-

Articles

Gourmand syndrome:
Eating passion associated with right anterior lesions
Marianne Regard, PhD, and Theodor Landis, MD

Article abstract-We present a new benign eating disorder associated with lesions involving parts of the right anterior cerebral hemisphere, This gourmandsyndrome describes a preoccupation with food and a preference for fine eating. Two exemplary case reports illustrate this new syndrome. Analysis of the clinical and anatomical data of 36 patients who displayed this behavior revealed, in 34, a strong association with lesion location in the right anterior part of the brain involving cortical areas, basal ganglia, or limbic structures. Our finding provides further evidence of a correlation between right hemispheric damage, eating, and other impulse control disorders. We conjecture that the serotonergic system subserves different functions in the left and right hemisphere.
NEUROLOGY 1997;48: 1185-1 190

Cerebral lesions associated with obsessivePathological eating behavior ranges from reduced to compulsive disorders centering around actions other excessive appetite, dysregulation of hunger and satithan eating implicate the frontal lobes, the basal ation signals, or odd food preferences. Neurologic disganglia, and cingulum, all sites that disturb the seroease is associated with a variety of eating disorders. tonergic and dopaminergic neurotransmitter sysWell documented are hyperphagia and anorexia in t e m ~ .Since ~ ~ ,there ~ ~ is a link between addictive beassociation with lesions, mostly tumors, involving haviors and diminished 5-HT metabolism, serotonin the ventromedial hypothalamu~.l-~ Eating disorders also occur in tumors within the temporal ~ o r t e x , ~ potentiators are used in the treatment of a wide variety of impulse control disorders with compulsive temporal lobe e p i l e p ~ y ,and ~ - ~advanced states of defeatures, such as pathological gambling,26 alcoholgenerative diseases with neuronal loss in the medial ism, a r ~ o n i s r nkleptomania, ,~~ aggression, and bulimtemporal lobe.s ia.14,28,29 Hyperorality is part of the Kliiver-Bucy syndrome Clinical observations and animal studies suggest which occurs in patients with bilateral mesial temporal the limbic structures and their connections are lesions,9-O as in temporal lobe epilepsy,ll herpes enstrongly involved in the regulation of appetite. Lecephalitis12 and Picks disease.13Eating problems may sions also be related to obsessive compulsive d i s o r d e r ~ . ~ ~ J ~ in the ventromesial hypothalamus, the amygdala, and the fiber bundle from the substantia nigra Iron deficiency, as in Pica disease, illustrates a to the basal ganglia alter the signal of satiation and dramatic behavior change, where patients display a consequently, food intake.4a30Cortical lesions cause morbid craving for unusual or unsuitable food, such eating disorders, typically when located in temporal as the ingestion of ice,16J7clay, laundry starch,l8 letand frontal association areas that are strongly contuce,lg or cigarette ashes.20 nected to basal and diencephalic systems controlling For some eating disorders, the underlying cause is appetite. a matter of controversy. Purely psychological explaWe report an altered eating habit as a consenations21of bulimia and anorexia nervosa have been quence of focal lesions that cannot be classified challenged by findings of altered serotonin and noramong known disorders, and is best characterized by adrenalin level^,^^,^^ suggesting trait-related disturthe name gourmand syndrome. The French word bances of neurotransmitter systems. However, it is gourmand describes someone who is heartily internot clear whether these alterations are pathogenetic ested in fine food and drink, or simply describes a or epiphenomena of these disorders. For example, food lover; the term gourmet is reserved for a food computer tomographies in anorexic patients may disconnoisseur. Although commonly not considered close ventricular and sulcular enlargement, but pathologic, gourmand eating may occasionally indithese structural changes could be the consequence of cate focal brain damage. In particular, passionate malnouri~hment.~~
Frum the University Hospital (Dr. Regard), Zurich and the HBpital Cantonal Universitaire de Geneve (Dr. Landis), Switzerland. Supported by the Swiss National Science Foundation grant Nr. 32-040682.94 and the EMDO Foundation. Resented a t the 17th Annual International Neuropsychology Society meeting, Vancouver, BC, Canada, February 1989. Received April 26, 1996. Accepted in final form November 19, 1996. Address correspondence and reprint requests to Dr. M. Regard, University Hospital, Department of Neurology, CH-8091 Zurich, Switzerland.
Copyright 0 1997 by the American Academy of Neurology

