Compulsive Eating: A Neuropsychologic to Certain Eating Disorders

Approach

John H. Rau and Richard S. Green

T

HE “EATING DISORDERS” represent a group of severe disturbances that have been largely refractory to a variety of medical, behavioral, and psychological treatment approaches. l--4 That they are not well understood is reflected by the considerable semantic and conceptual confusion to be found in the literature. With rare exceptions (e.g., Stunkard5*6) eating disorders have not been classified by variations in abnormal patterns in eating but rather by their consequences (viz. obesity or anorexia nervosa) or by the patient’s internal feeling state (viz. bulimia or anorexia). Obesity refers to an excess of body weight due to accumulation of fat. Exogenous obesity may be due to excessive caloric intake, while endogenous obesity may be due to metabolic disturbances. Obesity is thus a physical state, it is not an eating disorder, although it may be a consequence of one. Most obesity investigators have selected subjects on the basis of excessive weight, with the result that the findings have little direct relevance to the understanding of particular patterns of eating disturbances. Similarly, emaciation is a physical state, characterized by severe weight loss. When functional, such weight loss is sometimes referred to as anorexia nervosa.’ Anorexia nervosa is also not an eating disorder, although it may be a consequence of one. Studies of anorexia or anorexia nervosa have included patients on the basis of weight loss or malnutrition with no medical etiology, without considering variance in eating patterns, thus reducing these studies’ relevance in understanding problems in eating. Bulimia refers to an abnormal increase in the sensation of hunger, while, in contrast, anorexia refers to a lack or loss of appetite. These latter two inner feeling states may also stem from any one of several etiological antecedents. Bulimia has not been extensively studied. Major textbooks in psychiatry devote virtually no space to it. 7*8Bulimia is hardly mentioned in Hilda Bruch’s most recent review of the eating disorders.g Focusing on feelings about eating or its consequences rather than on the eating itself does not seem to have resulted either in the development of more effective treatments or in an improved theoretical understanding of eating problems. This article focuses on one particular pattern of disordered eating-compulsive eating. Compulsive eating involves irregular, unpredictable episodes of ego-dystonic excessive eating during which large quantities of food are consumed

From Long IslandJewish-Hillside Medical Center, Glen Oaks, N. Y. John H. Rau, Ph.D.: Senior Psychologist and Coordinator of Inpatient Services, Psvchology Department, Hillside Division: Richard S. Green, M.D.: Associate Director. Hillside Division: Long I.Fland Jewish&Hillside Medical Center. Requests for reprints should be addressed to J. H. Rau. Ph.D., Department Island Jewish-Hillside Medical Center, Glen Oaks, N. Y. 11004. 0 1975 by Grune &Stratton. Inc.

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“against the eater’s will.” By ego-dystonic we mean that the patient feels that his eating is unwanted and unacceptable, alien to his concept of himself and not within his control. Anticipation of losing control arouses anxiety and dread, while afterward feelings of guilt and shame occur along with a lowering of self-esteem. During an eating episode the patient may feel anxiety, guilt, and loathing and perceive the act of eating as something outside of himself-depersonalized and unreal. Compulsive eating must be clearly differentiated from overeating, which involves, in general, a regular psychogenically predictable increase in food intake over which the eater has some considerable measure of control, Compulsive eating must also be distinguished from episodic excessive eating, which is egosyntonic. To the extent that this latter form of eating is similar to a drunken celebration or spree, it could be called a binge. Neither BruchQ nor Stunkard5 regards binge eating as ego-syntonic, however. Bruch describes her anorexia nervosa patients as being “driven” by a “relentless pursuit of thinness.” When these patients eat, they experience feelings of dread, anxiety, guilt, and shame. Stunkard’s binge eaters similarly view their eating episodes as disturbing and unwanted and as evoking “severe discomfort and expressions of self-condemnation.” We prefer to restrict the use of the word binge to episodic ego-syntonic excessive eating and to use the phrase compulsive eating to describe ego-dystonic excessive eating episodes. Recently the authors have found that persons of varying weights with episodes of compulsive eating have shown cerebral dysrhythmias on electroencephalographic examinations (EEG) and that symptom remission occurred in 9 of 10 patients following the administration of anticonvulsant medication (diphenylhydantoin-Dilantin’O). An additional 8 patients with abnormal EEGs and compulsive eating have been interviewed and similarly treated pharmacologically. Five responded dramatically with symptom remission, while 3 had questionably positive responses. These investigations suggest the possibility that compulsive eating may have a neurologic etiology. This possibility, that episodes of compulsive eating or other eating disorders may be related to neurologic dysregulation, has been given only passing scattered interest in the recent literature. BruchQ does not discuss the issue at all, although fully one-quarter of her anorexic patients had episodes of excessive eating. She mentions a case of a man (also treated by Stunkard) whose eating episodes were clearly related to demonstratable organic brain syndrome following encephalitis when he was 12 years old.” Terzian et a1.12report a case of the Kltiver-Bucy syndrome in a man who also suffered from episodic excessive eating. Bulimia and obesity have been reported following temporal lobectomies by Grossman,13 Alajouanine et al.,14 and Sawa et a1.,15and following frontal lobotomy or accidental damage to the frontal neocortex by Kirschbaum,16 Hercaen,” and Hofstatter et al.ls GoorlQ reported 4 anorexic patients with abnormal EEGs indicating diencephalic dysfunction with similar findings observed in 11 of 15 relatives, suggesting a genetic neurologic defect. Balgura 2ohas suggested that recent animal research implicates hypothalamic factors in human eating disturbances. Similarly, Schacter’s researchzl presents evidence that obese persons behave like hyperphagic rats with lesions in the ven-

