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At the end of the 19th century, several authors became interested in the physical and psychological symptoms resulting from traumatic life events. Oppenheim presented 42 detailed clinical observations. He suggested the term "traumatic neurosis." Charcot, who was interested in male hysteria, published over 20 cases of traumatic hysteria between 1878 and 1893. The symptoms were considered to have a dynamic or functional origin. The role of horror and terror during the trauma was emphasized. However, Charcot opposed the idea of traumatic neuroses as specific syndromes as he considered them to be only an etiological form of hystero-neurasthenia. In The Tuesday Lessons (Les Leçons du Mardi), he presents several observations. They are surprising when compared with the current criteria for posttraumatic stress disorder (PTSD). Although he had rejected this new entity, a hundred years before the appearance of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised, Charcot described most of the symptoms mentioned for a diagnosis of PTSD such as intrusion (reliving the trauma, nightmares, and severe emotional distress), avoidance, negative changes in thinking and mood (negative thoughts, lack of interest, etc.), arousal, and reactivity (trouble sleeping, trouble concentrating, being easily startled or frightened, irritability, etc.).

The word hysteria originated in the Corpus Hippocraticum (c420 BCE) as a natural explanation for a variety of diseases in women linked in the Greco-Roman mind to an animate or inanimate womb, but which in the last five centuries has evolved to describe an elusive disorder of brain ± mind in men and women, currently referred to by neurologists as "functional neurological disorder". The Babylonians, Assyrians and Egyptians had no knowledge of brain or psychological function. Babylonian and Assyrian descriptions of disease and behaviour include only rare examples suggestive of modern hysteria. An earlier suggestion that the Greek concept of hysteria was transmitted from Egypt is not supported by recent evidence. The Greco-Roman civilisations had some knowledge of neuroanatomy, but little of nervous system function, conceived in terms of humors. The examples cited here suggestive of modern hysteria are relatively infrequent and fragmentary. The most plausible are attempts to separate the "sacred disease" from other causes of loss of consciousness. The great achievement of Greco-Roman medicine was in introducing natural causation, including causation linked to the womb, rather than gods or evil spirits. Nevertheless medicine, magic and religion have remained intertwined to varying degrees in all cultures up to the present time, despite the growth of modern scientific medicine. The study of hysteria in ancient civilisations adds interesting insight into the evolution of thinking about brain, psyche, mind and self. Babylonian and Egyptian medical and behavioural descriptions are based on observation. Greek and Roman accounts include some subjective aspects, probably linked to early attempts to understand identity, the psyche, intellectual and emotional functions. The great philosophical debate whether the latter resided in the head/brain (Plato) or the heart (Aristotle) has only been settled in the last few centuries, during which hysteria also became linked to brain ± mind. Our more recent increasing knowledge of brain function has also been accompanied by increasing interest in subjective feelings, thoughts, the inner life and subconscious mechanisms, suggesting we may have become more self-aware than in earlier civilisations, which in turn may perhaps influence the clinical presentation of hysteria. The study of hysteria may be one of the keys to a greater understanding of the relationship between brain and mind., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Chromosomal abnormalities involving 2q32q33 deletions are very rare and present with a specific phenotype. This case report describes a 37-year-old female patient with 2q32q33 microdeletion syndrome presenting with the characteristic features, but with the addition of secondary cognitive decline. Molecular karyotyping was performed on the patient and her parents. It revealed an 8.6 megabase deletion with the proximal breakpoint in the chromosome band 2q32.2 and the distal breakpoint in 2q33.1. The deletion encompassed 22 known genes, including theGLS,MYO1B,TMEFF2,PGAP1andSATB2genes. The observed deletion was confirmed using a paralogue ratio test. This case report provides further evidence that theSATB2gene, together withGLS,MYO1B,TMEFF2and possiblyPGAP1,is a crucial gene in 2q32q33 microdeletion syndrome. TheSATB2gene seems to be crucial for the behavioural problems noted in our case, but deletion of theGLS,MYO1BandTMEFF2genes presumably contributed to the more complex behavioural characteristics observed. Our patient is also, to our knowledge, the only patient with 2q32q33 microdeletion syndrome with secondary cognitive decline., (© The Author(s) 2016.)

