Chemical submission to commit robbery: A series of involuntary intoxications with flunitrazepam in Asian travellers in Brussels

Department of Emergency Medicine, Centre Hospitalier Universitaire Saint-Pierre, Brussels, Belgium, Université Libre de Bruxelles (ULB). Electronic address: .
Journal of Forensic and Legal Medicine (Impact Factor: 0.99). 10/2013; 20(7):918-921. DOI: 10.1016/j.jflm.2013.06.017
Source: PubMed

ABSTRACT Between January 17, 2003 and August 29, 2003, the Emergency Department admitted a patient who had been surreptitiously intoxicated and robbed of his valuables every Friday. The first cases were considered anecdotal, but criminal activity was rapidly suspected. The cohort includes 16 male Asian patients aged 28-50 years. All the victims had just arrived in Brussels through one of the main rail station of the town and were admitted via the emergency ambulance service from different locations in the centre of Brussels around the CHU Saint-Pierre Hospital. Haemodynamic parameters upon admission were within normal limits. The Glasgow Coma Scale was equal or higher than 9/15 in 14 of the 16 victims. Toxicology screening obtained in 12 patients revealed the presence of flunitrazepam, which was further quantified at levels ranging from 21 to 75 μg/l. One of the Japanese patients, who returned to Belgium afterwards for professional reasons, was approached by the police and accepted to press charges. This allowed the police to investigate and send undercover agents to the railway station on Friday afternoons and evenings. They found a person who was offering welcome cookies to Asian travellers. He arrived from Amsterdam and returned once his crime was committed. Flunitrazepam is well known as a rape drug. We report a series of victims in whom flunitrazepam was used to facilitate robbery.

  • [Show abstract] [Hide abstract]
    ABSTRACT: A confirmation procedure for the identification and quantification of gamma-hydroxybutyric acid (GHB) in urine is presented. This method is unique in that it does not involve the conversion of GHB to the gamma-butyrolactone (GBL). The urine samples were extracted using ethyl acetate, evaporated and derivatized with N, O-bis(trimethylsilyl)trifluoroacetamide (BSTFA) with 1% trimethylchlorosilane (TMCS), and analyzed by gas chromatography-mass spectrometry. Quantification was performed using selective ion monitoring (SIM), using GHB-d(6) as the internal standard. This method is simple and provides excellent linearity and sensitivity for GHB in urine.
    Forensic Science International 05/2000; 109(3):183-7. DOI:10.1016/S0379-0738(99)00221-2 · 2.12 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: EGD with conscious sedation is a safe procedure, but complications such as hypoxia can occur. The efficacy and safety of low-dose flunitrazepam (0.25 mg) was compared with a standard dose of flunitrazepam (0.5 mg) for moderate sedation during EGD. In a randomized, double-blind, placebo-controlled trial, 75 outpatients (40 men, 35 women, mean age 45 [11] years) undergoing screening EGD were randomly assigned to one of 3 treatment arms: 0.25 mg of flunitrazepam (F0.25 group), 0.5 mg of flunitrazepam (F0.5 group), or placebo (normal saline solution), each administered intravenously. Patient tolerance was scored by using self-assessment questionnaires with visual analogue scales. Cardiopulmonary complications were assessed by monitoring blood pressure, heart rate, oxygen saturation, and the electrocardiogram during the procedure. The patient tolerance scores in the F0.25 and F0.5 groups, respectively 2.1 (2.1) and 2.3 (2.5), were significantly lower than that for the placebo group (6.5 [3.0]); there was no significant difference between F0.25 and F0.5. Cardiopulmonary complications in the F0.25 group were significantly lower than in the F0.5 group. Oxygen desaturation (oxygen saturation < 90%) was noted in two of 25 patients in the F0.5 group. Post-procedure drowsiness was observed in two of 24 (8.3%) patients in the F0.25 group and 3 of 21 (14.3%) in the F0.5 group (p = 0.2438). Patient tolerance of EGD with low-dose flunitrazepam (0.25 mg intravenously) was similar to that with a standard dose (0.5 mg intravenously) and significantly better than in the placebo group. Oxygen desaturation was observed only in the group that received the standard dose, suggesting that sedation with low-dose flunitrazepam is efficacious and safe for EGD.
    Gastrointestinal Endoscopy 10/2003; 58(4):523-30. DOI:10.1016/S0016-5107(03)02005-4 · 4.90 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Several studies have shown that sleep deprivation produces deficits in learning tasks, but mechanisms underlying these effects remain unclear. Other lines of evidence indicate an involvement of brain GABA systems in cognitive processes. Here, we investigated the possibility that alterations in GABA(A) or benzodiazepine (BDZ) receptor binding might underlie avoidance deficits induced by sleep deprivation. Rats were deprived of sleep for 96 h using the platform method and then trained in a step-through inhibitory avoidance task, or allowed to recover sleep for 24 h before training (sleep rebound group). Thirty minutes after training, animals were given a retention test. Both sleep-deprived and sleep-recovered animals showed a significant impairment in avoidance responding compared to cage controls, and the sleep-deprived group performed significant worse than the sleep-recovered group. A separate group of animals was sacrificed either immediately after 96 h of sleep deprivation or after 96 h of sleep deprivation followed by 24 h of sleep recovery. [(3)H]muscimol and [(3)H]flunitrazepam binding were examined by quantitative autoradiography in 42 brain regions, including areas involved in cognitive processes. No significant differences among groups were found in any brain region, except for a reduction in [(3)H]flunitrazepam binding in the frontal cortex of sleep-recovered animals. These results confirm the deleterious effects of sleep loss on inhibitory avoidance learning, but suggest that such deficits cannot be attributed to altered GABA(A) or BDZ binding in brain.
    Brain Research 04/2005; 1037(1-2):157-63. DOI:10.1016/j.brainres.2005.01.005 · 2.83 Impact Factor