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tromedial nuclei of the hypothalamus. Hyperphagic rats eat fewer meals, eat more per meal, and eat at faster speeds than do normal rats,21*22findings not inconsistent with the concept of compulsive eating. Reeves and P1umz3 reported an obese patient with a neoplasm that precisely destroyed the ventromedial hypothalamus. She consumed up to 10,000 calories daily in a series of uncontrolled eating episodes. Other authors24-26 present data suggesting the possibility that some anorexic patients suffer from hypothalamic dysregulation. Stunkard5v6*” has also suggested this for obese patients in some of his papers. He classified obese persons into two main groups: night eaters and binge eaters. The night eater’s behavior was considered to be consistent with a disturbance in the satiation center of the hypothalamus, while the binge eater’s behavior was suggestive of a disturbance in the appetitive hypothalamic center. Crisp2’ found that 10% of his anorexic patients had had epileptic seizures, while Dallyzs found a history of epilepsy in 9% of his patients. Crisp et a1.2gfound that 15% of hospitalized anorexic nervosa patients had severely abnormal EEGs. A number of the authors’ patients have reported additional symptoms that have also surprisingly responded to pharmacologic intervention. These include episodic aggressive behavior, temper tantrums, irritability, insomnia, paresthesias, depression, and not infrequently other compulsive symptoms such as compulsive stealing or cleaning. Most patients were obsessed by thoughts of food and eating. These symptoms have not been extensively studied by persons interested in the eating disorders. Bruch,g however, mentions that stealing occurs primarily in binge eaters, while King,25 Thomae,30 and Ushakov31 all concur that stealing is an occasionally related sympton. The etiologic relationship between these symptoms and compulsive eating is not clear at this time. Nonetheless, the correlation between episodic impulse dyscontrol and episodic somatic symptoms with epileptiform EEG abnormalities (such as the 14 and 6 per second positive spike pattern) has been reported by a number of investigators.30-38 Such patterns are currently considered by some electroencephalographers as reflecting subcortical dysfunction, possibly involving thalamic or hypothalamic areas, among others.3g-41 There is, thus, considerable indirect evidence indicating the possibility of neurologic correlates to eating disorders, and it is not unreasonable to consider that episodic eating dyscontrol may also be a function of epileptiform subcortical cerebral dysrhythmias. This possibility stands in sharp contrast to the prevailing view that the eating disorders are psychogenically determined. Early psychoanalytic thinking was that bulimia and anorexia nervosa were symptoms that defended against women’s unconscious fears of impregnation and reflected their unconscious Oedipal conflicts.42-44 More recently, other analysts (viz. Bruchg and Selvini45) have disagreed with these earlier conceptions and have suggested that sexual problems are rarely found to be central conflicts in patients with anorexia nervosa. Moreover, the psychoanalytic model seems to be inconsistent with the fact that a small but substantial number of such patients are male. That more than one model can be explanatory of disturbances in eating is perhaps well illustrated by the case of “Laura,” called “Solitaire” in Robert Lindner’s well-known book The Fifty-Minute Hour.46 Lindner reported on his psychoanalytic treatment of this young woman with “bulimia.” Her primary

