852 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.2004.048819 on 16 May 2005. Downloaded from PAPER Brain lesions and eating disorders R Uher, J Treasure ............................................................................................................................... See end of article for J Neurol Neurosurg Psychiatry 2005;76:852–857. doi: 10.1136/jnnp.2004.048819 authors’ affiliations ....................... Correspondence to: Rudolf Uher, PO59 Eating Objective: To evaluate the relation between lesions of various brain structures and the development of Disorders Unit, Institute of eating disorders and thus inform the neurobiological research on the aetiology of these mental illnesses. Psychiatry, King’s College Method: We systematically reviewed 54 previously published case reports of eating disorders with brain London, De Crespigny damage. Lesion location, presence of typical psychopathology, and evidence suggestive of causal Park, London, SE5 8AF, UK; [email protected] association were recorded. Results: Although simple changes in appetite and eating behaviour occur with hypothalamic and brain Received 29 June 2004 stem lesions, more complex syndromes, including characteristic psychopathology of eating disorders, are Revised version received associated with right frontal and temporal lobe damage. 30 August 2004 Accepted Conclusions: These findings challenge the traditional view that eating disorders are linked to hypothalamic 17 September 2004 disturbance and suggest a major role of frontotemporal circuits with right hemispheric predominance in ....................... the pathogenesis. ating disorders, including anorexia and bulimia nervosa, into four categories: ‘‘anorexia nervosa’’ (underweight and are characterised by abnormal eating behaviour and either food or body related preoccupations or rituals, purging, Etypical psychopathological features, including fear of or hyperactivity), ‘‘atypical anorexia’’ (underweight without fatness, drive for thinness, and body image disturbance. In food or body weight related preoccupations, rituals, or most patients, there is no detectable focal brain abnormality. purging), ‘‘bulimia nervosa’’ (binge eating and/or purging Nonetheless, associations of anorexia and bulimia nervosa and either food or body weight related preoccupations or with history of perinatal complications12 and head injuries3 rituals without underweight), and ‘‘atypical bulimia’’ (hyper- suggest a role of cerebral pathology in some cases. A number phagia or binge eating but no food or body weight related of case studies describe eating disorders with intracranial preoccupations or rituals). In general, we refer as ‘‘typical’’ to tumours, injuries, or epileptogenic foci. However, many cases for which there is a record of food or body related clinical descriptions are limited to changes in appetite and preoccupations or rituals or when purging behaviour, food lack psychopathological features characteristic of eating restriction, or hyperactivity are intended to cause weight loss disorders. A previous review of 21 anorexia cases associated or prevent weight gain in the absence of objective overweight. with brain tumours found that only three of them fulfilled Evidence suggestive of causal association was noted if one formal diagnostic criteria.4 In the present paper, we provide a of the following criteria were fulfilled: 1) the onset of eating systematic review of published case reports and highlight disorder coincided with the occurrence of brain damage; 2) those relatively rare cases where typical eating disorders treatment directed at the lesion (surgical, antiepileptic) appear to be causally associated with localised brain damage. resulted in remission of the eating disorder; 3) brain injury http://jnnp.bmj.com/ coincided with remission of an eating disorder in a patient METHODS with previously established brain damage. The Web of Knowledge and Medline were searched for articles published up to April 2004 with any combination of RESULTS keywords: ‘‘eating disorders’’, ‘‘anorexia nervosa’’, ‘‘buli- Hypothalamic lesions mia’’, ‘‘binge eating’’, and ‘‘compulsive eating’’ with ‘‘brain There were 23 cases with brain lesions localised in the area of damage’’, ‘‘brain lesion’’, ‘‘tumor’’, ‘‘injury’’, and ‘‘epilepsy’’. the hypothalamus and the third ventricle (Table 1: cases 1– 6–24 We perused reference lists and performed citation searches 23). With one exception these were primary tumours. In on October 2, 2021 by guest. Protected copyright. for the identified articles. Cases in children under 7 years addition to abnormal eating behaviour, symptoms commonly were excluded. We found 54 case reports of eating disorders included diabetes insipidus, visual impairment, and unpro- related