related to preparatory processes. Copyright © 2015. Published by Elsevier B.V.
    Full-text · Article · May 2015 · Biological psychology
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