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Neurophysiology of conversion disorders: A historical perspective Neurophysiologie des troubles de conversion : perspective historique M. Crommelinck Institute of Neurosciences (IoNS), Catholic University of Louvain, 1200 Brussels, Belgium Received 4 October 2013; accepted 10 October 2013
KEYWORDS Conversion disorders; Hysteria; Historical perspective; Neuroimaging techniques; Cognitive neuropsychiatry
MOTS CLÉS Conversion ; Hystérie ; Histoire de la médecine ; Neuroimagerie ;
Summary The aim of this paper is to present a short historical perspective on the neurophysiological approach to hysteria and conversion disorders. The body of this paper will be constituted of three main parts. In the first part, we will present the significant progress due to some pioneers of neurology/psychiatry during the XIXth century. As we shall see, this period was particularly rich in personalities whose work gradually laid the foundations to a true medical approach to hysteria. In the first half of the XXth century, different factors have led to a long eclipse of the neurological approach to hysteria. In the second part, we will show how, by the 1960’s—1970’s, the conceptual and methodological advances in neurophysiology, as well as the turning point of cognitive sciences (and cognitive psychology in particular) allowed a gradual reinstatement of hysteria within the fields of neurology and clinical neurophysiology. Finally, and this is the third part of this paper, we will show how over the past three decades, an entirely new neurophysiological approach to hysteria and conversion disorders has emerged. © 2013 Elsevier Masson SAS. All rights reserved. Résumé Dans cet article, nous retrac ¸ons brièvement l’historique de l’approche neurophysiologique de l’hystérie ou des troubles conversifs. Il s’articule en trois parties. Dans une première partie, nous décrirons les progrès significatifs dus aux pionniers neurologues et psychiatres du 19e siècle. Nous verrons à quel point plusieurs personnalités ayant jeté les bases d’une approche véritablement médicale de l’hystérie ont contribué au développement scientifique de cette époque. Par contre, la première moitié du 20e siècle a connu une longue éclipse dans l’approche neurologique de l’hystérie. Dans la deuxième partie de l’article, nous montrerons comment, durant les années 1960 et 1970, les avancées conceptuelles en neurophysiologie et, surtout, l’avènement des neurosciences cognitives (et, plus particulièrement, de la
E-mail address: [email protected] 0987-7053/$ – see front matter © 2013 Elsevier Masson SAS. All rights reserved. http://dx.doi.org/10.1016/j.neucli.2013.10.126
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Neuropsychiatrie cognitive
neuropsychologie cognitive) ont permis de recadrer l’hystérie dans le champ de la neurologie et de la neurophysiologie clinique. Enfin, nous montrerons dans la troisième partie de cet article comment les 30 dernières années virent se développer une approche totalement nouvelle de l’hystérie et des troubles conversifs. © 2013 Elsevier Masson SAS. Tous droits réservés.
Introduction This paper aims to present a brief historical overview of the neurophysiology of hysteria or conversion disorders. Three main parts will constitute the body of this article. In the first part, we will present the significant progress due to some pioneers of neurology/psychiatry. As we shall see, the nineteenth century was particularly rich in personalities whose work gradually laid the foundations for a true medical approach to hysteria. In this era it was a question of causing some kind of epistemological break: i.e removing the disease from a tradition of thought, still alive at that time although dating back to Greek Antiquity, which described it as an affection of the uterus (etymologically ‘‘hysteria’’ comes from the Greek ustera, meaning matrix, uterus). Thus, to mention only one of the oldest sources, Plato [21] in Timaeus (91-c) evoked that ‘‘ whenever the matrix or womb, as it is called, which is an indwelling creature desirous of child-bearing, remains without fruit long beyond the due season, it is vexed and takes it ill; and by straying all ways through the body and blocking up the passages of the breath and preventing respiration it casts the body into the uttermost distress, and causes, moreover, all kinds of maladies; until the desire and love of the two sexes unite them’’. This design (also taken again by Hippocrates) of a ‘‘wandering’’ uterus, worried and frustrated, the source of all evils, placed for a long time hysteria in the heart of female sexuality, troubled and confused. . . the treatment often confining itself to ‘‘marriage’’! We also know that in the Middle Ages and until much later in the Classical Age, hysterics were often considered as witches possessed by the spirit of the devil and ended at the stake (see the famous case of the possessed of Loudun). The nineteenth century appears quite clearly as a turning point. It was necessary in this era to relocate the disease in the context of a more scientific, even experimental medicine recently theorized by Claude Bernard and to rely as much as possible on the anatomopathological method that had quickly demonstrated its relevance. At that time clinicians had the aim of providing a finer clinical picture of this protean disease, posing for the first time questions regarding its physiological and psychopathological basis and developing, still in a strong empirical manner, the first attempts at therapeutic measures. From those early days, we will consider, among many others, the names of Pierre Briquet, John Russell Reynolds, Jean-Martin Charcot and finally Sigmund Freud. During the first half of the twentieth century, two main sets of factors led to a long eclipse of the neurological approach to hysteria. Firstly, these were the excesses of dramatization and the suspicions of simulation in hysterical ‘‘patients’’ as well as the instrumentalization of the
body by the chief physician, all elements that marred the end of the career of J.M. Charcot at the Salpêtrière. Thus, J. Babinski (1857—1932), student and Charcot’s senior clinical assistant eventually excluded from the field of neurology psychic hysteria such as it had been identified by Charcot. The second factor is undoubtedly the birth, at the turn of the century, of Freudian psychoanalysis: this would come to focus on models and practices in psychodynamic terms, the hysterical neurosis becoming not only the psychoanalytic paradigm of the etiology of all forms of neurosis (repression as a defense mechanism following a psychic trauma and hysteria as a manifestation of the return of the repressed in the form of physical symptoms: hysterical conversion) but also the occasion of the setting-up of the ‘‘listening technique’’ (‘‘talking cure’’) and ‘‘free associations’’, after unsuccessful tests of hypnosis. Apart from a few sporadic references, study of conversion disorders thereby left neurological research and practice, to inhabit thereafter the field of psychiatry and psychopathology. Let us note only in passing an interesting contribution of I. Pavlov [20,27] (1849—1936) around the Thirties, which, within the framework of its associationist theories and of its ‘‘excitation-inhibition interaction’’ models of the cerebral cortex, makes the assumption that ‘‘a strong excitation of the instincts or the automatisms in subcortical centers may inhibit the activity of the cortex’’. This explains some pathological effects in hysteria in particular. In the second part of the article, we will show how, in the 1960’s—1970’s, the conceptual and methodological advances in neurophysiology, as well as the turning point of cognitive sciences (and cognitive psychology in particular) allowed a gradual reinstatement of the study of hysteria within the fields of neurology and clinical neurophysiology. Finally, and this is the third part of this paper, we will show how over the past three decades, an entirely new neurophysiological approach of hysteria or conversion disorders has developed. This is mainly due to two factors. The most important factor is probably the development of various functional human non-invasive brain imaging techniques allowing high-resolution assessment of the functional states of brain systems. The second factor is doubtless the publication by the American Society of Psychiatry of the Diagnostic and Statistical Manual of Mental Disorders (DSM). In DSMIII (1980), the clinical entity ‘‘hysteria’’ was dismantled into several diagnostic categories, more clearly identifying various syndromes and their articulation using statistical and quantitative axes (such as somatomorphic disorders and dissociative symptoms. . .). This made it possible for researchers to work on relatively homogeneous cohorts of patients.
