ICA IS DEFINED as the persistent eating of non-nutritive substances in an inappropriate and culturally unacceptable manner. To date, there is a lack of acceptable pathogenic mechanism underlying this behavior. Olanzapine, a commonly used antipsychotic, can block the central 5-HT2c and H1 receptors, therefore it has side-effects of increased bodyweight and appetite. There have been no reports, however, on pica occurring during olanzapine treatment. We here report on a schizophrenia patient who developed pica during the administration of olanzapine, which gradually remitted after this atypical antipsychotic had been discontinued.The present patient was a 35-year-old man with schizophrenia who had no medical or surgical diseases, eating disorders, drug abuse history or other psychiatric history. It had been 15 years since the first incidence and the patient had had several acute attacks during this period, but none of them resulted in pica. This time he developed negative symptoms of poor appetite, silence, social withdrawal; his medication had been changed from haloperidol 5 mg/day to olanzapine 10 mg/day, other medication remained unchanged. After he had taken olanzapine for 3 weeks, the negative symptoms and his appetite significantly improved without developing any positive symptoms. Of note, the patient started exhibiting pica by eating garbage, sand and pebble (based on the patient's statement, his behavior was unexplainable and uncontrollable, he just had a craving for eating them). The pica persisted for approximately 3 weeks. He was also found to have an increased appetite that even exceeded the amount of food that he could handle. No other hallucinations, delusions, or positive symptoms occurred. The patient also denied having intention of suicide or self-hurt. Nevertheless, the symptoms of pica persisted. Olanzapine was replaced by his previous medicine. After that, the pica gradually disappeared.Although we do not know the exact underlying mechanism of pica, there is increasing evidence that the craving for eating non-nutritional material could be considered as an obsessivecompulsive spectrum disorder.1 In addition, there are studies suggesting that some atypical antipsychotics may induce or aggravate the obsessive-compulsive symptoms.2 Given this, the mechanism of pica development in the present case could have been due to the blockade of olanzapine on the 5-HT2a receptors, resulting in an increase of dopamine release in the mid-brain and frontal cortex, and further causing the corticobasal ganglia dysfunction. In conclusion, the present case suggests that pica may occur during the use of olanzapine in schizophrenia patients, which is similar to obsessivecompulsive symptom. Further studies are warranted to explore the relationship between pica and the use of olanzapine.
Our institute serves as a centralized clinical laboratory for municipal and private hospitals in Taipei, a major international metropolis in the Asian region. Two key considerations leading to the development of our toxicology program are: a large number of foreign visitors and local residents returning from overseas trips may bring in chemicals which are less commonly seen in this region; and the lack of readily available assays for a large percentage of commonly used medicines, including prescription and over-the-counter drugs. Our toxicology screening program addresses the needs of both the Emergency Department Drug Screening and Drug of Abuse Screening. In Emergency Department Drug Screening, REMEDi HS is used as the general screening method. In Drug of Abuse Screening, the TDx is used for the initial screening of amphetamine-like substances and opiates, followed by REMEDi HS for the confirmation of positive samples. Emergency Department data collected at our institute over one year (September 1992 to August 1993) identified 57 different drugs in 713 samples. Opiates, narcotics and central stimulants accounted for 24% of the encountered drugs. Presently, there is no extensive reporting of misuse of benzodiazepines in this region. The detection of herbal ingredients like ephedrine and methylephedrine (from the Ma-Huang plant) in patient samples illustrates a large area often overlooked by western toxicology.
ObjectivePost weanling isolation-reared (IR) rats are featured with depressive phenotype, yet its mechanism is not clearly defined particularly in terms of the involvement of central 5-HT1A receptors. The present study aims to examine the effects of 5HT1A activation on forced swim test (FST) in IR rats following 5-HT depletion. MethodsSocial control (SOC) and IR rats received an intracerebraoventricular (ICV) injection of 5-HT depletion agent, 5,7-DHT. 14 days after the surgery, rats were assessed their performance in FST with or without the challenge with a 5-HT1A agonist, 8-OH-DPAT. Rats were then sacrificed for analyzing their 5-HT tissue levels and the expressions of their 5-HA1A receptors in prefrontal cortex (PFC), hippocampus (HPX), and amygdala (AMY). Results5,7-DHT decreased the tissue concentration of 5-HT in both IR and SOC rats. IR rats were more immobile and less sensitive to the lesion-induced immobility, however this effect was reversed by acute challenge of 8-OH-DPAT. 5,7-DHT lesion increased the expression of PFC 5-HT1A receptors. ConclusionThe integrity of central 5-HT system is developmentally crucial for the 5-HT1A-relevant depression profile in rats of social isolation.
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