to brain damage. Cases of obesity with brain lesions voked vomiting. have been reviewed elsewhere5 and are not included Three female cases were of apparently typical anorexia unless there is prominent behavioural disturbance or nervosa of the purging type (Table 1: cases 1–3). Case 1 psychopathology. appeared as typical in the initial phases with fear of fatness As most papers did not use formal diagnostic criteria, we and self induced vomiting; later it progressed into an atypical extracted the following symptoms from the case descriptions: scenario with spontaneous vomiting and good insight; underweight (less than 75% of body weight expected for the remission occurred after surgical removal of the tumour. height and age), vomiting (not self induced), binge eating Case 2 seems fairly characteristic with onset in adolescence, (eating unusually large amounts of food in a discrete time concern over becoming fat and cheating about eating; period), purging (self induced vomiting, laxative, or diuretic however, there was excessive sleepiness and it is unclear abuse for the purpose of weight control), preoccupations and whether vomiting was self induced or spontaneous. In case 3, rituals concerning food (calorie counting, specific eating anorexia developed on the background of severe personality rules, and unusual eating habits), preoccupations and rituals disorder with borderline, compulsive, and perfectionist concerning body weight and shape (intention to lose weight, features; after tumour removal, eating urges subsided but undue fear of fatness, body checking), hyperactivity (over the personality pathology persisted. It is notable that the exercising). Based on these symptoms, cases were classified onset of eating disturbance preceded neurological symptoms www.jnnp.com Brain lesions and eating disorders Table 1 Case reports of eating disorders associated with brain lesions Method of Case lesion Neurological number Author Year Syndrome Sex Age Onset Causal Lesion type Lesion location localisation Weight Vomiting Psychopathology symptoms 1 Wright23 1990 AN F 12 10 Y Germinoma Hypothalamus, CT, surgery Loss Y Body image, purging Headaches, third ventricle hypothyroidism 2 Hollatz15 1976 AN F 19 14 N Pinealoma Hypothalamus, Post mortem Loss Y Body image, food Hypersomnia third ventricle preoccupations, purging 3 Climo9 1982 AN F 23 N Craniopharyngioma Hypothalamus, Surgery Loss N Body image, binging, Diabetes insipidus third ventricle purging, obsessions 4 DeVile12 1995 A M 8 8 Y Craniopharyngioma Hypothalamus, MRI, surgery Loss N Headache, growth third ventricle hormone deficiency 5 DeVile12 1995 A M 13 13 Y Pinealoma Hypothalamus, MRI, biopsy Loss Y Visual impairment, third ventricle diabetes insipidus 6 White21 1977 A M 15 15 Y Glioma Hypothalamus, Surgery Loss Y Lack of concern Diabetes insipidus third ventricle 7 Nicholson18 1957 A F 9 7 N Pinealoma Hypothalamus, Post mortem Loss N Visual impairment, third ventricle diabetes insipidus, hyperthermia 8 Chipkevitch8 1993 A F 10 10 N Teratoma Hypothalamus, Post mortem Loss Y Lack of concern, Somnolence, diabetes third ventricle compulsive counting, insipidus hyperactivity 9 White22 1959 A F 62 59 N Postencephalopathic Hypothalamus Post mortem Loss Y Alcoholism Headaches atrophy 10 Lewis16 1963 A F 16 15 N Pinealoma Hypothalamus, Post mortem Loss N Diabetes insipidus, third ventricle, visual impairment midbrain 11 Lewin24 1972 A F 25 25 N Glioma Hypothalamus Post mortem Loss N Hirsutism 12 Daly10 1973 A F 22 21 N Pinealoma Hypothalamus Post mortem Loss Y Epilepsy, diabetes insipidus 13 Heron14 1976 A M 25 24 N Pinealoma Hypothalamus, PEG, biopsy Loss N Diabetes insipidus, third ventricle almost blind 14 Biebl7 1984 A M 15 13 N Pinealoma Hypothalamus, CT Loss Y Diabetes insipidus, third abd lateral visual impairment, ventricles incontinence 15 Lin17 2003 A M 19 19 N Germinoma Hypothalamus, MRI Loss Y Lack of concern Diabetes insipidus, ventricles hipopituitarism 16 Haugh13 1983 B F 26 24 Y Astroglioma Hypothalamus Post mortem Gain N Aggressive behaviour, Sleep disturbance hallucinations 17 Skorzewska20 1989 B M 11 11 Y Craniopharyngioma Hypothalamus, Surgery Gain N Binge eating, Visual impairment, third ventricle aggressive behaviour, headaches, emotional lability hipopituitarism, diabetes insipidus, hyperinsulinaemia 18 Skorzewska20 1989 B F 12 12 Y Craniopharyngioma Hypothalamus, Surgery Gain N Eating rituals, binge Visual impairment, third ventricle eating, aggressive headaches, behaviour, hipopituitarism, emotional lability hyperinsulinaemia 19 Skorzewska20 1989 B F 8 8 Y Craniopharyngioma Hypothalamus, Surgery Gain, Loss Y Binge eating, Headaches, diabetes www.jnnp.com third ventricle aggressive behaviour, insipidus, stealing hyperinsulinaemia 20 DePedro11