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Neurophysiology of conversion disorders: A historical perspective
‘‘Pioneering’’ neurologists and hysteria in the nineteenth century Pierre Briquet (1796—1881) Pierre Briquet [2,16,17] worked as a physician at the Hôpital de la Charité in Paris in 1846. In 1859, he published by J.B. Baillière an important 724-page essay entitled ‘‘Clinical and Therapeutic Treatise on Hysteria’’. He was received at the Academy of Medicine in 1860. If Pierre Briquet should be mentioned here it is first of all as one of the leading actors of the paradigm shift in the study of hysteria: he defended the essentially neurocerebral origin of the disease, rather than the ‘‘uterine’’ one. It should be noted that the ‘‘uterine theory’’ was still defended in the 1850s in particular by Pierre Adolphe Piorry (1794—1879) — at the Hôpital de la Charité — for whom the seat of hysteria was the ovary in women and the spermatic cord or testicles in men. The definition that Pierre Briquet gives of hysteria is as follows: ‘‘a neurosis of the brain, whose apparent phenomena consist mainly in the disruption of the vital acts which are the manifestation of emotional feelings and passions’’. Briquet thinks that the seat of hysteria is in what he calls ‘‘the emotional part of the brain’’, this part being distinct from ‘‘the intellectual part’’. He describes very carefully the many symptoms of this trouble (in men and women) and proposes a classification into 7 main categories among which he lists sensory disturbances (hyperesthesia, anesthesia), paralyses and ‘‘perversions of contractility’’, attacks, spasms and so on. P. Briquet continued to believe that hysteria was a disease that could affect all organs. Practicing a clinicopathological method (after post-mortem autopsy), he highlighted the absence of lesions.
John Russell Reynolds (1828—1896) Professor of Medicine at University College London and University College Hospital doctor, John Russell Reynolds was in close relation with the great British neurologist J.H. Jackson (1835—1911), who described the brain as working in a hierarchical form. Reynolds quickly became a medical authority, in particular in the field of epilepsy. In 1869, he published an important article on case studies of hysteria, ‘‘Remarks on paralysis and other disorders of motion and sensation dependent on idea’’ [22]. At the beginning of this article he wrote: ‘‘The object of this paper is to show that some of the most serious disorders of the nervous system, such as paralysis, spasm, pain, and otherwise altered sensations, may depend upon a morbid condition of emotion, of idea and emotion, or of idea alone’’. This is seen as a very clear statement of the importance of ideas and emotions in the etiology of motor or sensory symptoms of the disease. This hypothesis was to be later resumed by many authors such as Janet and Freud. It is interesting to note that Reynolds had extensive contacts with the French neurologist J.M. Charcot (having visited the Salpêtrière in 1877), whom as we shall see was interested in hysteria from the 1870’s onwards and who also proposed an etiological hypothesis based on ideation. In volume III of his complete works (21st lesson), Charcot mentioned
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this article by J.R. Reynolds and wrote: ‘‘It is well known without doubt that in certain circumstances, a paralysis could be produced by an idea and also that a contrary idea will be able to make it disappear, but between these two final events, how many intermediate links remain in the shadows. . .’’.
Jean-Martin Charcot (1825—1893) Hospital physician and student of Guillaume Duchenne (known as Duchenne de Boulogne, 1806—1875), J.-M. Charcot [4,8,9,12,15] was appointed to the Salpêtrière in late 1861 and taught anatomopathology at the University of Paris. He developed early neuropathology through clinicopathological methods (trying to match each pathology or symptom to a specific macro- or microscopic lesions). With Alfred Vulpian (1826—1887), he described the tremors of degenerative neuropathies, and established the anatomopathology of locomotor ataxia. From 1865 onwards, he began a series of studies on diseases of the nervous system, in particular in relation to the spinal cord. He described multiple sclerosis (1868) and in 1869, amyotrophic lateral sclerosis (‘‘maladie de Charcot’’) as well as locomotor ataxia (‘‘tabès syphilitique’’). The disorders of motor function were to remain a privileged set of themes in his clinical research. From the 1870’s onwards, the hospital administration designated the service as the ‘‘neighborhood of simple epileptics’’ where epileptics and hysterics were placed side by side (those with a diagnosis of insanity having been transferred to the Hôtel-Dieu from 1802). Charcot aimed to individualize hysteria as a clinical entity (such as Jackson had done for epilepsy) and devoted lessons to hemianesthesia or hyperesthesia. He distinguished the stereotypical stages of the ‘‘great hysteria’’ (aided by creation of the photographic laboratory at the Salpêtrière). He referred to hypnosis as a method for the experimental study of hysteria, and tried to apply the clinicopathological method. Around the 1880’s, a major turning point in its research and practice occurred. Firstly, Charcot established the inefficiency of the anatomopathological method in the case of hysteria, due to the lack of detectable post-mortem lesions (at least according to the means of that time). Then, along the same lines as Reynolds, Charcot adopted the hypothesis of ‘‘neuromuscular excitability triggered by psychic trauma, by an idea’’, a sort of ‘‘psychization’’ of hysteria, although his philosophy remained ‘‘positivist’’ and materialist. In 1882, he held the first chair of neurology. From 1884, he studied the ‘‘psychic paralyses’’. How does ‘‘ideation’’ interfere in such a spectacular way with body functioning? He affirmed that the substrate of paralysis is a ‘‘functional lesion’’ or a ‘‘dynamic cortical lesion’’ (sine materia). He turned to Théodule Ribot (1839—1916, doctor in philosophy from the École Normale Supérieure in Paris) who was to introduce the new experimental psychology in France, in creating the first chair of experimental psychology in the Sorbonne in 1885 and in the Collège de France from 1889. In 1883, Ribot published ‘‘Les maladies de la volonté’’ (The Diseases of the Will): the notion of ideo-motor activity was developed in this important book. Charcot attempts to clarify this border between organic and psychic notions of the disorder. In 1885, with Ribot and
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Pierre Janet in particular, Charcot founded the ‘‘Société de psychologie physiologique’’ (Society of Physiological Psychology) (first congress in 1889) which was constituted as an autonomous science, taking into account the first major advances of an emerging neuropsychology (including the location of the centers of language — P. Broca, 1861; C. Wernicke, 1873; the topography of cortical motor areas — G. Fritsch and E. Hitzig, 1870, D. Ferrier, 1876, and so on). It should emphasize the importance played by Pierre Janet (1859—1947). A philosopher and physician, he worked in Charcot’s department starting from 1885 and in 1889 published his important essay ‘‘L’automatisme psychologique — essai de psychologie expérimentale sur les formes inférieures de l’activité humaine’’ (The psychological automatism — experimental psychology essay on the lower forms of human activity). For Janet, hysteria was tied to ‘‘a narrowing of the field of consciousness’’. In the Salpêtrière, Charcot created a laboratory of experimental psychology for Janet. The challenge of creating this ‘‘Physiological Psychology’’ deserves comment. This was highlighted by G. Swain (French psychiatrist, 1945—1993) who wrote [12]: ‘‘It is the materialism that allows Charcot to pass without difficulty, without major epistemological obstacle and without the need for a conversion to another order of causality, from anatomopathology to psychology’’. Or put even more precisely: ‘‘A dualistic quartering between psychoanalytic perspective and biological perspective in psychiatry. . . had been rigorously inconceivable for Freud as for Charcot. Their materialism, their precisely ‘‘physiological’’ psychology that allows the new integrated design of cerebrospinal system, resulted in a true disqualification of the old problem of the relationships between soul and body, thought in terms of separated spheres by a solution of continuity’’.