Background: In the late 19th century, a man with a psychogenic movement disorder was evaluated by many of the Philadelphia neurologists associated with Silas Weir Mitchell. In 1885, prior to the development of movie cameras or projectors, the patient was photographed by pioneering photographer Eadweard Muybridge, in collaboration with neurologist Francis Dercum, using arrays of sequentially triggered single-image cameras. The photographic sequences are among the first motion picture sequences of patients with neurologic disorders., Methods: Examination of extant primary source documents concerning this patient, including published writings and photographic sequences by Muybridge and Dercum, the original clinical descriptions, Mitchell's documentation of the patient's later clinical course, and results of the autopsy., Results: Mitchell and his colleagues concluded that this was a "case of undoubted hysteria" in a man. Support for this contention includes the following: protracted course, spanning decades with temporary remissions; inconsistent character of the movement and features incongruous with typical "organic" tremors; complex, bizarre movements that are difficult to classify; increase in movements with attention; alteration in frequency of the movements with movement of the opposite arm; ability to trigger or temporarily stop the movements with unusual or nonphysiologic interventions; involvement of the opposite arm in a synchronous abnormal movement later in the course; remission with hypnotic suggestion; absence of other neurologic signs; and normal brain autopsy., Conclusion: The clinical history, serial examinations, photographic documentation, and autopsy results support Mitchell's contention that this was a case of male hysteria, or, in modern terminology, a psychogenic movement disorder., (© 2015 American Academy of Neurology.)

Hysteria has served as an important driving force in the development of both neurology and psychiatry. Jean Martin Charcot's devotion to mesmerism for treating hysterical patients evoked the invention of psychoanalysis by Sigmund Freud. Meanwhile, Joseph Babinski took over the challenge to discriminate between organic and hysterical patients from Charcot and found Babinski's sign, the greatest milestone in modern neurological symptomatology. Nowadays, the usage of the term hysteria is avoided. However, new terms and new classifications are complicated and inconsistent between the two representative taxonomies, the DSM-IV and ICD-10. In the ICD-10, even the alternative term conversion disorder, which was becoming familiar to neurologists, has also disappeared as a group name. The diagnosis of hysteria remains important in clinical neurology. Extensive exclusive diagnoses and over investigation, including various imaging studies, should be avoided because they may prolong the disease course and fix their symptoms. Psychological reasons that seem to explain the conversion are not considered reliable. Positive neurological signs suggesting nonorganic etiologies are the most reliable measures for diagnosing hysteria, as Babinski first argued. Hysterical paresis has several characteristics, such as giving-way weakness or peculiar distributions of weakness. Signs to uncover nonorganic paresis utilizing synergy include Hoover's test and the Sonoo abductor test.

The main objective of this paper is to present the importance of hysteria on Babinski's oeuvre, and the conceptions of pithiatism from Babinski until the one of conversion disorder. Babinski gave a mental basis for hysteria in the place of Charcot's encephalopatic one, and several important semiotic tools to differentiate organic from hysterical manifestations based on studies from 1893-1917/8. His teachings were spread worldwide, and in Brazil they were also appreciated in the work on hysteria by Antonio Austregesilo, the first Brazilian neurology chairman. The neurobiological basis of hysteria conceived by Charcot is nowadays reappraised, and Babinski's neurosemiological contribution is everlasting. The patients believed to be hysterical, and the two outstanding neurologists, Charcot and Babinski, gave support for the development of the modern neurology.