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symptoms consisted of “episodes of depression during which she would be seized by an overwhelming compulsion to gorge herself.” After more than 2 years of intensive psychoanalysis, four times a week, the patient became aware of her Oedipal conflicts and their relation to her eating. More specifically, her eating was viewed as a substitute for her sexual hunger for her father and for her wish to be impregnated by him. However, there was no report that her episodic compulsion to eat was affected by this insight, and no follow-up data were presented. Since Lindner and his patient were excellent observers and he presented an articulate description of her symptoms, treatment, and some history, it is possible to reanalyze the data to assess whether a neurological etiology could be supported. The following summarizes the pertinent information about Laura. Her age was not disclosed. She apparently was a young woman, most likely in her twenties. The episodic nature of her symptoms was described as follows: “It seems to come out of nowhere. I’ve tried to discover what touches it off, what leads up to it, but I can’t. Suddenly it hits me. . . . It seems I can be doing anything at the time, painting, working at the Gallery, cleaning the apartment, reading or talking to someone.” She referred to these episodes as “fits” and felt she was a “victim of forces beyond her ken or control.” As she put it, “It’s a frenzy, a fit, something automatic and uncontrollable. I want to stop it, but I can’t.” The ego-dystonic nature of these episodes was, thus, clearly described. Lindner stated that he was unable to ascertain any pattern to her eating or any relationship between these episodes and other current events in her life. In her words, her eating episodes began as follows: “Something, I don’t know what to call it, starts to ache; something right in the center of me feels as if it’s opening up, spreading apart maybe. . . . Then the emptiness starts to throb-at first softly like a fluttering pulse. . . . But then the pulsing turns into a regular beat; and the beat gets stronger and stronger.” The moment she became aware of the “hole opening inside” she became anything I “terrified” and began compulsively to eat: “I eat and eat-everything, can find to put in my mouth. I eat until my jaws get numb with chewing. I get sick with eating and still eat-fighting the sickness with swallowing, retching, vomiting-but always eating more and more.” Thus a possible preictal stage seems to be followed by the onset of what Lindner himself refers to as “seizures of uncontrollable hunger, the furious eating.” The episode ends with the patient usually losing consciousness, suggesting a postictal phenomenon. As she describes it: “Most of the time I eat myself into unconsciousness. I think I reach a state of drunkenness, or something very like it. Anyhow, I pass out. . . . No matter how the ‘fit’ ends, it’s followed by a long sleep, sometimes for as much as two whole days and nights.” At a later point, Lindner describes her as being amnestic for episodes. “As always, she had only a vague, confused memory of events during her seizure, recollecting them hazily through a fog of total intoxication. Until I recounted the episode, she had no clear remembrance of my visit and thought she had dreamed my presence in her room. Of the portion that concerned her pitiful imitation of pregnancy, not the slightest memorial trace remained.” Laura describes awakening as “coming out of a fog.” In between episodes, she imposed an ascetic regime on herself that “kept her fashionably thin.” She had repetitive dreams nightly, but was amnestic for most

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of their content. She had difficulty in controlling her impulses, once grabbing the analyst physically and at another time cutting her wrists. She was described as having a “histrionic talent” and used the therapy sessions as means of venting her enormous rage and anger at her parents. Her interpersonal relationships were poor and characterized by impermanence, bitchiness, and variation. Her father had deserted her mother when Laura was in the sixth grade. Her mother was a cripple, paralyzed from some unknown illness after having three children. The salient characteristics, then, of Laura’s syndrome consisted of an episodic, ego-dystonic, nonpredictable, irregular “seizure” involving compulsive eating preceded by an apparent aura and followed by a probable postictal phase involving loss of consciousness, amnesia, and confusion. That these episodes may thus have been an epileptic equivalent is a viable hypothesis from the data. Interestingly, both Lindner and Laura may have unconsciously viewed her problems in this vein, since the words fit and seizure appear frequently throughout the report. The possibility that patients previously classified as anorexia nervosa or obese patients with psychogenic determinants can also be seen as neurologically dysfunctional is further illustrated by the following two summaries of case histories obtained on patients seen by the authors. CASE