Sigmund Freud (1856—1939) We would like to make here a brief reference to ‘‘Freud the neurologist’’, before 1895, the date of publication of the « Studies on Hysteria » with J. Breuer (1842—1925). As a reminder, S. Freud worked at the Salpêtrière in the service of Charcot from October 1885 to February 1886. At the end of his stay, Charcot encouraged him to make a comparative study of organic paralyses and hysterical paralyses. The article, written in French probably in the course of 1886, was to be published in the ‘‘Archives de Neurologie’’ (Archives of neurology, the journal created by Charcot) but several years later in 1893 under the title: ‘‘Quelques considérations pour une étude comparative des paralysies motrices organiques et hystériques’’ [11] (Some considerations for a comparative study of organic and hysterical motor paralyzes). In the fourth part of the article, Freud proposes a series of reflections on the concepts of injury and function (evoking the concepts of ‘‘functional lesions’’ developed by Charcot). He also argued that ‘‘that there may be functional alteration without concomitant organic lesion, without palpable lesion, even by means of the most careful analysis’’. The following paragraph is interesting, since one sees there appearing a first formulation of what the clinical neurophysiology of today could say about hysteria: ‘‘I will take the term « lesion of function or dynamic lesion » in its truest
sense: impaired function or dynamics, altering a functional property. Such a deterioration would be for example a decrease in excitability or physiological quality which in the normal state remains constant or varies within given limits’’. Finally, quoting P. Janet, Freud reintroduces psychology by evoking the ‘‘idea’’ or the ‘‘representation’’ of the limb affected by the paralysis. It is the ‘‘great affective value’’ associated with this representation that was supposed to be the cause of this abnormal variation of some ‘‘physiological quality’’, producing an ‘‘associative rupture’’ (dissociation) between the ‘‘misconceptions’’ and the other representations of the body. To Janet and Freud, this ‘‘representation’’ was unconscious.
Transition: a new horizon for hysteria, the cognitive sciences The great split between the late nineteenth century and the current approach did not occur out of the blue. Since the end of 1960s, neurophysiological and neurological approaches to hysteria gradually integrated the evolutions/ revolutions of the main areas constituting the nebula of ‘‘cognitive sciences’’. These changes were conceptual (theories, models, assumptions), methodological (new experimental designs — mental chronometry — sophisticated statistical analyzes) and technical (exponential growth of the techniques of functional neuroimaging for example). What are the different areas that have gradually converged to constitute today’s field of cognitive neurophysiology of hysteria? We will briefly mention the four following disciplines: • it is first of all necessary to mention psychology, of all whose domains are in the process of being reconfigured by the cognitive revolution. In short, it will be a question under investigation of integrating into the study of observable behaviors (‘‘behaviorism’’) the mental states and the modalities of information processing underlying all aspects of behaviors. The principal dimensions of behavior, i.e perceptions, actions, attention, intentions, representations, learning, emotions and motivations, language, consciousness, unconsciousness, and so on, that have been so widely studied in adults or in their ontogenetic development, will see their theoretical approach renewed by this ‘‘cognitive turn’’. It is well understood that these fundamental studies will be used as a basis under investigation of the disturbance of these psychological functions; • psychiatry that, after a significant pharmacologicallydominated period, now integrates a cognitive-behavioral perspective. By defining and categorizing the symptoms in views of standardization (DSM), it will allow a more objective approach and the constitution of more homogeneous groups of patients; • neurophysiology, fundamental as well as clinical (neurology), has gradually become a cognitive science, even in the most basic aspects of molecular and cellular research (since one speaks today about the ‘‘cognitive neurosciences’’). It has the ambition to link within the same chain of causalities, neural structures (in terms of
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Neurophysiology of conversion disorders: A historical perspective neural networks), their mode of operation (in terms of information processing) and the emergent functions produced (in terms of mental and behavioral states) in normal as well as in pathological situations (see for example M. Gazzaniga [13] as the editor of ‘‘The cognitive neurosciences’’ series by the MIT Press); • finally, the domain of philosophy of which one of the most active fields is that of ‘‘philosophy of mind’’. In particular, in the heart of its concerns one finds the important program of naturalization of mind. In particular, concerning the conversion disorders, one can refer to de Vigermont [7]. Now, what are the main themes that, within these areas and in a transdisciplinary manner, have gradually constituted the theoretical frame of a neurophysiology of hysteria? The situation is particularly complex since virtually every dimension of behavior can be affected and appear in one or another form of hysterical disorder, as a symptom or as a mechanism. In parallel, the multiple neural networks underlying these dimensions can be affected. Thus, perceptual and motor functions, but also drive and memory are among the main components of hysterical symptomatology; affective and emotional functions but also attentional, representational and executive functions constituting some of the possible mechanisms involved in the etiology and pathophysiology. Thomas Sydenham (1624—1698), a contemporary English physician of T. Willis and W. Harvey had already underlined this ‘‘protean’’ aspect of the disease in the seventeenth century. On the subject of hysteria he wrote: ‘‘This disease is a Proteus who takes an infinity of different forms: it is a chameleon who varies his colors endless [. . .] Its symptoms are not only great in numbers and varied, yet they have this peculiarity among all diseases: that they do not follow any rule or any uniform type, and are just confused and irregularly assembled; hence it is difficult to give the history of hysterical affection’’. The multifaceted aspect of the disease (i.e, the wide range of functions involved and the variability in time) becomes yet more complex due to some rather vague conditions like ‘‘vulnerable personality or personality susceptible to suggestion’’ but also due to social and cultural factors. Taken together, these elements make it particularly difficult to have an indepth understanding of the neural mechanisms that underlie it. If today this sometimes-elusive aspect of the disease requires that clinicians adopt a subtle approach, contemporary research has nevertheless the ambition of highlighting ‘‘rules’’ or the pathophysiological principles underlying symptomatic manifestations. This is what we will briefly discuss in the last part of the article.
Neurophysiology of hysteria today: overview and issues This overview has been mainly established from experimental papers or reviews [1,14,19,23,26]. In order to identify the pathophysiological hypotheses of hysteria, clinical neurophysiology is now implementing
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the models, methodologies and techniques of the current scientific approach. It should be emphasized that since the 1970’s, remarkable developments, both formal and empirical, have occurred; e.g: significant advances in the general theories of cognitive functions involved in hysteria, implementation of sophisticated cognitive tasks, spatial and temporal resolutions of imaging techniques; study of connectivity and so on. In a very schematic way, we will organize this section into 4 main parts. First of all we will quote some of the methods and techniques used in current research. Then we will mention the principal elements of hysterical symptomatology. In the third part, we will try to identify the main etiological hypotheses, both in terms of disturbed functions and in terms of dysfunction of the neural networks that underlie these functions. Finally, we will introduce a theoretical discussion concerning two principal models that are now trying to account for the facts observed in the field of hysterical paralysis. One needs from the start to draw the reader’s attention to the very schematic character aspect of this overview. The contributions of the specialists in the present issue of the journal will provide for each their domains of expertise, the state of the art both in terms of experimental data and theoretical interpretations.
Methodologies First let us raise one of the main methodological difficulties: given the protean nature of the disease, the researcher is often trying to work on single cases, well documented and which meet all the criteria of inclusion in the experimental design (in particular the absence of neurological and/or psychiatric co-morbidity), but in this approach he has problems of interpretation (including statistical thresholds of functional neuroimaging) as well as the issue of generalization of the data collected. Alternatively the researcher may work on larger cohorts, with of course a better statistical reliability but with the risk of weakening the validity of the results due to the heterogeneity of symptomatology. The principal techniques used involve multiple functional brain imaging methods: electroencephalography (EEG) and magnetoencephalography (MEG), sensory or motor evoked potentials (EPs), positron emission tomography (PET) and functional magnetic resonance imagery (fMRI). Comparisons have been made between: • patients and control subjects, between patients in remission and symptomatic situation [19]; • healthy subjects simulators and patients [23]; • healthy subjects under hypnosis, patients and controls [1,10]. A variety of tasks have been implemented (we will mention here only a few of them as examples): passive stimulation, odd-ball paradigm, intention-preparation-execution of a movement, go/no-go paradigm, motor imagery of a segment (hand); recall of traumatic memories; gender judgment of expressive faces, etc.
