No abstract

We used psychophysiologic techniques to assess responses to imagery of psychologically stressful past experiences in medication-free Vietnam combat veterans classified, on the basis of DSM-III-R criteria into posttraumatic stress disorder (PTSD; n = 7) or non-PTSD anxiety disorder (anxious; n = 7) groups. Scripts describing each individual's combat experiences were recorded and played back in the laboratory. Ss were instructed to imagine the events the scripts portrayed while heart rate, skin conductance, and frontalis electromyogram were recorded. PTSD Ss' physiologic responses were higher than those of anxious Ss. A discriminant function derived from a previous study of PTSD and mentally healthy combat veterans identified 5 of the 7 current PTSD Ss as physiologic responders and all 7 of the anxious Ss as nonresponders. Results of this study replicate and extend results of the previous study and support the validity of PTSD as a separate diagnostic entity.

We assessed the heart rate, skin conductance, and left lateral frontalis electromyographic responses of World War II (WWII) and Korean War male veterans to recollection of their combat experiences by using a script-driven imagery technique previously validated in Vietnam veterans (Pitman et al., 1990;Pitman, Orr, Forgue, de Jong, & Claiborn, 1987). Medication-free subjects were classified on the basis of criteria from the revised third edition of the Diagnostic and Statistical Manual of Mental Disorders into posttraumatic stress disorder (PTSD; n = 8) and non-PTSD (« = 12) groups, which did not differ in overall combat exposure or severity of personal combat events. PTSD subjects' physiological responses during personal combat imagery were markedly larger than those of non-PTSD subjects', even though the self-reported emotional responses of the two groups were comparable. A physiological discriminant function derived from Vietnam veterans (Orr et al., 1990) correctly classified 7 of the 8 PTSD subjects (sensitivity was 88%) and 12 of the 12 non-PTSD subjects (specificity was 100%; p < .001).Much of the impetus behind the inclusion of posttraumatic stress disorder (PTSD) in the modern psychiatric nomenclature (American Psychiatric Association, 1980) came from the recognition of the readjustment problems of Vietnam veterans during the decade following that conflict. Indeed, PTSD is sometimes misunderstood to be synonymous with the psychiatric problems of Vietnam veterans. Actually, PTSD can result from any combat or noncombat event that is "outside the range of usual human experience and that would be markedly distressing to almost anyone" (American Psychiatric Association, 1987, p. 250). The Vietnam War had no monopoly on such events. The psychiatric response to the stress of warfare has been recognized for centuries and has been variously described as irritable heart syndrome, shell shock, traumatic war neurosis, operational fatigue, and combat exhaustion (Schnurr, 1991;Trimble, 1984). Clinical evidence confirms the occurrence of Diagnostic and Statistical Manual of Mental Disorders (3rd ed.;

CX516, a positive modulator of the glutamatergic alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor, improves performance in tasks requiring learning and memory in animals. CX516 was added to clozapine in 4-week, placebo-controlled, dose-finding (N = 6) and fixed-dose (N = 13) trials. CX516 was tolerated well and was associated with moderate to large, between-group effect sizes compared with placebo, representing improvement in measures of attention and memory. These preliminary results suggest that CX516 and other "ampakines" hold promise for the treatment of schizophrenia.

Ninety patients with schizophrenia or schizoaffective disorder according to DSM-III-R criteria participated in this double-blind, exploratory, dose-ranging trial. After a single-blind washout period of 4 to 7 days, patients were randomly assigned to receive one of four fixed doses of the new antipsychotic, ziprasidone 4 (N = 19), 10 (N = 17), 40 (N = 17), or 160 (N = 20) mg/day or haloperidol 15 mg/day (N = 17) for 4 weeks. A dose-response relationship among ziprasidone groups was established for improvements in Clinical Global Impression Severity (CGI-S) score (p = 0.002) but not in Brief Psychiatric Rating Scale (BPRS) total score (p = 0.08). The intent-to-treat analysis of mean changes from baseline in the BPRS total, BPRS Psychosis core, and CGI-S scores demonstrated that ziprasidone 160 mg/day was comparable with haloperidol in reducing overall psychopathology and positive symptoms and was superior to ziprasidone 4 mg/day. Despite the small sample size and short duration of the trial, the improvement in CGI-S with both ziprasidone 160 mg/day and haloperidol 15 mg/day was statistically significantly greater than with ziprasidone 4 mg/day (p = 0.001 andp = 0.005, respectively). The percentage of patients classified as responders on both the BPRS total (> or = 30% improvement) and CGI-Improvement (score of 1 or 2) scales in the ziprasidone 160 mg/day group was similar to that in the haloperidol group and nonsignificantly greater than that in the ziprasidone 4 mg/day group. On all assessments of clinical efficacy, the improvements associated with ziprasidone 4 mg/day, 10 mg/day, and 40 mg/day were similar. Concomitant benztropine use at any time during the study was less frequent with ziprasidone 160 mg/day (15%) than with haloperidol (53%). Haloperidol was associated with a sustained hyperprolactinemia, unlike ziprasidone, where only transient elevations in prolactin that returned to normal within the dosing interval were observed. Ziprasidone was well tolerated, and the incidence of adverse events was similar in all groups. The results of this study suggest that ziprasidone 160 mg/day is as effective as haloperidol 15 mg/day in reducing overall psychopathology and positive symptoms of an acute exacerbation of schizophrenia or schizoaffective disorder but has a lower potential to induce extrapyramidal symptoms.