1185

Figure. CT of Patient 1 showing a n acute hemorrhagic infarct in the territory of the right middle cerebral artery involving the right internal capsule and basal ganglia (right side on image corresponds to right hemisphere).

eating has diagnostic significance when it occurs in previously normal eaters and is associated with
other organic behavioral alterations. Prior to report-

ing the findings of a prospective study, we describe two patients who m a d e us aware of this condition.
Case reports. Patient 1. This 48-year-old right-handed man with treated high blood pressure, non-insulin dependent diabetes mellitus, and a chronic smokers bronchitis was admitted because of the sudden onset of a left hemiparesis. CT showed a fresh hemorrhagic infarction in the territory of the right middle cerebral artery including the right internal capsule and basal ganglia (figure). Neurologic and mental status examination revealed a severe left sensory-motor hemisyndrome, a left spatial hemineglect, a behavior syndrome with disinhibition and aggression, and impaired figural memory31and figural fluency.32 The patient had been an average eater. Not especially concerned with food, he ate what his wife brought to the table. He occasionally went to restaurants and had no particular food preferences. His main preoccupation was his profession as a well known local political journalist. He had no particular weight problems and did not follow any diet. He was slightly overweight (body mass index [BMI] = 29). (BMI is calculated by dividing body weight in kilograms by height in meters squared.) When asked what bothered him most, he instantly replied that he found the hospital food awful, that he felt perfectly healthy, and that he had nothing else on his mind but good, tasty, food served in a nice restaurant. During hospitalization, he wrote in his diary . . . sex I start to really miss, and it is time for a real hearty dinner, e.g. a good sausage with hash browns or some spaghetti bolognese, or risotto and a breaded cutlet, nicely decorated, or a scallop of game in cream sauce with Spatzle (a swiss and southern german speciality). Always just eat and drink! What a connoisseur I am, and now I am dried up here, just like in the desert. Where is the next oasis? With date trees and lamb-roast or couscous and mint tea, the moroccan way, real fresh . . . His left hemiparesis recovered partially, and after 4 months he was able to take up part-time work. Rather
1186 NEUROLOGY 48 May 1997

than resuming his job as a political news journalist, which was kept open for him, he left that job and chose to write columns on eating, which he subsequently did successfully. He also wrote about his experience a s a patient. . . . due to my paresis I cant hold a fork, i.e., I can only eat food which needs no cutting. How nicely surprised I was when the good sausage was served already cut as ordered, together with the potatoes. From another excerpt of an article he wrote seven months later: . . . a few more words on dining out. In my city are about 20 Italian restaurants, whereof only about 5 to 6 are really superb, where one can get great pasta, pizza and vino. For my more exotic pleasures there are 3 Chinese, one Korean and one Japanese place available. His family was struck by his outgoing and eating-oriented behavior, which they initially attributed to his new job. However, they noted that the only conversations that aroused him were about food, and his desires for meals prepared at home became more precise and exotic. He often left home to dine out. He gained three kilograms of weight in one year. Patient 2. This 55-year-old ambitextrous man was admitted because of severe headache and a sudden weakness of the left arm and face. CT revealed a hemorrhage in the right anterior basal ganglia with edema compressing the right lateral ventricle and small old periventricular hypodense areas. Within a few days, his left hemiplegia recovered, but his behavior was altered. He made sexual advances to the nurses and ate goodies even during examinations. Mental status examination revealed impaired figural memory and figural fluency, mild extinction of left visual and tactile stimuli, and left-sided asterognosis. MRI 5 months later showed residuals of the bleeding in the right putamen, in the external capsule, and in the right rostromedial temporal lobe. Previously, he was a very active businessman and sportsman, concerned about his looks, but not especially concerned with fine eating. He had no real food preferences, and preferred a tennis match to a fine dinner. He did not follow any diet but payed attention to his weight. He was a tall, athletic man (BMI = 22.7) who did not subsequently gain weight, as measurec! at a follow-up ex-