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Brief description of symptomatology
Interpretations and discussions about hysterical paralysis
The usually cited symptoms concern: • sensory functions: somesthesia (anesthesia, paresthesia, hyperesthesia), vision (blindness, scotoma), hearing (deafness), etc; • motor function loss: paralysis, hemiplegia, monoplegia, dystonia, weakness, spasms, gait disturbance — or new movements: myoclonus, tremor, etc; • memory functions: retrograde autobiographical or episodic amnesia, etc.
Etiology Let us see now what are the key assumptions concerning the factors involved in the etiology and pathophysiology of hysterical disorders. They relate to various functions: emotion, attention, representation, executive control and also to the neural networks that underlie these functions: • emotional functions: the supposed etiology most often makes reference to traumatic emotional events, stressful, or events with high emotional value. The neurocognitive models of emotions are thus important in the development of theoretical assumptions concerning the genesis of the disorder. See in particular the models of K. Scherer (with the development of a theory of integration of the components ‘‘Component Process Model’’), J. Panksepp (hypothalamus), J. LeDoux (amygdala), A. Damasio (limbic system and cortex); • attentional functions: the attention could be too intensely focused on a morbid representation (obsession) and separated from other functions (‘‘compartmentalization’’); or conversely, is it an attentional weakness, a sort of ‘‘negligence’’ (sensory-motor or cognitive) worn by the patient to the affected limb (‘‘la belle indifférence’’) or in terms of a mnesic trace? For neurocognitive models of attention see in particular, the works of M. Posner and S. Hillyard from the 1970’s; • representational functions: is there a disorder of the mental representations of the body or some parts (impaired body image, body schema, motor imagery default)? For neurocognitive models of mental imagery, see in particular all the works of S. Kosslyn since 1980; • executive functions: a large number of questions arise here as much as possible hypotheses. Thus, is there a defect of inhibition, or hypercontrol, mental rigidity, loss of conscious control with the profit of an unconscious control, major dissociation of cognitive components, weakening of the will (implicit or explicit), some deficits in the genesis of motor intentions; finally, are there predispositions or grounds (genetically determined or acquired) promoting the development of hysterical symptoms (presence of characteristics more integrated in a ‘‘hysterical personality’’? Here also there exists a very abundant literature concerning the neurocognitive models of executive functions).
According to Nowak and Fink [19], two major ‘‘theoretical models’’ are put forward to give an account for the main data of the literature.
The concept of ‘‘active inhibition of motor areas by the limbic system’’ The limbic areas (namely the orbitofrontal cortex and the anterior cingulate cortex, the amygdala) seem to play an important role in the inhibition (unconscious) of the process of preparing and executing the action in hysterical patients. Thus striato-thalamocortical premotor loops (involved in the genesis of intentional movements and also in motor learning) would be the target of an inhibitory action from the limbic system [18,25]. Traumatic emotional factors or stressful events would sensitize (within the meaning of the paradigm of sensitization developed notably by Kandel et al.) the limbic system and, consequently would inhibit the sensory-motor processes (at a relatively high level of processing). Recently, Voon et al. [24] shows a significant increase in activity in the right amygdala during the observation of expressive faces in hysterical patients compared to controls, the connectivity of this limbic structure with the right supplementary motor area (SMA) being reinforced.
The concept of ‘‘disorder of the conceptualization of movement’’ More recent works [3,5,6], on the basis of different tasks (motor imagery, go-nogo paradigm), defend another explanatory model, taken again by Nowak and Fink [19] under the term of ‘‘disorder of the conceptualization of movement’’. Thus, de Lange et al. [6] interpret the symptoms of hysterical paralysis as a result of an increased self-control (enhanced self-monitoring) of the motor behavior. The motor imagery of the paralyzed limb involves an activation of the ventromedial prefrontal areas and the superior temporal cortex, which are normally deactivated during the preparation and execution of a movement. The data of Cojan et al. [5], although obtained in a different task (go-nogo), are interpreted in the same direction (‘‘our results reveal that conversion does not involve an active inhibition of motor outputs by anterior or medial regions’’). The ventromedial prefrontal cortical areas (vmPFC) and the posterior cingulate cortex (PCC), activated during the preparation of a movement of the affected limb, form an intrinsic part of a network providing a ‘‘default mode’’(normally presenting a reduction in activity during cognitive tasks). This debate will probably be more deeply addressed by different contributors in the present issue on the conversion disorders.
Disclosure of interest The author declares that he has no conflicts of interest concerning this article.
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Neurophysiology of conversion disorders: A historical perspective
References [1] Bell V, Oakley DA, Halligan PW, Deeley Q. Dissociation in hysteria and hypnosis: evidence from cognitive neuroscience. J Neurol Neurosurg Psychiatry 2011;82:332—9. [2] Briquet P. Traité Clinique et thérapeutique de l’hystérie. Paris: J.-B. Baillière et fils; 1859. p. 724 [About Paul Briquet, we consulted the following articles and books: Mai F.M. & Merskey H., 1980; Mai F.M.; Edelman N., 2003 (especially Chapter 3 : Le triomphe de l’encéphale)]. [3] Burgmer M, Konrad C, Jansen A, et al. Abnormal brain activation during movement observation in patients with conversion paralysis. Neuroimage 2006;29:1336—43. [4] Charcot JM. There is an abundant literature on the life and work of J.M. Charcot. We consulted more particularly: C. Drèze, 2001; A. Lellouch, 2004 (A. Lellouch has published numerous interesting articles and books on Charcot, especially on Charcot and geriatrics); N. Edelman, 2003; M. Gauchet & G. Swain, 1997. [5] Cojan Y, Waber L, Carruzzo A, Vuilleumier P. Motor inhibition in hysterical conversion paralysis. Neuroimage 2009;47:1026—37. [6] de Lange FP, Roelofs K, Toni I. Increased self-monitoring during imagined movements in conversion paralysis. Neuropsychologia 2007;45:2051—8. [7] de Vigermont F. L’hystérie : ne plus vouloir pouvoir, ne plus pouvoir vouloir. Philosophiques 2006;33:197—215. [8] Drèze C. Charcot 1825—1893. Louvain Med 2001;120:33—66. [9] Edelman N. Les métamorphoses de l’hystérie. Du début du XIXe siècle à la Grande guerre. Paris: Ed. La Découverte; 2003. p. 346. [10] Faymonville ME, Boly M, Laureys S. Functional neuroanatomy of the hypnotic state. J Physiol (Paris) 2006;99:463—9. [11] Freud S. Quelques considérations pour une étude comparative des paralysies motrices organiques et hystériques. In: « Résultats, idées problèmes I — 1890—1920 ». PUF; 1984. p. 45—59. [12] Gauchet M, Swain G. Le vrai Charcot. Les chemins imprévus de l’inconscient. Paris: Calmann-Lévy; 1997. p. 284. [13] Gazzaniga M. (ed). ‘‘The cognitive neurosciences’’. MIT Press. (since 1995, four successive editions).
