Prepulse inhibition (PPI) is an operational measure of sensorimotor gating that is reduced in several neuropsychiatric disorders that are characterized by deficits in inhibition or gating of intrusive or irrelevant stimuli. Clinically, panic disorder (PD) patients have been described as having difficulties in inhibition of responding to sensory and cognitive events. Because such difficulties may be due to failures in early stages of information processing, we examined PPI in patients with PD. Acoustic startle reactivity, habituation, and PPI (30-, 60-, 120-, 240-, and 2,000-ms interstimulus intervals) were assessed in patients with panic disorder (m/f = 10, 10) and age- and gender-matched healthy controls (m/f = 11, 10). PD patients were assessed with structured clinical interview for DSM-IV criteria with benzodiazepine treatment as an exclusion criterion. Panic disorder patients exhibited normal startle reactivity, reduced habituation, and significantly reduced PPI in the 30-, 60-, and 240-ms prepulse conditions. Within the PD group, the patients with high trait and state anxiety exhibited less PPI than patients with low trait and state anxiety. Furthermore, in PD patients, decreased PPI correlated significantly with high trait but not state anxiety. These data indicate that early stages of sensory information processing are abnormal in patients with PD. These observed deficits in PPI could reflect a more generalized difficulty in suppressing or gating information in panic disorder. The correlation between high trait anxiety and deficient PPI supports the hypothesis that sensorimotor gating abnormalities are an enduring feature of subjects with PD.

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Serotonin (5-HT) release is the primary pharmacological mechanism of 3,4-methylenedioxymethamphetamine (MDMA, 'ecstasy') action in the primate brain. Dopamine release and direct stimulation of dopamine D2 and serotonin 5-HT2A receptors also contributes to the overall action of MDMA. The role of 5-HT1A receptors in the human psychopharmacology of MDMA, however, has not yet been elucidated. In order to reveal the consequences of manipulation at the 5-HT1A receptor system on cognitive and subjective effects of MDMA, a receptor blocking study using the mixed beta-adrenoreceptor blocker/5-HT1A antagonist pindolol was performed. Using a double-blind, placebo-controlled within-subject design, 15 healthy male subjects were examined under placebo (PL), 20 mg pindolol (PIN), MDMA (1.6 mg/kg b.wt.), MDMA following pre-treatment with pindolol (PIN-MDMA). Tasks from the Cambridge Neuropsychological Test Automated Battery were used for the assessment of cognitive performance. Psychometric questionnaires were applied to measure effects of treatment on core dimensions of Altered States of Consciousness, mood and state anxiety. Compared with PL, MDMA significantly impaired sustained attention and visual-spatial memory, but did not affect executive functions. Pre-treatment with PIN did not significantly alter MDMA-induced impairment of cognitive performance and only exerted a minor modulating effect on two psychometric scales affected by MDMA treatment ('positive derealization' and 'dreaminess'). Our findings suggest that MDMA differentially affects higher cognitive functions, but does not support the hypothesis from animal studies, that some of the MDMA effects are causally mediated through action at the 5-HT1A receptor system.

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Most aortic aneurysms have a degenerative genesis and show a slow expansion over years. Only a few patients with a rapid progression of mycotic or inflammatory aneurysm during some weeks or months have been reported. We report a patient with a rapidly growing symptomatic infrarenal aneurysm with a maximal diameter of 53 mm, which developed over a 5-month period from a normal aorta and did not feature typical signs of degenerative, inflammatory, or mycotic aneurysm. The aneurysm was successfully treated by endovascular repair. A complete shrinking of the aneurysm sac was demonstrated during a few weeks postoperatively. Because the patient received chemotherapy with docetaxel, cisplatin, and 5-fluorouracil for metastatic gastric carcinoma 1 year before the aneurysm occurred, we postulate that chemotherapy induced a rapid expansion of the aorta in this patient.