HISTORIES

Nun, a 25-year-old, 5’3” female college graduate, weighed 79 lb and was emaciated. She had been in intensive psychoanalytically oriented psychotherapy for 5 years because of family difficulties. She and her therapist understood that her compulsive eating, her throwing up afterward, and her use of laxatives were symptoms of an underlying problem. When this problem was “worked out,” the expectation was that her eating problems would subside. She was referred by a colleague who was aware of the previous research. She described her eating episodes as follows: “1 feel suddenly that my head is going to split open. . _. I feel I may go crazy unless 1 get something to eat. . . _I will eat anything I can find. If I am on the street, I will go to the nearest food store and buy crackers or candy, open the box and drop it into my handbag and start eating. . As soon as that is finished, 1 must have something else.” She would consume enormous quantities of food, feel terribly bloated and satiated; finally she vomited and then slept. Talking about this evoked tremendous feelings of shame and guilt. She described her need to be thin as a way of putting money in the bank. Her compulsive eating started at age 151,s. Since then she periodically decreased her weight in order to ensure herself that she would not become obese. She felt completely ineffective in controlling her eating. She was obsessed by thoughts about food. She had also been a compulsive stealer who had been frequently apprehended in major department stores. She was bright, articulate, and in touch with her feelings. Her EEG revealed I4 + 6 per second positive spikes in the right-temporal occipital area. She was placed on diphenylhydantoin, 100 mg t.i.d. Two weeks later she reported a “miracle.” She had no further compulsive eating episodes, she no longer compulsively stole, and she was less obsessed by thoughts of food. After 6 months she remains symptom-free and is approaching normal weight. Paul, a 23-year-old male college student, weighed 307 lb when first seen. He had been referred by a colleague who was acquainted with the previous research. He had been grossly overweight for many years; as an adolescent he had a complete evaluation for endocrine dysfunction, which was negative. He was unhappy about his weight, but felt he could do nothing about it. Episodically he would get an uncontrollable urge to eat. Anticipation of these episodes elicited anxiety and dread; following them he experienced guilt and shame. His compulsive eating behavior differed from that of the preceeding patient. He started by eating a large but normal meal at a restaurant; then he went somewhere else to another restaurant where he consumed a second large but normal meal. tram there he continued restaurant-hopping until the episode ended or his money ran out. At no time, therefore, did he behave in a socially inappropriate manner. He also reported frequent paresthesias ofhands and/or arms and rare long-lasting headaches. He had never been seen in therapy. His EEG showed marked diffuse paroxy-

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smal slowing and minimally expressed 14 + 6 per second positive spikes in the right midtemporalposterior temporal occipital area. He was treated with diphenylhydantion, 100 mg t.i.d. After 8 weeks he had lost 22 lb without attempting to diet. He stopped taking the medicine when he experienced some considerable difficulty adjusting to the idea of being thin, and he is now in psychotherapy. He reported no further episodes and experienced remission of the paresthesias when taking the medicine; he reported return of such episodes and paresthesias when he stopped. His weight is now 310 lb, mainly because he resumed his compulsive eating.