amination 1 year later, despite his acquired eating passion. Five weeks after the stroke, we asked him to write down his experiences as a patient. To our astonishment his writing almost exclusively contained reflections about fine eating. He wrote, . . . after I could stand on my feet again, I dreamt to go downtown and sit down in this well known restaurant. There I would get a beer, sausage and potatoes. Slowly, my diet improved again and thus did quality of life. The same day after discharge, my first trip brought me to this restaurant, and here I was ordering potatoe [sic] salad, sausage and a beer. I feel wonderful. My spouse anxiously registers everything I eat and nibble. It irritates me. A few steps down the street, we enter a coffee-house. My hand is reaching for pastry, my wifes hand reaches between. Through the window I see my bank, damn, if I chose, I could buy all the pastry I wanted, including the whole store. The creamy pastry slips from the foil, like a mermaid, I take a bite. From now on, it will be more difficult to put me under stress. At home, after five weeks in the hospital, his social behavior was appropriate again, but the family was struck by his eating passion. His conversation centered around his food fantasies, and he grasped every occasion to dine out, being concerned more by quality than quantity of food. Although he resumed his previous business and sport activities, he seemed less engaged.

Methods. Initiated by the above two observations, we conducted a prospective study of the frequency of and, particularly, the clinical and anatomical correlates of this altered eating behavior. A special checklist was constructed with questions regarding a patients previous and current eating behavior, and this checklist was presented in a semistandardized interview during the neuropsychological examination. The checklist assessed present and earlier eating habits including food quantity, number of meals a day, subjective quality of eating, specific preferences, presence of preoccupation with acts centering around eating (i.e., food shopping, preparation, dining rituals, restaurant selection, etc.), time of onset, medical and social circumstances and course. If a patient was a passionate eater, family members and caretakers were interviewed with the same checklist and the information compared with the medical history and findings. Gourmandeating as a neurological sign was diagnosed when the following criteria were fulfilled:
1) eating habit consisting of a) normal hunger and satiation signals, b) persistent food craving, c) consumption of food of distinct preference, typically of fine quality and average quantity, d) preoccupation with acts centering around food and eating, e) the habit is not experienced as a pathological symptom; 2) evidence of a single cerebral lesion; 3) onset of eating passion associated with cerebral lesion; 4) absence of other medical or social conditions inducing changes in diet or appetite (e.g., medications, endocrine, and metabolic disorders); 5) no history of previous eating disorders or other neurological or psychiatric illness.

Results. Of the consecutively referred patients to our neuropsychology unit, we assessed 723 patients with

known or suspected single cerebral lesions during a survey period of three years. Seventy one percent of these patients (513/723) had focal lesions that could be assigned to one of the four anatomical areas: 33% were located in the left anterior and 28% in the right anterior quadrant, 21% in the left posterior and 18% in the right posterior quadrant. Although lesions were more frequently located in the anterior quadrants, they were equally distributed between the two hemispheres. Among this patient population, we observed 36 patients who presented with the gourmand syndrome. Many patients spontaneously reported their preoccupation with eating and believed that the alteration was a positive consequence of their cerebral affection. Fourteen were women, 22 were men, and 35 were right-handed. Mean age was 43.6 years (range: 15-77). Mean time since symptom onset was 8.1 months. Most patients were assessed during hospitalization, within 1 to 3 weeks after the incidence. 17 patients were investigated after neurosurgery (mean 15.5 months). All underwent a complete neurological evaluation including the comprehensive neuropsychology examination used i n our unit, EEG, and laboratory tests. Lesion sites were confirmed by CT, MRI, or surgery. Seven of the 36 patients were considered mildly obese (range of BMI = 28-30); the other patients had a BMI within normal ranges. Except for one patient (case 1) who had diabetes, all other patients laboratory screenings were negative, indicating normal metabolic and endocrine functions. Neurologic findings. The prominent neurologic findings indicated focal right-sided damage. Left-sided hemisyndromes (9 sensory-motor, 6 motor only) were most frequent, followed by left-sided visual-field defects (5 hemianopia, 4 quandrantanopia). Ten patients had epileptic seizures (7 complex partial seizures of focal right temporal origin). In 12 patients with abnormal mental status, neurological examination was normal. Neuropsychological findings. Besides the gourmand eating, mental status examination revealed other behavior changes and cognitive abnormalities as summarized in table 1. The most prominent cognitive symptoms were visual-spatial dysfunctions. Of the 26 patients with impaired memory, 24 had impaired learning and recall of figures, a finding associated with dysfunction of the right temporal region. Ten patients recalled a geometric figure by 90 degrees rotated, a sign associated with right temporo-basal lesions.33 Poor performance in figural fluency, associated with right anterior lesions (frontal, temporal or b ~ t h ) , was ~ ~diagnosed ,~~ in 26 patients, whereas only 6 patients also performed low on verbal fluency. Twelve patients had a left hemispatial neglect and although rare, other isolated perceptive dysfunction was present. Besides the eating passion, most of the other behavioral changes observed also reflected diminished impulse control, i.e., hyperverbality, heightened aggression and drive, affective lability, and indifference. Such maniforme neuropsychiatric alterations in brain-damaged patients have been observed in association with lesions in the basal forebrain of the right ~ i d e . Two ~ ~ -were ~ ~ depressed, another two showed compulsive behavior, and one suffered a psychotic episode. Lesion etiology. The causes of these clinical symptoms were tumors in 14 patients (12 gliomas), cerebro-vascular
May 1997 NEUROLOGY 48 1187