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[14] Harvey SB, Stanton BR, David AS. Conversion disorder: towards a neurobiological understanding. Neuropsychiatr Dis Treat 2006;2:13—20. [15] Lellouch A. Charcot, Freud et l’inconscient. Un nouveau paradigme médical est-il né à Paris à la Salpêtrière entre 1880—1890 ? Hist Sci Med 2004;38(4):411—8. [16] Mai FM. Le « traité de l’hystérie » de Paul Briquet. Bibliothèque interuniversitaire de santé, Paris Descartes, C23, 71—73. [17] Mai FM, Merskey H. Briquet’s treatise on hysteria. Arch Gen Psychiatry 1980;37:1401—5. [18] Marschall JC, Halligan PW, Fink GR, Wade DT, Frackowiak RJS. The functional anatomy of a hysterical paralysis. Cognition 1997;64:B1—8. [19] Nowak D, Fink G. Psychogenic movement disorders: aetiology, phenomenology, neuroanatomical correlates and therapeutic approaches. Neuroimage 2009;47:1015—25. [20] Pavlov I. Essai d’une interprétation physiologique de l’hystérie. Encephale 1933;22:285—93 [The references to the assumptions of I. Pavlov are given in P. Vuilleumier, 2005; see also H. Wallon, 1963, from which the citation is extracted]. [21] Plato. The Timaeus. Perseus digital library, G.R. Crane Ed., Tufts University. [22] Reynolds JR. Remarks on Paralysis and other disorders of motion and sensation, dependant on idea. Br Med J 1869;2:483—5. [23] Stone J, Zeman A, Simonotto E, et al. fMRI patients with motor conversion symptoms and controls with simulated weakness. Psychosom Med 2007;69:961—9. [24] Voon V, Brezing C, Gallea C, Ameli R, Roelofs K, LaFrance Jr WC, Hallett M. Emotional stimuli and motor conversion. Brain 2010;133:1526—36. [25] Vuilleumier P, Chicherio C, Assal F, Schwartz S, Slosman D, Landis T. Functional neuroanatomical correlates of hysterical sensorimotor loss. Brain 2001;124:1077—90. [26] Vuilleumier P. Hysterical conversion and brain function, S. Laureys. Prog Brain Res 2005;150:309—29. [27] Wallon H. L’associationnisme de Pavlov. Enfance, vol. 16; 1963 [No.◦ 1-2].
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Neurophysiology of conversion disorders: A historical perspective Neurophysiologie des troubles de conversion : perspective historique M. Crommelinck Institute of Neurosciences (IoNS), Catholic University of Louvain, 1200 Brussels, Belgium Received 4 October 2013; accepted 10 October 2013
KEYWORDS Conversion disorders; Hysteria; Historical perspective; Neuroimaging techniques; Cognitive neuropsychiatry
MOTS CLÉS Conversion ; Hystérie ; Histoire de la médecine ; Neuroimagerie ;
Summary The aim of this paper is to present a short historical perspective on the neurophysiological approach to hysteria and conversion disorders. The body of this paper will be constituted of three main parts. In the first part, we will present the significant progress due to some pioneers of neurology/psychiatry during the XIXth century. As we shall see, this period was particularly rich in personalities whose work gradually laid the foundations to a true medical approach to hysteria. In the first half of the XXth century, different factors have led to a long eclipse of the neurological approach to hysteria. In the second part, we will show how, by the 1960’s—1970’s, the conceptual and methodological advances in neurophysiology, as well as the turning point of cognitive sciences (and cognitive psychology in particular) allowed a gradual reinstatement of hysteria within the fields of neurology and clinical neurophysiology. Finally, and this is the third part of this paper, we will show how over the past three decades, an entirely new neurophysiological approach to hysteria and conversion disorders has emerged. © 2013 Elsevier Masson SAS. All rights reserved. Résumé Dans cet article, nous retrac ¸ons brièvement l’historique de l’approche neurophysiologique de l’hystérie ou des troubles conversifs. Il s’articule en trois parties. Dans une première partie, nous décrirons les progrès significatifs dus aux pionniers neurologues et psychiatres du 19e siècle. Nous verrons à quel point plusieurs personnalités ayant jeté les bases d’une approche véritablement médicale de l’hystérie ont contribué au développement scientifique de cette époque. Par contre, la première moitié du 20e siècle a connu une longue éclipse dans l’approche neurologique de l’hystérie. Dans la deuxième partie de l’article, nous montrerons comment, durant les années 1960 et 1970, les avancées conceptuelles en neurophysiologie et, surtout, l’avènement des neurosciences cognitives (et, plus particulièrement, de la
E-mail address: [email protected] 0987-7053/$ – see front matter © 2013 Elsevier Masson SAS. All rights reserved. http://dx.doi.org/10.1016/j.neucli.2013.10.126
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Neuropsychiatrie cognitive
neuropsychologie cognitive) ont permis de recadrer l’hystérie dans le champ de la neurologie et de la neurophysiologie clinique. Enfin, nous montrerons dans la troisième partie de cet article comment les 30 dernières années virent se développer une approche totalement nouvelle de l’hystérie et des troubles conversifs. © 2013 Elsevier Masson SAS. Tous droits réservés.
Introduction This paper aims to present a brief historical overview of the neurophysiology of hysteria or conversion disorders. Three main parts will constitute the body of this article. In the first part, we will present the significant progress due to some pioneers of neurology/psychiatry. As we shall see, the nineteenth century was particularly rich in personalities whose work gradually laid the foundations for a true medical approach to hysteria. In this era it was a question of causing some kind of epistemological break: i.e removing the disease from a tradition of thought, still alive at that time although dating back to Greek Antiquity, which described it as an affection of the uterus (etymologically ‘‘hysteria’’ comes from the Greek ustera, meaning matrix, uterus). Thus, to mention only one of the oldest sources, Plato [21] in Timaeus (91-c) evoked that ‘‘ whenever the matrix or womb, as it is called, which is an indwelling creature desirous of child-bearing, remains without fruit long beyond the due season, it is vexed and takes it ill; and by straying all ways through the body and blocking up the passages of the breath and preventing respiration it casts the body into the uttermost distress, and causes, moreover, all kinds of maladies; until the desire and love of the two sexes unite them’’. This design (also taken again by Hippocrates) of a ‘‘wandering’’ uterus, worried and frustrated, the source of all evils, placed for a long time hysteria in the heart of female sexuality, troubled and confused. . . the treatment often confining itself to ‘‘marriage’’! We also know that in the Middle Ages and until much later in the Classical Age, hysterics were often considered as witches possessed by the spirit of the devil and ended at the stake (see the famous case of the possessed of Loudun). The nineteenth century appears quite clearly as a turning point. It was necessary in this era to relocate the disease in the context of a more scientific, even experimental medicine recently theorized by Claude Bernard and to rely as much as possible on the anatomopathological method that had quickly demonstrated its relevance. At that time clinicians had the aim of providing a finer clinical picture of this protean disease, posing for the first time questions regarding its physiological and psychopathological basis and developing, still in a strong empirical manner, the first attempts at therapeutic measures. From those early days, we will consider, among many others, the names of Pierre Briquet, John Russell Reynolds, Jean-Martin Charcot and finally Sigmund Freud. During the first half of the twentieth century, two main sets of factors led to a long eclipse of the neurological approach to hysteria. Firstly, these were the excesses of dramatization and the suspicions of simulation in hysterical ‘‘patients’’ as well as the instrumentalization of the
body by the chief physician, all elements that marred the end of the career of J.M. Charcot at the Salpêtrière. Thus, J. Babinski (1857—1932), student and Charcot’s senior clinical assistant eventually excluded from the field of neurology psychic hysteria such as it had been identified by Charcot. The second factor is undoubtedly the birth, at the turn of the century, of Freudian psychoanalysis: this would come to focus on models and practices in psychodynamic terms, the hysterical neurosis becoming not only the psychoanalytic paradigm of the etiology of all forms of neurosis (repression as a defense mechanism following a psychic trauma and hysteria as a manifestation of the return of the repressed in the form of physical symptoms: hysterical conversion) but also the occasion of the setting-up of the ‘‘listening technique’’ (‘‘talking cure’’) and ‘‘free associations’’, after unsuccessful tests of hypnosis. Apart from a few sporadic references, study of conversion disorders thereby left neurological research and practice, to inhabit thereafter the field of psychiatry and psychopathology. Let us note only in passing an interesting contribution of I. Pavlov [20,27] (1849—1936) around the Thirties, which, within the framework of its associationist theories and of its ‘‘excitation-inhibition interaction’’ models of the cerebral cortex, makes the assumption that ‘‘a strong excitation of the instincts or the automatisms in subcortical centers may inhibit the activity of the cortex’’. This explains some pathological effects in hysteria in particular. In the second part of the article, we will show how, in the 1960’s—1970’s, the conceptual and methodological advances in neurophysiology, as well as the turning point of cognitive sciences (and cognitive psychology in particular) allowed a gradual reinstatement of the study of hysteria within the fields of neurology and clinical neurophysiology. Finally, and this is the third part of this paper, we will show how over the past three decades, an entirely new neurophysiological approach of hysteria or conversion disorders has developed. This is mainly due to two factors. The most important factor is probably the development of various functional human non-invasive brain imaging techniques allowing high-resolution assessment of the functional states of brain systems. The second factor is doubtless the publication by the American Society of Psychiatry of the Diagnostic and Statistical Manual of Mental Disorders (DSM). In DSMIII (1980), the clinical entity ‘‘hysteria’’ was dismantled into several diagnostic categories, more clearly identifying various syndromes and their articulation using statistical and quantitative axes (such as somatomorphic disorders and dissociative symptoms. . .). This made it possible for researchers to work on relatively homogeneous cohorts of patients.