The foregoing suggests that models for the eating disorders based solely on dynamic considerations may not be sufficiently explanatory for compulsive eating and that alternative models should be given serious consideration. One such alternative view is that compulsive eaters have a primary neurologic disorder similar to epilepsy. Common symptoms consist of discrete, episodic, ego-dystonic compulsive eating, usually preceded by auralike sensations and followed by other symptoms similar to epileptic postictal events. These patients’ EEGs are usually characterized by positive or negative spikes or sharp waves and are regarded as abnormal. The patients respond with symptom remission, usually within 1 week, to diphenylhydantoin. To this extent, at least, episodic compulsive eating can be regarded as a bonafide disease as defined by a medical model. Unfortunately, unanswered questions concerning the etiology, location, form, and nature of such a neurological cerebral disturbance arise without difficulty. So far no one specific EEG pattern associated with these episodes has been found, although they do share the essential quality of an epileptiform abnormality (viz. the presence of a high-amplitude aperiodic discharge: “spike”). The fact that diphenylhydantoin is an effective medication tends to obscure rather than clarify questions related to locus. This is because the medication is thought to be effective by preventing the spread of excessive neuronal discharges from one or more existing sites to other locations. *’ Thus the information obtained from EEG tracings does not necessarily shed light on the locus in the central nervous system that may influence the onset or cessation of an eating episode. Two possible methods by which such a neurological dysregulation could affect eating suggest themselves. The first is that the cerebral dysrhythmias specijicully effect the hypothalamus, resulting in either an increased excitation in the appetitive center or an increased inhibition of the satiation center. The second possibility is that the primary neurological disorder results in episodic excessive increases in the patient’s general drive state. (In contrast, the former theory postualtes a specific disorder in one or more centers directly controlling eating behavior.) Factors in the patient’s personality or life experience could determine the choice of the behavior by which the increase in drive state is expressed. Thus compulsive eating can be conceived as a psychobiological concatenation of neurologic and psychological factors. This latter possibility is similar to that advanced by Epstein48 and Mitchell4Q for fetish behavior. These two ways of conceptualizing neurologic dysregulation do lead to a number of clearly different hypotheses. For example, the latter view seems to call for marked similarity in the premorbid personalities or early life experiences of compulsive eaters, while the former view is more compatible with marked variance among the personality structures of these patients.

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Despite common symptoms possibly attributable to neurologic dysregulation, these patients seem to vary psychologically in the ways in which they cope or attempt to cope with a primary dysregulation in their drive states, no matter how conceptualized. Their defensive strategies produce secondary psychogenic reactive disorders of varying types and of varying intensity. Some, like Laura, maintain themselves on Spartan regimes, anticipating the occurrence of bouts of uncontrollable eating. That is, they maintain an emaciated state between episodes as insurance against the knowledge that at some future time they will eat compulsively. Unlike the typically described anorexia nervosa patient, many of these people recognize and accept that they are, in fact, thin. Other patients use reaction formation and denial as defenses against overwhelming feelings of shame and embarrassment. They often fast between episodes. It is very difficult for patients to talk about their eating, because it is associated with concern over loss of control and the potential threat of being exposed to the public as a “pig” or “hog.” Alternatively, by simple Pavlovian conditioning, any eating may become associated with a loss of control and become inhibited by feelings of shame and guilt. These patients often behave in remarkable ways to avoid being publicly labeled as overeaters. Some only buy enough food for one ordinary meal; others do not permit food in the house at all, or refuse to go out to eat. If such patients have had many years of psychoanalytically oriented therapy, they often feel additional shame, since they have been told, explicitly or implicitly, that the “real” problem is their underlying oral greediness of their incestuous sexual feelings, and not their eating. In these patients such treatment may serve as an iatrogenic source of additional negative self-esteem. (One other problem in the psychological treatment of these patients is that disturbances in their interpersonal relationships are often seen as the cause rather than the result of their eating disturbances. For example, one patient broke up with her boyfriend and returned to her home, only to eat compulsively later. Inquiry revealed that she had provoked a disturbance in this relationship so that she could give in to her eating compulsion in a socially appropriate place.) Other patients do not defend themselves against the neurologic dysregulation in their drive states. They gradually become obese and corrrespondingly apathetic and depressed about themselves and their interpersonal adaptation. From time to time they may try to diet, join Weight-Watchers, or take amphetamines, but they soon give up, as these methods are at best transiently helpful as to weight and entirely useless in treating a primary neurologic disorder. If the disturbance has lasted a number of years, such persons adapt to the idea of being obese, and the idea is no longer as ego-dystonic as at first. Some of these patients have stopped taking their medication even after an extended weight loss because of the difficulties they have in adjusting to a self-concept of “not obese.” These patients need psychotherapy that is focused on helping them through this difficult phase. Schacter 5o has suggested that obese persons are relatively insensitive to internal appetitive cues and are in fact externally stimulus-bound. That is, when food is available, obese persons are more likely to eat more than normals would eat, whether or not they are “hungry.” In contrast, obese compulsive eaters seem to eat excessively in direct response to internal stimuli originating from neurologic dysregulation. It is not known how many of Schacter’s subjects may have

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been compulsive eaters. In the future, consideration should be given to separating obese subjects into groups depending on their eating patterns prior to assessing their responses to varying stimuli. SUMMARY

