different to those of their previous illness. Also in support for an iatrogenic cause is the finding that nine patients suffering from prolonged withdrawal symptoms, 5-42 months after stopping benzodiazepines, did not have psychophysiologial reactions characteristic of either anxiety or conversion hysteria but, conversely, were hard to distinguish from a normal control group (Higgitt et al., 1990). Some, though not all, patients with prolonged withdrawal problems develop significant depression typically within the first 3 months of abstinence (Olajide and Lader, 1984). However, the prolonged withdrawal syndrome and return of anxiety probably occur commonly together. Although the underlying mechanisms of benzodiazepine dependence are still not entirely understood, research in animals points to the clinical potential for the benzodiazepine antagonist flumazenil (Ro 15-1788) to reverse benzodiazepine dependence and tolerance and prevent withdrawal (Whitwam, 1988). Administration of flumazenil reverses tolerance and dependence to benzodiazepines (Gonsalves and Gallager, 1985) but precipitates recognizable withdrawal symptoms . However, if given during chronic treatment flumazenil can, by similarly reversing tolerance, prevent subsequent withdrawal syndromes in primates (Gallager, Heninger and Heninger, 1986) and in rats (Baldwin, Hitchcott and File, 1990). One explanation for this is the antagonism and depletion of an endogenous benzodiazepine receptor ligand with inverse agonist and thus anxiogenic activity by the antagonist flumazenil (Baldwin, Hitchcott and File, 1990). However, levels of the proposed 'anxiety peptide' ligand associated with diazepam binding inhibitor (DBI) were not found to be increased by the administration of diazepam in rats (Ball et al., 1987). An alternative explanation is that chronic