Hysteria has generated the most heated debates among physicians, from antiquity to the present day. It has been long confused with neuroses and neurological pathologies such as Parkinson's disease and epilepsy, principally associated with women and sexual disorders. The clinical manifestations must first be seen in their historical context, as interpretation varies according to the time period. Recently, the Diagnostic and Statistical Manual of Mental Disorders by the American Psychiatric Association marked a break in the consensus that previously seemed to apply to the concept of hysteria and approach to the clinical manifestations. The clinical manifestations of hysteria are numerous and multifaceted, comprising 3 main classifications: paroxysms, attacks, and acute manifestations; long-lasting functional syndromes, and visceral events. Each main classification can be subdivided into several subgroups. The first main group of paroxysms, attacks, and acute manifestations includes major hysterical attacks, such as prodrome, trance and epileptic states, minor hysterical attacks such as syncope and tetany, twilight states, paroxysmal amnesia, and cataleptic attacks. The second group includes focal hysterical symptoms, paralyses, contractures and spasms, anesthesia, and sensory disorders. Visceral manifestations can be subdivided into spasms, pain, and general and trophic disorders. The diversity of the symptoms of hysteria and its changing clinical presentation calls into question the same hysterical attacks and the same symptoms, which have had only a few differences for over 2,000 years. A new definition of hysteria should be proposed, in that it is a phenomenon that is not pathological, but physiological and expressional.

Babinski, 'Chef de Clinique' of Charcot from 1885 to 1887, fully supported the ideas of his teacher on hysteria and thought that a dynamic brain cortical lesion is the cause of the disease. After Charcot's death in 1893, Babinski gradually revised his position. In a first step, he described many neurological signs in order to clearly distinguish hysterical manifestations from the organic disorders of the central nervous system. The most famous one bears his name, the Babinski sign, an inversion of the plantar cutaneous reflex, testifying to a lesion of the pyramidal tract. In a second step, he defined what remained of hysteria and proposed in 1901 to abandon the term 'hysteria' in favor of the neologism 'pithiatism', defined as a pathologic state resulting in disorders which can be very accurately reproduced by suggestion, and can disappear by persuasion. Babinski therefore retained the exclusive etiological role of suggestion and refuted, unlike Dejerine, the role of emotion. He also sought to separate pithiatism from simulation, but ambiguously he made pithiatics 'semi-malingerers'. During the Great War, with Froment, he described physiopathic disorders and separated them from pithiatic disorders and simulation. After being accepted by many French neurologists, pithiatism, the word as well as the concept, gently died out. There remained little more than a few philosophical uses (especially by Jean-Paul Sartre and Maurice Merleau-Ponty) or metaphorical ones. What remains of the work of Babinski in the field of hysteria is not so much the creation of pithiatism as the masterly description of neurological signs to formally exclude an organic lesion of the nervous system or simulation before looking like hysteria disorders.

Medical humanities is the interdisciplinary field of humanities (literature, philosophy, ethics, history, and religion), social science (anthropology, cultural studies, psychology, and sociology), and the arts (literature, theater, film, and visual arts), and their application to medical education and practice. In this chapter, the concept of 'hysteria' is put into a medical humanities perspective. We review the concept of hysteria concisely. Two novels and one autobiographical story are used as material in order to study how 'hysteria' is represented in literary work. Madame Bovary (Gustave Flaubert), Hedda Gabler (Henrik Ibsen), and A Story in an Almost Classical Mode (Harold Brodkey) were searched for elements that are characteristic of hysteria. Excessive emotion, dramatics, attention-seeking behavior, physical symptoms of unknown and unidentifiable organic causes, self-centered behavior, and flirtatious behavior are the six elements used to operationalize hysteria. It was found that these elements were present in both a quantitative and qualitative manner in the literary works examined. Acknowledging some limitations and suggesting some research areas and clinical implications, we conclude that literary works are useful in analyzing concepts in medicine. Also, more generally, using literary works seems to have a positive impact on readers, healthcare providers, and researchers in the healthcare domain. Studying novels and related literary work contributes to the body of knowledge of medical humanities.