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Neurophysiology of conversion disorders: A historical perspective
‘‘Pioneering’’ neurologists and hysteria in the nineteenth century Pierre Briquet (1796—1881) Pierre Briquet [2,16,17] worked as a physician at the Hôpital de la Charité in Paris in 1846. In 1859, he published by J.B. Baillière an important 724-page essay entitled ‘‘Clinical and Therapeutic Treatise on Hysteria’’. He was received at the Academy of Medicine in 1860. If Pierre Briquet should be mentioned here it is first of all as one of the leading actors of the paradigm shift in the study of hysteria: he defended the essentially neurocerebral origin of the disease, rather than the ‘‘uterine’’ one. It should be noted that the ‘‘uterine theory’’ was still defended in the 1850s in particular by Pierre Adolphe Piorry (1794—1879) — at the Hôpital de la Charité — for whom the seat of hysteria was the ovary in women and the spermatic cord or testicles in men. The definition that Pierre Briquet gives of hysteria is as follows: ‘‘a neurosis of the brain, whose apparent phenomena consist mainly in the disruption of the vital acts which are the manifestation of emotional feelings and passions’’. Briquet thinks that the seat of hysteria is in what he calls ‘‘the emotional part of the brain’’, this part being distinct from ‘‘the intellectual part’’. He describes very carefully the many symptoms of this trouble (in men and women) and proposes a classification into 7 main categories among which he lists sensory disturbances (hyperesthesia, anesthesia), paralyses and ‘‘perversions of contractility’’, attacks, spasms and so on. P. Briquet continued to believe that hysteria was a disease that could affect all organs. Practicing a clinicopathological method (after post-mortem autopsy), he highlighted the absence of lesions.
John Russell Reynolds (1828—1896) Professor of Medicine at University College London and University College Hospital doctor, John Russell Reynolds was in close relation with the great British neurologist J.H. Jackson (1835—1911), who described the brain as working in a hierarchical form. Reynolds quickly became a medical authority, in particular in the field of epilepsy. In 1869, he published an important article on case studies of hysteria, ‘‘Remarks on paralysis and other disorders of motion and sensation dependent on idea’’ [22]. At the beginning of this article he wrote: ‘‘The object of this paper is to show that some of the most serious disorders of the nervous system, such as paralysis, spasm, pain, and otherwise altered sensations, may depend upon a morbid condition of emotion, of idea and emotion, or of idea alone’’. This is seen as a very clear statement of the importance of ideas and emotions in the etiology of motor or sensory symptoms of the disease. This hypothesis was to be later resumed by many authors such as Janet and Freud. It is interesting to note that Reynolds had extensive contacts with the French neurologist J.M. Charcot (having visited the Salpêtrière in 1877), whom as we shall see was interested in hysteria from the 1870’s onwards and who also proposed an etiological hypothesis based on ideation. In volume III of his complete works (21st lesson), Charcot mentioned
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this article by J.R. Reynolds and wrote: ‘‘It is well known without doubt that in certain circumstances, a paralysis could be produced by an idea and also that a contrary idea will be able to make it disappear, but between these two final events, how many intermediate links remain in the shadows. . .’’.
Jean-Martin Charcot (1825—1893) Hospital physician and student of Guillaume Duchenne (known as Duchenne de Boulogne, 1806—1875), J.-M. Charcot [4,8,9,12,15] was appointed to the Salpêtrière in late 1861 and taught anatomopathology at the University of Paris. He developed early neuropathology through clinicopathological methods (trying to match each pathology or symptom to a specific macro- or microscopic lesions). With Alfred Vulpian (1826—1887), he described the tremors of degenerative neuropathies, and established the anatomopathology of locomotor ataxia. From 1865 onwards, he began a series of studies on diseases of the nervous system, in particular in relation to the spinal cord. He described multiple sclerosis (1868) and in 1869, amyotrophic lateral sclerosis (‘‘maladie de Charcot’’) as well as locomotor ataxia (‘‘tabès syphilitique’’). The disorders of motor function were to remain a privileged set of themes in his clinical research. From the 1870’s onwards, the hospital administration designated the service as the ‘‘neighborhood of simple epileptics’’ where epileptics and hysterics were placed side by side (those with a diagnosis of insanity having been transferred to the Hôtel-Dieu from 1802). Charcot aimed to individualize hysteria as a clinical entity (such as Jackson had done for epilepsy) and devoted lessons to hemianesthesia or hyperesthesia. He distinguished the stereotypical stages of the ‘‘great hysteria’’ (aided by creation of the photographic laboratory at the Salpêtrière). He referred to hypnosis as a method for the experimental study of hysteria, and tried to apply the clinicopathological method. Around the 1880’s, a major turning point in its research and practice occurred. Firstly, Charcot established the inefficiency of the anatomopathological method in the case of hysteria, due to the lack of detectable post-mortem lesions (at least according to the means of that time). Then, along the same lines as Reynolds, Charcot adopted the hypothesis of ‘‘neuromuscular excitability triggered by psychic trauma, by an idea’’, a sort of ‘‘psychization’’ of hysteria, although his philosophy remained ‘‘positivist’’ and materialist. In 1882, he held the first chair of neurology. From 1884, he studied the ‘‘psychic paralyses’’. How does ‘‘ideation’’ interfere in such a spectacular way with body functioning? He affirmed that the substrate of paralysis is a ‘‘functional lesion’’ or a ‘‘dynamic cortical lesion’’ (sine materia). He turned to Théodule Ribot (1839—1916, doctor in philosophy from the École Normale Supérieure in Paris) who was to introduce the new experimental psychology in France, in creating the first chair of experimental psychology in the Sorbonne in 1885 and in the Collège de France from 1889. In 1883, Ribot published ‘‘Les maladies de la volonté’’ (The Diseases of the Will): the notion of ideo-motor activity was developed in this important book. Charcot attempts to clarify this border between organic and psychic notions of the disorder. In 1885, with Ribot and
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Pierre Janet in particular, Charcot founded the ‘‘Société de psychologie physiologique’’ (Society of Physiological Psychology) (first congress in 1889) which was constituted as an autonomous science, taking into account the first major advances of an emerging neuropsychology (including the location of the centers of language — P. Broca, 1861; C. Wernicke, 1873; the topography of cortical motor areas — G. Fritsch and E. Hitzig, 1870, D. Ferrier, 1876, and so on). It should emphasize the importance played by Pierre Janet (1859—1947). A philosopher and physician, he worked in Charcot’s department starting from 1885 and in 1889 published his important essay ‘‘L’automatisme psychologique — essai de psychologie expérimentale sur les formes inférieures de l’activité humaine’’ (The psychological automatism — experimental psychology essay on the lower forms of human activity). For Janet, hysteria was tied to ‘‘a narrowing of the field of consciousness’’. In the Salpêtrière, Charcot created a laboratory of experimental psychology for Janet. The challenge of creating this ‘‘Physiological Psychology’’ deserves comment. This was highlighted by G. Swain (French psychiatrist, 1945—1993) who wrote [12]: ‘‘It is the materialism that allows Charcot to pass without difficulty, without major epistemological obstacle and without the need for a conversion to another order of causality, from anatomopathology to psychology’’. Or put even more precisely: ‘‘A dualistic quartering between psychoanalytic perspective and biological perspective in psychiatry. . . had been rigorously inconceivable for Freud as for Charcot. Their materialism, their precisely ‘‘physiological’’ psychology that allows the new integrated design of cerebrospinal system, resulted in a true disqualification of the old problem of the relationships between soul and body, thought in terms of separated spheres by a solution of continuity’’.
