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Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

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8. Marijuana, Hallucinogens, and Club Drugs 171(Bubser Keseberg, Notz, & Griffiths, 1992), and this is likely the cause <strong>of</strong> itsability to reinforce and cause dependence. Furthermore, persisting memory deficitshave been demonstrat<strong>ed</strong> (Curran & Monaghan, 2001).TreatmentThe most dangerous effects <strong>of</strong> ketamine are behavioral. Individuals maybecome withdrawn, paranoid, and physically sloppy. In the event <strong>of</strong> dealingwith an individual who is intoxicat<strong>ed</strong> on ketamine, the physician must treatthe individual symptomatically. Calm reassurance and a low-stimulation environmentare usually most helpful. The patient should be plac<strong>ed</strong> in a part <strong>of</strong> theclinic or emergency room with the least amount <strong>of</strong> light and stimulation. Ifnecessary, the patient may be given benzodiazepines to control the associat<strong>ed</strong>anxiety (Graeme, 2000). Neuroleptics should be avoid<strong>ed</strong>, because the sideeffectpr<strong>of</strong>ile may cause discomfort and possibly exacerbate the patient’s agitat<strong>ed</strong>state.Ketamine is an addictive drug. There are numerous reports <strong>of</strong> individualswho have become dependent on the drug and use it daily (Galloway et al.,1997; Jansen, 1990). Such dependence should be treat<strong>ed</strong> in the same manner asany other chemical dependence. The clinician should do a careful evaluation inorder to discern other psychological conditions. These should be dealt with inthe most clinically exp<strong>ed</strong>itious manner.HistoryGHBGHB was first synthesiz<strong>ed</strong> in the mid-1970s by Dr. H. Laborit, a Frenchresearcher interest<strong>ed</strong> in exploring the effects <strong>of</strong> gamma-aminobutyric acid(GABA) in the brain. Laborit was attempting to manufacture a GABA-likeagent that would cross the blood–brain barrier (Vickers, 1969). During the1980s, GHB was widely available in health food stores. It came to the attention<strong>of</strong> authorities in the late 1980s as a drug <strong>of</strong> abuse, and the Food and DrugAdministration (FDA) bann<strong>ed</strong> it in 1990, after reports <strong>of</strong> several poisoningswith the drug (Chin, Kreutzer, & Dyer, 1992). In the past decade, it hasbecome more widely known as a drug <strong>of</strong> abuse associat<strong>ed</strong> with nightclubs andraves.GHB is known as “liquid Ecstasy,” and in Great Britain as GBH, or “grievousbodily harm.” It can be found, occurring naturally, in many mammaliancells. In the brain, the highest amounts are found in the hypothalamus andbasal ganglia (Gallimberti et al., 1989). It is likely that it is itself a neurotransmitter(Galloway et al., 1997). GHB is closely link<strong>ed</strong> to GABA and is both aprecursor and a metabolite <strong>of</strong> GABA (Chin et al., 1992).

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