At the end of the 19th century, neurasthenia and hysteria were considered distinct diseases. Specifically, neurasthenia was regarded as a disease of the body, whereas hysteria was regarded as a disease of the psyche. However, immediately before World War I, due to their common characteristics, both hysteria and neurasthenia were thought to be 'functional diseases'. Moreover, it was suggested that heredity and the presence in both of the predisposing condition called 'nervous weakness' were other shared factors. Nervous weakness was considered essential for the definition of neurasthenia, but it was also considered a precondition for the development of hysteria. Because of this, it is still difficult to demarcate a line between neurasthenia and hysteria; therefore, the two diseases should be considered as sharing a common borderland with each other.

In the paper below we present the clinical case of a 48 year old female with various symptoms associated with functional visual disturbance -constricted tubular visual fields, wich lasts from 6 years; the extensive clinical and paraclinical ophthalmological investigations ruled out the presence of an organic disorder. In the present, we suspect a diagnosis of hysteria, still uncertain, wich represented over time a big challenge in psychology and ophthalmology. The mechanisms and reasons for hysteria are still not clear and it could represent a fascinating research theme. The tunnel, spiral or star-shaped visual fields are specific findings in hysteria for patients who present visual disturbance. The question of whether or not a patient with hysterical visual impairment can or cannot "see" is still unresolved.

This article provides a neurobiological account of symptoms that have been called 'hysterical', 'psychogenic' or 'medically unexplained', which we will call functional motor and sensory symptoms. We use a neurobiologically informed model of hierarchical Bayesian inference in the brain to explain functional motor and sensory symptoms in terms of perception and action arising from inference based on prior beliefs and sensory information. This explanation exploits the key balance between prior beliefs and sensory evidence that is mediated by (body focused) attention, symptom expectations, physical and emotional experiences and beliefs about illness. Crucially, this furnishes an explanation at three different levels: (i) underlying neuromodulatory (synaptic) mechanisms; (ii) cognitive and experiential processes (attention and attribution of agency); and (iii) formal computations that underlie perceptual inference (representation of uncertainty or precision). Our explanation involves primary and secondary failures of inference; the primary failure is the (autonomous) emergence of a percept or belief that is held with undue certainty (precision) following top-down attentional modulation of synaptic gain. This belief can constitute a sensory percept (or its absence) or induce movement (or its absence). The secondary failure of inference is when the ensuing percept (and any somatosensory consequences) is falsely inferred to be a symptom to explain why its content was not predicted by the source of attentional modulation. This account accommodates several fundamental observations about functional motor and sensory symptoms, including: (i) their induction and maintenance by attention; (ii) their modification by expectation, prior experience and cultural beliefs and (iii) their involuntary and symptomatic nature.

Mass hysteria or collective hysteria usually begins when an individual shows a hysteric manifestation in front of others in the same group who later contagiously acquire the same symptoms. The underlying pathogenesis of mass hysteria is still unknown. It has been demonstrated that the mirror neuron system (MNS) provides an important neural substrate for humans' ability to imitate and there is an inhibitive component of MNS keeping us from imitating everything we see. We proposed that the inhibitive component for MNS automatic imitation may not function well in individuals of the group that results in the outbreaks of mass hysteria. We also provide evidences from emotional contagion, gender difference and treatment in mass hysteria to support this hypothesis.

It has been suggested that hysteria had waned and was an old-fashioned, stigmatizing and false concept, reflecting the incapacity of the medical community to establish a diagnosis in certain situations. Nowadays, however, those disturbances, now referred to as conversion or dissociative disorders, still remain a frequent and incapacitating condition that every clinician faces. These past decades, several studies have tried to better describe their clinical presentation and their neurobiological mechanisms, with the help of the development of new neuroimaging techniques. If the neurobiological correlates are now better understood, efficient treatments are still lacking and only a multidisciplinary (general practitioners, neurologists and psychiatrists) and individually-tailored therapy might be beneficial to the patients.

