Six‐month open trial of haloperidol as an adjunctive treatment for anorexia nervosa: A preliminary report

Cassano, Giovanni Battista; Miniati, Mario; Pini, Stefano; Rotondo, Alessandro; Banti, S.; Borri, C.; Camilleri, Valeria; Mauri, Mauro

doi:10.1002/eat.10130

Cited by 53 publications

(34 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For instance, stimulants such as methylphenidate or the antidepressant bupropion frequently affect food intake and promote weight loss (Anderson et al, 2002;Goldfield et al, 2007). In AN, small studies using the dopamine D2 antagonist haloperidol or the dopamine D2 partial agonist aripiprazole suggested beneficial effects on core symptoms of AN (Cassano et al, 2003;Trunko et al, 2011). Importantly, the stimulant amphetamine increased, whereas haloperidol decreased brain response in a human temporal difference model paradigm (Menon et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Anorexia Nervosa and Obesity are Associated with Opposite Brain Reward Response

Frank

Reynolds

Shott

et al. 2012

Neuropsychopharmacol

279

255

View full text Add to dashboard Cite

Anorexia nervosa (AN) is a severe psychiatric disorder associated with food avoidance and malnutrition. In this study, we wanted to test whether we would find brain reward alterations in AN, compared with individuals with normal or increased body weight. We studied 21 underweight, restricting-type AN (age M 22.5, SD 5.8 years), 19 obese (age M 27.1, SD 6.7 years), and 23 healthy control women (age M 24.8, SD 5.6 years), using blood oxygen level-dependent functional magnetic resonance brain imaging together with a rewardconditioning task. This paradigm involves learning the association between conditioned visual stimuli and unconditioned taste stimuli, as well as the unexpected violation of those learned associations. The task has been associated with activation of brain dopamine reward circuits, and it allows the comparison of actual brain response with expected brain activation based on established neuronal models. A group-by-task condition analysis (family-wise-error-corrected Po0.05) indicated that the orbitofrontal cortex differentiated all three groups. The dopamine model reward-learning signal distinguished groups in the anteroventral striatum, insula, and prefrontal cortex (Po0.001, 25 voxel cluster threshold), with brain responses that were greater in the AN group, but lesser in the obese group, compared with controls. These results suggest that brain reward circuits are more responsive to food stimuli in AN, but less responsive in obese women. The mechanism for this association is uncertain, but these brain reward response patterns could be biomarkers for the respective weight state.

show abstract

Section: Discussionmentioning

confidence: 99%

Anorexia Nervosa and Obesity are Associated with Opposite Brain Reward Response

Frank

Reynolds

Shott

et al. 2012

Neuropsychopharmacol

279

255

View full text Add to dashboard Cite

show abstract

“…To date, no significant correlations have been found between DA or DA receptor gene alterations and the development, course and prognosis of AN (Bruins-Slot et al, 1998). Treatments using typical antipsychotics alone or in combination with psychotherapies, many of them evaluated in open trials and without placebo (PL) control, have usually failed (Dally, 1966;Vandereyken and Pierlot, 1982;Vandereyken, 1984;Ruggero et al, 2001;Cassano et al, 2003). More recently, atypical antipsychotics, olanzapine (OLA), risperidone and amisulpride, in particular, in either single cases or in small patient groups, had been shown to improve eating habits, weight and some psychopathological aspects of AN (depression, anxiety, obsessivity-compulsivity, psychoticism) (Hansen, 1999;Newman Tocker, 2000;Ridley-Siegert, 2000;La Via et al, 2000;Coates, 2000;Gaskill et al, 2001;Mehler et al, 2001;Ruggero et al, 2001;Leucht et al, 2002;Jensen and Mejihede, 2002;Powers et al, 2002;Carver et al, 2002;Ercan et al, 2003;Malina et al, 2003;Boachie et al, 2003;Pederson et al, 2003;Mangano et al, 2004;Barbarich et al, 2004;Mondraty et al, 2005;Attia et al, 2005;Hillebrand et al, 2005;Menaster, 2005;Bosanac et al, 2005).…”

