“Anorexia Saved My Life”: Coincidental AnorexiaNervosa and Cerebral Meningioma

Aileen O’Brien,1 Pippa Hugo,1 Simon Stapleton,2 and Bryan Lask1,3*

1 St. George’s Eating Disorder Service, London, England2 Department of Neurosurgery, Atkinson Morley Hospital, London, England

3 Huntercombe Manor Hospital, Berkshire, England

Accepted 9 April 2000

Abstract: Objective: We report on a 13-year-old girl with coincidental occult intracranialtumor and early-onset anorexia nervosa. Method: The cerebral meningioma was discoveredfortuitously as the result of a research project using SPECT imaging to locate a neurobiologi-cal substrate in patients with anorexia nervosa. Without SPECT, the meningioma would haveremained undiagnosed until it had become symptomatic. The two conditions appear to havebeen completely unrelated. Results and Discussion: The case highlights two important points.First, intracranial pathology should also be considered however certain is the diagnosis ofearly-onset anorexia nervosa. Second, neuroimaging plays an important part in diagnosingearly-onset anorexia nervosa, both from a clinical and a research prospective. © 2001 byJohn Wiley & Sons, Inc. Int J Eat Disord 30: 346–349, 2001.

Key words: intracranial tumor; anorexia nervosa; neuroimaging

INTRODUCTION

Occult intracranial tumors masquerading as early-onset anorexia nervosa have beenreported (Chipkevitch, 1994; de Vile, Sufraz, Lask, & Stanhope, 1995). Conversely, it is notuncommon for the diagnosis of early-onset anorexia nervosa to be missed because of therelentless pursuit of an intracranial explanation for the weight loss and change in behavior(Fosson, Knibbs, Bryant-Waugh, & Lask, 1987). We believe this to be the first report of acoincidental occult intracranial tumor and apparently unrelated early-onset anorexia ner-vosa.

CASE REPORT

Chloe, a 13-year-old girl, presented to our child and adolescent eating disorder servicewith a 5-month history typical of anorexia nervosa. Her symptoms included food restric-tion, excessive exercise, preoccupation with food and weight, and low mood. Chloe was

*Correspondence to: Bryan Lask, Eating Disorders Research Team, St. George’s Hospital Medical School, JennerWing, Cranmer Terrace, London SW17 ORE, United Kingdom. E-mail: blask@sghms.ac.uk

© 2001 by John Wiley & Sons, Inc.

Prod. #1683

described as a quiet child who lacked confidence but had always been conscientious, withgood relationships with family, teachers, and friends. She described psychopathologycharacteristic of anorexia nervosa including a fear of “becoming fatter” and a distortedbody image.

She had lost approximately 12 kg over a period of 6 months. At assessment, her weightwas 31 kg, height 155 cm, weight/height ratio 69%, body mass index (BMI) 12.9 (normalrange 20–25). She had been amenorrheic for 3 months. No precipitating factors could beestablished and there was no history of headaches, visual disturbances, or seizures. Onphysical examination, she was emaciated with poor peripheral circulation, faint pedalpulses, acrocyanosis, bradycardia, and hypotension. There were no abnormal features onneurological examination, and both fundi were normal. The Eating Disorder Examination(EDE; Bryant-Waugh, Cooper, Taylor, & Lask, 1996) confirmed the diagnosis of anorexianervosa.

The psychopathology consistent with a diagnosis of anorexia nervosa persisted andChloe was admitted to our inpatient unit. She responded well to conventional treatmentincluding refeeding, psychotherapy, and parental counseling. She gained 5.2 kg duringthe first 6 weeks. Hematological and biochemical investigations returned to normal. Aspart of our continuing investigations into the neurobiological basis of anorexia nervosa(Gordon, Lask, Bryant-Waugh, Christie, & Timimi, 1997), SPECT examination of regionalcerebral blood flow was conducted. Unexpectedly, this suggested a space-occupyinglesion. Magnetic resonance imaging (MRI) was reported as follows: “There is a largeextra-axial lesion arising from the right frontal area. This is causing compression of theunderlying frontal lobe but there is little oedema in the adjacent white matter. The lesionmeasures approximately 4.5 × 2.5 cm. and shows intense homogeneous enhancement. Thepost contrast images also show dural tails. No other significant abnormality. The appear-ances are in keeping with a large frontal meningioma.”

The tumor was removed 3 days later without complication. Histology confirmed thediagnosis of meningioma.

Having recovered from surgery, Chloe returned to the unit to resume her treatment.Although her distorted cognitions persisted, she seemed more determined to recover. Shestated, “anorexia saved my life.” Gradually, she regained weight and was eventuallydischarged from the inpatient unit 13 weeks after the surgery. For the next few weeks, shecontinued treatment in the outpatient clinic. During this time, she was able to maintainnormal weight with resumption of menses. The distorted cognitions characteristic ofanorexia nervosa resolved gradually over the 12 months after surgery.

At 2 year postoperative follow-up, there was no evidence of recurrence of the tumor onrepeat MRI and there were no features of anorexia nervosa.

DISCUSSION

Meningiomas in children and adolescents are rare. They account for less than 5% ofintracranial tumors in childhood (Germano, Edwards, Davis, & Schiffer, 1994). Theypresent with focal neurological deficits, seizures, and symptoms of raised intracranialpressure. Prognosis is reasonable. In children, there is an absence of the female prepon-derance found among adults. Meningiomas do not typically present with psychiatricsymptoms.