Background: Elevated Minnesota Multiphasic Personality Inventory (MMPI) scores on the hysteria (Hy) scale are reported in several forms of pain. Previous results were possibly biased by diagnostic heterogeneity (psychogenic, somatic and mixed pain syndromes included in the same index sample) or Hy heterogeneity (failure to differentiate Hy scores into clinically meaningful subscales, such as admission of symptoms [Ad] and denial of symptoms [Dn])., Methods: To overcome this drawback, 48 patients diagnosed as having a Diagnostic and Statistical Manual of Mental Disorders, 4th edn, Text Revision (DSM-IV-TR) diagnosis of "pain disorder associated with psychological factors" were compared with 48 patients experiencing somatic pain excluding psychological factors, and 42 somatic controls without pain., Results: MMPI Hy and hypochondriasis (Hs) scores were significantly higher in the pain disorder group than in control groups, who scored similarly. MMPI correction (K) scores and Dn scores were similar in the three groups, whereas Ad was significantly higher in the pain disorder group and lower and similar in the two control groups, respectively. In the pain disorder group, Ad and Dn were negatively correlated, whereas in control groups they were unrelated., Conclusions: These findings suggest that whereas a pattern of high Hs and Hy scores together with a normal K score might characterize patients with a pain disorder associated with psychological factors, elevated Hy scores per se do not indicate hysterical traits. In the pain disorder group, elevated Hy scores reflected the Ad subscale alone, indicating a strikingly high frequency of distressing somatic symptoms. They tend not to repress or deny the emotional malaise linked to symptoms, as the hysterical construct expects. The pain disorder designation should be considered a nonhysterical form of somatization.

Four patients with the diagnosis of hysterical hemiparesis and normal magnetic resonance imagings were referred to us for further evaluation. All were being treated with antidepressant or antianxiety drugs or both, with no benefit. In all 4 cases single photon emission computed tomography revealed decreased regional cerebral blood flow in frontal regions in cortical areas corresponding to their neurologic deficits. In all 4 cases improvement followed neurologic treatment. We suspect that reduced blood flow in frontal regions may have produced the neurologic deficits. We call these conditions "pseudohysterical hemiparesis."

The study aimed at comparison of quantitative indices of gait in patients with hysteria and organic dysbasia. Two groups of patients were studied - 28 patients with psychogenic dysbasia and 22 with organic gait disturbances (cerebellar ataxia in multiple sclerosis and post stroke hemiparesis). A control group included 10 healthy subjects. Space and temporal gait characteristics were investigated using an impregnation method (footprint), i.e. analysis of gait parameters by footprints. Step width (base) and length, step frequency and gait speed were assessed. All parameters were recorded both at normal speed and accelerated gait. At accelerated gait, changes of step base (SB) were in different directions: in patients with hysteria and controls SB decreased and in patients with organic dysbasia increased. SB index (ratio of SB at accelerated gait to that at normal speed) was <1 in 82% of patients with psychogenic dysbasia and 90% controls and >1 in 91% of patients with organic gait disturbances. Maximal differences were found between subgroups with psychogenic and organic ataxia and less marked differences - in paresis.

Postural stability or fluctuation of general centre of gravity (GCG) was investigated in 14 patients with hysteric motor disorders(alterations of statics and walking, pseudopareses) by means of stabilograph. Comparative groups included 7 patients with hemipareses of vascular origin, 7 patients with multiple sclerosis with spastico and atactic disturbances and 7 healthy individuals. The amplitudes of GCG fluctuations in both sagittal and frontal planes as well as their correlations were analysed. It was shown that amplitude of GCG vibration was maximal in hysteriac patients. However patterns of regulation of postural control in hysteriac patients (correlation of amplitudes of vibrations in sagittal and frontal planes) were similar to those of healthy individuals and differed significantly from organic models.