The view advanced here suggests that compulsive eating should be regarded as a separate psychiatric syndrome and not as an integral part of other eating disorders. The syndrome is characterized, in general, by a primary neurologic dysregulation and secondary psychological reactive disorder, which varies among different patients. This variation has led to considerable conceptual confusion and deprived these patients of a possible successful pharmacologic intervention. The confusion stems in part from the fact that persons who appear to be very different (vis. fat or thin) may be quite similar in that they both suffer from some common neurologic disease. They appear different because they resort to different psychological defense mechanisms. In contrast, confusion is more easily elicited when persons who appear to be very similar (viz. obese) are so for very different reasons. That is, excessive weight gain (or loss) is the final common pathology resulting from more than one possible etiology. It may now be possible to distinguish between neurogenic compulsive eating and other psychogenic or medically based eating disorders. The former may be amenable to successful pharmacologic treatment as well as psychological. REFERENCES 1. Bliss EL, Branch CH: Anorexia Nervosa: Its History, Psychology and Biology. New York, Harper & Row (Hoeber), 1960 2. Rackoff V: The psychiatric aspect of obesity. Modern Treatment 4:lll I-1 124, 1967 3. Kolb LC: in Noyes (ed): Modern Clinical psychiatry. Philadelphia, WB Saunders, 1968 4. Fenichel 0: The Psychoanalytic Theory of Neurosis. New York, W. Norton, 1945 5. Stunkard AJ, Grace WJ, Wolff HG: The night-eating syndrome: A pattern of food intake among certain obese patients. Am J Med 19:78, 1955 6. Stunkard AJ: Eating patterns and obesity. Psychiatr Q 33:289, 1959 7. Redlich FC, Freedman DX: The Theory and Practice of Psychiatry. New York, Basic Books, 1966 8. Mayer-Gross W. Slater E, Roth M: Clinical Psychiatry. Baltimore, Williams & Wilkins, 1960 9. Bruch H: Eating Disorders: Obesity, Anorexia Nervosa and the Person Within. New York, Basic Books, 1973 10. Green RS, Rau JH: Treatment of compulsive eating disturbances with anti-convulsant medication. J Am Psychiatry 131:428-432, 1974 11. Stunkard AJ: Hunger and satiety. J Am Psychiary 118:212-217,1961 12. Terzian H, Ore GD: Syndrome of Kltiver-

Bucy reproduced in man by bilateral removal of temporal lobes. Neurology 5:373-380, 1955 13. Grossman SP: Neurophysiologic aspects: Extrahypothalamic factors in the regulation of food intake, in Reichsman F (ed): Advances in Psychosomatic Medicine: Hunger and Satiety in Health and Disease, ~017. New York, S Karger, 1972 14. Alajouanine T, Villey R, Nehlil J, et al: Troubles de l’appetit et rhinenacephale. Presse Med61:1385-1400, 1957 15. Sawa M, Veki Y, Arita M, et al: Preliminary report on the amygdaloidectomy on the psychotic patients with interpretations of oralemotional manifestation in schizophrenics. Folia Psychiatr Neurol Jap 7:30!-329, 1954 16. Kirschbaum WR: Excessive hunger as a symptom of cerebral origin. J Nerv Ment Dis 113:95, 1951 17. Hercaen H: Mental symptoms associated with tumors of the frontal lobe, in Warren, Akert (eds): The Frontal Granular Cortex and Behavior. New York, McGraw-Hill, 1964 18. Hofstatter L, Smolik EA, Busch AK: Prefrontal lobotomy in the treatment of chronic psychosis. Arch Neurol Chicago 53:1255130, 1945 19. Goor E: EEG in anorexia nervosa. Br J Psychiatry 6349-35 I,1954 20. Balagura S: Neuropsychological aspects:

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Hypothalamic factors in the control of eating behavior, in Reichsman F (ed): Advances in Psychosomatic Medicine: Hunger and Satiety in Health and Disease, ~017. New York, S Karger, 1972 21. Schacter S: Some extraordinary facts about obese humans and rats. Am Psycho1 26129~144, 1971 22. Teitelbaum P, Campbell BA: Ingestion patterns in hyperphagic and normal rats. J Comp Physiol Psycho1 51:135-141.1958 23. Reeves AG, Plum F: Hyperphagia, rage and dementia accompanying a ventromedial hypothalamic neoplasm. Arch Neurol 20:616 624, 1969 24. Lundberg 0, Wolinder J: Anorexia nervosa and signs of brain damage. Int J Neuropsychiatry 3:1655173, 1967 25. King A: Primary and secondary anorexia nervosa syndromes. Br J Psychiatry 109:470479, 1963 26. Templar D: Anorexic humans and rats. Am Psycho1 26:935, 1971 27. Crisp AH: The possible significance of some behavioral correlates of weight and carbohydrate intake. J Psycho1 Res 11:117-131, 1967 28. Dally P: Anorexia Nervosa. New York, Grune 8~Stratton, 1969 29. Crisp AH, Fenton GW, Srotton L: A controlled study of the EEG in anorexia nervosa. Br J Psychiatry 114:1149-l 169, 1968 30. Thomae H: Anorexia Nervosa. BennStuttgart, Huber-Klett; New York, International Universities Press, 1961 31. Ushakov GK: Anorexia nervosa. in Howells JG (ed): Modern Perspectives in Adolescent Psychiatry. Edinburg. Oliver & Boyd, 1971 32. Struve FA, Klein DF, Saraf KR: Electroencephalographic correlates of suicide ideation and attempts. Arch Gen Psychiatry 21~363-365. 1972 33. Monroe R: Episodic behavioral disorders. Cambridge, Harvard University Press, 1970 34. Kellaway P, Crawley JW, Kagawa N: Paroxysmal pain and autonomic disturbances of cerebral origin; A specific electroclinical syndrome. Epilepsia 1:466-483, 1952 35. Kirschbaum WR, Stehle HC: Electroencephalographic studies of patients with peptic ulcer functional and gastric disorders.

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Electroencephalogr Clin Neurophysiol 4:380, 1952 36. Refsum S, Presthus J, Skulstod AA, et al: Clinical correlates of the 14 + 6 per second positive spikes: An electroencephalographic and clinical study. Acta Psychiatr Stand 35:330-344, 1960 37. Schwade ED, Geiger SG: Abnormal electroencephalographic findings in severe behavior disorders. Dis Nerv Syst 17:307-317, 1956 38. Shimada Y, Koizumi A, Namba M, et al: Statistical observation of six and fourteen per second positive spikes. Yonago Acta Med 5: 102 108, 1961 39. Walker AE, Marshall C: The contribution to clinical medicine. of depth recording Electroencephalogr Clin Neurophysiol 16:88- 89, 1964 40. Stephenson WA: Intracranial neoplasm associated with fourteen and six per second spikes. Neurology 1:372-376, 1951 41. Hehman KN, Vonderahe AR, Peters JJ: Effect of serotonin on behavior, electrical activity of the brain and seizure threshold of the newly hatched chick; with a note on the production of seizures presenting fourteen and six per second positive spikes. Neurology ll:lOl I- 1016, 1961 42. Wailer JV, Kaufman R, Deutsch F: Anorexia nervosa: A psychosomatic entity. Psychosom Med 23-16, 1940 43. Nemiah JC: Anorexia nervosa: A clinical psychiatric study. Medicine 29:225-268, 1950 44. Nemiah JC: Foundations of Psychopathology. New York, Oxford University Press, 1961 45. Selvini MP: Anorexia nervosa, in Arieti A (ed): Biennial of Psychiatry and Psychotherapy 1. New York, Basic Books, 1970 46. Lindner R: The Fifty-Minute Hour. New York, Rinehart, 1954 47. Goodman LS, Gilman A: The pharmacological basis of therapeutics. New York, CollierMacmillan, 1965 48. Epstein AW: Fetishism: A study of its psychopathology with particular reference to a proposed disorder in brain mechanism as an etiological factor. J Nerv Ment Dis 130:107 ~119, 1960 49, Metchell W: Epilepsy with fetism relived by temporal lobectomy. Lancet 2:626-630,1954 50. Schacter S: Emotion, Obesity and Crime. New York, Academic, 1971

Compulsive eating: a neuropsychologic approach to certain eating disorders.

Compulsive Eating: A Neuropsychologic to Certain Eating Disorders Approach John H. Rau and Richard S. Green T HE “EATING DISORDERS” represent a gr...
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