Table 1 Neuropsychological findings in 36 patients with gourmand syndrome

Table 2 Etiology and localization of lesions in 36 patients with gourmand syndrome

Etiology (n) Tumors (14) 12 Gliomas 1 Meningioma
1 Tuberculoma

N* Symptom
26 Memory dysfunctions: 24 figural-spatial (10 with 90 figure rotation) 2 verbal and figural 26 Impaired conceptual thinking: 20 figural 6 verbal and figural 21 Impaired visual perception: 12 left hemispatial neglect

Localization (n)/side/site

4R

Frontal Frontotemporal Temporal Frontotemporoparietal Temporoparietal Frontotemporal Arteria cerebri media Arteria cerebri posterior Frontotemporal

2R
5R

1R
1R 1L Vascular (12)

4 topographagnosia
5 various isolated visual defects
1 left astereognosis

7 Infarctions 5 Malformations

9 R 1R

(3 AVM, 2 aneurysms) 1 R

39 Altered behavior displays:

31 affective dyscontrol

1 R > L Anterior communicating artery Epilepsy (8)

12 maniforme
10 irritable-aggressive

7 Hippocampal sclerosis 6 R 1L 1 Cortical dysplasia

6 affect lability 2 depressive

1 psychotic episode

Amygdalo-hippocampectomy Amygdalo-hippocampectomyl (RH language dominant)

Frontotemporal Frontal Temporolimbic

1R
Trauma (2) 2 Concussions with hemorrhage 1R 1R

8 Miscellaneous 3 indifference

2 anosognosia 2 compulsive 1 reduced drive AVM = arteriovenous malformation; R = right; L right hemisphere.
=

left; RH

* Frequencies
symptoms.

do not correspond to sample size due to multiple

accidents in 12 patients (7 infarctions, 5 bleedings caused by malformations), focal seizures in 8 patients (7 had undergone selective amygdalo-hippocampectomy),38 head trauma with focal concussion, and hemorrhages in 2 patients (table 2). Localization. Based on the clinical findings, brain imaging and surgery reports, lesion location was situated in the right hemisphere in 33 patients (table 2). Of the remaining three, only one patient showed no damage to the right hemisphere. This patient was investigated after resection of a meningioma located in the frontotemporal region of the left hemisphere. In one patient subarachnoidal hemorrhage from a ruptured aneurysm of the anterior communicans artery caused bilateral, but predominantly right hemispheric, symptoms and in one patient a leftsided amygdalo-hippocampectomy was performed, but neuropsychological findings indicated non-dominant temporal lobe dysfunction, and lateralized tachistoscopic tests showed inversed dominance of the right hemisphere. The intrahemispheric lesion sites follow. Of the 14 tumors, 1 1 were located in the right anterior quadrant (frontal, temporal or both lobes, and 7 included basal regions, i.e., insula, basal ganglia, thalamus). In 2 cases with larger lesions, the parietal lobe also was injured. Of the 12 vascular lesions, 10 involved the right anterior quadrant only and 7 involved basal areas, mostly basal ganglia and capsule.
1188 NEUROLOGY 48 May 1997

Seven of the 8 epileptic foci originated in the right hippocampal area and 1in the right frontotemporal cortex. Of the 2 concussions, 1 was right frontal and 1 right hippocampal. In summary, among the 36 patients in whom the gourmand syndrome was observed, the lesions involved the right anterior region in 34 cases. In 30 instances, this region was the sole site of damage. Three lesions included the right posterior region and in two instances was limited to this area. Lesion sites were cortical and subcortical, i.e., in 23 instances, damage either included or was solely located in basal and limbic areas.