Objective: To clarify factors contributing to mass illness of sudden onset by studying an outbreak that was apparently triggered by a gaseous odor and that involved a rapid, extensive response by school and fire officials., Setting: Urban elementary school., Main Outcome Measure: A standardized student questionnaire was designed to identify potential illness predictors., Design: Four weeks following the outbreak, public health officials distributed the questionnaire to all students in regular classes in grades 3 through 6 (N = 319), representing 46% of the estimated 680 students present the day of the outbreak., Results: Seventy-seven percent of the students who completed the questionnaire reported that they experienced physical symptoms during the epidemic. A stepwise regression analysis demonstrated several independent variables that predicted the severity of illness, including the intensity of the odor smelled during the outbreak (P < .0001), becoming sick after the fire trucks arrived (P < .0001), and believing in an environmental cause for the illness (P < .002)., Conclusions: These results indicate that both psychological and environmental factors, real or perceived, may contribute to sudden-onset epidemics of hysteria. Moreover, the response intervention of officials may influence the extent of such outbreaks. Early recognition of psychological causes and dispersion of groups at risk could reduce morbidity and associated health care costs.

Hysteria covers a variety of patterns of illness. The common element is that the symptoms relate to mistaken thoughts of illness or disability. Physiological processes can give rise to regional symptoms, e.g. pain. The diagnosis requires positive psychiatric evidence.

A pattern that prevails in Freud's early texts and carries over into his life suggests a culturally-derived coherence in Freud's thinking and work. This pattern connects the early studies in neuro-anatomy, the description in Studies on Hysteria of the structure of hysterical neuroses, urban design in Vienna, antisemitism, and the role of bourgeois values in Freud's life. The theoretical basis for this view depends upon the work of cognitive psychologists who define thinking as pattern recognition. I propose that consideration of such features as the structure of physical space can lend additional dimensions to our understanding of Freud, and that a complex appreciation might include attention to recent interdisciplinary developments such as chaos theory, and lead to a redefinition of the notion of 'cultural context'.

Status epilepticus is a life-threatening disorder whose early recognition is essential. Non-epileptic seizures (pseudoseizures, hysterical seizures) may be confused with true epileptic seizures presenting a diagnostic dilemma which can result in inappropriate, expensive and potentially harmful treatment. We describe a male patient with no prior history of epilepsy who presented with status epilepticus and developed multiple types of non-epileptic seizures during his hospital stay.

Of 167 patients referred to a unit treating severe behaviour disorders after brain injury, 54 showed clinical features closely resembling those of gross hysteria as described by Charcot. Close correlation was found with very diffuse insults (hypoxia and hypoglycaemia), but not with severity of injury or with family or personal history of hysterical or other psychiatric disorder. The findings may have implications for the understanding of the nature of hysteria.

We have reviewed the charts of 45 neuro-ophthamological patients diagnosed with 79 monocular visual field or visual acuity losses secondary to non-organic etiology. Our aim was to determine the percentage of patients that have improvement in vision. As part of the protocol, all patients had magnetic resonance images, pattern visual evoked potentials, and flash electroretinography in addition to complete neuro-ophthalmological examinations. A single physician performed both the initial and follow-up examinations of all patients. Thirty-three percent of these patients had visual field defects only, 62% had both visual field defects and visual acuity defects, and 5% had only visual acuity defects. After organic disease was ruled out, all were given a timetable for recovery and clear reassurance regarding their prognoses for visual recovery. Seventy-eight percent of these patients showed improvement or were normal, while 22% showed no improvement. Younger patients without obvious psychiatric disorder had better prognoses than older patients.

A self-control study was conducted among 92 inpatients for the purpose of the establishment of the relationship between psychoactive and body weight, with the latter measured once a week, stepwise regression (alpha = 0.3) revealed: increase or decrease of body weight was associated not only with the kinds of medicines administered, but also with the types of the diseases, living standard, and therapeutic effects. The mechanism of body weight increase was explored and some suggestions were also given with regard to the prevention of the increase of body weight.

Over a 5-year period 17% of admissions to an epilepsy unit in a psychiatric hospital had pseudoseizures; 42% of these patients also had concurrent epilepsy. Memory deficits were common both in those with pseudoseizures along (50%) and in those with concurrent epilepsy (62%). EEG abnormalities were more common in both groups with pseudoseizures than in a control group of patients with anxiety and affective disorders. Of specific EEG abnormalities only paroxysmal events occurred significantly more frequently in those with concurrent epilepsy than in those with pseudoseizures and in complicated cases of seizure disorder, the presence of cerebral pathology cannot be relied on to distinguish between epileptic and pseudo-seizures.