Sigmund Freud (1856—1939) We would like to make here a brief reference to ‘‘Freud the neurologist’’, before 1895, the date of publication of the « Studies on Hysteria » with J. Breuer (1842—1925). As a reminder, S. Freud worked at the Salpêtrière in the service of Charcot from October 1885 to February 1886. At the end of his stay, Charcot encouraged him to make a comparative study of organic paralyses and hysterical paralyses. The article, written in French probably in the course of 1886, was to be published in the ‘‘Archives de Neurologie’’ (Archives of neurology, the journal created by Charcot) but several years later in 1893 under the title: ‘‘Quelques considérations pour une étude comparative des paralysies motrices organiques et hystériques’’ [11] (Some considerations for a comparative study of organic and hysterical motor paralyzes). In the fourth part of the article, Freud proposes a series of reflections on the concepts of injury and function (evoking the concepts of ‘‘functional lesions’’ developed by Charcot). He also argued that ‘‘that there may be functional alteration without concomitant organic lesion, without palpable lesion, even by means of the most careful analysis’’. The following paragraph is interesting, since one sees there appearing a first formulation of what the clinical neurophysiology of today could say about hysteria: ‘‘I will take the term « lesion of function or dynamic lesion » in its truest
sense: impaired function or dynamics, altering a functional property. Such a deterioration would be for example a decrease in excitability or physiological quality which in the normal state remains constant or varies within given limits’’. Finally, quoting P. Janet, Freud reintroduces psychology by evoking the ‘‘idea’’ or the ‘‘representation’’ of the limb affected by the paralysis. It is the ‘‘great affective value’’ associated with this representation that was supposed to be the cause of this abnormal variation of some ‘‘physiological quality’’, producing an ‘‘associative rupture’’ (dissociation) between the ‘‘misconceptions’’ and the other representations of the body. To Janet and Freud, this ‘‘representation’’ was unconscious.
Transition: a new horizon for hysteria, the cognitive sciences The great split between the late nineteenth century and the current approach did not occur out of the blue. Since the end of 1960s, neurophysiological and neurological approaches to hysteria gradually integrated the evolutions/ revolutions of the main areas constituting the nebula of ‘‘cognitive sciences’’. These changes were conceptual (theories, models, assumptions), methodological (new experimental designs — mental chronometry — sophisticated statistical analyzes) and technical (exponential growth of the techniques of functional neuroimaging for example). What are the different areas that have gradually converged to constitute today’s field of cognitive neurophysiology of hysteria? We will briefly mention the four following disciplines: • it is first of all necessary to mention psychology, of all whose domains are in the process of being reconfigured by the cognitive revolution. In short, it will be a question under investigation of integrating into the study of observable behaviors (‘‘behaviorism’’) the mental states and the modalities of information processing underlying all aspects of behaviors. The principal dimensions of behavior, i.e perceptions, actions, attention, intentions, representations, learning, emotions and motivations, language, consciousness, unconsciousness, and so on, that have been so widely studied in adults or in their ontogenetic development, will see their theoretical approach renewed by this ‘‘cognitive turn’’. It is well understood that these fundamental studies will be used as a basis under investigation of the disturbance of these psychological functions; • psychiatry that, after a significant pharmacologicallydominated period, now integrates a cognitive-behavioral perspective. By defining and categorizing the symptoms in views of standardization (DSM), it will allow a more objective approach and the constitution of more homogeneous groups of patients; • neurophysiology, fundamental as well as clinical (neurology), has gradually become a cognitive science, even in the most basic aspects of molecular and cellular research (since one speaks today about the ‘‘cognitive neurosciences’’). It has the ambition to link within the same chain of causalities, neural structures (in terms of
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Neurophysiology of conversion disorders: A historical perspective neural networks), their mode of operation (in terms of information processing) and the emergent functions produced (in terms of mental and behavioral states) in normal as well as in pathological situations (see for example M. Gazzaniga [13] as the editor of ‘‘The cognitive neurosciences’’ series by the MIT Press); • finally, the domain of philosophy of which one of the most active fields is that of ‘‘philosophy of mind’’. In particular, in the heart of its concerns one finds the important program of naturalization of mind. In particular, concerning the conversion disorders, one can refer to de Vigermont [7]. Now, what are the main themes that, within these areas and in a transdisciplinary manner, have gradually constituted the theoretical frame of a neurophysiology of hysteria? The situation is particularly complex since virtually every dimension of behavior can be affected and appear in one or another form of hysterical disorder, as a symptom or as a mechanism. In parallel, the multiple neural networks underlying these dimensions can be affected. Thus, perceptual and motor functions, but also drive and memory are among the main components of hysterical symptomatology; affective and emotional functions but also attentional, representational and executive functions constituting some of the possible mechanisms involved in the etiology and pathophysiology. Thomas Sydenham (1624—1698), a contemporary English physician of T. Willis and W. Harvey had already underlined this ‘‘protean’’ aspect of the disease in the seventeenth century. On the subject of hysteria he wrote: ‘‘This disease is a Proteus who takes an infinity of different forms: it is a chameleon who varies his colors endless [. . .] Its symptoms are not only great in numbers and varied, yet they have this peculiarity among all diseases: that they do not follow any rule or any uniform type, and are just confused and irregularly assembled; hence it is difficult to give the history of hysterical affection’’. The multifaceted aspect of the disease (i.e, the wide range of functions involved and the variability in time) becomes yet more complex due to some rather vague conditions like ‘‘vulnerable personality or personality susceptible to suggestion’’ but also due to social and cultural factors. Taken together, these elements make it particularly difficult to have an indepth understanding of the neural mechanisms that underlie it. If today this sometimes-elusive aspect of the disease requires that clinicians adopt a subtle approach, contemporary research has nevertheless the ambition of highlighting ‘‘rules’’ or the pathophysiological principles underlying symptomatic manifestations. This is what we will briefly discuss in the last part of the article.
