Naltrexone in organic bulimia: A preliminary report

Abstract

Multiple lines of experimental evidence point to the involvement of endogenous opiates in appetite regulation. Post brain injury patients often exhibit driven eating behaviour. Since this problem fails to respond to behaviour modification, appetite suppressants, lithium, or any other usual approach, the use of the oral narcotic antagonist, Naltrexone, was given to three such patients. Naltrexone binds multiple opiate receptor sites in the hypothalamus, including the kappa receptors which have been implicated in appetite regulation, the use of this narcotic antagonist in hypothalamic hyperphagia appears to be a rational approach to this intractable problem. In this open trial, lasting from 4 1/2 to 9 months, the minimal effective dose appeared to be in the range of 100 mg per day. No side-effects (for example elevations in liver enzymes) were noted. All of the patients had an improved sense of well-being and their behaviours were less difficult to manage when on the Naltrexone. The significance of this preliminary trial is that narcotic antagonists may have a role in the treatment of brain-injured patients with bulimia. Also, Naltrexone may be useful in treating other maladaptive behavioural consequences of head trauma such as stealing, manipulation, demandingness, and depression. Likewise, the effects on the deranged endocrine system, such as the hypogonadism, are significant and deserve further exploration.

Time interval of oral feeding recovery as a prognostic factor in severe traumatic brain injury

“…The mean Barthel Index (BI) score was 82.4 (range 25-100) and the mean Mini Mental State (MMS) score was 26 (range [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30]. According to the MMS scores, the patients were divided into three groups: group 1 (n ¼ 33) with MMS scores from 0-10; group 2 (n ¼ 8) with scores from 11-20; group 3 (n ¼ 2) with scores from 21-30; the latter score indicated no dementia.…”

“…The Klùver-Bucy syndrome is characterized by the presence of three or more of the following signs and symptoms: increased oral activity, hypersexuality, hypermetamorphosis (extreme attention lability), memory disorders, placidity, loss of people recognition and bulimia [23]. Patients with severe TBI often exhibit driven eating behaviour, the so called organic bulimia [24,25], different from the nervous bulimia described in psychiatric disorders, according to the DSM-IV classification [26]. In clinical practice, weight gain is often observed in patients with severe TBI sequelae and it may be due to an increase in appetite and/or to little physical activity.…”

A Variant of the Kleine‐Levin Syndrome following Head Trauma

“…2). Hyperphagia and the problems of driven food-seeking behavior have been described following posttraumatic hypothalamic lesion [3] or with hypothalamic damage following surgery for craniopharyngioma [20].…”

Unilateral Temporal Lobe Damage and the Partial Kluver–Bucy Syndrome

“…The picture is similar in traumatic hypothalamic injury. Skorwezska et al (1989) describe the problems of driven food-seeking behaviour in three patients with hypothalamic damage following surgery for craniopharyngioma while Childs (1987) describes three such patients in intensive rehabilitation following head injury. Critchley (1962) described megaphagia as part of the Kleine-Levin syndrome, a condition characterized by periodic episodes of hypersomnolence and increased appetite.…”