Two cases of multiple personality were studied neurophysiologically and neuropsychologically. Bilateral frontal (Right greater than Left) and left temporal dysfunction was present in both cases, on neuropsychological indicators. Both cases on EEG analysis, were in a state of relative left hemisphere activation, across all cerebral regions and task conditions. The one case who was cured with hypnotherapy, after recovery showed normal left hemisphere functions neuropsychologically but remained in a state of relative left hemisphere activation electrophysiologically. This is in contrast to women with chronic hysteria who exhibit relative right hemisphere activation in all regions and across all conditions. Both patients were unmedicated throughout. A neurophysiological model to account for these findings is presented.

During the period 1962-1986, 54 patients received the diagnosis hysterical visual impairment, i.e. 1 out of every 631 patients admitted to our department. Isolated visual acuity impairment was the most common symptom, followed by combined visual acuity impairment and visual field constriction, whereas isolated visual field constriction occurred most infrequently. The mean age of the patients in the first group was significantly lower than that of the patients in the latter group. A questionnaire sent to all patients in 1987 was answered by 41 patients. Twenty-one of these (51%) felt that their visual function now was good, whereas 20 (49%) claimed that their visual function was still poor. Nine patients (22%) were disabled because of their visual problems. Twenty-nine of the patients who answered the questionnaire were re-examined. Sixteen of these (55%) still showed visual impairment at the follow-up, while 13 (45%) showed complete disappearance of visual complaints. The younger patients appeared to have a better prognosis than the older ones.

The torque during isokinetic knee extensions and flexions was determined in repeated tests at 3 speeds of angular rotation in 25 patients with pareses considered to be hysterical after relevant examinations and follow-up. The torque records were combined with surface EMG from the quadriceps and the hamstring muscles in some patients. Besides the weakness, 3 signs were observed that are not usually seen in patients with pareses due to verified peripheral or central lesions. These signs were: Enlarged variability of torque in repeated tests of the same movement (larger than 20% of maximum torque in 22 patients). Higher torque in fast movements than in slow movements (8 patients). Force production in knee flexion less than that expected from the weight of leg and lever arm due to restraining activation of the quadriceps muscle (12 patients). The restraint was present although there was no spasticity. The signs reflect inconsistent and contradictory motor performance that is not compatible with a genuine paresis. Thus, they aid the identification of weakness of functional origin.

At the start of this lecture, I invited you to indulge with me in a "dessert" of speculations. I hope it has been a sufficiency, not a surfeit. In summary, we have examined a hypothetical model of some dissociations of consciousness and the expression of unconscious symptoms in adults; we then explored some possible conditions that would account for the development of separate mental streams. In the course of this exploration we were led to question some basic assumptions about the unity of the self, and we proposed some possible mechanisms by which lateral specialization develops in children. This model of the development of lateral specialization has some implications for the study of evolution of the human brain and consciousness. It would seem useful to examine the relationship between the evolution of the commissural systems and the evolution of different capacities for consciousness. According to this model, the full development of lateral specialization depends upon the later myelination of the commissures, which makes possible the autonomy and competition between hemispheres. By this means, only minimal differences between hemispheres need to be specified genetically, since the rest of lateralization can be produced by progressive differentiation, through interactions with the environment. Thus man's eternal, internal struggle may be the price paid for the evolution of lateral specialization.