Neurophysiology of hysteria today: overview and issues This overview has been mainly established from experimental papers or reviews [1,14,19,23,26]. In order to identify the pathophysiological hypotheses of hysteria, clinical neurophysiology is now implementing
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the models, methodologies and techniques of the current scientific approach. It should be emphasized that since the 1970’s, remarkable developments, both formal and empirical, have occurred; e.g: significant advances in the general theories of cognitive functions involved in hysteria, implementation of sophisticated cognitive tasks, spatial and temporal resolutions of imaging techniques; study of connectivity and so on. In a very schematic way, we will organize this section into 4 main parts. First of all we will quote some of the methods and techniques used in current research. Then we will mention the principal elements of hysterical symptomatology. In the third part, we will try to identify the main etiological hypotheses, both in terms of disturbed functions and in terms of dysfunction of the neural networks that underlie these functions. Finally, we will introduce a theoretical discussion concerning two principal models that are now trying to account for the facts observed in the field of hysterical paralysis. One needs from the start to draw the reader’s attention to the very schematic character aspect of this overview. The contributions of the specialists in the present issue of the journal will provide for each their domains of expertise, the state of the art both in terms of experimental data and theoretical interpretations.
Methodologies First let us raise one of the main methodological difficulties: given the protean nature of the disease, the researcher is often trying to work on single cases, well documented and which meet all the criteria of inclusion in the experimental design (in particular the absence of neurological and/or psychiatric co-morbidity), but in this approach he has problems of interpretation (including statistical thresholds of functional neuroimaging) as well as the issue of generalization of the data collected. Alternatively the researcher may work on larger cohorts, with of course a better statistical reliability but with the risk of weakening the validity of the results due to the heterogeneity of symptomatology. The principal techniques used involve multiple functional brain imaging methods: electroencephalography (EEG) and magnetoencephalography (MEG), sensory or motor evoked potentials (EPs), positron emission tomography (PET) and functional magnetic resonance imagery (fMRI). Comparisons have been made between: • patients and control subjects, between patients in remission and symptomatic situation [19]; • healthy subjects simulators and patients [23]; • healthy subjects under hypnosis, patients and controls [1,10]. A variety of tasks have been implemented (we will mention here only a few of them as examples): passive stimulation, odd-ball paradigm, intention-preparation-execution of a movement, go/no-go paradigm, motor imagery of a segment (hand); recall of traumatic memories; gender judgment of expressive faces, etc.
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Brief description of symptomatology
Interpretations and discussions about hysterical paralysis
The usually cited symptoms concern: • sensory functions: somesthesia (anesthesia, paresthesia, hyperesthesia), vision (blindness, scotoma), hearing (deafness), etc; • motor function loss: paralysis, hemiplegia, monoplegia, dystonia, weakness, spasms, gait disturbance — or new movements: myoclonus, tremor, etc; • memory functions: retrograde autobiographical or episodic amnesia, etc.
Etiology Let us see now what are the key assumptions concerning the factors involved in the etiology and pathophysiology of hysterical disorders. They relate to various functions: emotion, attention, representation, executive control and also to the neural networks that underlie these functions: • emotional functions: the supposed etiology most often makes reference to traumatic emotional events, stressful, or events with high emotional value. The neurocognitive models of emotions are thus important in the development of theoretical assumptions concerning the genesis of the disorder. See in particular the models of K. Scherer (with the development of a theory of integration of the components ‘‘Component Process Model’’), J. Panksepp (hypothalamus), J. LeDoux (amygdala), A. Damasio (limbic system and cortex); • attentional functions: the attention could be too intensely focused on a morbid representation (obsession) and separated from other functions (‘‘compartmentalization’’); or conversely, is it an attentional weakness, a sort of ‘‘negligence’’ (sensory-motor or cognitive) worn by the patient to the affected limb (‘‘la belle indifférence’’) or in terms of a mnesic trace? For neurocognitive models of attention see in particular, the works of M. Posner and S. Hillyard from the 1970’s; • representational functions: is there a disorder of the mental representations of the body or some parts (impaired body image, body schema, motor imagery default)? For neurocognitive models of mental imagery, see in particular all the works of S. Kosslyn since 1980; • executive functions: a large number of questions arise here as much as possible hypotheses. Thus, is there a defect of inhibition, or hypercontrol, mental rigidity, loss of conscious control with the profit of an unconscious control, major dissociation of cognitive components, weakening of the will (implicit or explicit), some deficits in the genesis of motor intentions; finally, are there predispositions or grounds (genetically determined or acquired) promoting the development of hysterical symptoms (presence of characteristics more integrated in a ‘‘hysterical personality’’? Here also there exists a very abundant literature concerning the neurocognitive models of executive functions).
According to Nowak and Fink [19], two major ‘‘theoretical models’’ are put forward to give an account for the main data of the literature.
The concept of ‘‘active inhibition of motor areas by the limbic system’’ The limbic areas (namely the orbitofrontal cortex and the anterior cingulate cortex, the amygdala) seem to play an important role in the inhibition (unconscious) of the process of preparing and executing the action in hysterical patients. Thus striato-thalamocortical premotor loops (involved in the genesis of intentional movements and also in motor learning) would be the target of an inhibitory action from the limbic system [18,25]. Traumatic emotional factors or stressful events would sensitize (within the meaning of the paradigm of sensitization developed notably by Kandel et al.) the limbic system and, consequently would inhibit the sensory-motor processes (at a relatively high level of processing). Recently, Voon et al. [24] shows a significant increase in activity in the right amygdala during the observation of expressive faces in hysterical patients compared to controls, the connectivity of this limbic structure with the right supplementary motor area (SMA) being reinforced.
The concept of ‘‘disorder of the conceptualization of movement’’ More recent works [3,5,6], on the basis of different tasks (motor imagery, go-nogo paradigm), defend another explanatory model, taken again by Nowak and Fink [19] under the term of ‘‘disorder of the conceptualization of movement’’. Thus, de Lange et al. [6] interpret the symptoms of hysterical paralysis as a result of an increased self-control (enhanced self-monitoring) of the motor behavior. The motor imagery of the paralyzed limb involves an activation of the ventromedial prefrontal areas and the superior temporal cortex, which are normally deactivated during the preparation and execution of a movement. The data of Cojan et al. [5], although obtained in a different task (go-nogo), are interpreted in the same direction (‘‘our results reveal that conversion does not involve an active inhibition of motor outputs by anterior or medial regions’’). The ventromedial prefrontal cortical areas (vmPFC) and the posterior cingulate cortex (PCC), activated during the preparation of a movement of the affected limb, form an intrinsic part of a network providing a ‘‘default mode’’(normally presenting a reduction in activity during cognitive tasks). This debate will probably be more deeply addressed by different contributors in the present issue on the conversion disorders.
Disclosure of interest The author declares that he has no conflicts of interest concerning this article.
Please cite this article in press as: Crommelinck M. Neurophysiology of conversion disorders: A historical perspective. Neurophysiologie Clinique/Clinical Neurophysiology (2014), http://dx.doi.org/10.1016/j.neucli.2013.10.126
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Neurophysiology of conversion disorders: A historical perspective
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Please cite this article in press as: Crommelinck M. Neurophysiology of conversion disorders: A historical perspective. Neurophysiologie Clinique/Clinical Neurophysiology (2014), http://dx.doi.org/10.1016/j.neucli.2013.10.126