Discussion. We present a new eating disorder in patients with focal brain damage. Most patients with the gourmand syndrome had clinical and anatomical evidence of a unilateral right-sided lesion, mainly involving anterior cortico-limbic regions. The strong clinical-anatomical correlation suggests that gourmand-eating can represent a neurological sign of diagnostic value. The eating behavior does not correspond t o any known category of eating disorders. At most, it could be classified as a benign, non-disabling form of hyperphagia, but with a specific preference for fine food. The gourmand syndrome reflects reduced cortical control of visceral impulses. Some of the phenomenologic and biological features of gourmand-eating overlap with other addictive and obsessive disorders. Thus, anatomical and

neurochemical models, although primarily developed for substance abuse, may help in understanding the syndrome. Of special interest are the notions developed for craving, a state provoked by stimulus deprivation or by exposure to a related stimulus.39Neural mechanisms of positive reinforcement are activated by a stimulant and suggested as the biological basis of psychological dependence. Addictive substances additionally activate mechanisms that suppress pain and distress signals.40 Since non-addictive stimulants, such as food, may also produce craving and the negative experience of withdrawal symptoms, similar mechanisms are presumably activated. Positive reinforcement depends on the activation of the dopamine system; negative reinforcement is less well understood, although it may rely on different transmitter systems. According t o Wise,4o although the biochemical mechanisms of the two processes differ, medial forebrain bundle fibers are involved in both. The anatomical substrates of eating disorders are the basal ganglia and cortico-limbic areas, i.e., the same regions involved in other obsessive compulsive disorders and associated with satiation, activation, and appetite.41 The above explanations do not explain the association of passionate eating with the right hemisphere. Similar lateral asymmetry occurs in affective disorders with compulsive features not related to eatinP2 and in disabling eating disorders. Griffith and Hochfound that tumors producing anorexia were twice as often located in the right than in the left hemisphere. Braun and C h ~ u i n a r d reviewed ~~ the neurologic literature on anorexia and presented evidences for anorexia being a right-hemispheric disorder. Intense hunger occurred in a patient with a lesion in the right temporal lobe.45We are not aware of a laterality analysis of ventrolateral hypothalamic lesions, but Flynn et al.46 reported hyperphagia in a patient with a tumor in the right hypothalamic region. Although bilateral mesial temporal damage typically causes compulsive eating in the KluverBucy syndrome, I ~ e r reported n ~ ~ a woman who developed the syndrome after a gunshot wound destroying the medial temporal lobe and the frontal lobe of the right hemisphere only. The association of eating disorders with behavior alterations reflecting reduced impulse control suggests a common anatomical correlate. Anatomical studies have confirmed a strong association between behavioral changes and lesion location in right anterior region^.^^,^^,^^ Clinical findings and animal research suggest that neurotransmitter systems may be asymmetrically distrib~ted~ but l,~~ neurochemical studies of human brain tissues investigating hemispheric differences are rare. Arato et al.,50.51 comparing left and rightsided postmortem brain tissue, found significantly higher right hemisphere serotonin metabolite content and increased imipramine binding in samples of the medial and orbital frontal regions. Although this result needs further study, the finding of an asymmetric distribution of serotonin is well in accord with

the clinical evidence and implies that a normally asymmetric system may be rendered more imbalanced by unilateral right hemispheric lesions. This is supported by a recent PET study by Mann et al.,52 who found asymmetric serotonin activations in the prefrontal cortex of healthy subjects. We hypothesize that lesion localization is the primary factor of this new syndrome of altered eating habit. Heightened appetite induced by medications, especially by steroids and anticonvulsants, can be ruled out as a major cause, because centrally active drugs were prescribed independently of lesion site. Furthermore, the patients with space-occupying lesions investigated after operation were not taking steroids, and the patients with surgical treatment of seizures were on the same medication before and after the surgery.

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