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Investigation of the potential role for endogenous opiates as a modulator of anxiety states has yielded variable results. Increased plasma [3-endorphin has been reported accompanying surgical stress (Pickar et al 1982) and with high anxiety ratings in women during menstruation (Veith et al 1984). Can" et al (1986) found no significant change in plasma [3-endorphin during lactate infusion before and after treatment with alprazolam in panic disorder patients or controls but did note a slight decrease in 13-endorphin over time secondary to acclimatiza~'ion. Dager et al (1989) found higher 13-endorphin levels in panic disorder than in depressed patients and a slight decrease in plasma [3-endorphin during lactate infusion in panic disorder patients, depressed patients, and controls. George et al (1989) found significantly higher

We reportpilot fMRIdata on brainactivityin humanmotherslistening to a cryingbaby. Since animal data suggestthat maternalbehavioris impairedby cingolateablations,we hypothesizedthat motherswould have cingulateactivation,especiallyanteriorly,with this provocation. Fourbiologicalmothershavinga youngestchildless thanage fourwere studiedwith fMIU while they listenedto reeordedbaby cries (active condition)alternatingwith white noises whose temporalfeatures and averageintensitymatchedthoseof thecries(controIcondition).Weused a pairedt-test (P

Method:Patients (n = 243) with a diagnosisof panic disorderwere randomizedto treatmentwith fluoxetineor placebo.primary outcome measureswerechangein totalpanicattackfrequencyandCGI-improvement.Otherassessmentsincludedclinicianandpatient-ratedversionsof the panic and phobic disorder change scale, a phobia rating scale, HAMA,HAMD-21,andSheehanDisabilityscale.Correlationsbetween outcomesin individualsymptomdomainsand overallclinicaloutcome were determined,as were patternsof response.

Prostaglandins are thought to act as neuromodulators of both central catecholamine and endocrine systems. Abnormalities of these systems have been described in affective disorders, in general, and in agoraphobia with panic attacks, in particular. This study measured basal prostaglandin-E (PGE) cerebrospinal fluid (CSF) levels in 20 patients with agoraphobia with panic attacks and 10 nonpsychiatric controls. In a subgroup of patients and controls, CSF levels of adrenocorticotrophic hormone (ACTH) and corticotropin-releasing factor (CRF) were also measured. There was no significant difference in CSF PGE levels between patients and controls. However, patients with higher depression scores had lower CSF PGE levels. CSF PGE levels tended to correlate with CSF ACTH, but not CSF CRF in the patient group, in general, and in the female patients, in particular. These findings do not support an abnormality in basal CNS PGE production in agoraphobia with panic attacks, but suggest further study of the PGE modulatory effect on the hypothalamic-pituitary-adrenal axis in this disorder.