Nonetheless, there have been a number of case reports of patients with cerebral tumors

Comorbid Brain Tumor 347

associated with symptoms suggestive of anorexia nervosa, but very few cases have com-pletely fulfilled diagnostic criteria. Chipkevitch (1994) reviewed 21 cases in which theapparent diagnosis of anorexia nervosa preceded the discovery of a central nervoussystem lesion. Of the 21 cases, 19 proved to be tumors. Two thirds of the patients werefemale and the majority were in their teens. One can appreciate a higher index of suspi-cion for anorexia nervosa in this group. However, only two of these fulfilled criteria foranorexia nervosa outlined in the 3rd Rev. ed. of the Diagnostic and Statistical Manual ofMental Disorders (DSM-III-R; American Psychiatric Association, 1987) and symptomsimproved following treatment of the tumor. The majority of tumors were hypothalamicin origin, which accounted for the disordered eating.

De Vile et al. (1995) described three cases, all boys, with atypical presentations ofanorexia nervosa. Two had hypothalamic tumors and one had a brainstem tumor. Com-puted tomographic (CT) scans did not show any abnormality and the diagnosis was madeusing MRI. In each case, the symptoms misdiagnosed as anorexia nervosa resolved aftersurgery. In their review of organic disease mimicking an eating disorder, Wright, Smith,and Mitchell (1990) described a 12-year-old girl with depression and “additional charac-teristics of an atypical eating disorder.” CT scanning revealed a large pituitary mass anda germinoma was excised. Depression and poor appetite persisted, but these were attrib-utable to the continuing treatment including radiotherapy and repeat hospitalizations.

These reports have in common (1) the fact that the tumors impinged on the brain stem,hypothalamus, or pituitary, thus having the potential for affecting appetite regulation,and (2) the diagnosis of anorexia nervosa was suspect. The symptoms suggestive ofanorexia nervosa were due most likely to the location of the tumor. In contrast, our patientfulfilled the diagnosis of anorexia nervosa both before and after removal of the menin-gioma and there was nothing to suggest the presence of brain pathology. Frontal cognitivedeficits were reported in some emaciated patients with anorexia nervosa in some studies(Fox, 1981) but not in others (Touyz, Beamount, & Johnstone, 1986). Russell and Roxanas(1990) suggested that many of the behavioral characteristics of anorexia nervosa (e.g.,lying, deceitfulness, poor self-care, and apparent failure to learn from experience) aresuggestive of frontal lobe impairment. They concluded, however, that the role of frontallobe deficits in anorexia nervosa patients remains contentious, but would be expected tobe determined nutritionally. Detailed neuropsychometry before and after surgery re-vealed no frontal lobe deficit in our patient.

Our patient’s eating disorder does not appear to have been linked to either the natureor the site of the tumor. Her gradual recovery commenced before diagnosis of the me-ningioma and her abnormal cognitions persisted for several months after its removal. Webelieve that the co-occurrence of these disorders is coincidental and, given the rarity ofboth conditions, extraordinary. Despite the size of the meningioma, Chloe displayed nosigns of a space-occupying lesion. Its discovery was purely fortuitous, relating to a re-search project. Anorectic psychopathology persisted after its removal, but Chloe appearedto be far more motivated to recover from anorexia nervosa. Had the SPECT scan not beenconducted, the tumor would probably have remained undiagnosed until it had donesevere with possible irreparable damage. This case illustrates the need for constant clinicalvigilance and it is a sobering reminder that even in typical cases unlikely events can occur.

Chloe gave full consent to the publication of this paper. We thank the Hebdon Lodge nursing teamand the Atkinson Morley neurosurgical unit for their skilled care.

348 O’Brien et al.

REFERENCES

American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders (3rd Rev. ed.).Washington, DC: Author.

Bryant-Waugh, R., Cooper, P., Taylor, C., & Lask, B. (1996). The use of the Eating Disorder Examination withchildren: A pilot study. International Journal of Eating Disorders, 19, 391–398.

Chipkevitch E. (1994). Brain tumours and anorexia nervosa syndrome. Brain and Development, 175–179.De Vile, C.J., Sufraz, R., Lask, B.D., & Stanhope, R. (1995). Occult intracranial tumours masquerading as early

onset anorexia nervosa. British Medical Journal, 311, 1359–1360.Fosson, A., Knibbs, J., Bryant-Waugh, R., & Lask, B. (1987). Early onset anorexia nervosa. Archives of Disease in

Childhood, 621, 114–118.Fox, C. (1981). Neuropsychological correlates of anorexia nervosa. International Journal of Psychiatry and

Medicine, 12, 285–290.Germano, I., Edwards, M., Davis, R., & Schiffer, D. (1994). Intra-cranial meningiomas of the first two decades of

life. Journal of Neurosurgery, 80, 447–453.Gordon, I., Lask, B., Bryant-Waugh, R., Christie, D., & Timimi, S. (1997). Childhood onset anorexia nervosa:

Towards identifying a biological substrate. International Journal of Eating Disorders, 22, 159–166.Russell, J., & Roxanas, M. (1990). Psychiatry and the frontal lobes. Australian and New Zealand Journal of

Psychiatry, 24, 113–132.Touyz, S., Beaumont, P., & Johnstone, L. (1986). Neuropsychological correlates of eating disorders. International

Journal of Eating Disorders, 5, 1025–1034.Wright, K., Smith, M.S., & Mitchell, J. (1990). Organic diseases mimicking atypical eating disorders. Clinical

Pediatrics, 29, 325–328.

Comorbid Brain Tumor 349