ness of its antagonists in treatment of PD patients is even more exiting . As James L. Abelson writes in his review article a "non-sedating, non-addicting anxiolytics have been a kind of pharmacological holy grail ."1 The most common adverse effect, as reported by Dr. Kramer group, was orthostatic dizziness (21%), followed by muscle pain, nausea and headaches (12%).6 Among currently used anxiolitic agents, as described in Dr. Westenbergs article9, Tricyclic Antidepressants, such as cloripramine and imipramine cause jitterness syndrome, i.e. exacerbation of symptoms in the first week of treatment, a major cause of dropout, as well as anticholinergic side effects. Benzodiazepines often induce daytime sedation. Serotonin reuptake inhibitor fluvoxamine is one of the few clinically successive agents without major side effect. Furthermore, research data suggest that the mechanism of its action can shed light on CCK-4 role in panic disorder. In discussion of his ground breaking study on the effect of CCK-4 on panic disorder patients Bradwejn at al emphasized importance of investigation of possible blockage of CCK-4 induced attacks by known antipanic medications.3 The evidence of CCK interaction with other neurotransmitter systems was first established in animal studies, which showed that anxiogenic action of CCK can be antagonized by benzodiazepines and 5-HT3 receptor antagonists. The Bradwejns group tested imipramine effects on CCK-4 challenge, and the in most recent study another research group concentrated its efforts on fluvoxamine(van Megen et al., 1997).8 The authors hypothesis was based on circumstantial evidence of interaction between 5-HT and CCK-containing neuronal pathways in earlier animal studies. Twenty six patients were given fluvoxamine or placebo for eight weeks in a double blind manner starting with 50 mg and increasing the dose to 150 mg daily by the end of second week. The single blind challenge with 50 g of CCK-...