In an attempt to validate recent assertions that the strongest indicators of hysteria are the "positive" findings in the neurological examination, seven of the most accepted features (history of hypochondriasis, secondary gain, la belle indifference, nonanatomical sensory loss, split of midline by pain or vibratory stimulation, changing boundaries of hypalgesia, giveaway weakness) were sought in 30 consecutive neurology service admissions with acute structural nervous system damage. All subjects showed at least one of these findings; most presented three or four. The presence of these "positive" findings of hysteria in patients with acute structural brain disease invalidates their use as pathognomonic evidence of hysteria. A second, retrospective study on the misdiagnosis of hysteria demonstrated that women, homosexual men, the psychiatrically ill, and patients presenting plausible psychogenic explanations for their illness are most liable to be misdiagnosed. Certain disorders, particularly movement disorders and paralysis, are most often mislabeled as hysteria. A diagnosis of hysteria must be made with great caution as it so often proves incorrect.

To study the neurophysiological mechanisms of neurasthenia, hysterical neurosis and obsession neurosis with a view to the practical employment of the results, the authors examined 100 patients and 40 normal subjects using the method of evoked potentials (EP). EP changes indicated an neurasthenia-related decrease in the functional activity of the cortex, weakening of its inhibitive functions and an increase in the reactivity of the system of negative-emotional support. Patients with hysterical neurosis displayed the greatest excitability of the structures of the projective pathways and insufficiency of programme-integrating effects of the higher portions of the brain. Neurosis of obsessive states was characterized by an increase in the activity of specific cortical zones and, to a larger degree, of the centres of negative-emotional reactivity. The time-course of EP during treatment is outlined. The findings obtained may serve as additional criteria in the diagnosis and treatment of neurosis.

Patients with "hysterical" neurologic symptoms have long puzzled neurologists and psychiatrists. "Hysteria" has recently been subdivided into conversion and somatoform disorder. We applied computerized EEG frequency analysis to 10 patients with diagnosed conversion disorder, 10 somatoform disorder patients, and 10 control subjects. One minute EEG samples composed of 4 sec epochs were recorded from left frontal (F7-C3), right frontal (F8-C4), left posterior (T5-01) and right posterior (T6-02) derivations. Spectral power was calculated for 4 bands (0.25-4HZ, 4.25-8Hz, 8.25-13Hz, and 13.25-30Hz), and for the full frequency range. Low (0.25-8Hz) and high (8.25-30Hz) frequency bands were compared to determine high/low power ratios on the left and right (PHLL) and (PHLR), ratios of left/right front (PLRF) and posterior (PLRP) power, mean alpha frequency deviation frontally (FLRF) and posteriorly (FLRP), and mobility of left and right frontal power (MOLF and MORF). No significant differences were found between conversion disorder patients and controls in PHLL, PHLR, PLRP, and MORF. PLRF, FLRF and MOLF differed significantly between patients and controls. Power and frequency ratios of right frontal mobilities suggested a decrease in high frequency power, reduction in mean alpha frequency, and lower predominant frequency in the right frontal area in somatoform disorder patients as compared to controls, but significance was not reached. Somatoform and conversion disorder patients differed significantly in these spectral measures. These observations suggest that the two "hysterical" disorders may have distinct pathophysiology, and may be due to eventually identifiable cerebral dysfunction in some cases.

The authors have found that disturbances of general sensitivity are characteristic of not only patients with hysterical neurosis, but also of patients with neurasthenia. The clinical structure and the time course of those disturbances in both groups of the patients were found to be rather close. In general, they differ substantially from the sensitivity disturbances in neuroses described earlier. The leading mechanism of the development of those sensitivity disturbances consists in an impairment of the function of the limbico-reticular complex structures.

The follow-up findings were studied in 102 patients with long-standing (2-17 years) neuroses (neurasthenia, 49 cases, hysterical neurosis, 53 cases) and compared with those in 40 patients with acute forms of these diseases. The results of the study point out to factors predisposing to an unfavourable course of the illness. Ii is noted that in most cases, protracted neuroses develop in individuals with definite personality characteristics and numerous variants of "biological insufficiency", such as aggravated heredity, frequent colds in childhood, attendant somatic pathology, etc. Some risk factors have been emphasized including a prolonged influence of psychotraumatic circumstances on these patients, their late application for help to the psychiatrist and late initiation of the adequate treatment.