Section: Introductionmentioning

confidence: 98%

Olanzapine therapy in anorexia nervosa: psychobiological effects

Brambilla

Segura-Garcia

Fassino

et al. 2007

International Clinical Psychopharmacology

119

131

View full text Add to dashboard Cite

Dopamine impairments occur in anorexia nervosa. The aim of this study was to see whether treatment with the atypical dopamine antagonist antipsychotic olanzapine improves the disorder. Thirty anorexics, 18 restricted and 12 bingeing-purging, underwent a 3-month course of cognitive behavioral therapy, plus at random and double-blinded oral olanzapine (2.5 mg for 1 month, 5 mg for 2 months) in half and oral placebo in the other half of them. BMI, psychopathological aspects (eating disorder inventory, Hamilton Rating Scale, Buss-Durkee Rating Scale, Yale Brown Cornell for Eating Disorders Rating Scale, temperament-character inventory), and homovanillic acid blood concentrations for dopamine secretion, were monitored at baseline and then monthly during the trial. At the end of the trial BMI, total eating disorder inventory, total Yale Brown Cornell for Eating Disorders Rating Scale, Buss-Durkee Rating Scale, Hamilton Rating Scale scores and in olanzapine-treated patients the subitems of eating disorder inventory ineffectiveness and maturity fear, of Buss-Durkee Rating Scale direct aggressiveness, of temperament-characteristic inventory persistence had improved significantly. When stratified for anorexia nervosa subtype, BMI changes were significant among anorexia nervosa bingeing-purging patient, 'depression' (Hamilton Rating Scale) and 'direct aggressiveness' (Buss-Durkee Rating Scale) among anorexia nervosa bingeing-purging patients, 'persistence' (temprerament-characteristic inventory), among anorexics restricted patients, with a trend toward significance for obsessivity-compulsivity (Yale Brown Cornell for Eating Disorders Rating Scale). homovanilic acid blood levels increased significantly in the cognitive behavioral therapy+olanzapine group. No correlations were observed between homovanilic acid concentrations and psychopathological parameters. The pharmacological treatment can significantly improve specific aspects of anorexia nervosa.

show abstract

“…Altered DA secretion has been suggested to be involved in the etiopatogenesis of ED symptomatology [6,7,9,30-34]. However, specific treatments in the past with classical psychotropic drugs acting on DA secretion and receptor functions have not yielded positive results [5,35-37]. More recently, atypical psychotropic drugs including olanzapine, quetiapine, risperidol, clozapine, aripiprazole have been administered [5,38], again, with inconsistent effects.…”

Section: Discussionmentioning

confidence: 99%

Lack of efficacy of psychological and pharmacological treatments of disorders of eating behavior: neurobiological background

et al. 2014

View full text Add to dashboard Cite

BackgroundTreatments of eating disorders result too often in partial psychological and physical remission, chronicization, dropout, relapse and death, with no fully known explanations for this failure. In order to clarify this problem, we conducted three studies to identify the biochemical background of cognitive-behavioural psychotherapy (CBT), individual psychology brief psychotherapy (IBPP), and psychotherapy-pharmacotherapy with CBT + olanzapine in anorexics (AN) and bulimics (BN) by measuring the levels of plasma homovanillic acid (HVA) for dopamine secretion, plasma 3-methoxy-4-hydroxy-phenylglycol (MHPG) for noradrenalin secretion, and platelet [3H]-Paroxetin-binding Bmax and Kd for serotonin transporter function. The data were then compared with psychopathological and physical alterations.MethodsStudy 1 investigated the effects of 4 months of CBT on plasma HVA, MHPG and [3H]-Par-binding in 14 AN-restricted, 14 AN-bingeing/purging, and 22 BN inpatients. Study 2 investigated the effects of 4 months of IBPP on plasma HVA in 15 AN and 17 BN outpatients. Study 3 investigated the effect of 3 months of CBT + olanzapine (5 mg/day) in 30 AN outpatients. The data were analyzed using one-way ANOVA for repeated measures for the changes between basal and post-treatment biological and psychological parameters, two-way ANOVA for repeated measures for the differences in the psychobiological data in the 3 groups, Spearman’s test for the correlations between basal and final changes in the psychological and biological scores.ResultsStudy 1 revealed significant amelioration of the psychopathology in the AN and BN patients, no effects on HVA, MHPG or Paroxetin binding Kd, and a significant increase in Par-binding Bmax only in the BN patients. Study 2 revealed a significant effect of IBPP on psychopathology in the AN and BN patients, and a significant increase in HVA only in the BN patients. Study 3 revealed a significant positive effect of CBT + olanzapine therapy on the psychopathology and increased HVA values. No correlations were observed in the 3 groups between biological and psychological effects of the three treatments.ConclusionsOur data advance suggestions on the mechanism of action of the three therapies; however, the lack of correlations between biochemical and psychological effects casts doubt on their significance.Clinical Trials.gov. Identifier NCT01990755.

show abstract

Six‐month open trial of haloperidol as an adjunctive treatment for anorexia nervosa: A preliminary report

Abstract: These preliminary data suggest that low doses of haloperidol might be effective as an adjunctive treatment for patients with severe AN-R. Larger controlled studies are warranted to confirm these data.

Cited by 53 publications

References 22 publications

Anorexia Nervosa and Obesity are Associated with Opposite Brain Reward Response

Anorexia Nervosa and Obesity are Associated with Opposite Brain Reward Response

Olanzapine therapy in anorexia nervosa: psychobiological effects

Lack of efficacy of psychological and pharmacological treatments of disorders of eating behavior: neurobiological background

Contact Info

Product

Resources

About